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1,000 | Predictive characteristics of holter-based postinfarction risk stratifiers appear superior to electrophysiological testing. | Prevalent low-frequency (PLF) oscillation of heart rate and turbulence slope (TS) are both powerful postmyocardial infarction (MI) risk factors. Abnormal composite risk stratifier (CRS) was defined as abnormal PLF or abnormal TS when PLF was not analyzable. We compared the predictive power of CRS with the previously published predictive value of conventional electrophysiological (EP) testing based on the presence of nonsustained ventricular tachycardia (NSVT) and inducibility of sustained ventricular tachycardia/fibrillation (VT/VF) during programmed ventricular stimulation (PVS). PLF and TS were calculated from baseline Holter recordings in the placebo population of European Amiodarone Infarction Myocardial Infarction Trial (EMIAT trial) (n = 633; LVEF </= 40%; 87 deaths; 22-month follow-up). Previously established cut-off values of PLF >/= 0.1 Hz and TS </= 2.5 ms/RR were used. The clinical characteristics of the EMIAT population were similar to those of the Multicenter Unsustained Tachycardia Trial (MUSTT trial). Therefore, we compared the predictive power of CRS and conventional PVS using the values of 35% VT/VF inducibility during PVS in NSVT patients, and a 33% and 50% increase in all-cause and arrhythmic mortality, respectively, associated with VT/VF inducibility in MUSTT. Projecting the predictive power of PVS in MUSTT into the EMIAT population yielded a sensitivity of 13.8% and 14.0% and positive predictive value (PPV) of 27.9% and 14.0% for all-cause and arrhythmic mortality, respectively, whereas an abnormal CRS was associated with sensitivities of 46.0% and 46.5% and PPV of 37.4% and 18.7%. Compared with the noninvasive Holter-based CRS, invasive PVS appears inferior in the identification of high-risk post-MI patients with left ventricular dysfunction. |
1,001 | Defibrillation effects of intravenous nifekalant in patients with out-of-hospital ventricular fibrillation. | Nifekalant (NF), a pure K(+) channel blocker developed in Japan, has been reported to be effective in the treatment of life-threatening ventricular arrhythmias. We studied its efficacy in 18 men and 4 women with out-of-hospital ventricular fibrillation (VF) admitted to our emergency department between August 2001 and March 2004. The number of DC shocks delivered for out-of-hospital VF, serum Na(+) and K(+), arterial blood pH, and base excess were compared in 8 patients treated with NF, 0.3 mg/kg i.v. followed by a continuous intravenous (group N) versus 14 patients treated with lidocaine, 2 mg/kg, i.v. (group C). The two groups were similar with respect to their baseline characteristics. Sinus rhythm returned in 5 of 8 patients in group N versus 2 of 14 patients in group C (P < 0.05). These seven patients were admitted to the intensive care unit, though all died within 1 month. The results of this study suggest that NF may be effective in defibrillation of out-of-hospital VF, though controlled studies are needed to confirm our observations. |
1,002 | Detection of atrial fibrillation by implanted devices with wireless data transmission capability. | Remote telemetry may facilitate the management of implantable devices. We tested the reliability of a new automatic, wireless home monitoring (HM) system that archives data every 24 hours. We retrospectively analyzed archival data from 276 consecutive pacing system implants to define temporal atrial fibrillation (AF) patterns and associated ventricular rate. An "AF day" was defined by a >20%/24 hour mode switch (MS) duration, irrespective of the MS number. Management decisions resulting from transmissions were noted. A pilot study confirmed that 89% of 22,356 transmissions were successful, of which >90% were received in <5 minutes. Data integrity was 100% preserved. Overall, AF developed in 29 patients (10.5%), representing a total of 645 AF days (mean = 22.2 +/- 29.6 AF, median = 9 days), over 12 +/- 2 months of monitoring. AF was infrequent (<AF 30 days/year) in 80% of patients. When AF did occur, 83% patients had >/=1 day during which the AF burden was >50% of 24 hours. Ventricular rates during 645 AF days in 29 patients averaged 95.1 +/- 9.9 beats/min (median = 94 beats/min). Ventricular rates were >80 beats/min in 25 +/- 30 AF days (median = 11 days). HM enabled rapid anticoagulation decisions. In recipients of implantable devices, automatic wireless telemetry with HM was efficient and reliable. Its application may overcome some current challenges in AF management by early notification and precise measurement of both AF burden and ventricular rate during AF. |
1,003 | Serum troponin I and myoglobin after monophasic versus biphasic transthoracic shocks for cardioversion of persistent atrial fibrillation. | This study compared the effects of standard monophasic versus biphasic direct current shocks for cardioversion of atrial fibrillation (AF) on the release of cardiac troponin I (cTnI) and myoglobin (Myo). We randomized 48 patients with persistent AF (mean age = 61.4 +/- 10.7 years, 33 men) to monophasic (45.2%) or biphasic (54.8%) cardioversion. Plasma concentrations of cTn1 and Myo were measured before, and 6 and 24 hours after the procedure. Cardioversion was significantly more effective (88% vs 100%, P < 0.04) and required less energy (348.1 +/- 254.1 vs 187.6 +/- 105.3 J; P < 0.001) in the biphasic than the monophasic group. A significant increase in mean plasma cTnI concentration over 24 hours (0.23 +/- 0.18 vs 0.41 +/- 0.37 ng/mL, P < 0.04), and mean Myo concentration were recorded in the monophasic group over the first 6 hours following the procedure (38.2 +/- 14.2 vs 221.9 +/- 51.3 ng/mL, P < 0.001), whereas no significant increase was observed in the biphasic group. Increases in cTnI and Myo in the monophasic group correlated closely with the cumulative energy delivered (Spearman correlation coefficient r = 0.58, P = 0.004 for Myo and r = 0.67, P < 0.001 for cTnI). In addition, there was a positive correlation between cumulative cardioversion energy load and increase in Myo and cTnI indexed with left ventricular mass (r = 0.45, P < 0.02 for Myo and r = 0.47, P = 0.01 for cTnI). It is concluded that in cardioversion of AF, biphasic are more effective than monophasic and may cause less myocardial injury. |
1,004 | No correlation between atrial natriuretic peptide concentrations and echocardiographic measurements of left atrial size or left ventricular size and function in patients with persistent atrial fibrillation. | Atrial fibrillation (AF) may be associated with activation of atrial natriuretic peptide (ANP). The exact trigger for the release of ANP is still being debated. Atrial volume, pressure, and wall stretch are considered to be the main determinants of ANP activation. The aim of the study was to evaluate plasma ANP concentrations in patients with persistent AF and to analyze the echocardiographic determinants of ANP concentration in this group. The study population included 67 patients, 59 +/- 7 years of age, with a median AF duration of 5.5 months (range 0.1-12). The relationship between plasma ANP concentrations and echocardiographic left atrial (LA) diameter and volume, and left ventricular (LV) diameter and ejection fraction (EF) was analyzed by logistic regression analysis. The median baseline plasma ANP concentration was 63 pg/mL (range 21-126) in the study group versus 34 pg/mL (range 16-73) in a control group. The mean left antero-posterior atrial dimension, LA volume, LV enddiastolic diameter, and LVEF were 48 mm, 104 mL, 52 mm, and 54%, respectively. A significant linear positive correlation was found between plasma ANP concentration and maximal LA volume (r = 0.62, P < 0.01). A negative correlation was found between LVEF and plasma ANP concentration (r =-0.42, P = 0.01). However, by multivariate regression analysis, no echocardiographic parameter was an independent predictor of plasma ANP concentration. Plasma ANP concentrations were independent of echocardiographic measurements of LA size or LV size and function in patients with persistent AF. |
1,005 | [Treatment of life-threatening cardiac arrhythmias]. | Tachyarrhythmias represent a frequent problem in intensive care medicine. However, considerable uncertainty prevails among physicians regarding optimal pharmacotherapy, due also to numerous negative study results on chronic antiarrhythmic therapy. Moreover, in an emergency situation, the physician faces the dilemma of treating a potentially life-threatening arrhythmia as quickly as possible while simultaneously ensuring adequate diagnostic work-up, which will be decisive for long-term therapy once the patient has survived the crisis. The differential diagnosis between supraventricular and ventricular tachycardias is primarily facilitated by knowledge of a few salient points from the patient's history and 12-lead electrocardiography. This overview presents the most important principles for treating these arrhythmias. Interventional therapy principles (overstimulation, ablation) play an increasing role in these considerations. New insights on the pathogenesis of "malignant" arrhythmias and implementation of new concepts such as defibrillation by lay responders with the automatic external defibrillator will substantially influence emergency treatment of tachyarrhythmias in the coming years. |
1,006 | Prevention of sudden cardiac death: the role of the implantable cardioverter-defibrillator. | Sudden cardiac death, usually due to fatal ventricular tachyarrhythmias, results in the loss of 300,000-400,000 lives each year in the United States. Implantable cardioverter-defibrillator therapy has revolutionized both the secondary and, increasingly, the primary prevention of sudden cardiac death. In the last decade, subcutaneous pectoral implantation with transvenous lead placement has lessened perioperative risk considerably, raising the benefit/risk ratio for many candidates. As a consequence, the list of approved indications for implantable cardioverter-defibrillator therapy has expanded rapidly in recent years. Current devices offer tiered therapy utilizing bradycardia pacing, anti-tachycardia pacing, low-energy cardioversion, and high-energy defibrillation. Hybrid therapy, combining device, drugs and radiofrequency catheter ablation as required, has become the standard of care for reducing both appropriate and inappropriate shocks. As implantation rates continue to rise, so will the number of patients presenting with electrical storm. The dilemma of how our society will cope with the enormous projected costs of implantable cardioverter-defibrillator therapy has yet to be resolved. |
1,007 | N,N,N',N'-tetrakis(2-pyridylmethyl)-ethylenediamine improves myocardial protection against ischemia by modulation of intracellular Ca2+ homeostasis. | N,N,N',N'-Tetrakis(2-pyridylmethyl)-ethylenediamine (TPEN), a transition-metal chelator, was recently found to protect against myocardial ischemia-reperfusion injury. The goals of this study were to investigate the in vivo antiarrhythmic and antifibrillatory potential of TPEN in rats and guinea pigs and to study the in vitro effects of TPEN on calcium homeostasis in cultured newborn rat cardiac cells in normoxia and hypoxia. We demonstrated on an in vivo rat model of ischemia-reperfusion that TPEN abolishes ventricular fibrillation incidence and mortality and decreases the incidence and duration of ventricular tachycardia. To elucidate the mechanism of cardioprotection by TPEN, contraction, synchronization, and intracellular calcium level were examined in vitro. We have shown for the first time that TPEN prevented the increase in intracellular Ca(2+) levels ([Ca(2+)](i)) caused by hypoxia and abolished [Ca(2+)](i) elevation caused by high extracellular Ca(2+) levels ([Ca(2+)](o)) or by caffeine. Addition of TPEN returned synchronized beating of cardiomyocytes desynchronized by [Ca(2+)](o) elevation. To discover the mechanism by which TPEN reduces [Ca(2+)](i) in cardiomyocytes, the cells were treated with thapsigargin, which inhibits Ca(2+) uptake into the sarcoplasmic reticulum (SR). TPEN successfully reduced [Ca(2+)](i) elevated by thapsigargin, indicating that TPEN did not sequester Ca(2+) in the SR. However, TPEN did not reduce [Ca(2+)](i) in the Na(+)-free medium in which the Na(+)/Ca(2+) exchanger was inhibited. Taken together, the results show that activation of sarcolemmal Na(+)/Ca(2+) exchanger by TPEN increases Ca(2+) extrusion from the cytoplasm of cardiomyocytes, preventing cytosolic Ca(2+) overload, which explains the beneficial effects of TPEN on postischemic cardiac status. |
1,008 | Successful resuscitation after sudden death in a one year old infant who sustained a blunt chest injury after a fall from 10 m. | Sudden cardiac arrest due to blunt anterior chest wall impact (Commotio Cordis) usually occurs in young athletes who are struck by a baseball or other projectile in the precordium. Survival is extremely rare if the induced ventricular fibrillation (VF) is not defibrillated immediately at the scene. We report here a rare case of a one-year-old infant survivor of cardiac arrest caused by blunt chest impact during an accidental fall from a fourth story window. Eye witnesses reported to have seen him land on the front of his chest directly onto the plastic rain cover on the ground floor. He was transferred to a nearby hospital within minutes, where ventricular fibrillation was recorded. Immediate cardiopulmonary resuscitation and defibrillation and was successful. He recovered without any subsequent sequelae. To the best of our knowledge, this rare incident represents the first time that an infant has survived such cardiac arrest in these circumstances that has been recorded in the literature. This has implications for the management of paediatric fall injuries. |
1,009 | Prehospital thrombolysis perfomed by a ship's nurse with on-line physician consultation. | Prehospital thrombolysis for acute ST-elevation myocardial infarction (STEMI) has been shown to improve recovery from myocardial function. We describe prehospital thrombolytic treatment in two patients suffering from STEMI complicated by ventricular fibrillation (VF) on a passenger ship. The importance of a functioning Emergency Medical Service (EMS) system providing guidance for paramedical personnel is discussed briefly. Both our patients survived and returned back to normal life. It is concluded that EMS physician guided prehospital thrombolytic treatment may offer an important therapeutic option for nurses or paramedics in locations out of reach of ordinary EMS services. |
1,010 | Influence of dobutamine on the variables of systemic haemodynamics, metabolism, and intestinal perfusion after cardiopulmonary resuscitation in the rat. | Global left ventricular dysfunction after successful resuscitation from cardiac arrest may be treated successfully with dobutamine but the effects on intestinal perfusion are unknown.</AbstractText>In 24 male Sprague-Dawley rats ventricular fibrillation was induced. After 4 min of untreated cardiac arrest, precordial chest compression was performed for 4 min; adrenaline (epinephrine) (90 microg kg(-1)) was injected, followed by defibrillation. Return of spontaneous circulation was achieved in 18 animals, which were allocated to receive saline 0.9% (control group, n = 6), dobutamine at 5 microg kg(-1) min(-1) (n = 6) or dobutamine at 10 microg kg(-1) min(-1) (n = 6). Measurements of haemodynamic variables and intestinal tonometer P(CO2) were made before induction of ventricular fibrillation and 15, 30, 60, and 120 min postresuscitation.</AbstractText>At 120 min postresuscitation, mean aortic pressure was 82 +/- 20, 104 +/- 19, and 113 +/- 15 mmHg for the control group, the dobutamine (5 microg kg(-1) min(-1)) group and the dobutamine (10 microg kg(-1) min(-1)) group (P < 0.05 for comparison of the dobutamine (10 microg kg(-1) min(-1)) group versus the control group). Respective abdominal aortic blood flow was 107 +/- 16, 133 +/- 49, and 145 +/- 18 ml min(-1) kg(-1) (P < 0.05 for comparison of the dobutamine (10 microg kg(-1) min(-1)) group versus the control group), and superior mesenteric artery blood flow was 25 +/- 9, 28 +/- 8, and 33 +/- 8 ml min(-1) kg(-1). Arterial lactate was significantly higher (P < 0.05) in the control group (2.3 +/- 0.6 mmol l(-1)) than in the dobutamine (5 microg kg(-1) min(-1)) group (1.6 +/- 0.3 mmol l(-1)) and dobutamine (10 microg kg(-1) min(-1)) group (1.5 +/- 0.3 mmol l(-1)). Tonometrically derived P(CO2) gap was highly elevated at 15 min of postresuscitation and returned to prearrest level at 120 min postresuscitation in all groups.</AbstractText>Dobutamine enhances the recovery of global haemodynamic and metabolic variables early after cardiac arrest.</AbstractText> |
1,011 | Effects of intravenous arginine vasopressin on epicardial coronary artery cross sectional area in a swine resuscitation model. | Although arginine vasopressin (AVP) has been shown to be a promising drug during cardiopulmonary resuscitation (CPR), concern has been raised about the potential for AVP-mediated vasoconstriction of the coronary arteries. In a prospective, randomized laboratory investigation employing an established porcine model, the effects of AVP on haemodynamic variables, left anterior descending (LAD) coronary artery cross sectional area employing intravascular ultrasound (IVUS), and return of spontaneous circulation were studied. During sinus rhythm, the LAD coronary artery cross sectional area was measured by IVUS at baseline, and 90 s and 5 min after AVP (0.4 U/kg IV). Following a 60 min recovery, ventricular fibrillation was induced. At 4 min, chest compressions were initiated; AVP (0.4 U/kg IV) was injected at 5.5 min, and defibrillation performed at 8 min. LAD coronary artery cross sectional area was measured by IVUS at the pre-arrest baseline, 90 s after drug injection during CPR, and 5 min after return of spontaneous circulation. Compared with baseline, the mid-LAD coronary artery cross sectional area increased significantly (P<.05) 90 s and 5 min after AVP administration (9.2+/-.5mm2 versus 10.7+/-.6mm2 versus 11.7+/-.6mm2, respectively) during normal sinus rhythm. Similarly during ventricular fibrillation and CPR plus AVP, the mid-LAD coronary artery cross sectional area increased at 90 s after AVP compared with baseline (9.5+/-.6mm2 versus 11.0+/-.7mm2; P<.05). Moreover, the cross sectional area increased further 5 min after return of spontaneous circulation (9.5+/-.6mm2 versus 14.0+/-.8mm2, P<.05). In conclusion, in this experimental model with normal coronary arteries, AVP resulted in significantly increased LAD coronary artery cross sectional area during normal sinus rhythm, during ventricular fibrillation with CPR, and after return of spontaneous circulation. |
1,012 | The evolution of serum astroglial S-100 beta protein in patients with cardiac arrest treated with mild hypothermia. | To study the effects of mild hypothermia on the 24h concentration of serum astroglial of S-100 beta protein in patients who survived cardiac arrest (CA).</AbstractText>A prospective, randomised, clinical study in a university teaching hospital.</AbstractText>Sixty-one resuscitated patients were randomised into two prospective studies, known as the short study period (SSP) (n = 33 patients) and the long study period (LSP) (n = 28 patients). In the SSP study, patients older than 18 years of age and surviving asystole or pulseless electrical activity were included. In the LSP study, patients with ventricular fibrillation (VF) or non-perfusing ventricular tachycardia (VT) aged between 18 and 75 years were included. In each of the study groups, the patients were further randomised into either normothermic or hypothermic subgroups. The standard supportive therapy was similar, only the devices used to reduce the body temperature and the period of hypothermia were different. Serum samples for the measurement of astroglial S-100 beta protein were collected at admission and 24h later.</AbstractText>During the first 24h after the cardiac arrest, the concentration of astroglial serum S-100 beta protein decreased significantly in the hypothermic cohort. In the normothermic cohort, the decrease of serum astroglial S-100 beta protein was less pronounced and even increased in the normothermic LSP group.</AbstractText>Induced mild hypothermia reduced the 24h astroglial serum S-100 beta protein concentration and might play a neuroprotective effect after cardiac arrest.</AbstractText> |
1,013 | Layperson positioning of defibrillation electrodes guided by pictorial instructions. | Correct positioning of defibrillation electrodes is essential to achieve sufficient transmyocardial current to depolarize a critical mass of myocardium, and thus terminate ventricular fibrillation (VF).</AbstractText>To evaluate the pictures on the self-adhesive defibrillation electrodes in guiding laypersons to place the electrodes in the recommended position.</AbstractText>Defibrillation electrodes from five manufactures (Access Cardio Systems, Schiller, Medtronic, Cardiac Science and Philips) were included in the study and compared with electrodes with a lateral view picture, designed for the study, showing the placement of the apical electrode. A total of 150 laypersons without any experience or training in use of a defibrillator participated in the study. The participants placed randomly selected electrodes on the chest of a resuscitation manikin without any guidance apart from the pictures on the electrodes. The distances of the electrodes from the recommended positions were measured.</AbstractText>The proportion of participants who placed both electrodes within 5 cm from recommended position varied from 8% to 36% with the different electrodes. Usually, the apical electrode was placed too anteriorly. Electrodes placed with help of the lateral instruction picture, (designed for the study), showing the placement of the apical electrode were placed significantly more often within 5 cm than any of the others (64%, 95% confidence interval 44-80, P < 0.05).</AbstractText>The current practice in designing pictures on the electrodes does not seem to be optimal in showing the recommended position of the apical electrode as recommended by Guidelines 2000. It is suggested that by showing a lateral view in the instructions, success in placing the apical electrodes correctly can be improved.</AbstractText> |
1,014 | Evaluating the quality of prehospital cardiopulmonary resuscitation by reviewing automated external defibrillator records and survival for out-of-hospital witnessed arrests. | Without an easy method to monitor the performance of prehospital cardiopulmonary resuscitation (CPR), earlier studies have not been able to assess the quality of CPR. In this study, we have used a new approach to evaluate prehospital CPR performance and the impact on outcome using data retrieved from the automatic external defibrillators (AED).</AbstractText>Electrocardiography (ECG) and voice records from AED data cards from 633 out-of-hospital cardiac arrests (OHCA) were reviewed. Fifty-two witnessed cardiac arrests in ventricular fibrillation (VF) requiring post-shock CPR underwent an independent, structured review by two physicians. The adequacy of prehospital CPR was defined on the basis of noticeable deflection of the ECG with chest compressions, the actual number of chest compressions delivered per minute, and the continuity of prehospital CPR at the scene and during transport. Outcome measures included return of spontaneous circulation (ROSC) and survival to hospital admission and discharge.</AbstractText>The quality of prehospital CPR was judged as adequate in 15 (29%, 95%; CI: 18-42%) and inadequate in 37 (71%, 95%; CI: 58-82%) of the consensus. Adequate CPR performance resulted in a higher rate of ROSC at the scene (53% versus 8%, 95% CI of the difference 14-76%), and survival to hospital discharge (53% versus 8%, 95% CI of the difference 14-76%). Two reviewers agreed on whether CPR was adequate in 92.3% of cases, with a kappa of 0.82.</AbstractText>The quality of prehospital CPR is associated with a greater likelihood of survival in witnessed VF arrests in need of post-shock CPR. The potential of widely available electrocardiography and voice records in AEDs in providing a convenient and real-time evaluation of prehospital CPR should be explored further.</AbstractText> |
1,015 | Emergency trans-oesophageal ventricular pacing in a child. | We report our experience with an 8-year-old boy with complete atrioventricular block and syncopal bradycardia who required urgent pacing. Each attempt to cross the tricuspid valve with a femoral lead triggered ventricular standstill, followed by fibrillation, and pacing through the coronary sinus failed. Successful ventricular pacing was finally achieved through the oesophagus, allowing subsequent implantation of a transvenous pacemaker. |
1,016 | Effects of transient myocardial ischemia on the ventricular defibrillation threshold. | Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT).</AbstractText>The purpose of this study was to determine the effects of transient regional left ventricular (LV) ischemia on the DFT.</AbstractText>Ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and DFT were measured under nonischemic conditions (control) in 26 pigs weighing 25-35 kg. Myocardial ischemia was then induced by occlusion of the mid left anterior descending coronary artery, and measurements of ERP and VFT were repeated after 2 minutes of occlusion. The coronary artery ligation was released immediately after the onset of VF and DFT was measured.</AbstractText>LV ERP was unchanged by ischemia (199 +/- 19 ms at control vs. 200 +/- 22 ms under ischemic conditions, P = 0.799), whereas VFT was significantly lower during coronary occlusion (10.7 +/- 5.4 mA vs. 37.7 +/- 13 mA, P = 0.000). Brief myocardial ischemia caused a significant increase in DFT (13.5 +/- 12.6 J after coronary occlusion vs. 6.8 +/- 6.8 J at control, P = 0.023). The duration of coronary occlusion was not correlated with the amounts of energy required to defibrillate (P = 0.526).</AbstractText>This experimental study shows that transient myocardial ischemia markedly increases the DFT, suggesting that specific defibrillation algorithms should be designed for recipients of implantable defibrillators at risk of myocardial ischemia.</AbstractText> |
1,017 | Thyrotoxic periodic paralysis complicated by near-fatal ventricular arrhythmias. | A 35-year-old Chinese man presented with acute thyrotoxic periodic paralysis complicated by near-fatal cardiac arrhythmias due to persistent hypokalaemia, despite maximum potassium supplementation. He was eventually resuscitated with external cadioversion. In this unusual case of severe refractory hypokalaemia leading to ventricular fibrillation in a patient with underlying thyrotoxicosis, the potential dangers concerning the use of dextrose infusion and beta-adrenergic agent for resuscitation are highlighted. |
1,018 | The burden of atrial fibrillation: should we abandon antiarrhythmic drug therapy? | Atrial fibrillation (AF) is the most common sustained arrhythmia, exacting a substantial toll in cardiovascular morbidity and mortality. Until recently, the prevailing philosophy has been that restoration and maintenance of normal sinus rhythm, as opposed to control of ventricular response rate, was the optimal approach to treatment of AF. A series of landmark trials (AFFIRM, RACE, STAF, and PIAF) have called this strategy into question, suggesting outcomes are equivalent with both approaches. These data do not mean that rhythm control is not beneficial, but highlight the limitations of current therapies to achieve and maintain sinus rhythm. Limitations of the rhythm-control strategy may be related to our difficulty in accurately documenting symptomatic benefit from this approach, the lack of efficacy and excessive adverse-effect burden associated with currently available antiarrhythmic agents, and selection biases in the enrollment of patients in clinical trials of rhythm control versus rate control, making the trials incompletely representative of the population eligible for therapy. New pharmacologic agents under development feature increased atrial selectivity or multi-channel-blocking properties (or both). As a result, these compounds may be more effective in prolonging atrial refractoriness and may also have reduced proarrhythmic potential. It is premature to abandon the concept of rhythm control in AF until we have trials designed to include younger and highly symptomatic patients, more sensitive tools to measure symptomatic improvement, and safer, more effective antiarrhythmic agents. |
1,019 | C-reactive protein and microalbuminuria are associated with atrial fibrillation. | Atrial fibrillation (AF) is associated with an increased risk for cardiovascular disease. It is important to detect AF at an early stage and to search for new pathophysiological pathways to intervene. We hypothesized that microalbuminuria and C-reactive protein (CRP), a marker of generalized vascular damage and inflammation, respectively, are associated with AF.</AbstractText>Standard 12-lead electrocardiograms were recorded in 7546 subjects (mean age 49+/-13 years, 51% male). AF was defined according to Minnesota codes. The urinary albumin excretion rate was measured as the mean of two 24-h urine collections and microalbuminuria was defined as an albumin excretion rate between 30 and 300 mg per 24 h. High-sensitive CRP was dichotomized (low: three lowest quartiles, CRP<2.87 mg/l vs. high: highest quartile, CRP>2.87 mg/l). Data are expressed as odds ratios (95% confidence intervals).</AbstractText>AF was present in 75 (1.0%) subjects. In multivariate analysis, an age >60 years, the presence of ischemic heart disease, left ventricular hypertrophy, elevated CRP level (1.79 [1.07-2.97], p=0.03) and microalbuminuria (1.93 [1.10-3.37], p=0.02) were significantly associated with AF. Surprisingly, the combination of elevated CRP and the presence of microalbuminuria showed an even higher association with AF after adjusting for all cardiovascular risk factors (3.80 [1.89-7.63], p<0.001).</AbstractText>An elevated CRP level and microalbuminuria are associated with AF. Moreover, the combination of both indicates a fourfold higher association with the presence of AF in a population at large.</AbstractText> |
1,020 | Improved resuscitation outcome in emergency medical systems with increased usage of sodium bicarbonate during cardiopulmonary resuscitation. | The use of sodium bicarbonate (SB) in cardiopulmonary resuscitation (CPR) is controversial. This study analyzes the effects of SB use on CPR outcome in the Brain Resuscitation Clinical Trial III (BRCT III), which was a multicenter randomized trial comparing high-dose to standard-dose epinephrine during CPR. Sodium bicarbonate use in BRCT III was optional.</AbstractText>The entire BRCT III database was reviewed. Analysis included only patients who arrested out of the hospital and whose time from collapse to initiation of ACLS was no longer than 30 min (total n = 2122 patients). Sodium bicarbonate use by the 16 participating study sites was analyzed. The study sites were divided according to their SB usage profile: 'low SB user' sites administered SB in less than 50% of CPRs and their first epinephrine to SB time exceeded 10 min; and 'high SB user' sites used SB in over 50% of CPRs and their first epinephrine to SB time was <10 min.</AbstractText>Sites' SB usage rates ranged between 3.1% and 98.2% of CPRs. Sodium bicarbonate usage rates correlated inversely with the sites' intervals from collapse (r = - 0.579 P = 0.018) from initiation of ACLS (r = - 0.685 P = 0.003) and from first epinephrine (r = - 0.611 P = 0.012) to SB administration. Mean ROSC rate in the 'high SB user' sites was 33.5% (CI = 30.0-37.0) compared to 25.7% (CI = 23.1-28.4) in the 'low SB user' sites. In the 'high SB user' sites, hospital discharge rate was 5.3% (CI = 3.6-7.0) compared to 3% (CI = 2.0-4.0) in the 'low SB user' sites, and 5.3% (CI = 3.6-7.0) had a favorable neurological outcome compared to 2.1% (CI = 1.2-3.0) in the 'low SB user' sites. Collapse to ACLS interval was 8.5 min (CI = 8.1-9.0) in the 'high SB user' sites compared to 10.2 min (CI = 9.8-10.6) in the 'low SB user' sites, and their ACLS to first epinephrine interval was 7.0 min (CI = 6.5-7.5) compared to 9.7 min (CI = 9.3-10.2). Multivariate regression analysis found that belonging to 'high SB user' sites independently increased the chances for ROSC (OR 1.36, CI 1.08-1.7) and for achieving a good neurological outcome (OR 2.18, CI 1.23-3.86).</AbstractText>Earlier and more frequent use of SB was associated with higher early resuscitability rates and with better long-term outcome. Sodium bicarbonate may be beneficial during CPR, and it should be subjected to a randomized clinical trial.</AbstractText> |
1,021 | CPR before defibrillation in out-of-hospital cardiac arrest: a randomized trial. | Current resuscitation guidelines recommend that defibrillation be undertaken as soon as possible in patients suffering a cardiac arrest where the cardiac rhythm is either ventricular fibrillation (VF) or ventricular tachycardia (VT). Evidence from animal and clinical studies suggests that outcomes may be improved if a period of cardiopulmonary resuscitation (CPR) is given prior to defibrillation. The objective of this study was to determine if 90 seconds of CPR before defibrillation improved survival.</AbstractText>Patients suffering non-paramedic witnessed VF/VT cardiac arrest were randomized to receive either 90 seconds of CPR before defibrillation (treatment) or immediate defibrillation (control). The study was carried out in Perth, Western Australia between June 2000 and June 2002. The primary endpoint was survival to hospital discharge with secondary endpoints of return of spontaneous circulation (ROSC) and survival at 1 year.</AbstractText>A total of 256 patients underwent randomization. Baseline characteristics including response intervals were similar in both groups. Survival to hospital discharge in the CPR first group was 4.2% (5/119) compared with 5.1% (7/137) for the immediate defibrillation group (OR 0.81; 95%CI. 0.25-2.64). No difference in those achieving ROSC was observed between the groups (OR 1.16; 95% CI 0.49-2.80).</AbstractText>Ninety seconds of CPR before defibrillation does not improve overall survival in patients suffering VF/VT cardiac arrests. Further studies to evaluate various aspects of this treatment strategy are required as published outcomes to date are inconclusive.</AbstractText> |
1,022 | Gender differences in electrophysiologic effects of mental stress and autonomic tone inhibition: a study in health individuals. | Gender differences exist in electrophysiologic properties and the occurrence of certain arrhythmias. Mental stress may trigger serious arrhythmias, including ventricular tachycardias and ventricular fibrillation. This study investigates gender differences in the electrophysiologic effects on different levels of the cardiac conduction system elicited by mental stress and autonomic tone inhibition.</AbstractText>Twenty-three healthy volunteers (11 male and 12 female) participated in the study. Electrophysiologic and hemodynamic variables were measured at baseline, during mental stress produced by Stroop's color word conflict test (CWT), and after autonomic tone inhibition (ATI) with propranolol (0.15 mg/kg) and atropine (0.02 mg/kg). During CWT, men showed shorter QT and JT durations, whereas women had shorter refractoriness in the atrial tissue and AV node. After ATI, no gender differences in sinus nodal properties were noted, whereas AV nodal refractoriness and conduction time became shorter in women, and QT and JT duration and the refractory period of the right ventricle were shorter in men.</AbstractText>In women, mental stress produces a pronounced effect on the AV node and on the sinus node. Men react with a more pronounced effect on ventricular electrophysiologic properties. Certain gender differences in cardiac electrophysiologic properties seem to be intrinsic. After ATI, women have a higher heart rate and shorter AV nodal refractoriness but longer QT and JT intervals and longer effective refractory periods in the right ventricle. These differences may partly explain why certain arrhythmias occur more often in women than in men.</AbstractText> |
1,023 | Further insights into the effect of quinidine in short QT syndrome caused by a mutation in HERG. | The principal aim of this study was to assess the efficacy of quinidine in suppressing IKr in vitro and in modulating the rate dependence of the QT interval in the "SQT1" form of the short QT syndrome.</AbstractText>Graded-intensity bicycle exercise testing was performed off drug in three patients and during oral quinidine in two patients with short QT syndrome and compared to a control group of healthy normal subjects. The in vitro effects of quinidine on currents in patch clamp technique were investigated. Off drugs QTpV3/heart rate correlation is much weaker in patients with short QT syndrome, and QTpV3 shortens less with heart rate increase compared to normal subjects. In addition to prolonging the QT interval into the normal range, quinidine restored the heart rate dependence of the QT interval toward a range of adaptation reported for normal subjects. Data from heterologous expression of wild-type and mutant HERG genes indicate the mutation causes a 20-fold increase in IC50 of d-sotalol but only a 5.8-fold increase in IC50 of quinidine.</AbstractText>Oral quinidine is effective in suppressing the gain of function in IKr responsible for some cases of short QT syndrome with a mutation in HERG and thus restoring normal rate dependence of the QT interval and rendering ventricular tachycardia/ventricular fibrillation noninducible.</AbstractText> |
1,024 | Assessment of markers for identifying patients at risk for life-threatening arrhythmic events in Brugada syndrome. | Risk stratification for life-threatening arrhythmic events in Brugada syndrome is not yet established. The aim of the present study was to examine the usefulness of various markers in predicting life-threatening arrhythmic events in the Brugada syndrome.</AbstractText>Forty-six patients with Brugada-type ECGs were categorized into the symptomatic (n=28) and asymptomatic (n=18) groups. Statistical analyses were performed with respect to the usefulness of the following markers: SCN5A mutation, pharmacologic challenge, ventricular fibrillation (VF) inducibility by programmed electrical stimulation, and late potential (LP) by signal-averaged ECG (SAECG). Comparison between the two groups revealed a significant difference only in LP positivity (92.6% vs 47.1%, P=0.0004). The symptomatic group had significantly lower RMS40, longer LAS40, and longer fQRSd compared with the asymptomatic group. A significant difference was noted, especially RMS40. The positive predictive value, negative predictive value, and predictive accuracy when setting a cutoff value of 15 microV were 92.0%, 78.9%, and 86.4%, respectively. Furthermore, patients with an RMS40 value <15 microV (n=25) showed significantly higher rates of VF recurrence compared with patients with an RMS40 value > or = 15 microV (n=19, P=0.047).</AbstractText>Regarding risk stratification for identifying high-risk patients in Brugada syndrome, only LP by SAECG was shown to be useful, suggesting the importance of RMS40 in predicting the history of life-threatening arrhythmic events and the recurrence of VF.</AbstractText> |
1,025 | Hypertension and hypertensive heart disease are associated with increased ostial pulmonary vein diameter. | Atrial fibrillation (AF) is associated with increased ostial pulmonary vein (PV) diameter and commonly with hypertension. We sought to investigate ostial PV anatomy in patients with and without AF with the goal of characterizing the relationship to hypertension and cardiovascular disease.</AbstractText>Ostial PV diameter was assessed by preprocedural spiral computed tomography in 100 AF patients undergoing a PV isolation procedure and in 24 age- and sex-matched non-AF control patients. Ostial diameter of 392 PVs in 100 AF patients was increased compared to 106 PVs in 24 non-AF controls (1.50 +/- 0.31 vs 1.20 +/- 0.31 cm, P <0.001) and diameters of individual PVs were uniformly affected (r=0.45-0.62, P <0.001). Left atrial dilation was associated with a larger PV diameter (1.56 +/- 0.32 vs 1.44 +/- 0.29 cm, P <0.01). PV diameter in AF patients with hypertension (1.55 +/- 0.32 cm), particularly if associated with left ventricular hypertrophy (1.66 +/- 0.37 cm), was larger compared to AF patients without hypertension (1.43 +/- 0.26 cm, P <0.01). PV diameter in control patients with hypertension (n=14) was larger than in those without hypertension (n=10, P <0.01). Patients with persistent AF had larger PV diameters (1.61 +/- 0.34 cm) than patients with paroxysmal AF (1.47 +/- 0.30 cm, P <0.01). Male gender (P <0.01), history of hypertension (P <0.01), and persistent AF (P <0.05) were identified as independent cofactors of increased ostial PV diameter.</AbstractText>PV dilation affects all PVs uniformly in AF patients. Hypertension and hypertensive heart disease in patients with and without AF are associated with PV dilation, supporting theories that impaired left ventricular diastolic function is associated with a stretch-induced PV arrhythmia mechanism.</AbstractText> |
1,026 | Evolution of our knowledge of sudden death due to commotio cordis. | Commotio cordis refers to circulatory arrest due to a nonpenetrating blow to the chest. First discovered in 1932 in a study using large rabbits, it came to the attention of clinicians who encountered children dying suddenly from a chest blow while engaging in sports activities. This review traces the history of commotio cordis, establishes the conditions necessary for sudden death from a nonpenetrating chest blow, and presents the first ECG record showing that a chest blow landing in the ventricular vulnerable period can produce ventricular fibrillation. The conditions necessary for sustaining ventricular fibrillation and numerous examples of sudden death by commotio cordis are presented. |
1,027 | Electrical characteristics of low atrial septum pacing compared with right atrial appendage pacing. | The study was designed to compare the electrical characteristics of atrial leads placed in the low atrial septum (LAS) with those placed in the right atrial appendage (RAA) associated with dual chamber pacing.</AbstractText>In 86 patients an active-fixation (St. Jude Medical's Tendril DX model 1388T) atrial lead was positioned in RAA and in 86 patients the same model atrial lead was placed in the LAS. Pacing thresholds, sensing thresholds, impedances and the Far Field paced R-Wave (FFRW) amplitude and timing were compared at 6 weeks and at 3 and 6 months.</AbstractText>The pacing threshold did not differ between groups. Sensed voltage of the P-wave was higher in the LAS compared with the RAA at 3 and 6 months (P=0.004). Impedance was higher in the LAS at 6 weeks and 3 months (P=0.002) but this difference was no longer significant at 6 months (P=0.05). The atrial sensed FFRW voltage was significantly higher in the LAS position compared with the RAA at 3 and 6 months follow-up (P=0.0002). FFRW voltage>1 mV was seen in 87% of the RAA pacing group and in 94% of the LAS pacing group (P=ns). The time between the ventricular pacing stimulus and the sensed FFRW in the atrium, (V spike-FFRW) in RAA was longer than in LAS at all follow-up measurements (P=0.006).</AbstractText>The electrical characteristics of LAS pacing makes this alternative position in the atrium safe and feasible. Though statistical differences were found in P-wave sensing (LAS higher voltage than in the RAA) and FFRW sensing was higher in the LAS compared with the RAA this did not interfere with the clinical applicability of the LAS as alternative pacing site.</AbstractText> |
1,028 | Effects of successful cardioversion of persistent atrial fibrillation on right ventricular refractoriness and repolarization. | Changes in ventricular refractoriness and repolarization after successful electrical cardioversion to sinus rhythm in persistent atrial fibrillation (AF) patients were studied.</AbstractText>In 33 AF patients with controlled ventricular response, right ventricular ERP (VERP) at three basic cycle lengths (600, 500, 400 ms), as well as monophasic action potential duration (MAPd(90)) at a drive cycle length of 500 ms, were measured just before, 20 min and 24 h after cardioversion. VERP at 600 ms changed from 241+/-19 ms to 249+/-21 ms to 253+/-24 ms (P<0.001), VERP at 500 ms changed from 234+/-19 ms to 242+/-22 ms to 246+/-23 ms (P<0.001) and VERP at 400 ms changed from 224+/-20 ms to 232+/-23 ms to 236+/-24 ms (P<0.001). MAPd(90) changed from 247+/-16 ms preconversion to 252+/-17 ms 20 min postconversion to 253+/-19 ms after 24 h (P<0.05). Change in refractoriness at 500 ms was well correlated with change of mean RR interval before and 20 min after conversion (R=0.616, P<0.001). There was no correlation between RR variability and VERP before cardioversion.</AbstractText>Restoration of sinus rhythm in persistent AF patients is followed by significant effects on ventricular refractoriness and repolarization related to cycle length change. No AF related ventricular electrophysiological alterations were found.</AbstractText> |
1,029 | [Complications of myocardial infarction]. | Most acute complications of myocardial infarction do not need emergency imaging, since they often result in death prior to hospital admission: ventricular fibrillation and tachycardia, papillary muscle or septal rupture, fissuration and tamponade. Imaging can play a role at distance of the acute phase (papillary muscle dysfunction, false aneurysm, development of a mural thrombus associated to left ventricular apical dyskinesis, with potential embolic complications). |
1,030 | [Causes and prognosis of syncope in patients with primary dilated cardiomyopathy]. | The causes of adverse prognosis of patients with primary dilated cardiomyopathy remain controversial. Classically, it is thought that syncope is associated with an increased risk of mortality. The aim of this study was to try and identify the causes and prognostic significance of syncope in patients with primary dilated cardiomyopathy. Sixty-five patients aged 31 to 80 with primary dilated cardiomyopathy were admitted for investigation of syncope. The average ejection fraction was 27 +/- 10%. Invasive and non-invasive investigations including complete electrophysiological investigations, were performed. Sustained monomorphic ventricular tachycardia was induced in 14 patients (21.5%), ventricular flutter or fibrillation was induced in 9 patients (14%), a supraventricular arrhythmia in 17 patients (26%), and a conduction defect alone or associated with another arrhythmia in 7 patients (11%). A pathological result of tilt testing was observed in 5 patients (8%). No cause of syncope could be demonstrated in 15 patients (23%). During follow-up (4 +/- 2 years) there was a mortality of 15% which was only correlated with the reduction in left ventricular ejection fraction. The authors conclude that there are many causes of syncope in primary dilated cardiomyopathy: ventricular arrhythmias represent only 35% of cases and do not impact on the prognosis; above all, left ventricular ejection fraction is the most important prognostic factor. |
1,031 | Life-threatening ventricular arrhythmia recognition by nonlinear descriptor. | Ventricular tachycardia (VT) and ventricular fibrillation (VF) are ventricular cardiac arrhythmia that could be catastrophic and life threatening. Correct and timely detection of VT or VF can save lives.</AbstractText>In this paper, a multiscale-based non-linear descriptor, the Hurst index, is proposed to characterize the ECG episode, so that VT and VF can be recognized as different from normal sinus rhythm (NSR) in the descriptor domain.</AbstractText>This newly proposed technique was tested using MIT-BIH malignant ventricular arrhythmia database. The relationship between the ECG episode length and the corresponding recognition performance was studied. The experiments demonstrated good performance of the proposed descriptor. An accuracy rate as high as 100% was obtained for VT/VF to be recognized from NSR; for VT and VF to be recognized from each other, the recognition accuracy varies from 84.24% to 100%. In addition, the results were compared favorably against those obtained using Complexity measure.</AbstractText>There is strong potential for using the Hurst index for malignant ventricular arrhythmia recognition in clinical applications.</AbstractText> |
1,032 | Pretreatment with ACE inhibitors improves acute outcome of electrical cardioversion in patients with persistent atrial fibrillation. | Persistent atrial fibrillation (AF) is difficult to treat. In the absence of class I or III antiarrhythmic drugs sinus rhythm is maintained in only 30% of patients during the first year after electrical cardioversion (ECV). One of the remodeling processes induced by AF is fibrosis, which relates to inducibility and maintenance of AF. The renin-angiotensin system may play a important role in this. The aim of this study was to investigate the role of angiotensin-converting enzyme (ACE) inhibitor use on efficacy of ECV, and occurrence of subacute recurrences.</AbstractText>One hundred-seven consecutive patients with persistent AF underwent ECV. In twenty-eight (26%) patients ACE inhibitors had been started before initiation of the present episode of AF ('pre-treated' patients).</AbstractText>ECV was successful in 96% of patients who were on ACE inhibitors before start of the present episode of AF compared to 80% of the patients not pre-treated (p = 0.04). After 1 month of follow-up 49% of the pre-treated patients and 50% of those not pre-treated with ACE inhibition were still in sinus rhythm (p=ns). Multivariate analysis showed that pre-treatment with ACE inhibitors and a smaller left atrial size were independent predictors of successful ECV (OR = 5.8, C.I. 1.3-26.1, and OR = 5.6, C.I. 1.2-25.3, respectively).</AbstractText>Pre-treatment with ACE inhibitors may improve acute success of ECV but does not prevent AF recurrences.</AbstractText> |
1,033 | Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter. | The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were administered nicotine (5 mg.kg(-1).day(-1) sc) for 1 mo using osmotic minipumps. High-resolution epicardial (1,792 bipolar electrodes) and endocardial Halo catheters were used to map activation during induced atrial rhythms. Nicotine promoted inducible sustained AFL at a mean cycle length of 134 +/- 10 ms in all MI dogs (n = 6) requiring pacing and electrical shocks for termination. No AFL could be induced in MI dogs (n = 6), control (non-MI) dogs (n = 3) not exposed to nicotine, and dogs with no MI and exposed to nicotine (n = 3). Activation maps during AFL showed a single reentrant wavefront in the right atrium that rotated either clockwise (60%) or counterclockwise (40%) around the crista terminalis and through the isthmus. Ablation of the isthmus prevented the induction of AFL. Nicotine caused a significant (P < 0.01) but highly heterogeneous increase in atrial interstitial fibrosis (2- to 10-fold increase in left and right atria, respectively) in the MI group but only a 2-fold increase in the right atrium in the non-MI group. Nicotine also flattened (P < 0.05) the slope of the epicardial monophasic action potential duration (electrical restitution) curve of both atria in the MI but not in non-MI dogs. Two-dimensional simulation in an excitable matrix containing an isthmus and nicotine's restitutional and reduced gap junctional coupling (fibrosis) parameters replicated the experiments. Chronic nicotine in hearts with MI promotes AFL that closely resembles typical human AFL. Increased atrial interstitial fibrosis and flattened electrical restitution are important substrates for the AFL. |
1,034 | Incomplete myocardial rupture after coronary embolism of an isolated single coronary artery. | An 82-year-old female was admitted to the coronary care unit with an anterior wall myocardial infarction and cardiogenic shock. She was in chronic atrial fibrillation without oral anticoagulation. Coronary angiography showed occlusion of the left main coronary artery which originated together with a normal right coronary artery from the right sinus of Valsalva. The advanced age, the presence of chronic atrial fibrillation not anticoagulated and the normal appearance of the remaining coronary arteries suggested a thromboembolic origin. Transthoracic echocardiography showed an abrupt interruption of the myocardial wall, in the apical portion of the interventricular septum, not communicating with the pericardial sac or right ventricular cavity suggesting the presence of an incomplete contained rupture of the myocardial wall at this location. She died in cardiogenic shock due to the extensive left ventricular damage. |
1,035 | Activation recovery time measurements in evaluation of global sequence and dispersion of ventricular repolarization. | Activation recovery time (ART), defined as the time from the earliest ventricular activation time to the end of T wave on unipolar electrograms, has been used as an index of myocardial repolarization time. However, it is unknown whether the ART can be used to estimate the global sequence and dispersion of ventricular repolarization as determined by the monophasic action potential (MAP) mapping technique.</AbstractText>Endocardial MAPs and unipolar electrograms were simultaneously recorded using the CARTO system from 34 +/- 12 left (n = 6) or right (n = 9) ventricular sites in 12 patients. End-of-repolarization (EOR) times from the MAPs and ARTs from the unipolar electrograms were calculated, based on which 15 sets of 3-dimensional maps of global EOR sequence and ART sequence were reconstructed. The ART sequence was consistent with the EOR sequence in 14 of 15 maps. In the 473 paired measurements obtained, the differences between the ART and the EOR time were 2 +/- 22 milliseconds (NS). A significant positive correlation between the ART and the EOR time was found in all the maps (r = 0.58 +/- 0.22). Agreement analyses showed that the differences between these 2 measurements were almost all within the range of mean difference +/- 2 SD for each individual map and for all the 473 recordings. The global dispersion of ART was 79 +/- 35 milliseconds, as compared with that of EOR time of 78 +/- 35 milliseconds (NS).</AbstractText>The ART from unipolar electrograms is a good estimate of EOR time measured from MAPs, suggesting the usefulness of the former in evaluation of global sequence and dispersion of ventricular repolarization.</AbstractText> |
1,036 | QT dispersion failed to estimate the global dispersion of ventricular repolarization measured using monophasic action potential mapping technique in swine and patients. | The aim of this study was to evaluate whether the QT dispersion measured from 12-lead electrocardiogram (ECG) can estimate the global dispersion of ventricular repolarization (DVR) measured using a monophasic action potential (MAP) mapping technique. Monophasic action potentials were recorded from 75 +/- 12 left ventricular sites in 10 pigs and from 48 +/- 16 left or right ventricular sites in 15 patients using the CARTO mapping system. The maximum DVRs in both end-of-repolarization and MAP duration among all the mapped sites were calculated and termed as global DVR for each measurement. QT intervals, QT peak and QT end , were measured from the 12-lead ECG, and QT dispersions; namely the differences between the maximum and the minimum of the QT peak and QT end were calculated. We found that QT dispersions were significantly smaller than (P < .05) and poorly correlated with the global DVRs both in pigs and patients. Bland-Altman agreement analysis demonstrated a marked variation of the differences and an obvious lack of agreement between the results obtained using the ECG and the MAP methods. In our patients, the global DVR increased markedly during ventricular tachycardia as compared with that during sinus rhythm (P < .05), whereas there was no significant difference in QT dispersion between these 2 subgroups. In conclusion, QT dispersion on the surface ECG could not estimate the global DVR measured using the MAP mapping technique. These findings are not consistent with some previously reported observations, suggesting the need for reappraisal of the electrophysiological implications of QT dispersion. |
1,037 | Factors associated with an increased chance of survival among patients suffering from an out-of-hospital cardiac arrest in a national perspective in Sweden. | To describe factors associated with an increased chance of survival among patients suffering from an out-of-hospital cardiac arrest in Sweden.</AbstractText>All patients suffering from an out-of-hospital cardiac arrest, which were not crew witnessed, in Sweden and in whom cardiopulmonary resuscitation (CPR) was attempted and who were registered in the Swedish Cardiac Arrest Registry. This registry covers about 85% of the Swedish population and has been running since 1990.</AbstractText>In all, 33,453 patients, 71% of whom had a cardiac etiology, were included in the survey. The following were independent predictors for an increased chance of survival in order of magnitude: (1) patients found in ventricular fibrillation (odds ratio [OR] 5.3, 95% confidence limits [CL] 4.2-6.8), (2) the interval between call for and arrival of the ambulance less than or equal to the median (OR 3.6, 95% CL 2.9-4.6), (3) cardiac arrest occurred outside the home (OR 2.2, 95% CL 1.9-2.7), (4) cardiac arrest was witnessed (OR 2.0, 95% CL 1.6-2.7), (5) bystanders performing CPR before the arrival of the ambulance (OR 2.0, 95% CL 1.7-2.4), and (6) age less than or equal to the median (OR 1.6, 95% CL 1.4-2.0). When none of these factors were present, survival to 1 m was 0.4%; when all factors were present, survival was 23.8%.</AbstractText>Among patients suffering from an out-of-hospital cardiac arrest, which were not crew witnessed, in Sweden and in whom CPR was attempted, 6 factors for an increased chance of survival could be defined. These include (1) initial rhythm, (2) delay to arrival of the rescue team, (3) place of arrest, (4) witnessed status, (5) bystander CPR, and (6) age.</AbstractText> |
1,038 | Role of permanent pacing to prevent atrial fibrillation: science advisory from the American Heart Association Council on Clinical Cardiology (Subcommittee on Electrocardiography and Arrhythmias) and the Quality of Care and Outcomes Research Interdisciplinary Working Group, in collaboration with the Heart Rhythm Society. | This advisory summarizes the current database on pacing modalities and algorithms used to prevent and terminate atrial fibrillation (AF). On the basis of the evidence indicating that ventricular pacing is associated with a higher incidence of AF in patients with sinus node dysfunction, a patient who has a history of AF and needs a pacemaker for bradycardia should receive a physiological pacemaker (dual chamber or atrial) rather than a single-chamber ventricular pacemaker. For patients who need a dual-chamber pacemaker, efforts should be made to program the device to minimize the amount of ventricular pacing when atrioventricular conduction is intact. Many pacemakers and implantable defibrillators have features designed to prevent AF and to terminate AF with rapid atrial pacing. The evidence to support their use is limited, although these algorithms appear to be safe and usually add little additional cost. For patients who have a bradycardia indication for pacing and also have AF, no consistent data from large randomized trials support the use of alternative single-site atrial pacing, multisite right atrial pacing, biatrial pacing, overdrive pacing, or antitachycardia atrial pacing. Even fewer data support the use of atrial pacing in the management of AF in patients without symptomatic bradycardia. At present, permanent pacing to prevent AF is not indicated; however, additional studies are ongoing, which will help to clarify the role of permanent pacing for AF. |
1,039 | [Myocardial ischemia and paroxysmal cardiac arrhythmia in different severity of bronchial asthma]. | The study was undertaken to define the prevalence and pattern of myocardial ischemia and cardiac arrhythmia in patients with persistent bronchial asthma (BA) in relation to its severity. Eighty-one patients with persistent BA, including 21 patients with mild BA, 39 with moderate BA, and 21 with severe BA, were examined. ECG and Holter 24-hour monitoring were performed. Myocardial ischemic episodes were detected in 33% of the patients with moderate BA and in 57% of the patients with severe BA. Silent and painful myocardial ischemia occurred at the equal rate in moderate BA and painful episodes predominated in severe BA. The incidence and degree of supraventricular and ventricular extrasystoles increased with the severity of BA. The paroxysms of ventricular tachycardia, atrial fibrillation and flutter appeared in the presence of BA concurrent with myocardial ischemia. |
1,040 | Cardiac wall motion abnormalities observed in a patient with transient hyperthyroidism. | A 74-year-old woman, with a history of hypertension and hyperlipidemia, was admitted to our hospital. She was found to have a sinus tachycardia with ST-segment elevations in leads II, III, (a)V(F), and V(3) through V(6) in electrocardiography, hypokinesis of the left ventricular apex by echocardiography, and normal findings on coronary angiography. Blood analysis revealed an increase in the creatine kinase MB fraction, a significant positive detection in troponin T, and transient elevations in the concentrations of free triiodothyronine, free thyroxine, thyroid globulin antibody, and thyroid peroxidase antibody. Defects in myocardial perfusion and fatty acid metabolism in the apical area were also demonstrated by myocardial scintigraphy. These data suggest that tako-tsubo syndrome or myocardial infarction may be induced in patients with mild and transient hyperthyroidism. |
1,041 | A case of the toxicity of pilsicainide hydrochloride with comparison of the serial serum pilsicainide levels and electrocardiographic findings. | We treated an 88-year-old man with aortic valvular stenosis/insufficiency and paroxysmal atrial fibrillation, who developed ventricular tachycardia due to pilsicainide toxicity. He was treated at the outpatient clinic of his local hospital, and was administered pilsicainide (100 mg/day) for atrial fibrillation. The electrocardiographic findings on admission to our hospital indicated wide QRS with frequent episodes of ventricular tachycardia. We diagnosed him as having pilsicainide toxicity because of a low cardiac output and renal dysfunction. His creatinine level was 2.4 mg/dL and the serum pilsicainide level was 2.42 microg/mL on admission. Fluid infusion and continuous hemodiafiltration were performed to achieve an early reduction in the serum pilsicainide level. His serum pilsicainide concentration was significantly decreased by these treatments, and the prolongation of the QTc and ventricular tachycardia improved in parallel to the decrease in the serum pilsicainide level. The changes in the serum pilsicainide level showed a significant positive correlation with the changes in the electrocardiographic findings (PQ, QRS, ST intervals, and QTc). Pilsicainide should be administered with great care to elderly patients, especially patients with cardiac dysfunction and renal dysfunction. Estimation of the serum level may be possible from the electrocardiographic findings if the pilsicainide toxicity occurs. |
1,042 | Brugada syndrome: report of the second consensus conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. | Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries. Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation. The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity. In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred. The report of the first consensus conference, published in 2002, focused on diagnostic criteria. The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data. |
1,043 | In vivo and in vitro antiarrhythmic effects of SSR149744C in animal models of atrial fibrillation and ventricular arrhythmias. | SSR149744C (2-butyl-3-{4-[3-(dibutylamino)propyl]benzoyl}-1-benzofuran-5-carboxylate isopropyl fumarate) is a new noniodinated benzofuran derivative structurally related to amiodarone and dronedarone that is currently undergoing clinical trials as an antiarrhythmic agent. As SSR149744C exhibits electrophysiological and hemodynamic properties of class I, II, III, and IV antiarrhythmic agents, the aim of this study was to evaluate its acute intravenous (IV) or oral (PO) antiarrhythmic activities in in vitro and in vivo animal models of atrial and ventricular arrhythmias. In vagally induced atrial fibrillation (AF) in anesthetized dogs, SSR149744C (3 and 10 mg/kg IV) terminated AF in all 7 dogs and prevented reinduction in 4 out of 7 dogs; effective refractory periods of right atrium were dose-dependently and frequency-independently lengthened. In low-K+ medium-induced AF models, SSR149744C (0.1 to 1 microM) prevented AF in isolated guinea pig hearts in a concentration-dependent manner. At the ventricular level, SSR149744C (0.1 to 10 mg/kg IV and 3 to 90 mg/kg PO) prevented reperfusion-induced arrhythmias in anesthetized rats with a dose-effect relationship, and, at doses of 30 to 90 mg/kg PO, it reduced early (0-24 hours) mortality following permanent left coronary artery ligature in conscious rats. The present results show that SSR149744C is an effective antiarrhythmic agent in atrial fibrillation and in ventricular arrhythmias. Like amiodarone and dronedarone, its efficiency in these animal models of arrhythmias is likely be related to its multifactorial mechanism of action. |
1,044 | Changes in demographic factors and mortality after out-of-hospital cardiac arrest in Sweden. | To describe changes between 1992 and 2003 in age, sex, factors at resuscitation and survival among patients suffering from out-of-hospital cardiac arrest in Sweden.</AbstractText>This was a prospective observational study including various ambulance organizations in Sweden. Patients suffering from out-of-hospital cardiac arrest between 1992 and 2003 included in the Swedish Cardiac Arrest Registry were followed for survival to 1 month.</AbstractText>In all 19 791 cases took part in the survey. There was a slight increase in mean age from 68 to 70 years (P = 0.025) and an increase of females from 29 to 32% (P = 0.0001). There was a change in witnessed status (P < 0.0001) with an increase in crew-witnessed cases and a decrease in non-witnessed cases. There was a decrease in cases of a cardiac etiology from 75 to 61% (P < 0.0001) and a decrease in the percentage found in ventricular fibrillation from 36 to 25% (P < 0.0001). When crew-witnessed cases were excluded the proportion receiving bystander cardiopulmonary resuscitation (CPR) increased from 30 to 42% (P < 0.0001). There was a slight increase in the overall proportion of patients hospitalized alive from 16 to 20% (P = 0.032). There was no significant change in the overall proportion of survivors at 1 month after cardiac arrest (4.5% in 1992 and 5.0% in 2003).</AbstractText>Among patients suffering from out-of-hospital cardiac arrest in Sweden some changes took place. The most important ones were a decrease in the proportion of patients found in ventricular fibrillation and an increase in the proportion of patients receiving bystander CPR. The proportion of patients admitted alive to hospital increased moderately, whereas the proportion of patients alive after 1 month remained unchanged.</AbstractText> |
1,045 | Tachycardia-induced cardiomyopathy: atrial fibrillation and congestive heart failure. | Tachycardia-induced cardiomyopathy occurs as a result of prolonged, excessive heart rates. Ventricular function may improve significantly upon control of the heart rate. We present a case of a patient with atrial fibrillation with rapid ventricular response who showed a dramatic improvement in left ventricular function following AV nodal ablation and insertion of a pacemaker. We also review the history and pathophysiology of tachycardia-induced cardiomyopathy. |
1,046 | Rate control vs. pulmonary vein isolation. | Atrial fibrillation (AF) is a frequent arrhythmia encountered in clinical practice. It can be asymptomatic in some patients but incapacitating in others. Regardless of symptoms, patients at increased risk of embolism need chronic anticoagulation. In patients with AF and a rapid ventricular response that cannot be controlled with drugs, interventional procedures are required. Radiofrequency catheter ablation of the atrioventricular junction with pacemaker implantation is an effective therapeutic approach that relieves the symptoms associated with a rapid and irregular rhythm. This approach can also improve left ventricular function in patients with tachycardia-induced cardiomyopathy. Due to the irreversible nature of this approach, it is more suitable for older patients and those with advanced left ventricular dysfunction. Many patients with a structurally normal heart have symptomatic paroxysmal AF refractory to antiarrhythmic agents. This form of AF is frequently initiated by premature atrial beats arising from the pulmonary veins. A catheter ablation technique is available to electrically isolate the pulmonary veins. This procedure can eliminate AF in many patients but can result in complications, including embolic events, pulmonary veins stenosis, and cardiac perforation. |
1,047 | Ablation therapy of supraventricular tachycardia in elderly persons. | Ablation of supraventricular tachycardia in elderly persons presents a challenging problem to electrophysiologists. Friable cardiac structures, prone to catheter perforation, comorbid cardiovascular disease, and the propensity to develop atrial fibrillation and thromboembolic complications, place these patients at high risk. Newer techniques for cardiac mapping and ablation, the establishment of precise ablation lines, and safer approaches to the ablation mechanism (particularly for atrial fibrillation) are presented in this review. In addition, a novel rapid ablation method to permanently cure atrial ventricular nodal re-entry tachycardia is demonstrated. |
1,048 | Role of electrophysiologic studies, signal-averaged electrocardiography, heart rate variability, T-wave alternans, and loop recorders for risk stratification of ventricular arrhythmias. | Ventricular tachycardia and fibrillation are major causes of morbidity and mortality after myocardial infarction. Frequently, sudden cardiac death is the first manifestation of such malignant rhythms. Optimal risk stratification strategies in this population are of utmost importance. In this review the authors discuss the background and clinical use of invasive tests, such as electrophysiologic study and implantable loop recorders, and noninvasive tests, such as signal-averaged electrocardiography, heart rate variability, and T-wave alternans. The utility, indications, and limitations of each test in clinical practice are discussed, especially for the purpose of postmyocardial infarction risk stratification in the elderly population. |
1,049 | [Defibrillators--end of sudden cardiac death?]. | The ventricular fibrillation is still the main cause of a sudden cardiac death, even though it was described 155 years ago in experiment (M. Hoffa 1849) and its therapy--defibrillation--has been known since 1947 (C. Beck). In Europe 2500 inhabitants suffer from cardiac arrest daily and 90% is caused by ventricular fibrillation. A key interval for an effective defibrillation seems to be 3-8 minutes from the begining of a cardiac arrest. Automated (automatized) external defibrillators (AED) have been used for last 15 years, especially in USA. However it is still unclear how many devices will be needed and where to place them. We don't know if they improve the prognosis of patients with out of hospital cardiac arrest during ventricular fibrillation. The individualisation of the risk of a sudden cardiac death has brought a new method to the clinical practise--implantation of cardioverter-defibrillator (ICD). Their efficacy in reduction of total mortality was verified first in the field of secondary prevention--in patients after cardiac arrest (AVID study) and than in the field of primary prevention--in patients with risk markers (left ventricle dysfunction, non sustained ventricular tachycardias) but without sustained malignant arrhythmia in anamnesis (MUSTT, CIDS, MADIT I, MADIT II). Defibrillators (external, automated, implantable) obviously don't mean the end of the sudden cardiac death. The incidence of sudden cardiac death can be reduced significantly with prevention (nutrition, prevention of CAD) and one attention should be drawn to the fact even in the future. |
1,050 | Noninvasive sudden death risk stratification by ambulatory ECG-based T-wave alternans analysis: evidence and methodological guidelines. | Extensive experimental and clinical evidence supports the utility of T-wave alternans (TWA) as a marker of risk for ventricular fibrillation. This entity appears to reflect the fundamental arrhythmogenic property of enhanced dispersion of repolarization. This relationship probably accounts for its relative ubiquity in patients with diverse types of cardiac disease, as has been recognized with the development of analytical tools. A basic premise of this review is that ambulatory ECG monitoring of TWA as patients experience the provocative stimuli of daily activities can expose latent electrical instability in individuals at heightened risk for arrhythmias. We will discuss the literature that supports this concept and summarize the current state of knowledge regarding the use of routine ambulatory ECGs to evaluate TWA for arrhythmia risk stratification. The dynamic, nonspectral modified moving average analysis method for assessing TWA, which is compatible with ambulatory ECG monitoring, is described along with methodological guidelines for its implementation. Finally, the rationale for combined monitoring of autonomic markers along with TWA will be presented. |
1,051 | Heart rate turbulence: a new predictor for risk of sudden cardiac death. | Initial acceleration and a subsequent deceleration of sinus rhythm following a ventricular ectopic beat with a compensatory pause has been termed heart rate turbulence (HRT). The changes in sinus rhythm are thought to be mediated by a baroreflex response to the lower stroke volume of the ectopic beat. HRT is vagally mediated and abolished by atropine, whereas beta-blockers have no effect. HRT has been shown to be an independent and powerful predictor of mortality after myocardial infarction. In patients on beta-blockers, it scores better than left ventricular ejection fraction (LVEF) in its predictive value. Two common measures of HRT are turbulence onset and turbulence slope. When both these measures are abnormal, it is as powerful a predictor of mortality as LVEF. HRT correlates with other indices of cardiac autonomic functions like baroreflex sensitivity and heart rate variability. A composite autonomic index including all these three has been shown to be a powerful predictor of mortality. In patients undergoing direct percutaneous intervention for myocardial infarction, HRT improves in those attaining successful reperfusion. Abnormal values for HRT have been noted in patients with dilated cardiomyopathy and Chagas disease. Diabetic and elderly individuals are more likely to have blunted HRT. HRT cannot be measured in patients lacking ventricular ectopic beats and in patients presenting with atrial fibrillation. |
1,052 | Exercise-induced ventricular arrhythmias and cardiovascular death. | Exercise-induced ventricular arrhythmias (EIVA) are frequently observed during exercise testing. However, the clinical guidelines do not specify their significance and so we examined this issue in our population.</AbstractText>A retrospective analysis of prospectively collected data was performed on 5754 consecutive male veterans referred for exercise testing at two university-affiliated Veterans Affairs Medical Centers. Exercise test responses were recorded and cardiovascular mortality was assessed after a mean follow-up of 6 +/- 4 years. EIVA were defined as frequent premature ventricular complexes (PVCs) constituting more than 10% of all ventricular depolarizations during any 30-second ECG recording, or a run of three or more consecutive PVCs during the exercise test or recovery.</AbstractText>EIVA occurred in 426 patients (7.4%). There were 550 (10.6%) cardiovascular deaths during follow-up. Seventy two (17%) patients with EIVA died of cardiovascular causes, whereas 478 (9.0%) of patients without EIVA died of cardiovascular causes (P < 0.001). Patients with EIVA had a higher prevalence of cardiovascular disease, resting PVCs, resting ST depression, and ischemia during exercise than patients without EIVA. In a Cox hazards model adjusted for age, cardiovascular disease, exercise-induced ischemia, ECG abnormalities, exercise capacity and risk factors, EIVA was significantly associated with time to cardiovascular death. The combination of both resting PVCs and EIVA was associated with the highest hazard ratio.</AbstractText>EIVA are independent predictors of cardiovascular mortality after adjusting for other clinical and exercise test variables; combination with resting PVCs carries the highest risk.</AbstractText> |
1,053 | Effect of reperfusion on P-wave duration and P-wave dispersion in acute myocardial infarction: primary angioplasty versus thrombolytic therapy. | Atrial fibrillation (AF) is a common arrhythmia occurring in about 10-20% of patients with acute myocardial infarction (AMI). P-wave dispersion (PWd) and P-wave duration (PWD) have been used to evaluate the discontinuous propagation of sinus impulse and the prolongation of atrial conduction time, respectively. This study was conducted to compare the effects of reperfusion either by thrombolytic therapy or primary angioplasty on P-wave duration and dispersion in patients with acute anterior wall myocardial infarction.</AbstractText>We have evaluated 72 consecutive patients retrospectively (24 women, 48 men; aged 58 +/- 12 years) experiencing acute anterior wall myocardial infarction (AMI) for the first time. Patients were grouped according to the reperfusion therapy received (primary angioplasty (PTCA) versus thrombolytic therapy). Left atrial diameter and left ventricular ejection fraction (LVEF) were determined by echocardiography in all patients. Electrocardiography was recorded from all patients on admission and every day during hospitalization. Maximum (P max) and minimum (P min) P-wave durations and P-wave dispersions were calculated before and after the treatment.</AbstractText>There were not any significant differences between the groups regarding age, gender, left ventricular ejection fraction, left atrial diameter and volume, cardiovascular risk factors, and duration from symptom onset to treatment. P-wave dispersions and P-wave durations were significantly decreased after PTCA [Mean P max was 113 +/- 11 ms before and 95 +/- 17 ms after the treatment (P = 0.007)]. Mean PWd was 46 +/- 12 ms before and 29 +/- 10 ms after the treatment (P = 0.001). Also, P max and PWd were significantly lower in PTCA group (for P max 97 +/- 22 ms vs 114 +/- 16 ms and for PWd 31 +/- 13 ms vs 55 +/- 5 ms, respectively).</AbstractText>Primary angioplasty reduces the incidence of AF by decreasing P max and P-wave dispersion.</AbstractText> |
1,054 | Assessment of left atrial volumes in sinus rhythm and atrial fibrillation using the biplane area-length method and cardiovascular magnetic resonance imaging with TrueFISP. | To determine whether the biplane area-length method can be used for the evaluation of left atrial volumes and ejection fraction with cardiovascular magnetic resonance imaging (CMR) by TrueFISP in normal subjects and patients with atrial fibrillation.</AbstractText>Atrial fibrillation is the most common arrhythmia in elderly patients. Left atrial size and volumes play an important role in predicting short and long-term success after cardioversion.</AbstractText>Fifteen healthy subjects (mean age 65.6+/-6.4 years) and 18 patients (mean age 67.2+/-8.8 years) with atrial fibrillation were examined by CMR (Magnetom, Siemens, Erlangen, Germany). Images were acquired by TrueFISP using the horizontal and vertical long-axis plane to measure left atrial end-diastolic and end-systolic areas and longitudinal dimensions. Volumes were determined with commercially available software. Left atrial end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and ejection fraction (EF) were determined by the biplane area-length method and compared to findings obtained by the standard short-axis method. Images were acquired and analyzed a second time in the patients with atrial fibrillation.</AbstractText>There was no difference in age between men and women (p=0.147) and healthy subjects and patients (p=0.128) included in the study. EDV and ESV were significantly higher and SV and EF significantly lower in patients with atrial fibrillation than in healthy subjects (p < or = 0.009), regardless of the method used. The values obtained for EDV and ESV by the biplane area-length method were significantly higher in both healthy subjects (p<0.001) and patients with atrial fibrillation (p<0.001) than those obtained by the standard short-axis approach, whereas SV (p> or = 0.057) and EF (p> or = 0.118) did not differ significantly. In the second investigation in patients with atrial fibrillation, ESV, SV, and EF did not differ significantly between the two methods (p> or =0.481). Assessment of interobserver variability revealed good agreement in the findings of the two observers, both in normal sinus rhythm and atrial fibrillation (overall variability 0.8+/-6.5%).</AbstractText>The biplane area-length method can be used in CMR images obtained by TrueFISP to assess left atrial volumes and ejection fraction in normal subjects and patients with varying cardiac cycle length, as in atrial fibrillation.</AbstractText> |
1,055 | Out-of-hospital cardiac arrest locations in a rural community: where should we place AEDs? | Early defibrillation improves survival for patients suffering cardiac arrest from ventricular fibrillation (VF) or ventricular tachycardia (VT). Automated external defibrillators (AEDs) should be placed in locations in which there is a high incidence of out-of-hospital cardiac arrest (OOHCA). The study objective was to identify high-risk, rural locations that might benefit from AED placement. A retrospective review of OOHCA in a rural community during the past 5.5 years was conducted. The OOHCAs that occurred in non-residential areas were categorized based on location. Nine hundred, forty OOHCAs occurred during the study period of which 265 (28.2%) happened in non-residential areas. Of these, 127 (47.9%) occurred in healthcare-related locations, including 104 (39.2%) in extended care facilities. No location used in this study had more than two OOHCAs. Most (52.1%) non-residential OOHCAs occurred as isolated events in 146 different locations. Almost half of the OOHCAs that occurred in non-residential areas took place in healthcare-related facilities suggesting that patients at these locations may benefit from AED placement. First responders with AEDs are likely to have the greatest impact in a rural community. |
1,056 | ["Highlights" in emergency medicine -- severe head trauma, polytrauma and cardiac arrest]. | According to scientific publications focusing on emergency medicine and published in international journals in the past few months, new and clinically important results can be identified. In patients with severe head trauma (SHT), application of hypertonic solutions is possible; long term outcome, however, is not improved by this measure. Prehospital capnometry is important, because otherwise up to 40 % of all mechanically ventilated patients are hypoventilated. In a study in 200 patients with prehospital cardiac arrest and ventricular fibrillation as initial cardiac rhythm, subgroup analysis (alarm-response time > 5 min) showed an increase in survival rate (14 % vs. 2 %), if defibrillation was proceeded by 3 min of conventional cardiopulmonary resuscitation (CPR) for reperfusion. If ACD ("active compression decompression")-CPR is combined with a specific ventilatory valve ("inspiratory impedance threshold device", ITD) which does not allow passive inspiration, survival rate after cardiac arrest is increased for up to 24 h. Such a device facilitates an increase in venous return to the heart during decompression of the thorax. High-dose adrenalin for intrahospital CPR in children is not associated with better survival but with worse outcome. Comparison of an emergency medical service (EMS) system from U.K. with paramedics and a physician-staffed German EMS system demonstrated that survival rate following prehospital cardiac arrest is markedly increased with doctors on board. The European multicentre trial comparing vasopressin vs. adrenalin as first vasopressor during CPR in 1219 patients did not reveal any differences between both groups. In subgroup analyses of patients with asystoly and prolonged CPR, vasopressin was superior without being associated with a benefit on neurological outcome. Further subgroup analyses revealed beneficial effects of amiodarone and thrombolysis during CPR. Thrombolysis during CPR apears to be associated with an increased rate of haemodynamic stabilisation without increased risk of bleeding complications. In a very clear advisory statement, the "International Liaison Committee on Resuscitation" (ILCOR) has recommended mild therapeutic hypothermia (i. e., cooling of cardiac arrest victims to 32 - 34 degrees C central body temperature for 12 - 24 h following cardiac arrest of cardiac etiology) not only for unconciuous patients with ventricular fibrillation as initial prehospital rhythm, but also for all other adult patients (other rhythms, intrahospital CPR) following cardiac arrest. In randomised controlled clinical trials, this therapy has markedly improved survival rate and neurological outcome. Such therapeutic cooling can be initiated nearly everywhere and with simple methods - like the infusion of ice-cold cristalloid solutions. |
1,057 | Effects of cyclic GMP and its protein kinase on the contraction of ventricular myocytes from hearts after cardiopulmonary arrest. | Hearts undergoing cardiopulmonary arrest and resuscitation have depressed function and may have changes in signal transduction. We hypothesized that the cyclic GMP (cGMP) signaling pathway would be altered in the post-resuscitation heart. This was studied in ventricular myocytes from 7 anesthetized open-chest rabbits. Cardiopulmonary arrest was achieved for 10 min through ventricular fibrillation and respirator shutdown. After cardiopulmonary arrest, respiration was resumed, the heart was defibrillated, and the heart recovered for 15 min. Seven additional rabbits served as controls. Myocyte function was measured via a video edge detector. Myocytes were treated with 8-bromo-cGMP (10(-5)-10(-6) mol/L) followed by KT5823 (10(-6) mol/L, cGMP protein kinase inhibitor). The baseline percent shortening was significantly depressed in the cardiac arrest myocytes compared with control (3.3 +/- 0.1 vs. 5.5 +/- 0.3%). Treatment with 8-Br-cGMP similarly and dose-dependently reduced cell contraction in both cardiac arrest (-24%) and control (-25%) myocytes. The negative effect of 8-Br-cGMP was partially reversed by KT5823 in control myocytes, but not in the arrest group, indicating reduced involvement of cGMP protein kinase. Multiple proteins were specifically phosphorylated when cGMP was present, but the degree of phosphorylation was significantly less in myocytes after cardiac arrest. The data suggested that the basal contraction was reduced, but the functional response to 8-Br-cGMP was preserved in myocytes from cardiopulmonary arrested hearts. The results also indicated that the action of cGMP appeared to be mainly through non-cGMP protein kinase pathways in the post-resuscitation heart. |
1,058 | Hepatotoxicity during rapid intravenous loading with amiodarone: Description of three cases and review of the literature. | Atrial fibrillation is the most common arrhythmia after cardiac surgery. Amiodarone can effectively prevent and control postoperative atrial and ventricular fibrillation. Acute hepatic damage after intravenous amiodarone, which can be fatal, is not well recognized. We describe three cases of acute hepatocellular injury after intravenous amiodarone administration in critically ill patients. Another 25 published cases and six cases reported to the Swiss Pharmacovigilance Center (Swissmedic) are discussed.</AbstractText>This study consisted of a series of three case reports and review of the literature.</AbstractText>: This study was conducted at an operative critical care unit at the University Hospital Basel, Switzerland.</AbstractText>Three hemodynamically compromised patients after open heart surgery developed significant increases of transaminases (up to more than 100-fold of the upper limit of normal) shortly after the introduction of intravenous amiodarone. INTERVENTIONS AND MEASUREMENT: Cessation of intravenous amiodarone and of other potentially hepatotoxic drugs.</AbstractText>Liver parameters significantly improved or returned to normal in all three patients, even after start of oral amiodarone in two patients.</AbstractText>Amiodarone is a highly effective antiarrhythmic agent for the treatment and prevention of atrial and ventricular arrhythmias. Acute liver damage after intravenous amiodarone, possibly induced by the solubilizer polysorbate 80, is rare but potentially harmful. Amiodarone loading should therefore be adapted to the necessity of an immediate effect of the drug, and liver function should be monitored closely in critically ill patients. Oral maintenance therapy with amiodarone is possible, even in patients who developed liver disease during intravenous loading.</AbstractText> |
1,059 | Vasopressin for cardiac arrest: a systematic review and meta-analysis. | The current guidelines for cardiopulmonary resuscitation recommend vasopressin as an alternative to epinephrine for the treatment of adult shock-refractory ventricular fibrillation. The objective of this study was to determine the effectiveness of vasopressin in the treatment of cardiac arrest.</AbstractText>We performed a systematic review and meta-analysis of 1519 patients with cardiac arrest from 5 randomized controlled trials that compared vasopressin and epinephrine. Two reviewers conducted a systematic search of electronic databases, complemented by hand searches, to identify randomized trials. Reviewers evaluated the quality of the trials, extracted data, and derived pooled estimates using a random-effects model.</AbstractText>There were no statistically significant differences between the vasopressin and epinephrine groups in failure of return of spontaneous circulation (risk ratio [RR], 0.81; 95% confidence interval [CI], 0.58-1.12), death before hospital admission (RR, 0.72; 95% CI, 0.38-1.39), death within 24 hours (RR, 0.74; 95% CI, 0.38-1.43), death before hospital discharge (RR, 0.96; 95% CI, 0.87-1.05), or combination of number of deaths and neurologically impaired survivors (RR, 1.00; 95% CI, 0.94-1.07). Subgroup analysis based on initial cardiac rhythm showed no statistically significant difference in the rate of death before hospital discharge between the vasopressin and epinephrine groups in any of the 3 subgroups: ventricular fibrillation or ventricular tachycardia (RR, 0.97; 95% CI, 0.79-1.19), pulseless electrical activity (RR, 1.02; 95% CI, 0.95-1.10), or asystole (RR, 0.97; 95% CI, 0.94-1.00).</AbstractText>There is no clear advantage of vasopressin over epinephrine in the treatment of cardiac arrest. Guidelines for Advanced Cardiac Life Support should not recommend vasopressin in resuscitation protocols until more solid human data on its superiority are available.</AbstractText> |
1,060 | Long-term prognosis of individuals with right precordial ST-segment-elevation Brugada syndrome. | Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of ST-segment elevation in the right precordial leads and an increased risk of sudden cardiac death as a result of ventricular fibrillation. Controversy exists with regard to risk stratification and therapeutic management, particularly in asymptomatic individuals.</AbstractText>A total of 212 individuals (mean age, 45+/-6 years) with a type 1 Brugada ECG pattern were studied. Of these, 123 (58%) were asymptomatic, 65 (31%) had > or =1 syncope of unknown origin, and 24 (11%) had to be resuscitated because of ventricular fibrillation. In 125 individuals (59%), a spontaneous type 1 ECG was recorded. In the remaining, drug challenge with a class I antiarrhythmic agent unmasked a Brugada ECG. The mean ST elevation was 2.3+/-1.2 mm in symptomatic patients and 1.9+/-1.5 mm in asymptomatic individuals (P=0.04). During a mean follow-up of 40+/-50 months, 4 of the 24 patients (17%) with aborted sudden cardiac death and 4 of 65 (6%) with a prior syncope had a recurrent arrhythmic event, whereas only 1 of 123 asymptomatic individuals (0.8%) had a first arrhythmic event. Four of 9 patients with arrhythmic events during follow-up were not inducible during programmed electrical stimulation. A previous history of aborted sudden death or syncope and the presence of a spontaneous type 1 ECG were predictors of adverse outcome.</AbstractText>The present study reports data on a large population of individuals with a type 1 Brugada ECG pattern with the longest follow-up reported so far. A very low incidence of severe arrhythmic events, particularly in asymptomatic individuals, was found during follow-up. In the presence of very few arrhythmic events on follow-up, programmed electrical stimulation showed very little accuracy in predicting outcome.</AbstractText> |
1,061 | Targeted modification of atrial electrophysiology by homogeneous transmural atrial gene transfer. | Safe and effective myocardial gene transfer remains elusive. Heterogeneous ventricular gene delivery has been achieved in small mammals but generally with methods not readily transferable to the clinic. Atrium-specific gene transfer has not yet been reported. We hypothesized that homogeneous atrial gene transfer could be achieved by direct application of adenoviral vectors to the epicardial surface, use of poloxamer gel to increase virus contact time, and mild trypsinization to increase virus penetration.</AbstractText>We "painted" recombinant adenovirus encoding the reporter gene Escherichia coli beta-galactosidase directly onto porcine atria. Investigational variables included poloxamer use, trypsin concentration, and safety. Using the painting method, we modified the atrial phenotype with an adenovirus expressing HERG-G628S, a long-QT-syndrome mutant. Our results showed that application of virus with poloxamer alone resulted in diffuse epicardial gene transfer with negligible penetration into the myocardium. Dilute trypsin concentrations allowed complete transmural gene transfer. After trypsin exposure, echocardiographic left atrial diameter did not change. Left atrial function decreased on postoperative day 3 but returned to baseline by day 7. Tissue tensile strength was affected only in the 1% trypsin group. HERG-G628S gene transfer prolonged atrial action potential duration and refractory period without affecting ventricular electrophysiology.</AbstractText>We show complete transmural atrial gene transfer by this novel painting method. Adaptation of the method could allow application to other tissue targets. Use with functional proteins in the atria could cure or even prevent diseases such as atrial fibrillation or sinus node dysfunction.</AbstractText> |
1,062 | Comparison of the effects of metoclopramide and domperidone on HERG channels. | Torsades de pointes (TdP) is a potentially fatal form of ventricular arrhythmia that occurs under conditions where cardiac repolarization is delayed (as indicated by prolonged QT intervals from electrocardiographic recordings). A likely mechanism for QT prolongation and TdP is blockade of the rapid component of the cardiac delayed rectifier K(+) current (I(Kr)), which is encoded by HERG (human ether-a-go-go-related gene). The gastroprokinetic agent cisapride is a potent blocker of HERG currents and serious cardiac arrhythmias and deaths from TdP and ventricular fibrillation have been reported in patients taking cisapride. The aim of the present study was to compare the effects of the gastroprokinetic agents domperidone and metoclopramide on HERG channels transiently expressed in human embryonic kidney (HEK 293) cells using the whole-cell configuration of the patch-clamp technique. Both domperidone and metoclopramide concentration-dependently blocked HERG currents, and the following values were calculated for IC(50) (the concentrations causing half-maximal inhibition) and n (the Hill coefficient): 57.0 nmol/l and 0.99 for domperidone, 5.4 micromol/l and 0.95 for metoclopramide. The observation that the extent of block of HERG currents by domperidone increased at more positive membrane potentials whereas block of HERG currents by metoclopramide displayed a smaller degree of voltage dependency seems to indicate that domperidone and metoclopramide have distinct binding sites on HERG channels. In conclusion, the potency for block of HERG currents is about 100-fold lower for metoclopramide when compared to domperidone. |
1,063 | Prevalence of diastolic dysfunction as a possible cause of dyspnea in the elderly. | Symptoms in patients with heart failure and preserved left ventricular ejection fraction may be caused by isolated diastolic dysfunction. The purpose of this study was to assess the prevalence of diastolic dysfunction as a potential cause of dyspnea in a sample of elderly subjects, as well as of isolated diastolic dysfunction as a potential cause of dyspnea in a subgroup with a preserved left ventricular ejection fraction and normal lung function.</AbstractText>A total of 152 subjects with dyspnea underwent echocardiography, electrocardiography, and lung function testing. Subjects with normal lung function test results (n = 60) underwent cardiac magnetic resonance imaging, chest radiography, bicycle exercise tests, and blood tests. Left ventricular diastolic function was assessed by a variety of echocardiographic/Doppler techniques.</AbstractText>Of 129 subjects with dyspnea, 81 (63%) had signs of lung disease or 'obvious' cardiac disease. In the remaining 48 subjects, 32 (67%) had a potential cardiac/noncardiac cause of dyspnea. In all subjects with dyspnea, 1% to 11% had diastolic dysfunction, and in the 48 remaining subjects, 0% to 10% had isolated diastolic dysfunction, depending on the definition used.</AbstractText>The frequency of diastolic dysfunction was low in the sample of elderly subjects with dyspnea as well as in the subgroup of persons with no signs of lung disease, left ventricular systolic dysfunction, atrial fibrillation, or valvular heart disease. Diastolic dysfunction was infrequent as a possible cause of dyspnea, and coexisting potential causes of dyspnea were often present.</AbstractText> |
1,064 | [Predictive value of coagulative molecular markers for thromboembolism in patients with nonvalvular atrial fibrillation: prospective five-year follow-up study]. | Nonvalvular atrial fibrillation is a known risk factor for thromboembolism. This study investigated the use of coagulation markers to predict thromboembolism in nonvalvular atrial fibrillation patients.</AbstractText>One hundred thirty nonvalvular atrial fibrillation patients (104 males, 26 females, mean age 63.7 +/- 10.7 years) treated at the Sendai Cardiovascular Center from April 1996 to August 1997 were enrolled in this study. Coagulation markers such as prothrombin fragment 1 + 2, thrombin-antithrombin III complex and D-dimer were measured, and the patients were followed up prospectively to October 2001.</AbstractText>One hundred and twenty-six patents (100 males, 26 females, chase rate 96.9%) were included in this investigation based on the medical chart and telephone interview. During five-year follow-up, 16 patients had thromboembolism accidents (3.25%/year) and two were suspected to die of thromboembolism. Three patients died of malignant disease, four of heart disease, and five of other diseases. Eight (25.8%) of the 31 patients with high levels of thrombin-antithrombin III complex and 6 (33.3%) of 18 patients with high levels of D-dimer suffered thromboembolism accidents. High thrombin-antithrombin III complex and D-dimer were statistically positive predictive markers for thromboembolism in patients with nonvalvular atrial fibrillation (p < 0.05).</AbstractText>Coagulation markers such as thrombin-antithrombin III complex and D-dimer can predict thromboembolism accidents in nonvalvular atrial fibrillation patients.</AbstractText> |
1,065 | [Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone]. | Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone. The cardiovascular symptoms of thyrotoxicosis were described more than two hundred years ago and remained the basis of diagnosis in modern medicine. Myocardium, peripheral circulation and sympathetic nerve system, all affecting cardiovascular hemodynamics, are influenced by thyroid hormones in many ways. Sub-clinical hyperthyroidism is characterized by suppressed thyroid stimulating hormone and normal free triiodothyronine and free thyroxine levels. Cardiovascular symptoms: elevation of heart rate, myocardial contractility, stroke volume, myocardial oxygen consumption, systolic blood pressure and reduction in systemic vascular resistance and diastolic blood pressure can be often seen even in case of subclinical hyperthyroidism. Thyrotoxicosis exacerbates the symptoms of a preexisting heart disease, but it can also cause complaints in case of a structurally normal heart. The most common cardiac complications are arrhythmias (mainly atrial fibrillation), heart failure and hypertension. Amiodarone is used for the treatment and prevention of several arrhythmias. It is safely applicable even in case of left ventricular dysfunction. The more common application is limited by its side effects that can develop even at low doses and may involve several organs (thyroid gland, lungs, liver, heart, nerve system among others). The complex effect of amiodarone on thyroid function ranges from mild abnormalities of thyroid function tests to overt thyrotoxicosis or hypothyroidism. |
1,066 | Doppler tissue analysis of atrial electromechanical coupling in paroxysmal atrial fibrillation. | The aim of this study was to: (1) evaluate atrial electromechanical coupling using M-mode Doppler tissue; and (2) test its clinical impact for detecting atrial abnormalities in paroxysmal atrial fibrillation (AF). Using Doppler tissue, the time intervals from the onset of P wave until the backward motions of the right and left atrioventricular rings in the apical 4-chamber view corresponding to the atrial contractions were measured. In paroxysmal AF group, these intervals were significantly longer than in the control group. Using the criteria that an abnormal time interval from the onset of P wave until the backward motion of the left atrioventricular ring is longer than 112 milliseconds, the sensitivity, the specificity, and the positive predictive values for paroxysmal AF are 73%, 93%, and 93%, respectively. This parameter is affected in patients with paroxysmal AF and should be useful for detecting atrial impairment related to paroxysmal AF. |
1,067 | Noninvasive prediction of complications with anteroseptal acute myocardial infarction by left ventricular Tei index. | Tei index has been proposed as a noninvasive and simple index that enables the evaluation of global left ventricular (LV) function and prediction of patient prognosis. However, its use to predict complications with acute myocardial infarction (AMI) is not fully investigated. Therefore, the purpose of this study was to investigate whether or not LV Tei index allows noninvasive prediction of complications with AMI.</AbstractText>In all, 80 consecutive patients with anteroseptal AMI were enrolled. LV Tei index was measured at the time of admission as (a - b)/ b , where a is the interval between cessation and onset of mitral filling flow and interval b is the aortic flow ejection time. Subsequent complications including cardiac death, shock, congestive heart failure, ventricular tachycardia/fibrillation, paroxysmal atrial fibrillation/flutter, advanced atrioventricular block requiring pacing, pericardial effusion, and LV aneurysm during the 30 days after the onset of AMI were prospectively evaluated and compared with the initial Tei index at admission.</AbstractText>Complications developed in 31 of 80 (39%) patients with AMI. The Tei index was significantly increased for patients with complications compared with those without them (0.69 +/- 0.16 vs 0.50 +/- 0.11, P < .0001). When Tei index > or = 0.59 was used for the criteria, the sensitivity, specificity, and overall accuracy to predict subsequent complications were 77%, 86%, and 85%, respectively.</AbstractText>In patients with anteroseptal AMI, LV Tei index at arrival to the hospital in the acute phase allows noninvasive prediction of subsequent complications.</AbstractText> |
1,068 | Anti-HERG activity and the risk of drug-induced arrhythmias and sudden death. | Drug-induced QTc-prolongation, resulting from inhibition of HERG potassium channels may lead to serious ventricular arrhythmias and sudden death. We studied the quantitative anti-HERG activity of pro-arrhythmic drugs as a risk factor for this outcome in day-to-day practice.</AbstractText>All 284,426 case reports of suspected adverse drug reactions of drugs with known anti-HERG activity received by the International Drug Monitoring Program of the World Health Organization (WHO-UMC) up to the first quarter of 2003, were used to calculate reporting odds ratios (RORs). Cases were defined as reports of cardiac arrest, sudden death, torsade de pointes, ventricular fibrillation, and ventricular tachycardia (n = 5591), and compared with non-cases regarding the anti-HERG activity, defined as the effective therapeutic plasma concentration (ETCPunbound) divided by the HERG IC50 value, of suspected drugs. We identified a significant association of 1.93 (95% CI: 1.89-1.98) between the anti-HERG activity of drugs, measured as log10 (ETCPunbound/IC50), and reporting of serious ventricular arrhythmias and sudden death to the WHO-UMC database.</AbstractText>Anti-HERG activity is associated with the risk of reports of serious ventricular arrhythmias and sudden death in the WHO-UMC database. These findings are in support of the value of pre-clinical HERG testing to predict pro-arrhythmic effects of medicines.</AbstractText> |
1,069 | Predictors of mortality in patients with acute myocardial infarction and cardiogenic shock. | Although cardiogenic shock (CS) is the leading cause of death for acute myocardial infarction (AMI) patients, reliable predictive factors in the acute stage, such as cardiovascular peptides, have not yet been identified.</AbstractText>In 42 consecutive AMI patients with CS on admission, successfully treated by primary percutaneous coronary intervention (PCI) within 12 h of onset, related factors including brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), renin, aldosterone, catecholamines, and adrenomedullin, were investigated 24 h from onset, as well as the 1-year mortality rates. During the 12-month follow-up period, 15 patients died from cardiovascular causes (group D). There were no significant differences in patient characteristics, angiographic findings, and left ventricular systolic function between group D subjects and the survivors (group S: n=27). Multivariate analysis identified high levels of adrenomedullin as an independent predictor of 1-year mortality (risk ratio: 6.42, 95% confidence interval, 1.49-43.31, p<0.05).</AbstractText>The acute-phase plasma concentration of adrenomedullin may be a reliable predictor of mortality in patients with AMI complicated by CS and successfully treated by direct PCI, as may be BNP concentration, peak-creatine kinase value, and ventricular fibrillation.</AbstractText> |
1,070 | Termination of resuscitative efforts for out-of-hospital cardiac arrests. | To determine the rate of termination of resuscitative efforts for out-of-hospital cardiac arrest patients and whether variability exists among different base hospitals providing online medical control (OLMC).</AbstractText>This was an observational one-year study that included all adult patients in the city of Los Angeles with nontraumatic, out-of-hospital cardiac arrests with attempted resuscitative efforts by paramedics. OLMC was provided by 13 base hospitals. The main outcome measure was the incidence of termination of resuscitative efforts on scene as directed by OLMC.</AbstractText>Of 1,700 patients, 151 (9%) had resuscitative efforts terminated on scene via direction by OLMC. Patients pronounced on scene were statistically more likely to be older, be found in an extended care facility, have an unwitnessed arrest, and present in asystole. Two base hospitals were more likely to terminate resuscitative efforts via OLMC than all others. Incidence at base hospital A was 37% (odds ratio, 18.6; 95% confidence interval = 11.7 to 30.0; p < 0.0001); incidence at base hospital B was 14% (odds ratio, 3.3; 95% confidence interval = 1.9 to 5.5; p < 0.0001), and incidence at all other base hospitals was 5%. Cardiac arrest patients handled by base hospital A were more likely to be found in ventricular fibrillation; those patients handled by base hospital B had shorter emergency medical services response times and were more likely to be found in an extended care facility. All other characteristics of cardiac arrest patients were not significantly different among the base hospitals.</AbstractText>There is significant variability in Los Angeles, depending on the particular base hospital that provides OLMC, in pronouncement of death and termination of resuscitative efforts for medical cardiac arrest in the field. Given potential ethical, logistical, and economic concerns, efforts to assure consistency in the practice of discontinuing resuscitative efforts in the field is warranted.</AbstractText> |
1,071 | Potential impact of a targeted cardiopulmonary resuscitation program for older adults on survival from private-residence cardiac arrest. | Traditional cardiopulmonary resuscitation (CPR) training programs do not target older adults who are most likely to witness private-residence cardiac arrests and do not reliably result in a bystander who is likely to perform CPR in the event of an arrest. This study was performed to compare targeted CPR training programs for older adults (older than 50 years) that 1) increase numbers of CPR-trained bystanders of private-residence cardiac arrest or 2) increase the percentage of trained bystanders of private-residence cardiac arrest who perform CPR. A simultaneous outcome was to estimate the minimal significant survival benefit associated with each of the training programs.</AbstractText>A probabilistic simulation model was developed in Fortran95 that incorporated key out-of-hospital cardiac arrest elements, including witnessed arrests, CPR-trained witness, CPR provision, and impact of CPR on ventricular fibrillation. Input data were derived from published or publicly available data, including a large prospective cohort study of outcomes in Oakland County, MI. Monte Carlo simulation (n = 10,000) and sensitivity analyses (n = 40) were used to assess median and the empiric 95% confidence intervals [CIs] for incremental survival with either intervention.</AbstractText>The baseline model, calibrated to the characteristics of the input-data community, established that, for private-residence cardiac arrests, 40.8% of cardiac arrest bystanders were trained in CPR; however, only 25.7% performed CPR. This yielded 4.81% survival (95% CI = 4.72 to 4.89). Modeling the impact on the baseline training level with increased CPR performance among trainees indicated that 75% of private-residence trained bystanders would need to perform CPR in order to reach a minimally significant improvement in survival (5.02%; 95% CI = 4.94 to 5.15). Similarly, targeted CPR training that would result in a significant survival benefit (to 5.01%; 95% CI = 4.93 to 5.09) would require that 70.8% of bystanders be trained.</AbstractText>CPR training programs that focus on yielding 75% of trainees who perform CPR in the event of witnessing an arrest would have equivalent results to mass CPR training programs that result in 70% of bystanders being trained in CPR. However, the minimal survival benefit associated with these programs (around 0.2%) may prove either method costly with minimal effect.</AbstractText> |
1,072 | Cardiac rate normalization in chronic atrial fibrillation: comparison of long-term efficacy of treatment with amiodarone versus AV node ablation and permanent His-bundle pacing. | Chronic atrial fibrillation (AF) is a common arrhythmia with significant morbidity and mortality. AF has been the subject of considerable attention and intensive clinical research in recent years. Current opinion on the management of AF favors the restoration and maintenance of normal ventricular rhythm. This has several potential benefits, including the alleviation of arrhythmia-associated symptoms and hemodynamic improvements. Maintenance of frequents normalization of ventricular rhythm (NVR) can be achieved with antiarrhythmic drug therapy or with AV node radiofrequency ablation (RFA) and permanent ventricular pacing. Recent interest has focused on the use of class III antiarrhythmic agents, such as amiodarone hydrochloride. This investigation compared amiodarone to AV node RFA and permanent pacing of the His-bundle area in maintaining NVR in patients with resistant chronic AF. After 12 months of treatment with amiodarone (200 to 400 mg/d) 30 % of patients remained in NVR, 30 % were in transitional phase of improvement, and 40 % showed negative effect. Only a few patients in this group developed ocular or hepatic side effects. On one year follow-up was achieved in 100 % of cases without any clinically significant side effects being seen. In conclusion, analysis of the results of this study suggests that low-dose amiodarone is well tolerated in the management of chronic AF in a selected patient population. The more aggressive interventional radiofrequency ablation technique is significantly more effective and more reliable in the long-term clinical treatment of drug-resistant AF. |
1,073 | Autonomic profile and arrhythmic risk stratification after surgical repair of tetralogy of Fallot. | Severe ventricular arrhythmias represent one of the main causes of mortality after repair of tetralogy of Fallot. Their appearance is primarily caused by the large ventricular scar created by surgical intervention. However, the role of autonomic activity as a modulating factor should be considered. The aim of our study was to evaluate this activity in a low-risk group of patients operated on for TOF and its correlation with the occurrence of sustained ventricular tachycardia.</AbstractText>The study group included 38 patients with a mean age of 31 +/- 10 years, selected out of 76 subjects operated on for total correction of tetralogy of Fallot. After a mean interval of 21.9 +/- 6 years from surgical procedure, they underwent electrocardiography, echocardiography, and time domain heart rate variability (HRV) analysis obtained by 24-hour Holter monitoring. Thirty-five healthy subjects comprised the control group for HRV analysis. During a mean follow-up of 6.2 +/- 3 years, 8 patients experienced episodes of sustained ventricular tachycardia. Among different HRV parameters, the standard deviation of all normal beat intervals showed a significant reduction in this group of patients (91.7 +/- 19 versus 133.4 +/- 46, P < .02). Echocardiographic examination demonstrated an increased left ventricular end diastolic volume (85.6 +/- 55 versus 61.3 +/- 13 mL/m(2), P < .05) and a reduced left ventricle ejection fraction (53.9 +/- 9 versus 61.0 +/- 6 %, P < .01) in arrhythmic patients. QRS duration was similar in patients with or without sustained ventricular tachycardia.</AbstractText>Patients after surgical correction of tetralogy of Fallot, considered to be at low risk, showed a significant incidence of severe ventricular arrhythmias. HRV analysis seems to be a useful method for identifying arrhythmic patients, and the standard deviation of all normal beat intervals appears to be the more helpful index.</AbstractText> |
1,074 | Cerebrovascular risk factors and clinical classification of strokes. | Cerebrovascular risk represents a progressive and evolving concept owing to the particular distribution of risk factors in patients with ischemic stroke and in light of the newest stroke subtype classifications that account for pathophysiological, instrumental, and clinical criteria. Age represents the strongest nonmodifiable risk factor associated with ischemic stroke, while hypertension constitutes the most important modifiable cerebrovascular risk factor, confirmed by a host of epidemiological data and by more recent intervention trials of primary (HOT, Syst-Eur, LIFE) and secondary (PROGRESS) prevention of stroke in hypertensive patients. To be sure, a curious relationship exists between stroke and diabetes. Although the Framingham Study, The Honolulu Heart Program, and a series of Finnish studies reported a linear relationship between improved glucose metabolism and cerebral ischemia, the clinical and prognostic profile of diabetic patients with ischemic stroke remains to be fully understood. Our group, on the basis of TOAST classification--a diagnostic classification of ischemic stroke developed in 1993 that distinguishes five different clinical subtypes of ischemic stroke: large-artery atherosclerosis (LAAS), cardioembolic infarct (CEI), lacunar infarct (LAC), stroke of other determined origin (ODE), and stroke of undetermined origin (UDE), and now extensively used in clinical and scientific context--analysed the prevalence of cerebrovascular risk factors and the distribution of TOAST subtypes in more 300 patients with acute ischemic stroke in two consecutives studies that reported the significant association between diabetes and the lacunar subtype and a better clinical outcome for diabetic patients, most likely related to the higher prevalence of the lacunar subtype. Well-confirmed are the roles of cigarette smoking, atrial fibrillation, and asymptomatic carotid stenosis as cerebrovascular risk factors. Particularly interesting seems to be the function of inflammation markers (CRP, TNF-alpha, IL-1 beta, ISPs) as potential risk factors. Still elusive remains the association between cholesterol serum levels and stroke, on the basis of the epidemiological data regarding this causative relationship, confirmed only by the results of intervention trials (4S, LIPID, CARE, HPS, ASCOT). Ultimately, cerebrovascular risk appears peculiar owing to the unique relationship between some modifiable risk factors (mainly diabetes and cholesterol) and the possible preferential association with stroke subtypes and specific cerebrovascular risks. |
1,075 | Development of a substrate of atrial fibrillation during chronic atrioventricular block in the goat. | Atrial dilatation is an important risk factor for atrial fibrillation (AF). In the present study, we monitored the electrophysiological changes during progressive atrial dilatation in chronically instrumented goats.</AbstractText>In 8 goats, 2 screw-in leads with piezoelectric crystals were implanted transvenously in the right atrium. After 2 weeks, atrial diameter and effective refractory period were measured. AF paroxysms were induced by burst pacing to determine the baseline AF cycle length and stability of AF. After His-bundle ablation, the above measurements were repeated once a week. After 4 weeks of complete AV block, the free wall of the right atrium was mapped and the atrium was fixed in formalin for histological analysis. After His-bundle ablation, the ventricular rate decreased from 113.8+/-4.8 to 44.6+/-2.5 bpm. Right atrial diameter increased gradually by 13.5+/-3.9% during 4 weeks of AV block (P<0.01). The duration of induced AF paroxysms increased from 4.6 seconds to 6.4 minutes (P<0.05). Atrial effective refractory period and AF cycle length remained constant. Spontaneous paroxysms of AF were not observed. Atrial mapping during rapid pacing revealed that slow conduction (<30 cm/s) was present in 3.7+/-1.0% of the mapped area (control, 0.9+/-0.5%, P<0.05). Histological analysis showed hypertrophy without atrial fibrosis. Connexin40 and connexin43 expression was unchanged.</AbstractText>Chronic AV block in the goat leads to progressive atrial dilatation, prolongation of induced AF paroxysms, and local conduction delays. The increase in AF stability was not a result of a shortening of atrial refractoriness or atrial fibrosis.</AbstractText> |
1,076 | Cost-effectiveness of dual-chamber pacing compared with ventricular pacing for sinus node dysfunction. | Compared with single-chamber ventricular pacing, dual-chamber pacing can reduce adverse events and, as a result, improve quality of life in patients paced for sick sinus syndrome. It is not clear, however, how these benefits compare with the increased cost of dual-chamber pacemakers.</AbstractText>We used 4-year data from a 2010-patient, randomized trial to estimate the incremental cost-effectiveness of dual-chamber pacing compared with ventricular pacing and then projected these findings over the patients' lifetimes by using a Markov model that was calibrated to the first 5 years of in-trial data. To assess the stability of the findings, we performed 1000 bootstrap analyses and multiple sensitivity analyses. During the first 4 years of the trial, dual-chamber pacemakers increased quality-adjusted life expectancy by 0.013 year per subject at an incremental cost-effectiveness ratio of 53,000 dollars per quality-adjusted year of life gained. Over a lifetime, dual-chamber pacing was projected to increase quality-adjusted life expectancy by 0.14 year with an incremental cost-effectiveness ratio of approximately 6800 dollars per quality-adjusted year of life gained. In bootstrap analyses, dual-chamber pacing was cost-effective in 91.9% of simulations at a threshold of 50,000 dollars per quality-adjusted year of life and in 93.2% of simulations at a threshold of 100,000 dollars. Its cost-effectiveness ratio was also below this threshold in numerous sensitivity analyses that varied key estimates.</AbstractText>For patients with sick sinus syndrome requiring pacing, dual-chamber pacing increases quality-adjusted life expectancy at a cost that is generally considered acceptable.</AbstractText> |
1,077 | Survival from in-hospital cardiac arrest: the potential impact of infection. | The aim of this study was to examine the relationship between outcome from cardiac arrest and infection status at the time of in-hospital cardiac arrest.</AbstractText>This was a retrospective database review from a single resuscitation service supporting two major hospitals.</AbstractText>Two urban University Hospitals in London.</AbstractText>Data from 1436 in-patient cardiac arrest were available for analysis.</AbstractText>Nil.</AbstractText>Patients were classified into infected or non-infected groups by the resuscitation audit process and the hospitals diagnostic coding unit. Survival was followed according to the in-hospital Utstein timepoints. In addition, the data were examined by presenting the cardiac rhythm. Age and length of prior hospitalisation were recorded. Infection associated diagnoses appear to be increasing in prevalence. Initial survival from cardiac arrest was not affected by infection status, but this did have a substantial impact on chance of leaving the initial hospital (odds ratio 0.52, confidence intervals 0.3-0.8), or being discharged to home (odds ratio 0.48, confidence intervals 0.4-0.8). The outcome from ventricular fibrillation/pulseless ventricular tachycardia was worse for infected patients (odds ratio for home discharge 0.37, confidence intervals 0.2-0.9), although initial survival was not significantly different.</AbstractText>Infection may be becoming an increasingly important association with cardiac arrest in the hospitalised population. Initial survival from cardiac arrest is the same as for non-infected patients, but longer term survival is much poorer. Long-term survival from ventricular fibrillation or pulseless ventricular tachycardia is relatively poor, in spite of similar initial success.</AbstractText> |
1,078 | Characteristics and outcome among children suffering from out of hospital cardiac arrest in Sweden. | To evaluate the characteristics, outcome and prognostic factors among children suffering from out of hospital cardiac arrest in Sweden.</AbstractText>Patients aged below 18 years suffering from out of hospital cardiac arrest which were not crew witnessed and included in the Swedish cardiac arrest registry were included in the survey. This survey included the period 1990-2001 and 60 ambulance organisations covering 85% of the Swedish population (8 million inhabitants).</AbstractText>In all 457 children participated in the survey of which 32% were bystander witnessed and 68% received bystander CPR. Ventricular fibrillation was found in 6% of the cases. The overall survival to 1 month was 4%. The aetiology was sudden infant death syndrome in 34% and cardiac in 11%. When in a multivariate analysis considering age, sex, witnessed status, bystander CPR, initial rhythm, aetiology and the interval between call for, and arrival of, the ambulance and place of arrest only one appeared as an independent predictor of an increased chance of surviving cardiac arrest occurring outside home (adjusted odds ratio 8.7; 95% CL 2.2-58.1).</AbstractText>Among children suffering from out of hospital cardiac arrest in Sweden that were not crew witnessed, the overall survival is low (4%). The chance of survival appears to be markedly increased if the arrest occurs outside the patients home compared with at home. No other strong predictors for an increased chance of survival could be demonstrated.</AbstractText> |
1,079 | A probabilistic neural network as the predictive classifier of out-of-hospital defibrillation outcomes. | Although modern defibrillators are nearly always successful in terminating ventricular fibrillation (VF), multiple defibrillation attempts are usually required to achieve return of spontaneous circulation (ROSC). This is potentially deleterious as cardiopulmonary resuscitation (CPR) must be discontinued during each defibrillation attempt which causes deterioration in the heart muscle and reduces the chance of ROSC from later defibrillation attempts. In this work defibrillation outcomes are predicted prior to electrical shocks using a neural network model to analyse VF time series in an attempt to avoid defibrillation attempts that do not result in ROSC.</AbstractText>The 198 pre-shock VF ECG episodes from 83 cardiac arrest patients with defibrillation conversions to different outcomes were selected from the Oslo ambulance service database. A probabilistic neural network model was designed for training and testing with a cross validation method being used for the better generalisation performance.</AbstractText>We achieved an accuracy of 75% in overall prediction with a sensitivity of 84% and a specificity of 65% using VF ECG time series of an order of 1 s in length.</AbstractText>Pre-shock VF ECG time series can be classified according to the defibrillation conversion to a return of spontaneous circulation (ROSC) or No-ROSC.</AbstractText> |
1,080 | Intravenous amiodarone bolus for treatment of atrial fibrillation in patients with advanced congestive heart failure or cardiogenic shock. | The clinical course of patients with advanced organic heart disease is often complicated by the occurrence of atrial fibrillation. Slowing the ventricular rate and, if possible, restoration of normal sinus rhythm is crucial but difficult in the state of decreased ventricular function.</AbstractText>We included 78 consecutive patients with atrial fibrillation and heart rate above 135 beats min(-1) in an observational, uncontrolled study in the coronary care unit of a tertiary care center. Thirty-nine patients suffered from advanced congestive heart failure, 26 patients had pulmonary edema, and 13 patients were in cardiogenic shock. All patients were treated with 450 mg amiodarone given as a single intravenous bolus through a peripheral venous access without further infusion. Ventricular heart rate and cardiac rhythm were measured within 30 minutes after drug administration. Cardiac rhythm was monitored for 24 hours. The site of venous access was examined 30 minutes after drug administration and every 6 hours until the needle was removed after a maximum of 48 hours.</AbstractText>Twenty-five patients (32%) converted to normal sinus rhythm within 30 minutes. Another 15 (19%) reverted into sinus rhythm during the following 24 hours. Within 30 minutes after amiodarone administration, ventricular heart rate decreased significantly from 152 +/- 12 to 88 +/- 17 (p < 0.0001) beats min(-1) in patients who converted to sinus rhythm and from 157 +/- 14 to 98 +/- 16 beats min(-1) in patients who did not. The degree of reduction in heart rate was similar among patients presenting with exacerbated congestive heart failure, pulmonary edema, or cardiogenic shock. Systolic blood pressure decreased in two patients, from 115 to 80 mmHg and from 130 to 100 mmHg, but was reversible after 10 and 90 minutes respectively without specific intervention. No proarrhythmia or clinical relevant bradycardia was observed, and no inflammation detected at the site of venous access.</AbstractText>Amiodarone, given as a single intravenous bolus through a peripheral vein rapidly reduced ventricular rate and was well tolerated in patients with atrial fibrillation, even in the presence of congestive heart failure and cardiogenic shock.</AbstractText> |
1,081 | Effects of SEA0400, a Na+/Ca2+ exchange inhibitor, on ventricular arrhythmias in the in vivo dogs. | SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline), a novel and selective inhibitor of Na+/Ca2+ exchanger, was investigated for its possible antiarrhythmic effects on arrhythmias of Ca2+ overload induced by coronary ligation/reperfusion and by digitalis in the dog. SEA0400 (1.0 mg/kg) did not change the hemodynamics but slightly prolonged the QRS duration (P<0.05). Pre-ischemic administration (10 min before coronary occlusion) of SEA0400 (1.0 mg/kg) and post-ischemic administration (1 min before reperfusion) of SEA0400 (0.3, 1.0 and 3.0 mg/kg) had no effects on the incidence of ventricular fibrillation induced by coronary ligation/reperfusion. On the other hand, SEA0400 (3.0 mg/kg) decreased the arrhythmic ratio in the digitalis arrhythmias (P<0.01). However, atrioventricular block and cardiac standstill were induced in two digitalized dogs. In conclusion, SEA0400 has no significant antiarrhythmic effect on arrhythmias induced by coronary ligation/reperfusion, but has an obvious suppressing effect on tachyarrhythmias induced by digitalis in in vivo canine models. |
1,082 | Recurrent cardiac events in patients with idiopathic ventricular fibrillation, excluding patients with the Brugada syndrome. | The recurrence of cardiac events in patients with idiopathic ventricular fibrillation (VF) excluding patients with the Brugada syndrome is unclear since this entity remains present in previous studies.</AbstractText>Since 1992, 18 patients (72% male) with idiopathic VF out of 455 ICD implants were treated with an implantable cardioverter defibrillator (ICD). The mean age at first ICD implantation was 42 +/- 14 years. Brugada syndrome, as well as other primary electrical diseases (e.g. long QT), were systematically excluded in all patients by the absence of the typical electrocardiogram (ST elevation in the right precordial leads) at rest and/or after pharmacological tests (ajmaline, flecainide, or procainamide). Recurrence of cardiac events was prospectively assessed.</AbstractText>During a mean follow-up period of 41 +/- 27 months, VF recurrence with appropriate shock occurred in 7 patients (39%) covering a total of 27 shocks. The median time to first appropriate shock was 12 +/- 9 months. There were no deaths. In the electrophysiological study, 39% of patients were inducible, but inducibility failed to predict subsequent arrhythmic events. Forty-four percent of patients suffered 21 inappropriate shocks, which were caused by sinus tachycardia, atrial arrhythmias or lead malfunction.</AbstractText>Idiopathic ventricular fibrillation patients have a high recurrence rate of potentially fatal ventricular arrhythmias, excluding patients with the Brugada syndrome or other known causes. ICD prevents sudden cardiac death but inappropriate shocks remained a major issue in this young and active population.</AbstractText> |
1,083 | Use of automated external defibrillators in cardiac arrest: an evidence-based analysis. | The objectives were to identify the components of a program to deliver early defibrillation that optimizes the effectiveness of automated external defibrillators (AEDs) in out-of-hospital and hospital settings, to determine whether AEDs are cost-effective, and if cost-effectiveness was determined, to advise on how they should be distributed in Ontario.</AbstractText>Survival in people who have had a cardiac arrest is low, especially in out-of-hospital settings. With each minute delay in defibrillation from the onset of cardiac arrest, the probability of survival decreases by 10%. (1) Early defibrillation (within 8 minutes of a cardiac arrest) has been shown to improve survival outcomes in these patients. However, in out-of-hospital settings and in certain areas within a hospital, trained personnel and their equipment may not be available within 8 minutes. This implies that "first responders" should take up the responsibility of delivering shock. The first responders in out-of-hospital settings are usually bystanders, firefighters, police, and community volunteers. In hospital settings, they are usually nurses. These first responders are not trained in reading electrocardiograms and identifying abnormal heart rhythms restorable by defibrillation.</AbstractText>An AED is a device that can analyze a heart rhythm and deliver a shock if needed. Thus, AEDs can be used by first responders to deliver early defibrillation in out-of-hospital and hospital settings. However, simply providing an AED would not likely improve survival outcomes. Rather, AEDs have a role in strengthening the "chain of survival," which includes prompt activation of the 911 telephone system, early cardiopulmonary resuscitation (CPR), rapid defibrillation, and timely advanced life support. In the chain of survival, the first step for a witness of a cardiac arrest in an out-of-hospital setting is to call 911. Second, the witness initiates CPR (if she or he is trained in CPR). If the witness cannot initiate CPR, or the first responders of the 911 system (e.g., firefighters/police) have arrived, the first responders initiate CPR. Third, the witness or first responders apply an AED to the patient. The device reads the patient's heart rhythm and prompts for shock when indicated. Fourth, the patient is handed over to the advanced life-support team with subsequent admission to an intensive care unit in a hospital. The use of AEDs requires developing and implementing a program at sites where the cardiac arrest rate is high, where a number of potential first responders are trained and retained, and where patients are transferred to an advanced care facility after initiating resuscitation. Obviously, placing an AED at a site where no cardiac arrests are likely to occur would be futile, as would placing an AED at a site where no one knows how to use it. Moreover, abandoning patients after initial resuscitation by not transferring them to an advanced care facility would negate all earlier efforts. Thus, it is important to identify the essential components of an AED program that might also optimize the effectiveness of AED use.</AbstractText>There is a large body of literature on the use of AEDs in various settings ranging from closed environments such as hospitals, airlines, and casinos to open places such as sports fields and highways. There is little doubt regarding the effectiveness and safety of AEDs to treat people in cardiac arrest. It is intuitive that these devices should be provided in hospitals in areas that are not readily accessible to the traditional responders, the "code blue team." Similarly, it is intuitive to provide AEDs in out-of-hospital settings where the risk of cardiac arrest is high and a response plan involving trained first responders in the use of AEDs is in place. Thus, the Medical Advisory Secretariat reviewed the literature and focused on the components of an AED program in out-of-hospital settings that maximize the effectiveness and cost-effectiveness of the program in the management of cardiac arrest. Search engines included MEDLINE, EMBASE, EconLit and Web sites of other agencies that assess health technologies. Any study that reported results of an AED program in an out-of-hospital setting was included. Studies that did not use AEDs, had a physician-assisted emergency response plan, did not have a program for the use of AEDs, or did not include cardiac arrest as an outcome were excluded.</AbstractText>A total of 133 articles were identified; 62 were excluded after reviewing titles and abstracts. Of the 71 articles reviewed, 8 reported findings of 2 large studies, the Ontario Prehospital Advanced Life Support (OPALS) study and the Public Access Defibrillation (PAD) trial. These studies examined the effect of a community program to respond to cardiac arrest with and without the use of AEDs. Their authors had reported a significant reduction in overall mortality from cardiac arrest with the use of AEDs. Factors That Improve the Effectiveness of an AED Program The PAD trial investigators reported a significant improvement in survival (P = .03) after providing AEDs in public access areas and training volunteers in CPR compared with training volunteers in CPR only. The OPALS study investigators reported odds ratios (ORs) and 95% confidence intervals (CIs) for significant predictors of survival, which were age (OR [age per 10 year], 0.8; CI, 0.8-0.9), arrest witnessed by bystander (OR, 3.9; CI, 2.7-5.5), CPR initiated by bystander (OR, 3.7; CI, 2.6-5.1), CPR initiated by first responder (OR, 1.6; CI, 1.1-2.3), and emergency medical service response within 8 minutes (OR, 3.0; CI, 1.8-5.1). The last 3 variables are modifiable and thus may improve the effectiveness of an AED program. For example, the rate of bystander-initiated CPR was only 14% in the OPALS study, but it was 100% in the PAD trial. This was because PAD trial investigators trained community volunteers whereas the OPALS study investigators did not. Cost-Effectiveness A systematic review of the literature suggests that cost-effectiveness varies from setting to setting. Most of the studies have estimated cost-effectiveness in American settings from a societal perspective; therefore, the results are not applicable to this report. However, results from this review suggest that the incidence of cardiac arrest in out-of-hospital setting in Ontario is 59 per 100,000 people. The mean age of cardiac arrest patients is 69 years. Eighty-five percent of these cardiac arrests occur in homes. Of all the cardiac arrests, 37% have heart rhythm abnormalities (ventricular tachycardia or ventricular fibrillation) that are correctable by delivering shock through an AED. Thus, in an out-of-hospital setting, general use of AEDs by laypersons would not be cost-effective. Special programs are needed in the out-of-hospital setting for cost-effective use of AEDs. One model for the use of AEDs in out-of-hospital settings was examined in the OPALS study. Firefighters and police were trained and provided with AEDs. The total initial cost (in US dollars) of this program was estimated to be $980,000. The survival rate was 3.9% before implementing the AED program and 5.2% after its implementation (OR, 1.33; 95% CI, 1.03-1.7; P = .03). Applying these estimates to cardiac arrest rates in Ontario in 2002, one would expect 54 patients of the total 1,395 cardiac arrests to survive without AEDs compared with 73 patients with AEDs; thus, 19 additional lives might be saved each year with an AED program. It would initially cost $51,579 to save each additional life. In subsequent years, however, total cost would be lower (about $50,000 per year), when it would cost $2,632 to save each additional life per year. One limitation of the OPALS study was that the authors combined emergency medical service response time and application of an AED into a single variable. Thus, it was not possible to tease out the independent effects of reduction in response time and application of an AED on the small improvement in survival. Nevertheless, the PAD study found that when response time was fixed, the application of AED improved survival. There are other delivery models for AEDs in casinos, sports arenas, and airports. The proportion of cardiac arrest at these sites out of the total cardiac arrests in Ontario is between 0.05% and 0.4%. Thus, an AED placed at these sites would likely not be used at all. Of the 85% cardiac arrests that occur in homes, 56% occur in single residential dwellings (houses), 23% occur in multi-residential dwellings (apartments/condominiums), and 6% occur in nursing homes. There is no program in place except the 911 system to reach these patients. Accordingly, the Medical Advisory Secretariat examined the cost-effectiveness of providing AEDs in hospitals, office buildings, apartments/condominiums, and houses. The results suggested that deployment of AEDs in hospitals would be cost-effective in terms of cost per quality adjusted life year gained. Conversely, deployment of AEDs in office buildings, apartments, and houses was not cost-effective. An exception, however, was noted for people at high risk of sudden cardiac arrest; these were patients with a left ventricular ejection fraction less than or equal to 0.35.</AbstractText>The OPALS study model appears cost-effective, and effectiveness can be further enhanced by training community volunteers to improve the bystander-initiated CPR rates. Deployment of AEDs in all public access areas and in houses and apartments is not cost-effective. Further research is needed to examine the benefit of in-home use of AEDs in patients at high risk of cardiac arrest.</AbstractText> |
1,084 | Implantable cardioverter defibrillators. Prophylactic use: an evidence-based analysis.<Pagination><StartPage>1</StartPage><EndPage>74</EndPage><MedlinePgn>1-74</MedlinePgn></Pagination><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">The use of implantable cardiac defibrillators (ICDs) to prevent sudden cardiac death (SCD) in patients resuscitated from cardiac arrest or documented dangerous ventricular arrhythmias (secondary prevention of SCD) is an insured service. In 2003 (before the establishment of the Ontario Health Technology Advisory Committee), the Medical Advisory Secretariat conducted a health technology policy assessment on the prophylactic use (primary prevention of SCD) of ICDs for patients at high risk of SCD. The Medical Advisory Secretariat concluded that ICDs are effective for the primary prevention of SCD. Moreover, it found that a more clearly defined target population at risk for SCD that would be likely to benefit from ICDs is needed, given that the number needed to treat (NNT) from recent studies is 13 to 18, and given that the per-unit cost of ICDs is $32,000, which means that the projected cost to Ontario is $770 million (Cdn). Accordingly, as part of an annual review and publication of more recent articles, the Medical Advisory Secretariat updated its health technology policy assessment of ICDs.</AbstractText><AbstractText Label="CLINICAL NEED" NlmCategory="OBJECTIVE">SUDDEN CARDIAC DEATH IS CAUSED BY THE SUDDEN ONSET OF FATAL ARRHYTHMIAS, OR ABNORMAL HEART RHYTHMS: ventricular tachycardia (VT), a rhythm abnormality in which the ventricles cause the heart to beat too fast, and ventricular fibrillation (VF), an abnormal, rapid and erratic heart rhythm. About 80% of fatal arrhythmias are associated with ischemic heart disease, which is caused by insufficient blood flow to the heart. Management of VT and VF with antiarrhythmic drugs is not very effective; for this reason, nonpharmacological treatments have been explored. One such treatment is the ICD.</AbstractText><AbstractText Label="THE TECHNOLOGY" NlmCategory="METHODS">An ICD is a battery-powered device that, once implanted, monitors heart rhythm and can deliver an electric shock to restore normal rhythm when potentially fatal arrhythmias are detected. The use of ICDs to prevent SCD in patients resuscitated from cardiac arrest or documented dangerous ventricular arrhythmias (secondary prevention) is an insured service in Ontario. Primary prevention of SCD involves identification of and preventive therapy for patients who are at high risk for SCD. Most of the studies in the literature that have examined the prevention of fatal ventricular arrhythmias have focused on patients with ischemic heart disease, in particular, those with heart failure (HF), which has been shown to increase the risk of SCD. The risk of HF is determined by left ventricular ejection fraction (LVEF); most studies have focused on patients with an LVEF under 0.35 or 0.30. While most studies have found ICDs to reduce significantly the risk for SCD in patients with an LVEF less than 0.35, a more recent study (Sudden Cardiac Death in Heart Failure Trial [SCD-HeFT]) reported that patients with HF with nonischemic heart disease could also benefit from this technology. Based on the generalization of the SCD-HeFT study, the Centers for Medicare and Medicaid in the United States recently announced that it would allocate $10 billion (US) annually toward the primary prevention of SCD for patients with ischemic and nonischemic heart disease and an LVEF under 0.35.</AbstractText><AbstractText Label="REVIEW STRATEGY" NlmCategory="METHODS">The aim of this literature review was to assess the effectiveness, safety, and cost effectiveness of ICDs for the primary prevention of SCD. The standard search strategy used by the Medical Advisory Secretariat was used. This included a search of all international health technology assessments as well as a search of the medical literature from January 2003-May 2005. A modification of the GRADE approach (1) was used to make judgments about the quality of evidence and strength of recommendations systematically and explicitly. GRADE provides a framework for structured reflection and can help to ensure that appropriate judgments are made. GRADE takes into account a study's design, quality, consistency, and directness in judging the quality of evidence for each outcome. The balance between benefits and harms, quality of evidence, applicability, and the certainty of the baseline risks are considered in judgments about the strength of recommendations.</AbstractText><AbstractText Label="SUMMARY OF FINDINGS" NlmCategory="RESULTS">Overall, ICDs are effective for the primary prevention of SCD. Three studies - the Multicentre Automatic Defibrillator Implantation Trial I (MADIT I), the Multicentre Automatic Defibrillator Implantation Trial II (MADIT II), and SCD-HeFT - showed there was a statistically significant decrease in total mortality for patients who prophylactically received an ICD compared with those who received conventional therapy (Table 1). Table 1:Results of Key Studies on the Use of Implantable Cardioverter Defibrillators for the Primary Prevention of Sudden Cardiac Death - All-Cause MortalityStudy, * YearPopulationNFollow-up, MonthsMortality, ICD† Group, %Mortality, Control Group, %Hazard Ratio (95% CI)PNNT†MADIT, 1996 (2)Ischemic1962715.838.60.46 (0.26-0.82).0094PriormyocardialinfarctionConventional therapy54% relative reductionEjection fraction ≤ 0.35NSVT†EP† +MADIT II, 2002 (3)Ischemic12322014.219.80.69(0.51-0.93).01618PriormyocardialinfarctionConventional therapy31% relative reductionEjection fraction ≤ 0.30SCD-HeFT, 2005 (4)Ischemic & Nonischemic25216022290.77 (0.62-0.96).00713Optimal therapyEjection fraction < 0.3523% relative reduction*MADIT I: Multicentre Automatic Defibrillator Implantation Trial I; MADIT II: Multicentre Automatic Defibrillator Implantation Trial II; SCD-HeFT: Sudden Cardiac Death in Heart Failure Trial.†EP indicates electrophysiology; ICD, implantable cardioverter defibrillator; NNT, number needed to treat; NSVT, nonsustained ventricular tachycardia. The NNT will appear higher if follow-up is short. For ICDs, the absolute benefit increases over time for at least a 5-year period; the NNT declines, often substantially, in studies with a longer follow-up. When the NNT are equalized for a similar period as the SCD-HeFT duration (5 years), the NNT for MADIT-I is 2.2; for MADIT-II, it is 6.3.</AbstractText><AbstractText Label="GRADE QUALITY OF THE EVIDENCE" NlmCategory="UNASSIGNED">Using the GRADE Working Group criteria, the quality of these 3 trials was examined (Table 2). Quality refers to the criteria such as the adequacy of allocation concealment, blinding and follow-up. Consistency refers to the similarity of estimates of effect across studies. If there is important unexplained inconsistency in the results, our confidence in the estimate of effect for that outcome decreases. Differences in the direction of effect, the size of the differences in effect, and the significance of the differences guide the decision about whether important inconsistency exists. Directness refers to the extent to which the people interventions and outcome measures are similar to those of interest. For example, there may be uncertainty about the directness of the evidence if the people of interest are older, sicker or have more comorbidity than those in the studies. As stated by the GRADE Working Group, the following definitions were used to grade the quality of the evidence: HIGH: Further research is very unlikely to change our confidence n the estimate of effect.MODERATE: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.LOW: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.VERY LOW: Any estimate of effect is very uncertain.Table 2:Quality of Evidence - MADIT I, MADIT II, and SCD-HeFT*TrialDesignQualityConsistencyDirectness†Quality GradeMADIT IRCTImbalance in β-blocker usage between study arms.The overall number of patients from which the study was drawn was not reported.Selection bias may have occurred since patients were selected for randomization if they did not respond to procainamide, thereby introducing a potential bias into the medication arm.Specific details regarding allocation concealment and blinding procedures were not provided.Single-chamber ICD used in study.Trial started with transthoracic implants, and then switched to nontransthoracic implants.Ischemic cardiomyopathy only.5-year NNT = 2.The overall number of Moderate patients from which the study was drawn was not reported.Selection bias may have occurred since patients were selected for randomization if they did not respond to procainamide, thereby introducing a potential bias into the medication arm.ModerateMADIT IIRCT~ 90% of patients were recruited ≥6 months post-MI; 20% of control group died after mean 20-month follow-up.How and where patients recruited?Specific details regarding allocation concealment/blinding procedures not provided.Subset had MADIT I criteria; post hoc analysis of incomplete data suggested "weak-moderate evidence that ICD effect greater in inducible than noninducible patients in MADIT II." (5;6)First study to assess both single- and dual-chamber ICD devices for primary prevention.Programming of device and medications left to the discretion of the patients' physician.Higher rate of hospitalization for new or worsened heart failure in the group receiving the ICDs compared to conventional therapy (19.9% versus 14.9% respectively).Ischemic cardiomyopathy only.5-year NNT = 6.How and where patients Weak recruited?Subset had MADIT I criteria.WeakSCD-HeFTRCTStatistically significant difference in β-blocker usage between treatment groups at last follow-up.Drug arms double-blinded.Shock-only single-lead device. Antitachycardia pacing not permitted.Ischemic and nonischemic cardiomyopathy.There was a statistically significant difference in terms of the NYHA prespecified subgroups analysis. The NYHA subgroups were prespecified a priori and the results of the interaction tests were significant. Yet, ICD treatment had a significant benefit in patients in NYHA class II but not in those in NYHA class III. (ABSTRACT TRUNCATED)</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><CollectiveName>Medical Advisory Secretariat</CollectiveName></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2005</Year><Month>09</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>Canada</Country><MedlineTA>Ont Health Technol Assess Ser</MedlineTA><NlmUniqueID>101521610</NlmUniqueID><ISSNLinking>1915-7398</ISSNLinking></MedlineJournalInfo></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2012</Year><Month>10</Month><Day>18</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>1</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23074465</ArticleId><ArticleId IdType="pmc">PMC3382404</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>GRADE Working Group. Br Med J. 2004;328:1490–1497. Grading quality of evidence and strength of recommendations.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC428525</ArticleId><ArticleId IdType="pubmed">15205295</ArticleId></ArticleIdList></Reference><Reference><Citation>Moss AJ, Hall WJ, Cannom DS, Daubert JP, Higgins SL, Klein H, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med. 1996;335:1933–1940.</Citation><ArticleIdList><ArticleId IdType="pubmed">8960472</ArticleId></ArticleIdList></Reference><Reference><Citation>Moss AJ, Zareba W, Hall WJ, Klein H, Wilber D, Cannom DS, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346:877–883.</Citation><ArticleIdList><ArticleId IdType="pubmed">11907286</ArticleId></ArticleIdList></Reference><Reference><Citation>Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, et al. Amiodarone or an implantable cardioverter defibrillator for congestive heart failure. Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) N Engl J Med. 2005;352:225–237.</Citation><ArticleIdList><ArticleId IdType="pubmed">15659722</ArticleId></ArticleIdList></Reference><Reference><Citation>Centers for Medicare and Medicaid Services. Letter to Guidant. Available from: www.cms.hhs.gov/coverage/download/id39-4.pdf. (Accessed Nov. 2003)</Citation><ArticleIdList><ArticleId IdType="pubmed">12049095</ArticleId></ArticleIdList></Reference><Reference><Citation>Centers for Medicare and Medicaid Services. National Coverage Analysis: Tracking Sheet. Available from www.cms.hhs.gov/ncdr/trackingsheet.asp?id=39. (Accessed Feb 2003)</Citation></Reference><Reference><Citation>Zipes DP. Epidemiology and mechanisms of sudden cardiac death. Can J Cardiol. 2005;21:37A–40A.</Citation><ArticleIdList><ArticleId IdType="pubmed">15953943</ArticleId></ArticleIdList></Reference><Reference><Citation>Myerburg JJ, Mitrani R, Interian A, Castellanos A. Frequency of sudden cardiac death and profiles of risk. Am J Cardiol. 1997;80(5B):10F–19F.</Citation><ArticleIdList><ArticleId IdType="pubmed">9291445</ArticleId></ArticleIdList></Reference><Reference><Citation>Myerburg RJ. Sudden cardiac death: exploring the limits of our knowledge. J Cardiovasc Electrophysiol. 2001;12:369–381.</Citation><ArticleIdList><ArticleId IdType="pubmed">11291815</ArticleId></ArticleIdList></Reference><Reference><Citation>Huikuri HV, Castellanos A, Myerburg RJ. Sudden death due to cardiac arrhythmias. N Engl J Med. 2001;345:1473–1482.</Citation><ArticleIdList><ArticleId IdType="pubmed">11794197</ArticleId></ArticleIdList></Reference><Reference><Citation>Kannel WB, Doyle JT, McNamara PM. Precursors of sudden coronary death: factors related to the incidence of sudden death. Circulation. 1975;51:606–611.</Citation><ArticleIdList><ArticleId IdType="pubmed">123182</ArticleId></ArticleIdList></Reference><Reference><Citation>Reichenbach DD, Moss NS, Meyer E. Pathology of the heart in sudden cardiac death. Am J Cardiol. 1977;39:865–869.</Citation><ArticleIdList><ArticleId IdType="pubmed">871113</ArticleId></ArticleIdList></Reference><Reference><Citation>Myerburg RJ, Kessler KM, Caastellanos A. Sudden cardiac death: structure, function, and time-dependence of risk. Circulation. 1992;85(suppl I):2–10.</Citation><ArticleIdList><ArticleId IdType="pubmed">1728501</ArticleId></ArticleIdList></Reference><Reference><Citation>Doyle JT, Kannel WB, McNamara RM, Quickenton R, Gordon T. Factors related to suddenness of death from coronary heart disease: combined Albany-Framingham studies. Am J Cardiol. 1976;37:1073–1078.</Citation><ArticleIdList><ArticleId IdType="pubmed">132115</ArticleId></ArticleIdList></Reference><Reference><Citation>Packer M. Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. Circulation. 1992;85(suppl I):50–56.</Citation><ArticleIdList><ArticleId IdType="pubmed">1728505</ArticleId></ArticleIdList></Reference><Reference><Citation>Cobb LA, Fahrenbruch CE, Lolsufka M, Copass MK. Changing incidence of out-of-hospital ventricular fibrillation, 1980-2000. JAMA. 2002;288:3008–3013.</Citation><ArticleIdList><ArticleId IdType="pubmed">12479765</ArticleId></ArticleIdList></Reference><Reference><Citation>Waien SA, Stiell IG. Cardiac arrest care and emergency medical services. Naylor CD, Slaughter PM, . Toronto: Institute for Clinical Evaluative Sciences. 1999:283–300. In. editors. Cardiovascular Health and Services in Ontario: An ICES Atlas.</Citation></Reference><Reference><Citation>Moss AJ, Cannom DS, Daubert JP, Hall WJ, Higgins SL, Klein H, et al. Multicenter Automatic Defibrillator Implantation Trial II (MADIT II): design and clinical protocol. Ann Noninvasive Electrocardiol. 1999;4:83–91.</Citation></Reference><Reference><Citation>Bigger JT, Fleiss JL, Kleiger R, Miller JP, Rolnitzky LM. The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction. Circulation. 1984;69:250–258.</Citation><ArticleIdList><ArticleId IdType="pubmed">6690098</ArticleId></ArticleIdList></Reference><Reference><Citation>Cooklin M. Devices for the management of ventricular arrhythmias in cardiac failure. Heart Fail Rev. 2002;7:301–310.</Citation><ArticleIdList><ArticleId IdType="pubmed">12215734</ArticleId></ArticleIdList></Reference><Reference><Citation>Multicenter Postinfarction Research Group. N Engl J Med. 1983;309:331–336. Risk stratification and survival after myocardial infarction.</Citation><ArticleIdList><ArticleId IdType="pubmed">6866068</ArticleId></ArticleIdList></Reference><Reference><Citation>Buxton AE, Lee KL, DiCarlo L, Gold MR, Greer GS, Prystowsky EN, et al. Electrophysiologic testing to identify patients with coronary artery disease who are at risk for sudden death. N Engl J Med. 2000;342:1937–1945.</Citation><ArticleIdList><ArticleId IdType="pubmed">10874061</ArticleId></ArticleIdList></Reference><Reference><Citation>Tchou PJ. Ventricular Tachycardia. Topol EJ, editor. Philadelphia, PA: Lippincott Williams and Wilkins. 20021498:1479. In. editor. Textbook of Cardiovascular Medicine.</Citation></Reference><Reference><Citation>Doval H, Nul DR, Grancelli HO, Varini SD, Soifer S, Corrado G, et al. Nonsustained ventricular tachycardia in severe heart failure. Circulation. 1996;94:3198–3203.</Citation><ArticleIdList><ArticleId IdType="pubmed">8989129</ArticleId></ArticleIdList></Reference><Reference><Citation>Teerlink JR, Jalaluddin M, Anderson S, Kukin ML, Eichhorn EJ, Francis G, et al. Ambulatory ventricular arrhythmias in patients with heart failure do not specifically predict an increased risk of sudden death. Circulation. 2000;101:40–46.</Citation><ArticleIdList><ArticleId IdType="pubmed">10618302</ArticleId></ArticleIdList></Reference><Reference><Citation>Maggioni AP, Zuanetti G, Franzosi MG, Roveli F, Santoro E, Staszewsky L, et al. Prevalence and prognostic significance of ventricular arrhythmias after acute myocardial infarction in the fibrinolytic era: GISSI-2 results. Circulation. 1993;87:312–322.</Citation><ArticleIdList><ArticleId IdType="pubmed">8093865</ArticleId></ArticleIdList></Reference><Reference><Citation>Rouleau JL, Talajic M, Sussex B, Potvin L, Warnica W, Davies RF, et al. Myocardial infarction patients in the 1990s - their risk factors, stratification and survival in Canada. J Am Coll Cardiol. 1996;27:1119–1127. The Canadian Assessment of Myocardial Infarction (CAMI) Study.</Citation><ArticleIdList><ArticleId IdType="pubmed">8609330</ArticleId></ArticleIdList></Reference><Reference><Citation>Singh SN, Karasik P, Hafley GE, Pieper KS, Lee KL, Wyse DG, et al. Electrophysiologic and clinical effects of angiotensin-converting enzyme inhibitors in patients with prior myocardial infarction, nonsustained ventricular tachycardia, and depressed left ventricular function. Am J Cardiol. 2001;87(6):716–720. MUSTT Investigators. Multicenter UnSustained Tachycardia Trial.</Citation><ArticleIdList><ArticleId IdType="pubmed">11249889</ArticleId></ArticleIdList></Reference><Reference><Citation>Singh SN, Fisher SG, Carson PE, Fletcher RD, et al. Prevalence and significance of nonsustained ventricular tachycardia in patients with premature ventricular contractions and heart failure treated with vasodilator therapy. J Am Coll Cardiol. 1998;32:942–947.</Citation><ArticleIdList><ArticleId IdType="pubmed">9768715</ArticleId></ArticleIdList></Reference><Reference><Citation>Singh S, Fletcher RD, Fisher S. Veterans Affairs Congestive Heart Failure Antiarrhythmic Trial. Am J Cardiol. 1993;72:99F–102F. and the CHF STAT Investigators.</Citation><ArticleIdList><ArticleId IdType="pubmed">8237838</ArticleId></ArticleIdList></Reference><Reference><Citation>Makikallio TH, Barthel P, Schneider R, Bauer A, Tapanainen JM, Tulppo MP, et al. Prediction of sudden cardiac death after acute myocardial infarction: role of Holter monitoring in the modern treatment era. Eur Heart J. 2005;26:762–769.</Citation><ArticleIdList><ArticleId IdType="pubmed">15778204</ArticleId></ArticleIdList></Reference><Reference><Citation>Buxton AE, Marchlinski FE, Waxman HL, Flores BT, Cassidy DM, Josephson ME. Prognostic factors in nonsustained ventricular tachycardia. Am J Cardiol. 1984;53:1275–1279.</Citation><ArticleIdList><ArticleId IdType="pubmed">6711427</ArticleId></ArticleIdList></Reference><Reference><Citation>Cripps T, Bennett D, Camm J, Ward DE. Inducibility of sustained monomorphic ventricular tachycardia as a prognostic indicator in survivors of recent myocardial infarction: a prospective evaluation in relation to other prognostic variables. J Am Coll Cardiol. 1989;14:289–296.</Citation><ArticleIdList><ArticleId IdType="pubmed">2754119</ArticleId></ArticleIdList></Reference><Reference><Citation>Bourke JP, Richards DA, Ross DL, Wallace EM, McGuire MA, Uther JB. Routine programmed electrical stimulation in survivors of acute myocardial infarction for prediction of spontaneous ventricular tachyarrhythmias during followup: results, optimal stimulation protocol and cost-effective screening. J Am Coll Cardiol. 1991;18:780–788.</Citation><ArticleIdList><ArticleId IdType="pubmed">1907984</ArticleId></ArticleIdList></Reference><Reference><Citation>Crandall BG, MOrris CD, Cutler JE, Kudenchuk PJ, Peterson JI, Liem LB, et al. Implantable cardioverter defibrillator therapy in survivors of out of hospital sudden cardiac death without inducible arrhythmias. J Am Coll Cardiol. 1993;21:1186–1192.</Citation><ArticleIdList><ArticleId IdType="pubmed">8459075</ArticleId></ArticleIdList></Reference><Reference><Citation>Zoni-Berisso M, Molini D, Mela GS, Vecchio C. Value of programmed ventricular stimulation in predicting sudden death and sustained ventricular tachycardia in survivors of acute myocardial infarction. Am J Cardiol. 1996;77:673–680.</Citation><ArticleIdList><ArticleId IdType="pubmed">8651115</ArticleId></ArticleIdList></Reference><Reference><Citation>Furukawa T, Rozanski JJ, Nogami J, Moroe K, Gosselin AJ, Lister JW. Time dependent risk and predictors for cardiac arrest recurrence in survivors of out of hospital cardiac arrest with chronic coronary artery disease. Circulation. 1989;80:599–608.</Citation><ArticleIdList><ArticleId IdType="pubmed">2766512</ArticleId></ArticleIdList></Reference><Reference><Citation>Moss AJ. Implantable cardioverter defibrillator therapy. Circulation. 2000;101:1638–1640. The sickest patients benefit the most.</Citation><ArticleIdList><ArticleId IdType="pubmed">10758042</ArticleId></ArticleIdList></Reference><Reference><Citation>Cannom DS, Pyrstowsky EN. Management of ventricular arrhythmias: detection, drugs and devices. JAMA. 1999;281:172–179.</Citation><ArticleIdList><ArticleId IdType="pubmed">9917122</ArticleId></ArticleIdList></Reference><Reference><Citation>Stevenson WG, Khan H, Sager P. Identificaton of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction. Circulation. 1993;88:1647–1670.</Citation><ArticleIdList><ArticleId IdType="pubmed">8403311</ArticleId></ArticleIdList></Reference><Reference><Citation>Blanchard SM, Walcott GP, Wharton JM, Ideker RE. Why is catheter ablation less successful than surgery for treating ventricular tachycardia that results from coronary artery disease? Pacing Clin Electrophysiol. 1994;17(pt 1):2315–2335.</Citation><ArticleIdList><ArticleId IdType="pubmed">7885941</ArticleId></ArticleIdList></Reference><Reference><Citation>Pinski SL, Chen PS. Implantable Cardioverter Defibrillators. Textbook of Cardiovascular Medicine. In: Topol EJ, editor. Philadelphia: Lippincott Williams and Wilkins. 2002. pp. 1597–1614. In. editor. Second ed.</Citation></Reference><Reference><Citation>Spath MA, O’Brien BJ. Cost effectiveness of implantable cardioverter defibrillator therapy versus drug therapy for patients at high risk of sudden cardiac death. Pharmacoeconomics. 2002;20:727–738.</Citation><ArticleIdList><ArticleId IdType="pubmed">12201792</ArticleId></ArticleIdList></Reference><Reference><Citation>Parkes J, Bryant J, Milne R. Health Technology Assessment. 26. Vol. 4. Winchester, England: 2000. Implantable cardioverter defibrillators: Arrhythmias; pp. i–60. A rapid and systematic review.</Citation><ArticleIdList><ArticleId IdType="pubmed">11086270</ArticleId></ArticleIdList></Reference><Reference><Citation>Antiarrhythmics Versus Implantable Defibrillators (AVID) Investigators. N Engl J Med. 1997;337:1576–1583. A comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from near fatal ventricular arrhythmias.</Citation><ArticleIdList><ArticleId IdType="pubmed">9411221</ArticleId></ArticleIdList></Reference><Reference><Citation>Kuck KH, Cappato R, Siebels J, Ruppel R. Randomized comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from cardiac arrest: Cardiac Arrest Study Hamburg (CASH) Circulation. 2000;102:748–754.</Citation><ArticleIdList><ArticleId IdType="pubmed">10942742</ArticleId></ArticleIdList></Reference><Reference><Citation>Connolly SJ, Gent M, Roberts RS, Dorian P, Roy D, Sheldon RS, et al. Canadian Implantable Defibrillator Study (CIDS): a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. 2000;101:1297–1302.</Citation><ArticleIdList><ArticleId IdType="pubmed">10725290</ArticleId></ArticleIdList></Reference><Reference><Citation>Connolly SJ, Hallstron AP, Cappato R, Schron EB, Kuck KH, Zipes DP, et al. Meta-analysis of the implantable cardioverter defibrillator secondary prevention trials. Eur Heart J. 2000;21:2071–2078.</Citation><ArticleIdList><ArticleId IdType="pubmed">11102258</ArticleId></ArticleIdList></Reference><Reference><Citation>Eisenberg MS, Horwood BT, Cummins RO, Reyolds-Haertle R, Hearne TR. Cardiac arrest and resuscitation. Ann Emerg Med. 1990;19:179–186.</Citation><ArticleIdList><ArticleId IdType="pubmed">2301797</ArticleId></ArticleIdList></Reference><Reference><Citation>Zivin A, Bardy GH. Implantable defibrillators and antiarrhythmic drugs in patients at risk for lethal arrhythmias. Am J Cardiol. 1999;84(9 SUPPL. 1):63–68.</Citation><ArticleIdList><ArticleId IdType="pubmed">10568662</ArticleId></ArticleIdList></Reference><Reference><Citation>Wilber KJ, Kall JG, Kopp DE. What can we expect from prophylactic implantable defibrillators? Am J Cardiol. 1997;80(5B):20F–27F.</Citation><ArticleIdList><ArticleId IdType="pubmed">9291446</ArticleId></ArticleIdList></Reference><Reference><Citation>Blue Cross Blue Shield Technology Evaluation Center Assessment Program. Blue Cross Blue Shield 2005;Volume 19(Number 19) Use of implantable cardioverter defibrillators for prevention of sudden death in patients at high risk for ventricular arrhythmia.</Citation></Reference><Reference><Citation>National Institute for Clinical Excellence. Implantable cardioverter defibrillators for arrhythmias (review of technology appraisal 95) Available from: www.nice.org.uk/TA095. (Accessed May 2005)</Citation></Reference><Reference><Citation>Desai AS, Fang JC, Maisel WH, Baughman KL. Implantable defibrillators for the prevention of mortality in patients with nonischemic cardiomyopathy: a meta-analysis of randomized controlled trials. JAMA. 2004;292:2874–2879.</Citation><ArticleIdList><ArticleId IdType="pubmed">15598919</ArticleId></ArticleIdList></Reference><Reference><Citation>Centers for Medicare and Medicaid Services. National Coverage Analysis: Decision Memo of Implantable Defibrillators (CAG-00157R3) Available from: www.cms.hhs.gov/mcd/viewdecisionmemo.asp?id=148. (Accessed May 2005)</Citation></Reference><Reference><Citation>Newman D. When is an ICD indicated in the primary prevention of sudden death: a review of the evidence. Lecture - Arrhythmia and Electrophysiology. 2003. Available from: www.fac.org.ar/tcvc/llave/c027/newman.htm. (Accessed June 2005)</Citation></Reference><Reference><Citation>Klein H, Auricchio A, Reek S, Geller C. New primary prevention trials of sudden cardiac death in patients with left ventricular dysfunction: SCDHeFT and MADIT II. Am J Cardiol. 1999;83:91D–97D.</Citation><ArticleIdList><ArticleId IdType="pubmed">10089848</ArticleId></ArticleIdList></Reference><Reference><Citation>Bryant J, Brodin H, Loveman E, Payne E, Clegg A. The clinical effectiveness and cost effectiveness of implantable cardioverter defibrillators for arrhythmias. Jan, 2004. Available from: www.nice.org.uk/page.aspx?o=259000 .</Citation><ArticleIdList><ArticleId IdType="pubmed">17234018</ArticleId></ArticleIdList></Reference><Reference><Citation>Kadish A, Dyer A, Daubert JP, Quigg R, Estes NAM, Anderson KP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med. 2004;350:2151–2158.</Citation><ArticleIdList><ArticleId IdType="pubmed">15152060</ArticleId></ArticleIdList></Reference><Reference><Citation>Hohnloser SH, Kuck KH, Dorian P, Roberts RS, Hampton JR, Hatala R, et al. Prophylactic use of an implantable cardioverter defibrillator after acute myocardial infarction. N Engl J Med. 2004;351:2481–2488.</Citation><ArticleIdList><ArticleId IdType="pubmed">15590950</ArticleId></ArticleIdList></Reference><Reference><Citation>Raviele A, Bongiorni MG, Brignole M, Cappato R, Capucci A, Gaita F, et al. Which strategy is “best” after myocardial infarction? The Beta-blocker Strategy plus Implantable Cardioverter Defibrillator Trial: rationale and study design. Am J Cardiol. 1999;83(5B)(111D):104D.</Citation><ArticleIdList><ArticleId IdType="pubmed">10089851</ArticleId></ArticleIdList></Reference><Reference><Citation>Steinbeck G, Andresen D, Senges J, et al. Immediate Risk Stratification Improves Survival (IRIS): study protocol. Europace. 2004;6:392–399.</Citation><ArticleIdList><ArticleId IdType="pubmed">15294263</ArticleId></ArticleIdList></Reference><Reference><Citation>Sanders G, Hlatky MA, Owens DK. Cost effectiveness of implantable cardioverter defibrillators. N Engl J Med. 2005;353:1471–1480.</Citation><ArticleIdList><ArticleId IdType="pubmed">16207849</ArticleId></ArticleIdList></Reference><Reference><Citation>Goldman L. Cost-effectiveness in a flat world - can ICDs help the United States get rhythm? N Engl J Med. 2005;353:1513–1515.</Citation><ArticleIdList><ArticleId IdType="pubmed">16207856</ArticleId></ArticleIdList></Reference><Reference><Citation>Al-Khatib SM, Anstrom KJ, Eisenstein EL, Peterson ED, Jollis JG, Mark DB, et al. Clinical and economic implications of the multicenter automatic defibrillator implantation trial-II. N Engl J Med. 2005;142:593–600.</Citation><ArticleIdList><ArticleId IdType="pubmed">15838065</ArticleId></ArticleIdList></Reference><Reference><Citation>Pauker SG, Estes NAM, Salem DN. Preventing sudden cardiac death: can we afford the benefit? Ann Intern Med. 2005;142:664–666.</Citation><ArticleIdList><ArticleId IdType="pubmed">15838073</ArticleId></ArticleIdList></Reference><Reference><Citation>McClellan MB, Tunis SR. Medicare coverage of ICDs. N Engl J Med. 2005;352:222–224.</Citation><ArticleIdList><ArticleId IdType="pubmed">15659721</ArticleId></ArticleIdList></Reference><Reference><Citation>Blue Cross Blue Shield Technology Evaluation Center Assessment Program. Blue Cross Blue Shield 2004;Volume 19(Number 5) Special report: cost-effectiveness of implantable cardioverter defibrillators in a MADIT II population.</Citation><ArticleIdList><ArticleId IdType="pubmed">15241900</ArticleId></ArticleIdList></Reference><Reference><Citation>Redfield MM, Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289:194–202.</Citation><ArticleIdList><ArticleId IdType="pubmed">12517230</ArticleId></ArticleIdList></Reference><Reference><Citation>Jauhar S, Slotwiner DJ. The economics of ICDs. N Engl J Med. 2004;351:2542–2544.</Citation><ArticleIdList><ArticleId IdType="pubmed">15590958</ArticleId></ArticleIdList></Reference><Reference><Citation>Tu JV, Austin P, Naylor CD, Iron K, Zhang H. Acute myocardial infarction outcomes in Ontario. Naylor CD, Slaughter PM, . Cardiovascular Health and Services in Ontario: An ICES Atlas. Toronto: Institute for Clinical Evaluative Sciences. 1999:83–110. In. editors.</Citation></Reference><Reference><Citation>Sanders GD, Hlatky MA, Every NR, McDonald KM, Heidenreich PA, Parsons LS, et al. Potential cost-effectiveness of prophylactic use of the implantable cardioverter defibrillator or amiodarone after myocardial infarction. Ann Intern Med. 2001;135(10):870–883.</Citation><ArticleIdList><ArticleId IdType="pubmed">11712877</ArticleId></ArticleIdList></Reference><Reference><Citation>Plummer CJ, Irving RJ, McComb JM. Implications of national guidance for implantable cardioverter defibrillation implantation in the United Kingdom. Pacing Clin Electrophysiol. 2003;26:479–482.</Citation><ArticleIdList><ArticleId IdType="pubmed">12687872</ArticleId></ArticleIdList></Reference><Reference><Citation>Every NR, Hlatky MA, McDonald KM, Weaver WD, Hallstrom AP. Estimating the proportion of post-myocardial infarction patients who may benefit from prophylactic implantable defibrillator placement from analysis of the CAST registry. Cardiac Arrhythmia Suppression Trial. Am J Cardiol. 1998;82(5):683–685.</Citation><ArticleIdList><ArticleId IdType="pubmed">9732904</ArticleId></ArticleIdList></Reference><Reference><Citation>Hunt SA, Abraham WT, Chin MH, Feldman AM, Francis GS, Ganiats TG, et al. ACC/AHA 2005 guideline update for the diagnosis and management of chronic heart failure in the adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure) Available from: www.acc.org/clinical/guidelines/failure/index.pdf. (Accessed Dec 2005)</Citation><ArticleIdList><ArticleId IdType="pubmed">16160202</ArticleId></ArticleIdList></Reference><Reference><Citation>Swedberg K, Cleland J, Dargie H, Drexler H, Follath F, Komajda M, et al. Guidelines for the diagnosis and treatment of chronic heart failure. The Task Force for the Diagnosis and Treatment of CHF of the European Society of Cardiology. Available from: www.escardio.org/NR/rdonlyres/8A2848B4-5DEB-41B9-9A0A-5B5A90494B64/0/CHFFullTextehi205FVFW170505.pdf. (Accessed June 2005)</Citation><ArticleIdList><ArticleId IdType="pubmed">15901669</ArticleId></ArticleIdList></Reference><Reference><Citation>Tang AS, Ross H, Simpson CS, Mitchell LB, Dorian P, Goeree R, et al. Canadian Cardiovascular Society/Canadian Heart Rhythm Society position paper on implantable cardioverter defibrillator use in Canada. Can J Cardiol. 2005;21:11A–18A.</Citation><ArticleIdList><ArticleId IdType="pubmed">15953939</ArticleId></ArticleIdList></Reference><Reference><Citation>Arnold JMO, Liu P, Demers C, Dorian P, Giannetti N, Haddad H, et al. Canadian Cardiovascular Society consensus conference recommendations on heart failure 2006: diagnosis and management. Can J Cardiol. 2006;22:23–45.</Citation><ArticleIdList><ArticleId IdType="pmc">PMC2538984</ArticleId><ArticleId IdType="pubmed">16450016</ArticleId></ArticleIdList></Reference><Reference><Citation>Aetna. Cardioverter defibrillators. Clinical Policy Bulletins. Number 0585. Available from: www.aetna.com. (Accessed Apr 2005)</Citation></Reference><Reference><Citation>Zareba W. Late breaking clinical trials: noninvasive electrocardiology and outcome in MADIT II patients. North American Society of Pacing and Electrophysiology (NASPE) for the MADIT II Investigators. Available from: www.naspehighlights.org. (Accessed Feb 2003)</Citation></Reference></ReferenceList></PubmedData></PubmedArticle><PubmedBookArticle><BookDocument><PMID Version="1">21290759</PMID><ArticleIdList><ArticleId IdType="bookaccession">NBK7491</ArticleId></ArticleIdList><Book><Publisher><PublisherName>Academia</PublisherName><PublisherLocation>Moscow</PublisherLocation></Publisher><BookTitle book="mechano">Mechanosensitivity in Cells and Tissues</BookTitle><PubDate><Year>2005</Year></PubDate><AuthorList Type="editors" CompleteYN="Y"><Author ValidYN="Y"><LastName>Kamkin</LastName><ForeName>Andre</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Kiseleva</LastName><ForeName>Irina</ForeName><Initials>I</Initials></Author></AuthorList><Isbn>5769525908</Isbn></Book><ArticleTitle book="mechano" part="A1365">Mechano-Electric Feedback and Atrial Arrhythmias | Numerous clinical evidences as well as experimental studies show an increased vulnerability to atrial arrhythmias by acute stretch of the atrial walls. However, the mechanism by which atrial dilatation favours the development of sustained atrial tachyarrhythmias, such as atrial fibrillation (AF), is not fully understood. The effects of acute atrial dilatation on the substrate of atrial fibrillation were investigated in Langendorff-perfused rabbit heart. Increased atrial pressure resulted in a significant increase in vulnerability to AF, while release of the atrial stretch resulted in prompt cardioversion of AF. Atrial stretch has been shown to modulate the atrial vulnerable parameters. Stretch-induced shortening in atrial refractoriness and impairment of atrial conduction have been demonstrated. Atrial stretch through the modulation of the electrophysiological properties may not only favour the onset of arrhythmias but may also modulate the rate of reentrant arrhythmias. Cyclic variations in atrial volume following ventricular contraction modulate the atrial flutter cycle length and account for the spontaneous variability of the arrhythmia. |
1,085 | Rectilinear biphasic waveform defibrillation of out-of-hospital cardiac arrest. | The rectilinear biphasic (RLB) waveform has been shown to effectively defibrillate short-duration ventricular fibrillation (VF) at significantly lower energies than a monophasic damped sine (MDS) waveform. This article reports RLB waveform defibrillation effectiveness for patients presenting in VF during out-of-hospital cardiac arrest when compared with historical MDS effectiveness.</AbstractText>External RLB defibrillators were deployed in the Omaha Fire Department's emergency medical services (EMS) system. The RLB defibrillators delivered an escalating three-shock sequence of 120, 150, and 200 J. The results observed during the first year of full deployment were compared with the results observed during the previous year when only MDS defibrillators were deployed in the system. The MDS defibrillators delivered an escalating three-shock sequence of 200, 300, and 360 J. Defibrillation was defined as termination of VF for at least 5 seconds after a defibrillation shock.</AbstractText>There were 141 adult patients presenting in VF without trauma during the first year using RLB defibrillators. By comparison, there were 153 adult patients during the comparable year using MDS defibrillators. The 120-J RLB shocks had a significantly higher first-shock rate of successful VF termination (67%, 95% CI: 59%-75%) compared with the initial 200-J MDS shocks (48%, 95% CI: 40%-57%, p < 0.0025; odds ratio 2.14 [1.33-3.42]). The number of patients who were defibrillated to a return of spontaneous circulation with a sinus rhythm was significantly greater (25%, 95% CI: 18%-33%) when using the RLB defibrillator compared with using the MDS defibrillator (15%, 95% CI: 10%-22%, p = 0.05; odds ratio 1.85 [1.04-3.31]).</AbstractText>The RLB defibrillator terminated the VF of patients in out-of-hospital cardiac arrest with superior rates using significantly less energy compared with historical rates for a higher-energy MDS defibrillator.</AbstractText> |
1,086 | Protective effect of taurine against free radicals damage in the rat myocardium. | Free radicals are highly cytotoxic to the heart and are involved in ischemia/reperfusion injury. In this study, we tested the ability of taurine to neutralize the deleterious effects of free radicals generated ex vivo and in vitro. Taurine was added at a concentration of 0.1 mM to the drinking water of experimental rats during 6 months. The animal hearts were then isolated and submitted to regional ischemia and reperfusion; ventricular fibrillation was significantly reduced as compared to a control group of non-treated animals. Moreover, at a concentration of 1 mM, taurine provided significant cardio-protection against the deleterious effect of free radicals generated by the electrolysis of Krebs-Henseleit buffer. When isolated hearts were perfused with electrolysed buffer, extensive fiber necrosis occurred, as observed by staining with nitro blue tertrazolium, a soluble dye which yields a dark blue formazan stain in the presence of reducing agents This stain was barely detectable when taurine was added to the perfusing electrolysed buffer. To further understand the protecting mechanism of taurine, we used xanthine-xanthine-oxidase as a superoxide (O2-) generating system and monitored the O2- through yield O2--dependent cytochrome c reduction. We demonstrated that taurine did not affect this system, which indicated that it did not scavenge O2- directly. On the other hand, taurine inhibited the auto-oxidation of adrenaline to adrenochrome at pH 7.8 where this auto-oxidation is O2--independent and superoxide dismutase insensitive. We thus conclude that taurine acts as a potent, but non-specific, scavenger of free radicals that cause heart damage and protects against reperfusion-induced ventricular |
1,087 | Morphological detection algorithms for the automatic implantable cardioverter/defibrillator (AICD). | To prevent sudden cardiac death of patients who are at risk from long standing tachyarrhythmia the implantable cardioverter defibrillator (ICD) is the first choice therapy. ICDs use a range of electrostimuli up to defibrillation, which is a non synchronous high energy shock, whereas cardioversion is synchronous with the ECG. In order to know when and how to react, a detection algorithm, which analyses an intracardial electrocardiogram (ECG) and classifies the heart rhythm, is implemented in every ICD. All detection algorithms use the heart rate to classify the different heart rhythms roughly. If a tachycardia is detected, it is important to discriminate between a ventricular tachycardia, which is life threatening and a supraventricular tachycardia, which is much less threatening. To be able to make this distinction the detection algorithms analyse the behaviour of the heart cycle intervals, the ECG-morphology or in addition to the ventricular ECG, an atrial ECG. In this paper morphological algorithms will be evaluated and newly developed algorithms will be presented. Recent algorithms use the mathematical wavelet theory. The evaluation shows that these get better results than all but one of the simpler classical morphological algorithms. A new wavelet based algorithm, developed by the authors, exhibits the best detection results. |
1,088 | Effect of remodelling, stretch and ischaemia on ventricular fibrillation frequency and dynamics in a heart failure model. | The dynamics of ventricular fibrillation (VF) in the presence of heart failure (HF) are different from those in the normal heart. This has been attributed solely to HF-induced electrophysiologic remodelling. We hypothesized that acute stretch and ischaemia, which are normally present during VF, might contribute significantly to the altered VF dynamics in HF.</AbstractText>HF was induced in eight sheep by rapid ventricular pacing for 4-6 weeks. Eight sheep served as controls. Optical mapping of isolated hearts was performed during VF at low intraventricular pressure (0-5 mm Hg), high pressure (25-30 mm Hg, in six HF and six controls), and at low pressure after 5 min of global ischaemia (six HF, five controls). Maximum dominant frequency (DF(max)), singularity point (SP) density and number of SP lasting more than one revolution (rotors) were analyzed. Possible statistical interactions between HF and ischaemia (HF x ischaemia) or stretch (HF x stretch) were evaluated.</AbstractText>At low pressure, VF in HF was slower (13% reduction in DF(max)) and more organized than in control: 33% less SPs and 74% less rotors with 20% longer life spans. Acute stretch did not affect DF(max) but increased SP and rotors density similarly in both groups (no interaction HF x stretch). In controls, ischaemia caused a marked decrease in DF(max), SP density and incidence of rotors. However, in HF animals, the ischaemia-induced decrease in SP density was virtually abolished, indicating a significant interaction HF x ischaemia (p<0.005).</AbstractText>HF remodelling decreases VF rate and increases VF organization. Acute stretch partially reverses these effects by a mechanism that is independent of remodelling. The effects of acute ischaemia on VF dynamics are significantly attenuated in HF compared to normal hearts.</AbstractText> |
1,089 | Three-day magnesium administration prevents atrial fibrillation after coronary artery bypass grafting. | The efficacy of magnesium administration in preventing the occurrence of atrial fibrillation after coronary artery bypass grafting surgery remains controversial. Optimal dose and timing of the administration also await clarification. The purpose of this study was to assess the effect of 3-day postoperative infusion of magnesium on postoperative atrial fibrillation and to find factors that can influence the efficacy of this treatment.</AbstractText>After institutional review board approval, a retrospective study was conducted reviewing 200 consecutive patients who underwent isolated, initial coronary artery bypass grafting operation. The first 100 patients did not receive the prophylactic treatment, whereas the next 100 patients were treated with magnesium postoperatively. Patients in the magnesium-treated group received 10 mmol (2.47 g) of magnesium sulfate (MgSO4 * 7H2O) infused daily for 3 days after surgery.</AbstractText>The incidence of postoperative atrial fibrillation was 35% in the untreated group compared with 16% in the magnesium-treated group (p = 0.002). Multivariate logistic regression analysis revealed that advanced age, decreased left ventricular ejection fraction, and absence of magnesium therapy were independent predictors of postoperative atrial fibrillation. For patients receiving the magnesium therapy, advanced age and decreased ejection fraction were the independent factors that predicted the arrhythmia.</AbstractText>Postoperative 3-day magnesium infusion is effective in reducing the incidence of atrial fibrillation occurring after coronary artery bypass grafting surgery. However, in older patients or in patients with reduced left ventricular function, magnesium treatment alone is insufficient for prophylaxis of postoperative atrial fibrillation.</AbstractText> |
1,090 | Critical aortic stenosis in early infancy: surgical treatment for residual lesions after balloon dilation. | The optimal management for critical aortic stenosis in early infancy continues to challenge cardiologists and cardiac surgeons. We present a review of our experience with the surgical treatment of residual aortic valve disease after percutaneous balloon dilation for critical aortic stenosis in early infancy.</AbstractText>Since 1989, 11 of the 38 patients who survived aortic balloon dilation (28.9%) have undergone surgical treatment for residual aortic valve dysfunction. Median time from aortic balloon dilation to surgical intervention was 7 months (range 1 to 56 months). Residual aortic stenosis was the predominant problem in 8 patients and aortic regurgitation was predominant in 2 patients.</AbstractText>Aortic valvuloplasty was possible in 5 children; pulmonary autograft replacement of the aortic valve was performed in 6 children. Two children underwent a Ross-Konno procedure because of annulus hypoplasia and severe left ventricular outflow tract obstruction. Two early deaths occurred after a Ross-Konno procedure, both with findings of severe left ventricular fibroelastosis at the pathologic examination. Median follow-up time was 5 years (range 1 month to 11.9 years). No late deaths occurred. One patient with moderate-severe aortic valve regurgitation after aortic valvuloplasty underwent a successful Ross operation. All 9 patients are asymptomatic and are in good clinical condition.</AbstractText>We are convinced that the best aortic valve in the pediatric age group is the native one, provided it can function acceptably. However, in cases where conservative surgical treatment fails to yield a functional aortic valve, replacement of the valve is indicated, and the best aortic valve substitute in infants is the pulmonary autograft because of its potential for growth.</AbstractText> |
1,091 | Outcomes of patients with acute coronary syndromes and prior percutaneous coronary intervention: a pooled analysis of three randomized clinical trials. | We sought to characterize the outcomes of patients with a prior percutaneous coronary intervention (PCI) who presented with a non-ST-segment elevation acute coronary syndrome (ACS).</AbstractText>We analysed the 30 and 180 day outcomes of 3012 patients with prior PCI and 21 154 patients without prior PCI enrolled in three randomized ACS trials (GUSTO IIb, PURSUIT, and PARAGON-B). The median (25th, 75th percentile) interval between the prior PCI and randomization was 647 (123, 1585) days. Patients with prior PCI had significantly more adverse baseline clinical characteristics, left ventricular dysfunction, and multi-vessel coronary artery disease. After adjusting for baseline characteristics and treatment, we found that patients with prior PCI had a significantly lower mortality rate at 30 days [hazard ratio (HR), 0.60; 95% confidence interval (CI), 0.45-0.80; P=0.0006] and 180 days (HR, 0.81; 95% CI, 0.66-0.98; P=0.029). However, no difference was observed in the composite of death or myocardial infarction (MI) at 30 days (HR, 0.95; 95% CI, 0.83-1.08; P=0.42) or 180 days (HR, 1.01; 95% CI, 0.90-1.13; P=0.90). Patients with prior PCI had a higher rate of MI at 180 days (13.3 vs. 12.0%; P=0.045). Prior-PCI patients had lower incidences of in-hospital cardiogenic shock, congestive heart failure (CHF), and atrial fibrillation.</AbstractText>Patients with prior PCI who present with non-ST-segment elevation ACS have a lower mortality rate than those without prior PCI.</AbstractText> |
1,092 | Prognostic risk of atrial fibrillation in acute myocardial infarction complicated by left ventricular dysfunction: the OPTIMAAL experience. | The present study aimed to determine the frequency and the impact on clinical outcome of atrial fibrillation (AF) in patients with acute myocardial infarction (AMI) and left ventricular dysfunction.</AbstractText>In the OPTIMAAL trial, 5477 patients with AMI and signs of left ventricular dysfunction were included. At baseline, 655 patients (12%) had AF, and 345 (7.2%) developed new-onset AF during follow-up (2.7 +/- 0.9 years). Older patients, patients with history of angina and worse Killip class had and developed AF more frequently (P < 0.001). Patients with AF at baseline were at increased risk relative to those without AF for mortality [adjusted hazard ratio (HR) of 1.32, P = 0.001] and for stroke (HR 1.77, P < 0.001). New-onset AF was associated with increased subsequent mortality for the first 30 days following randomization (HR 3.83, P < 0.001) and the entire trial period (HR 1.82, P < 0.001). Risk of stroke was increased for the first 30 days (HR 14.6, P < 0.001) and for the whole trial period (HR 2.29, P < 0.001).</AbstractText>AF is frequently observed in patients with AMI complicated by heart failure. Current AF, and the development of new AF soon after AMI, is associated with increased risk of death and stroke.</AbstractText> |
1,093 | Prognostic influence of mitral regurgitation prior to a first myocardial infarction. | Mitral regurgitation (MR) following an acute myocardial infarction (AMI) confers an adverse prognosis during long-term follow-up. There are no studies evaluating the influence of pre-AMI MR in the short- and long-term prognosis of such patients. Our aim was to assess the prognostic value of pre-AMI MR in the short- and long-term follow-up of patients who suffered a first AMI and to assess its influence on left ventricular haemodynamics.</AbstractText>Sixty-eight consecutive patients with a first AMI and an echocardiographic study before AMI (<3 months) were included in the study. The pre-AMI echo was performed for various reasons. Of these 68 patients, 42 had pre-AMI MR (Group 1) and 26 showed no pre-AMI MR (Group 2). The presence of degenerative changes at the level of the mitral valve was confirmed in all cases. Patients with any other cause of MR were excluded. Clinical and echocardiographic variables for both phases (pre-AMI and post-AMI) were analysed and patients were followed up. Mean age was 75.5+/-9.5 years; there were 38 males (55.9%). There were no statistical differences in baseline clinical variables between the groups, except for the presence of pre-AMI atrial fibrillation, which was more frequent in Group 1 (21.4 vs. 0%; P = 0.01). After AMI, only end-diastolic left ventricular diameter was significantly larger in Group 1 (54.9 +/- 4.7 vs. 48.1 +/- 5.6 mm; P < 0.001). During long-term follow-up, median survival times were 912 days (interquartile range: 690 days) in Group 1 and 1423 days (interquartile range: 520 days) in Group 2 (Log-rank P = 0.02). The multivariable analysis showed that the presence of pre-AMI MR relates to a statistically significant relationship with a worse post-AMI evolution [relative risk (95% confidence interval): 3.8 (1.1-13.1); P = 0.037].</AbstractText>The present study shows that the presence of pre-AMI MR is an independent prognostic marker among those patients suffering a first AMI.</AbstractText> |
1,094 | Functional impact of rate irregularity in patients with heart failure and atrial fibrillation receiving cardiac resynchronization therapy. | Atrial fibrillation (AFib) with a rapid ventricular response may adversely impact cardiac performance, especially in patients with heart failure. However, it remains uncertain whether rhythm irregularity per se has unfavourable effects apart from tachycardia, and whether rate regularization alone can improve heart function.</AbstractText>Nine subjects with chronic AFib, atrioventricular nodal block, and symptomatic heart failure (ejection fraction 14-30%) were studied using a pressure-volume catheter. Ventricles were biventricularly paced (RV-apex, LV-lateral wall) at 80 or 120 min(-1) mean rate, using regular or irregular, Poisson-distributed stimulation. At 80 min(-1), ventricular function was similar between the two pacing modes. However, at 120 min(-1), irregular pacing impaired systolic (dP/dt(max): -8.2%, P<0.001) and diastolic function (dP/dt(min): +21%, P<0.001, LV end-diastolic pressure: +26%, P=0.007) compared with regular rate pacing. Contractile function during irregular pacing varied with the ratio of preceding/pre-preceding intercycle (RR) interval (dP/dt(max): 80 b.p.m.: r=0.69; 120 b.p.m.: r=0.74), whereas pre-load had little effect on instantaneous contractility.</AbstractText>In heart failure subjects with AFib, RR-interval irregularity worsens cardiac function at elevated but not at normal range heart rate. Overall rate control is most important in these patients while rate regularization of rapid AFib may impart additional benefits.</AbstractText> |
1,095 | Comparative assessment of right, left, and biventricular pacing in patients with permanent atrial fibrillation. | Left ventricular (LV) and biventricular (BiV) pacing are potentially superior to right ventricular (RV) apical pacing in patients undergoing atrioventricular (AV) junction ablation and pacing for permanent atrial fibrillation.</AbstractText>Prospective randomized, single-blind, 3-month crossover comparison between RV and LV pacing (phase 1) and between RV and BiV pacing (phase 2) performed in 56 patients (70+/-8 years, 34 males) affected by severely symptomatic permanent atrial fibrillation, uncontrolled ventricular rate, or heart failure. Primary endpoints were quality of life and exercise capacity. Compared with RV pacing, the Minnesota Living with Heart Failure Questionnaire (LHFQ) score improved by 2 and 10% with LV and BiV pacing, respectively, the effort dyspnoea item of the Specific Symptom Scale (SSS) changed by 0 and 2%, the Karolinska score by 6 and 14% (P<0.05 for BiV), the New York Heart Association (NYHA) class by 5 and 11% (P<0.05 for BiV), the 6-min walked distance by 12 (+4%) and 4 m (+1%), and the ejection fraction by 5 and 5% (P<0.05 for both). BiV pacing but not LV pacing was slightly better than RV pacing in the subgroup of patients with preserved systolic function and absence of native left bundle branch block. Compared with pre-ablation measures, the Minnesota LHFQ score improved by 37, 39, and 49% during RV, LV, and BiV pacing, respectively, the effort dyspnoea item of the SSS by 25, 25, and 39%, the Karolinska score by 39, 42, and 54%, the NYHA class by 21, 25, and 30%, the 6-min walking distance by 35 (12%), 47 (16%), and 51 m (19%) and the ejection fraction by 5, 10, and 10% (all differences P<0.05).</AbstractText>Rhythm regularization achieved with AV-junction ablation improved quality of life and exercise capacity with all modes of pacing. LV and BiV pacing provided modest or no additional favourable effect compared with RV pacing.</AbstractText> |
1,096 | [Effect of tetradrine on electrophysilogic changes caused by rising of left ventricular preload in guinea pigs]. | To investigate the changes of guinea pig heart electrophysiological properties caused by increasing left ventricular preload, and to assess the effects of tetradrine on these changes.</AbstractText>Working model preparation of guinea pig hearts in vitro was used, and the preload of left ventricle was increased by adjusting the prefusion pressure of left atria. The changes of heart electrophysiologic parameters including monophasic action potential duration (MAPD90), monophasic action potential amplitude (MAPA), effective refractory period (ERP) and ventricular fibrillation threshold (VFT) were observed before and after altering the preload of left ventricle, and compared in the absence and presence of tetradrine, streptomycin or verapamil.</AbstractText>The rising of left ventricular preload led to shortening of MAPD90, ERP, and to descent of MAPA, VFT (all P<0.01). Both Tetradrine and streptomycin inhibited these changes of heart electrophysiologic parameters caused by elevation of left ventricular afterload (all P<0.01). In contrast, verapamil had no effects on the preload-related electrophysiological changes (all P>0.05).</AbstractText>Electrophysiologic changes caused by increasing left ventricular preload may be inhibited by tetrandrine, through inhibition of stretch-activated ion channels.</AbstractText> |
1,097 | [A case of cardiogenic syncope in a drug-addict patient]. | Torsade de pointes is a polymorphic ventricular tachycardia, associated with prolonged QT interval and characterized by twisting of the mean electrical axis of the QRS complexes around an isoelectric line. The long QT syndrome can be divided into two categories, congenital and acquired. The congenital long QT syndrome may be caused by some gene mutation, whereas the acquired form is usually associated with drugs and electrolyte imbalance. It usually remains asymptomatic or causes presyncope, although it may degenerate into ventricular fibrillation and may cause sudden death. The different presentation depends on the polymorphism that characterizes genotypic and phenotypic expression of proteic channel subunits, and on drug toxicity that provoke subunit dysfunction. The case report presented here is an example of prolonged QT interval syndrome in a patient with cocaine abuse and electrolyte disturbances. |
1,098 | Induction of ventricular arrhythmias following mechanical impact: a simulation study in 3D. | Commotio cordis, mechanical induction of heart rhythm disturbances, including sudden cardiac death, in the absence of corresponding structural damage, has been reported with increasing frequency in young individuals participating in sporting activities. Recently, the electrophysiological changes during c. cordis have been attributed to mechano-electric feedback, and particularly, to the recruitment of stretch-activated ion channels. The underlying mechanisms, however, by which a mechanical impact results in ventricular fibrillation, remain unknown. This study employs a 3D realistic model of rabbit ventricular geometry and fiber orientation to elucidate the electrophysiological mechanisms involved in arrhythmia induction following acute mechanical stimulation of the heart. Impact effects are modeled through stretch-activated ion channel activation in a 3D region of the ventricles representing the impact profile. Both cation-nonselective and potassium-selective stretch-activated ion channels are recruited upon mechanical impact. The impact is administered at various coupling intervals following pacing at the apex. To aid in the interpretation of results, the effect of mechanical stimulation on single cell action potentials is also examined. The results demonstrate that the region of impact is characterized by different types of cellular responses, including generation of a new action potential, shortening, or lengthening of action potential duration. The impact induces sustained reentry only when (1) a new activation is elicited by mechanical stimulation (caused by activation of cation-nonselective stretch-activated ion channels), and (2) upon return to the original region of impact, this activation does not encounter an extension of action potential duration (prevented by activation of potassium-selective stretch-activated ion channels). |
1,099 | [Subclinical thyroid disease: subclinical hypothyroidism and hyperthyroidism]. | Subclinical hypothyroidism (SHT) and subclinical hyperthyroidism (SCH) are defined as normal serum free T4 and T3 levels associated with elevated (SHT) or subnormal (SCH) serum TSH levels, respectively. Symptoms and signs of thyroid dysfunction are scarce. The prevalence is low. In SHT, total cholesterol and LDL-C are modestly elevated and levothyroxine may influence the lipids levels. There is decreased cardiac contractility and increased peripheral vascular resistance that improve with treatment. SCH is associated with atrial fibrillation, increased cardiac contractility and left ventricular mass, diastolic and systolic dysfunction that can be reversed with beta-adrenergic antagonists. Bone density is reduced in SCH. Depression, panic disorders and alterations in cognitive testing are frequent in SHT. Treatment of SHT is recommended for serum TSH levels greater than 8 mU/L and presence of thyroid antibodies. Endogenous SCH should be treated for serum TSH levels less than 0.1 mU/L, in the presence of symptoms and in elderly patents. |
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