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1,300 | [Long survival with chronic ventricular fibrillation under support of uni-left-ventricular assist system]. | Few minutes of suspended malignant ventricular arrhythmia may be permitted for the patient with left ventricular assist system (LVAS). However, longer and continuous ventricular arrhythmia, especially ventricular fibrillation (Vf), may induce the low output of LVAS, which leads circulatory collapse immediately. Our presenting case is a female dilated cardiomyopathy patient who has been supported with LVAS. Four months after the LVAS installation, her electrocardiogram has changed to Vf without any symptoms. Her ventricular function has never recovered, even ventricular tachycardia. She has been a candidate of heart transplantation for more than 19 months with this rare hemodynamic condition (LVAS+Vf), like the Fontan circulation. Her performance status is limited due to deceasing of the LVAS flow, which caused by the change of her position: 2.5-2.9 l/min (lie down) to 2.0 l/min (rise). Her peak VO2/W is 6.9 ml/min/kg measured by the cardio-pulmonary exercise test. However, she has developed her general status by doing rehabilitation program and is able to walk for more than 100-150 meters. |
1,301 | Total failure to sense ventricular fibrillation with inappropriate defibrillator sensitivity adjustment. | Automatic Sensitivity Control, unique to St. Jude defibrillators, allows for programmable sensitivity threshold and refractory periods. However, inappropriate programming can lead to marked undersensing and potentially lethal complications. We report a case of complete failure to sense ventricular fibrillation with inappropriate sensitivity adjustments. Detailed review of the parameters with induction of ventricular fibrillation must be performed to assure adequate safety. |
1,302 | Resumption of atrioventricular conduction by levosimendan after radiofrequency ablation of the AV node: | We report the case of a patient in whom radiofrequency catheter ablation of the AV node was initially successfully performed for persistent atrial fibrillation with fast ventricular rate, but in whom atrioventricular conduction transiently resumes following therapy with levosimendan. Plausible hypothesis are discussed as well as potential implications. |
1,303 | Quantification of atrial tachyarrhythmia burden with an implantable pacemaker before and after pulmonary vein isolation. | Long-term efficacy of pulmonary vein (PV) ostial isolation for paroxysmal atrial fibrillation is difficult to assess. We evaluated the net duration of atrial tachyarrhythmia episodes (burden), atrial tachyarrhythmia episode frequency, and quality-of-life (QOL) before and after PV isolation in patients with an existing pacemaker featuring extensive diagnostic capabilities. Due to frequent recurrences of paroxysmal atrial fibrillation, PV isolation was performed 21 +/- 10 months following pacemaker implantation on 12 patients (57 +/- 5 years) with normal left ventricular function. Atrial tachyarrhythmia burden (ATB) and episode frequency were monitored daily by the device both pre- and postablation. QOL questionnaires were collected at ablation and 1, 3, and 6 months thereafter. Patients were followed for 20 +/- 9 and 11 +/- 9 months pre- and postablation, respectively. Membrane-active antiarrhythmic medications were discontinued after ablation in 8 of 12 patients. PV isolation resulted in a significant reduction of ATB from a median of 3.2 hours/day (preablation) to 0.2 hours/day (postablation, P < 0.01, Wilcoxon signed-rank test). The median tachyarrhythmia frequency was 6.4 episodes/day (preablation) and 0.3 episodes/day (postablation, P = 0.09). QOL measures significantly improved over the data collection intervals (P < 0.05). Tachyarrhythmia burden was positively associated with Symptom Checklist frequency and severity (P < 0.01). Significant long-term reductions in total ATB (symptomatic and asymptomatic) were observed. Furthermore, reductions in ATB were associated with improvements in QOL measures. Extensive monitoring capabilities in implantable devices help provide complete disclosure on the effect of PV isolation in paroxysmal atrial fibrillation patients. |
1,304 | Strategies for perioperative arrhythmias. | Rapid atrial arrhythmias affect close to one million elderly Americans who undergo cardiac or non-cardiac operations annually and have been associated with prolonged hospital stays. In contrast, bradyarrhythmias or ventricular arrhythmias severe enough to require treatment occur in less than 1% of patients who undergo all types of surgery, including cardiac. This article focuses on new issues leading to the improved understanding of the pathophysiology and mechanisms of post-operative atrial arrhythmias. New approaches directed at prophylaxis and acute therapy of atrial arrhythmias are discussed, as are recommendations to prevent thromboembolic events. Practice and research agenda are proposed. |
1,305 | Impact of nesiritide on health care resource utilization and complications in patients with decompensated heart failure. | To determine the impact of nesiritide on health care resource utilization and complications in patients hospitalized with decompensated heart failure.</AbstractText>Retrospective case-control study.</AbstractText>United States hospitals.</AbstractText>Two hundred sixteen patients hospitalized for decompensated heart failure.</AbstractText>One hundred eight patients who received a nesiritide infusion for a minimum of 12 hours during the first 48 hours after hospital admission were matched with 108 patients not receiving nesiritide. Health care resource utilization, consisting of hospital length of stay (LOS), rate of rehospitalization within 90 days, concomitant drugs administered, and laboratory and diagnostic tests, was determined for each hospital admission. Rates of adverse events also were recorded. Patients receiving nesiritide had a significantly shorter LOS in a critical care unit (p=0.03). General medical ward or step-down unit LOS was not different between the treatment groups. A favorable trend toward a lower rate of rehospitalization over the 90-day follow-up period was observed with nesiritide (p=0.07). The number of patients who developed life-threatening ventricular arrhythmias and hypotension was similar for both treatment groups. However, in patients receiving nesiritide, significantly less atrial fibrillation (p=0.03) and renal dysfunction (p=0.04) occurred compared with patients not receiving nesiritide.</AbstractText>Nesiritide therapy is associated with significant reductions in both health care resource utilization and complications in patients with decompensated heart failure.</AbstractText> |
1,306 | Isolated noncompaction of the left ventricular myocardium in an elderly patient. | Noncompaction of the ventricular myocardium (NVM) is a rare disorder of endomyocardial morphogenesis characterized by numerous, prominent trabeculations and deep intertrabecular recesses. It is commonly associated with congenital heart disease, but the isolated form (INVM) is not associated with other structural heart diseases. Clinical reports of INVM have been limited to a few case reports and small series of pediatric patients. INVM is considered to be a form of congenital abnormal endomyocardial morphogenesis caused by abnormal cessation of the embryonic development of the ventricular myocardium; most reported cases have been pediatric patients, and autopsy cases of elderly patients have been quite rare. In the present case, an elderly female had INVM associated with severely disturbed left ventricular (LV) function and an enlarged left ventricle similar to dilated cardiomyopathy. The echocardiogram showed prominent trabeculations and deep intertrabecular recesses of the LV walls, especially in the posterior and apical areas. LV contrast echocardiography revealed markedly protruberant trabeculations, which were also observed with computed tomography. Five years later, the patient died of refractory heart failure and ventricular fibrillation. The autopsy revealed numerous excessively prominent trabeculations in the LV myocardium, with deep intertrabecular recesses containing thrombi. |
1,307 | Brugada syndrome presenting with sustained monomorphic ventricular tachycardia. | Typically Brugada syndrome presents with either ventricular fibrillation or polymorphic ventricular tachycardia that may result in sudden death or syncope in patients without any structural heart disease. We report the case of a patient with Brugada syndrome who presented atypically with recurrent presyncope following physical exertion due to sustained monomorphic ventricular tachycardia, which appeared to be sensitive to both adenosine and catecholamine. He refused ICD implantation but remained asymptomatic on treatment with a beta-blocker. |
1,308 | Echocardiographic changes in patients with malignant phase hypertension: the West Birmingham Malignant Hypertension Register. | In order to study the echocardiographic abnormalities in consecutive patients with malignant phase hypertension (MHT), we reviewed echocardiograms of 31 patients (23 male; mean age 52+/-14 years) with MHT who were admitted to our unit. Trans-thoracic echocardiography was carried out in all patients, and echocardiographic measurements were compared with those of 39 patients (30 male; mean age 54+/-10 years) with controlled nonmalignant essential hypertension, and 32 (19 male; mean age 51+/-10 years) healthy normotensive volunteers. Patients with MHT had a significantly higher mean systolic and diastolic blood pressure (P<0.001) compared to the other two groups. MHT patients had significantly greater mean left atrial dimensions (P=0.002), as well as aortic root dimensions (P=0.01) and left ventricular (LV) dimensions (with the exception of the diastolic internal diameter) (P<0.001). MHT patients also had a mean larger LV mass and LV mass index (both P<0.001) when compared to the other two groups. The mean ejection fraction was also lower in the MHT group (P<0.001). In conclusion, patients with MHT have significant cardiac hypertrophy, in association with systolic dysfunction and dilated left atria, irrespective of the duration of known hypertension. These abnormalities may predispose MHT patients to cardiovascular complications including heart failure and cardiac arrhythmias, such as atrial fibrillation. |
1,309 | Failure to demonstrate myocardial protective effects of the ultra short-acting calcium antagonist clevidipine in a closed-chest reperfusion porcine model. | Restoration of myocardial perfusion is essential in acute myocardial infarction for the salvaging of myocardial tissue. However, reperfusion per se can provoke myocardial necrosis within the jeopardized tissue. Yet, no intervention has been successfully applied to the clinical situation in this matter. Clevidipine, an ultra-short acting calcium antagonist, has, in open-chest animal models, shown to reduce the extent of reperfusion injury. In the present study we intended to reproduce those findings in a closed-chest porcine model with a clinically applicable set up. Pigs were subjected to balloon occlusion of the left anterior descending coronary artery (LAD) for 45 minutes. During 25 minutes, starting 1 minute prior to reperfusion, clevidipine, Intralipid, or saline was infused antegradely into the endangered myocardium. As no significant effects on infarct size were achieved, the model was modified. In a second phase, different anesthesias were evaluated addressing the same issue. Nonetheless no significant effects on infarct size were observed. Different techniques of occluding LAD, in an open-chest model, were investigated in a third phase, and revealed no significant differences between the techniques. However, when comparing all the closed- versus open-chest models, significant reduction in infarct size by the use of clevidipine was only obtained in the open-chest models. We could not demonstrate any significant myocardial protective effect with clevidipine in our porcine, closed-chest, acute infarct, and reperfusion model. However, in a modified open-chest model we obtained significant reduction in infarct size. Further studies are required to explain the discrepancies. |
1,310 | Transvenous cryoablation of cardiac arrhythmias. | This study reports on the acute and long-term results of cryoablation in patients with supraventricular and ventricular tachycardia. One hundred fifty nine patients with cardiac arrhythmias (147 with supraventricular and 12 with ventricular tachycardia) were consecutively enrolled in our institution to undergo trnasvenous cryoablation with a new cryotechnology system (CryoCor trade mark ). This cryoablation system consists of a console, an articulating arm housing a pre-cooler, and a disposable sterile steerable bipolar 10-fr catheter. The N(2)O is used as a main refrigerant. The acute and chronic outcomes (after 15 months for patients with supraventricular tachycardia and 9 months for patients with ventricular tachycardia) were comparable to those using radiofrequency energy. From this study we concluded that transvenous cryoablation is a safe and effective therapy for the treatment of cardiac arrhythmias. |
1,311 | Limitations to antiarrhythmic drug use in patients with atrial fibrillation. | Of the antiarrhythmic agents currently marketed in Canada, 5 are commonly used to treat atrial fibrillation (AF). The impact of contraindications, warnings and precautions for the use of these drugs in patients with AF is not known. We evaluated the proportion of patients with AF for whom contraindications, warnings and/or precautions might limit the use of these commonly prescribed drugs and the proportion of patients actually receiving antiarrhythmic drugs despite the presence of contraindications and/or warnings.</AbstractText>A total of 723 patients with electrocardiographically confirmed, new-onset paroxysmal AF who were enrolled in the Canadian Registry of Atrial Fibrillation were used in this analysis. The 1996 Compendium of Pharmaceuticals and Specialties was used to obtain contraindications, warnings and precautions for use of 5 antiarrhythmic drugs: flecainide, quinidine, sotalol, amiodarone and propafenone. Proportions of patients with contraindications, warnings and/or precautions for use of any of these drugs owing to comorbid conditions or concomitant drug therapy were calculated, regardless of whether the drugs had been prescribed. We then calculated the proportion of patients taking each antiarrhythmic drug at 3 months despite contraindications and/or warnings.</AbstractText>At baseline, when conditions for contraindications and warnings were combined, 414 (57%), 235 (33%), 327 (45%), 285 (39%) and 272 (38%) patients had restrictions for the use of flecainide, quinidine, sotalol, amiodarone and propafenone respectively. Among 465 patients actually taking these medications at 3-month follow-up, 33.3% (2/6), 83.3% (40/48), 36.4% (92/253), 64.1% (25/39) and 34.5% (41/119) respectively had contraindications and/or warnings against their use. The burden of comorbid disease among patients with AF was noteworthy: 404 (56%) had structural heart disease, which included 227 (31%) with ischemic heart disease, 158 (22%) with left ventricular systolic dysfunction and 106 (15%) with heart failure.</AbstractText>The high burden of comorbid disease and concomitant drug use in a large proportion of patients with AF limits the suitability of existing antiarrhythmic drugs. Over one-third of patients with new-onset AF received antiarrhythmic drugs despite the presence of contraindications or warnings. Although such restrictions may not preclude the use of these drugs, the results demonstrate the need for new antiarrhythmic drugs with fewer limitations.</AbstractText> |
1,312 | Ventricular fibrillation frequency characteristics and time evolution in piglets: a developmental study. | Derived variables of ventricular fibrillation, such as the frequency distribution by fast Fourier transformation and its evolution over time, have been used to determine the optimum timing for defibrillation. We hypothesized that these frequency variables would differ among neonatal, young child and older child populations due to cardiac developmental and size differences. Such differences may have important implications for developing defibrillation algorithms for pediatric patients and for extrapolating adult defibrillation algorithms to children in VF.</AbstractText>Ventricular fibrillation was induced and recorded for 6 min in 4 kg (n = 11), 14 kg (n = 10), and 24 kg (n = 16) piglets, corresponding to neonatal, young child and older children. Mean, median, and dominant frequencies were computed in 30 s intervals and compared among weight classes.</AbstractText>All frequency variables in all weight groups showed first a decline at 1.25-1.75 min, followed by a gradual rise and plateau. There were significant differences for mean, median and dominant frequencies among weight classes. Specifically, 14 kg piglets showed higher frequency variables overall with a time evolution that was different from that of 4 and 24 kg piglets. Mean frequency showed the most stable time evolution with the least moment-to-moment variability.</AbstractText>The frequency waveform characteristics and time course are somewhat different in 14 kg piglets compared with 4 and 24 kg piglets. If similar differences are demonstrable among children of different weights and ages, AEDs designed to determine optimal timing of defibrillation shocks in adults by frequency waveform characteristics may require modification for use in children with VF.</AbstractText> |
1,313 | Effects of hypertonic versus isotonic infusion therapy on regional cerebral blood flow after experimental cardiac arrest cardiopulmonary resuscitation in pigs. | To evaluate the effects of hypertonic, isooncotic, and isotonic infusion therapy on cerebral blood flow (CBF) during and after cardiopulmonary resuscitation (CPR) from experimental cardiac arrest (CA).</AbstractText>In 32 domestic swine (13-23 kg) open chest CPR was initiated after 8 min of ventricular fibrillation. With the onset of CPR animals randomly received 2 ml/kg per 10 min of either hypertonic saline (HS: 7.2% NaCl), hypertonic-isooncotic HES-saline (HHS: 7.2% NaCl in 6% HES 200,000/0.5), isooncotic HES (6% HES 200,000/0.5), or isotonic (normal) saline (NS: 0.9% NaCl). Haemodynamic variables were monitored continuously, and coloured microspheres were used to measure CBF quantitatively before CA, during CPR, and 20, 90 and 240 min after restoration of spontaneous circulation (ROSC).</AbstractText>In HES/NaCl treated animals, CBF significantly decreased during CPR compared to the prearrest level (P < 0.01, respectively; MANOVA). In contrast, CBF was sustained during CPR in HS/HHS treated animals and significantly higher compared to animals receiving NS (P < 0.05, respectively). During recirculation severe postischaemic hypoperfusion as indicated by a decrease of CBF below the prearrest level, was present only in animals receiving HES and NS.</AbstractText>Hypertonic solutions (HS/HHS) applied during internal cardiac massage enhanced CBF during CPR and after ROSC.</AbstractText> |
1,314 | Electrical therapy for post defibrillatory pulseless electrical activity. | Defibrillation may convert ventricular fibrillation (VF) only to reveal profound mechanical dysfunction. Survival following this dysfunction, known as pulseless electrical activity (PEA) and electromechanical dissociation (EMD), is uncommon. We sought to evaluate an electrical therapy for primary post shock PEA following short duration VF.</AbstractText>Forty-eight episodes of VF, lasting 110 +/- 25 s, were induced in 16 anesthetized dogs. Following defibrillation, 35 episodes met PEA criteria (ABP < or = 36 mmHg diastolic and pulse pressure < or = 14 mmHg in the first 20 s post shock). These post defibrillation PEA episodes were either Not Treated (NT) or Treated (T) with packets of 4-20 monophasic 0.2 ms 50-100 Hz pulses of 20-60 V applied across the tip and coil of an integrated bipolar transvenous defibrillation lead positioned in the right ventricle. The therapeutic endpoint was return of spontaneous circulation (ROSC; self-sustained ABP > or = 60 mmHg diastolic and/or > or = 100 mmHg systolic) for over 2 min. In the Not Treated group, only 4 of 19 (21%) episodes spontaneously recovered to ROSC in 123 +/- 49 s while in the Treated group, 11 of 16 (69%) of the PEA episodes achieved ROSC in 102 +/- 92 s.</AbstractText>Electrical therapy increased the likelihood of ROSC in primary post defibrillation PEA three-fold (P < 0.01). Recovery occurred in the absence of thoracic compression, mechanical ventilation, or adjunctive drug therapy.</AbstractText> |
1,315 | Incidence of EMS-treated out-of-hospital cardiac arrest in the United States. | The potential impact of efforts to improve the chain of survival for out-of-hospital sudden cardiac arrest (SCA) is unclear in part because estimates of the incidence of treatable cases of SCA are uncertain. The aim of the investigation was to determine a representative national incidence of emergency medical services (EMS)-treated all-rhythm and ventricular fibrillation (VF) SCA as well as survival.</AbstractText>We used Medline to identify peer-reviewed articles published between 1 January 1980 and 31 March 2003 that reported a US community's EMS SCA experience. Inclusion criteria required the study to include at least 25 cases, report the total number of all-rhythm and/or ventricular fibrillation arrests, and provide information about population size and study duration. Incidence was computed by dividing the total number of SCA events by the product of the community's population and the study duration.</AbstractText>Reports from 35 communities met the inclusion criteria. A total of 35,801 all-rhythm EMS-treated cardiac arrests occurred during 62.11 million person-years of observation resulting in an overall incidence of 54.99 per 100,000 person-years. The incidence of ventricular fibrillation-rhythm SCA was 21.32 per 100,000 person-years. Sensitivity analyses generally produced similar results. Applying these results to the US population, 155,000 persons would experience EMS-treated all-rhythm SCA and 60,000 persons would experience EMS-treated ventricular fibrillation-rhythm SCA annually in the US. Survival was 8.4% for all-rhythm and 17.7% for ventricular fibrillation SCA.</AbstractText>The results provide a framework to assess opportunities and limitations of EMS care with regard to the public health burden of SCA.</AbstractText> |
1,316 | Preliminary in-hospital experience with a fully automatic external cardioverter-defibrillator. | Ventricular fibrillation (VF) and ventricular tachycardia (VT) are frequently present as initial rhythms during in-hospital cardiac arrest. Although ample evidence exists to support the need for rapid defibrillation, the response to in-hospital cardiac arrest remains without major advances in recent years. The delay between the arrhythmic event and intervention is still a challenge for clinical practice.</AbstractText>To analyze the performance and safety of in-hospital use of a programmable, fully automatic external cardioverter-defibrillator (AECD).</AbstractText>We conducted a prospective study at the Emergency Department of a university hospital. A total of 55 patients considered to be at risk of sustained VT/VF were included. Patients underwent monitoring of their cardiac rhythm by the AECD. Upon detection of a ventricular tachyarrhythmia, the AECD was programmed to automatically deliver shock therapy.</AbstractText>We recorded 19 episodes of VT/VF in 3 patients. The median time between the beginning of the arrhythmia and the first defibrillation was 33.4 s (21-65 s). One episode of spontaneous reversion of VT was documented 20 s after its origin and shock therapy was aborted. The defibrillation success was 94.4% (17/18) for the first shock and 100% (1/1) for the second shock. No case of inappropriate shock discharge was registered during the study period.</AbstractText>The AECD has the feasibility to combine long-term monitoring with automatic defibrillation safely and effectively. It presents the possibility of providing rapid identification of, and response to, in-hospital ventricular tachyarrhythmias.</AbstractText> |
1,317 | Treatment of atrial fibrillation by catheter-based procedures. | Catheter-based procedures have been developed with a view to reproduce or improve upon the excellent results of the Maze procedure in the treatment of atrial fibrillation (AF). Linear epicardial lesions created using minimally invasive techniques, or endocardial lesions to encircle the pulmonary veins (PV) have been associated with restoration of sinus rhythm in high percentages of carefully selected patients. The tricuspid-caval isthmus interruption procedure for atrial flutter is highly successful and, in patients who have both atrial flutter and fibrillation, prevents the development of AF when combined with antiarrhythmic agents. Modification of atrioventricular (AV) nodal conduction by eliminating the posterior atrial inputs to the AV node is performed to decrease the ventricular rate and alleviate symptoms during AF without the need for permanent pacing, though may be complicated by inadvertent AV block. AV junctional ablation and permanent pacing alleviates cardiac symptoms, improves quality-of-life, and reduces the use of health care resources. Its constraints include the inescapable need for anticoagulation, loss of AV synchrony, and life-long pacemaker-dependency. The variety of methods and results among published studies strongly emphasises the importance of patient selection, and the relative importance of substrate versus trigger. Possible complications of catheter ablation for AF include systemic thromboembolism, PV stenosis, pericardial effusion, cardiac tamponade, and phrenic nerve paralysis. These remain a matter of concern and stimulate research toward the development of less complex procedures. |
1,318 | Atrial fibrillation and heart failure: natural history and pharmacological treatment. | Atrial fibrillation (AF) is the most common sustained arrhythmia. Congestive heart failure (CHF), an increasingly frequent cardiovascular disorder affecting millions of people world-wide, has become the most important risk factor of AF in developed countries, as a result of ageing populations. Approximately two thirds of patients with CHF are >65 years of age and likely to have AF as a coexistent complication. Epidemiological surveys and large clinical trials in CHF provide strong evidence that AF is a marker of increased mortality. AF may compromise LV systolic function and worsen CHF through poor rate control, irregularity of ventricular response, and loss of atrial systolic activity. Furthermore, enhanced adrenergic stimulation in the setting of CHF facilitates AV conduction and promotes the progression of cardiomyopathy, and AF may worsen CHF as a consequence of the negative inotropic effects of drugs used to control the heart rate of rhythm, or of the proarrhythmic effects of drugs used to maintain sinus rhythm. This article reviews the putative mechanisms behind atrial remodelling due to long-standing AF, and the role of neuro-hormonal alterations in the atrial electrophysiologic and structural changes which facilitate its perpetuation. It also reviews and discusses various controlled trials of angiotensin-converting enzyme inhibitors and AT-1 receptor blockade in the perspective of AF treatment and prevention. Finally the role of specific antiarrhythmic drugs, the respective advantages and shortcomings of rate versus rhythm control in patients with AF and CHF, and the important issue of chronic anticoagulation are presented in the light of time-tested therapies, as well as new promising therapeutic approaches. |
1,319 | [Specific complications in the treatment with implantable cardioverter-defibrillators]. | Using implantable cardioverter-defibrillators in treatment of malignant ventricular arrhythmias revealed new complications specific to this therapy. Inappropriate therapy, arrhythmic storm and device related proarrhythmia belong to the most significant complications. The authors describe specific complications in a group of ICD patients, analyze their etiology and prognostic value. There are some recommendations for the management of specific complications.</AbstractText>138 consecutive patients underwent ICD implantation between 1994-2001. Median follow-up was 47,35 months. Average left ventricular ejection fraction was 38 +/- 14% and 71% of patients suffered from coronary artery disease. From the total of 2490 arrhythmic episodes 1490 were evaluated in detail. 253 episodes (17%) were classified as inappropriate therapy. The most common etiology of inappropriate therapy was atrial fibrillation with rapid ventricular response (68%), atrial flutter (13%) and sinus tachycardia (11%). After the therapeutic intervention, 65% of them remained free of inappropriate therapy. There were 38 arrhythmic storms in 19 patients as another serious complication.</AbstractText>All the observed arrhythmic episodes were ventricular tachycardias (p<0.04). Patients with arrhythmic storm in history had significantly lower survival (p<0.05). The risk factors of cardiac nonsudden death were: age >66 years, left ventricular ejection fraction <35% and arrhythmic storm history. The authors present recommendations for the treatment of the most common specific ICD complications.</AbstractText> |
1,320 | QT prolongation through hERG K(+) channel blockade: current knowledge and strategies for the early prediction during drug development. | Prolongation of the QT interval of the electrocardiogram is a typical effect of Class III antiarrhythmic drugs, achieved through blockade of potassium channels. In the past decade, evidence has accrued that several classes of drugs used for non-cardiovascular indications may prolong the QT interval with the same mechanism (namely, human ether-a-go-go-related gene (hERG) K(+) channel blockade). The great interest in QT prolongation is because of several reasons. First, drug-induced QT prolongation increases the likelihood of a polymorphous ventricular arrhythmia (namely, torsades de pointes, TdP), which may cause syncope and degenerate into ventricular fibrillation and sudden death. Second, the fact that several classes of drugs, such as antihistamines, fluoroquinolones, macrolides, and neuroleptics may cause the long QT syndrome (LQTS) raises the question whether this is a class effect (e.g., shared by all agents of a given pharmacological class) or a specific effect of single agents within a class. There is now consensus that, in most cases, only a few agents within a therapeutic class share the ability to significantly affect hERG K(+) channels. These compounds should be identified as early as possible during drug development. Third, QT prolongation and interaction with hERG K(+) channels have become surrogate markers of cardiotoxicity and have received increasing regulatory attention. This review briefly outlines the mechanisms leading to QT prolongation and the different strategies that can be followed to predict this unwanted effect. In particular, it will focus on the approaches recently proposed for the in silico screening of new compounds. |
1,321 | Cognitive impairment in survivors of out-of-hospital cardiac arrest. | The huge importance of rapid provision of care, especially early defibrillation, for survival of out-of-hospital cardiac arrest (OHCA) is well known. This prospective cohort study investigated cognitive functioning of OHCA survivors in relation to the time-related elements of the resuscitation.</AbstractText>Fifty-seven consecutive survivors, from a cohort of 308 witnessed OHCA patients with ventricular fibrillation as the initial rhythm, underwent extensive neuropsychologic examination, including tests of memory, attention, and executive functioning, 6 months after the resuscitation. Time-related aspects of the resuscitation were collected on scene. Cognitive functioning was studied in relation to the administration of cardiopulmonary resuscitation (CPR) prior to ambulance arrival, and time from collapse to start of CPR, defibrillation, and return of spontaneous circulation (ROSC).</AbstractText>Depending of the test, between 11% and 28% of survivors were cognitively impaired, while 58% scored unimpaired for all tests. Daily life activities were limited in 19% of the patients. Patients who received CPR prior to arrival of the ambulance showed a trend towards overall better cognitive functioning and significant better immediate memory and visuomotor tracking (P =.03 and P <.01). We found a weak correlation between the time to CPR, time to defibrillation, or time to ROSC and cognitive functioning.</AbstractText>The majority of survivors of OHCA with ventricular fibrillation as the initial rhythm are cognitively unimpaired. Long delays to ROSC are compatible with good cognitive outcome. Initiation and cessation of resuscitation efforts should not be based on the duration of circulatory arrest.</AbstractText> |
1,322 | In vitro atrial flow dynamics: normal conditions versus atrial fibrillation. | The flow dynamics in the atrium is poorly described. The reasons are principally due to the complicated geometry of the cavity and its contractility. The present in vitro study focuses on the description of the flow in the left atrium in normal conditions (NC) and in atrial fibrillation (AF). The final objective is to give leads to understand, from the hemodynamic point of view, complications in case of AF.</AbstractText>An atrio-ventricular dual activation system is used to simulate physiological flow in the left atrium. The cavities are compliant and transparent. Velocity measurements are performed with Particle Image Velocimetry. Systolic peak of the pulmonary venous flow is about 0.4 m s(-1) and diastolic peak 0.6 m s(-1) in magnitude. Vortices appear during diastasis and systole and are of normal size and duration. In early and late diastole, the ventricular filling (in NC and AF) and the atrial contraction (in NC only) create a characteristic flow pattern that consists in directed flow towards the mitral valve. In AF an increased resident time (500 ms versus 300 ms) and a slow helical flow pattern (about 0.1 m s(-1)), similar to what is measured using ultrasound echocardiography are observed.</AbstractText>This study uses atrial flow dynamics description to help understand why thromboembolisms occur in AF.</AbstractText> |
1,323 | Role of previous treatment with sulfonylureas in diabetic patients with acute myocardial infarction: results from a nationwide French registry. | The cardiovascular effects of sulfonylureas (SU) in diabetic patients are controversial and it has been suggested that diabetic patients with acute myocardial infarction while on SU were at increased risk.</AbstractText>To assess the in-hospital outcome of patients with acute myocardial infarction according to the use of SU at the time of the acute episode.</AbstractText>Of 443 intensive care units in France, 369 (83%) prospectively collected all cases of infarction admitted within 48 h of symptom onset in November 2000.</AbstractText>Among the 2320 patients included in the registry, 487 (21%) had diabetes, of whom 215 (44%) were on SU. Patients on SU were older and had a more frequent history of hyperlipidemia than those not receiving SU. Type and location of infarction were similar in the two groups, and there was no difference in Killip class on admission. In-hospital mortality was lower in patients on SU (10.2%) than in those without SU (16.9%) (p = 0.035). There was a trend toward less frequent ventricular fibrillation (2.3% vs 5.9%, p = 0.052). In two models of multivariate analyses, SU therapy was associated with decreased in-hospital mortality (model 1: relative risk: 0.44, p = 0.012; model 2: relative risk: 0.37, p = 0.020).</AbstractText>In this nationwide registry reflecting real-world practice, the use of sulfonylureas in diabetic patients was not associated with increased in-hospital mortality.</AbstractText>Copyright 2004 John Wiley & Sons, Ltd.</CopyrightInformation> |
1,324 | Thrombolysis and adjunctive therapy in acute myocardial infarction: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. | This chapter about antithrombotic therapy for acute myocardial infarction (MI) is part of the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following: For patients with ischemic symptoms characteristic of acute MI of < 12 h in duration, and ST-segment elevation or left bundle-branch block (of unknown duration) on the ECG, we recommend administration of any approved fibrinolytic agent (Grade 1A). We recommend the use of streptokinase, anistreplase, alteplase, reteplase, or tenecteplase over placebo (all Grade 1A). For patients with symptom duration < 6 h, we recommend the administration of alteplase over streptokinase (Grade 1A). For patients with known allergy or sensitivity to streptokinase, we recommend alteplase, reteplase, or tenecteplase (Grade 1A). For patients with acute posterior MI of < 12 h duration, we suggest fibrinolytic therapy (Grade 2C). In patients with any history of intracranial hemorrhage, closed head trauma, or ischemic stroke within past 3 months, we recommend against administration of fibrinolytic therapy (Grade 1C+). For patients with acute ST-segment elevation MI whether or not they receive fibrinolytic therapy, we recommend aspirin, 160 to 325 mg p.o., at initial evaluation by health-care personnel followed by indefinite therapy, 75 to 162 mg/d p.o. (both Grade 1A). In patients allergic to aspirin, we suggest use of clopidogrel as an alternative therapy to aspirin (Grade 2C). For patients receiving streptokinase, we suggest administration of either i.v. unfractionated heparin (UFH) [Grade 2C] or subcutaneous UFH (Grade 2A). For all patients at high risk of systemic or venous thromboembolism (anterior MI, pump failure, previous embolus, atrial fibrillation, or left ventricular thrombus), we recommend administration of IV UFH while receiving streptokinase (Grade 1C+). |
1,325 | Antithrombotic therapy in atrial fibrillation: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. | This chapter about antithrombotic therapy in atrial fibrillation (AF) is part of the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines. Grade 1 recommendations are strong and indicate that the benefits do, or do not, outweigh risks, burden, and costs. Grade 2 suggests that individual patients' values may lead to different choices (for a full understanding of the grading see Guyatt et al, CHEST 2004; 126:179S-187S). Among the key recommendations in this chapter are the following (all vitamin K antagonist [VKA] recommendations have a target international normalized ratio [INR] of 2.5; range, 2.0 to 3.0): In patients with persistent or paroxysmal AF (PAF) [intermittent AF] at high risk of stroke (ie, having any of the following features: prior ischemic stroke, transient ischemic attack, or systemic embolism, age > 75 years, moderately or severely impaired left ventricular systolic function and/or congestive heart failure, history of hypertension, or diabetes mellitus), we recommend anticoagulation with an oral VKA, such as warfarin (Grade 1A). In patients with persistent AF or PAF, age 65 to 75 years, in the absence of other risk factors, we recommend antithrombotic therapy with either an oral VKA or aspirin, 325 mg/d, in this group of patients who are at intermediate risk of stroke (Grade 1A). In patients with persistent AF or PAF < 65 years old and with no other risk factors, we recommend aspirin, 325 mg/d (Grade 1B). For patients with AF and mitral stenosis, we recommend anticoagulation with an oral VKA (Grade 1C+). For patients with AF and prosthetic heart valves, we recommend anticoagulation with an oral VKA (Grade 1C+); the target INR may be increased and aspirin added depending on valve type and position, and on patient factors. For patients with AF of > or = 48 h or of unknown duration for whom pharmacologic or electrical cardioversion is planned, we recommend anticoagulation with an oral VKA for 3 weeks before and for at least 4 weeks after successful cardioversion (Grade 1C+). For patients with AF of > or = 48 h or of unknown duration undergoing pharmacologic or electrical cardioversion, an alternative strategy is anticoagulation and screening multiplane transesophageal echocardiography (Grade 1B). If no thrombus is seen and cardioversion is successful, we recommend anticoagulation for at least 4 weeks (Grade 1B). For patients with AF of known duration < 48 h, we suggest cardioversion without anticoagulation (Grade 2C). However, in patients without contraindications to anticoagulation, we suggest beginning IV heparin or low molecular weight heparin at presentation (Grade 2C). |
1,326 | Atrial ionic remodeling induced by atrial tachycardia in the presence of congestive heart failure. | Atrial fibrillation (AF) and congestive heart failure (CHF) produce discrete forms of atrial ionic remodeling. The in vivo effects of atrial tachycardia (AT) remodeling are altered by CHF. This study evaluated underlying mechanisms at the level of ionic remodeling.</AbstractText>We studied 4 groups of dogs: (1) unpaced controls (CTLs); (2) CHF caused by 2-week ventricular tachypacing (VTP, 240 bpm); (3) AT (400 bpm x 7 days); and (4) CHF+AT (2-week VTP with AT for the last 7 days). CHF and CHF+AT groups equally increased left atrial pressure. AF duration was increased in all paced groups. Effective refractory period (ERP) was decreased by 42% in AT versus CTL but by only 24% in AT+CHF versus CHF. CHF reduced L-type Ca2+ (I(Ca)), transient-outward (I(to)), and the slow delayed-rectifier (I(Ks)) currents while increasing the Na+-Ca2+ exchanger (I(NCX)) and not affecting the inward-rectifier (I(K1)) current. AT reduced I(to) and I(Ca) while increasing I(K1) and leaving I(Ks) unaltered. The addition of AT to CHF failed to alter I(to), I(Ks), or I(NCX) beyond the effect of CHF alone, decreased I(Ca) slightly compared with CHF alone, but had smaller effects on I(Ca) and I(K1) compared with AT alone. Thus, CHF+AT, as would occur in a CHF patient who develops AF, produced an ionic remodeling pattern different from that of CHF or AT alone and from what would have been predicted from additive effects of CHF and AT.</AbstractText>The presence of CHF alters AT-induced ionic remodeling. Thus, the ionic remodeling caused by cardiac arrhythmias in the presence of cardiac pathology is not necessarily predictable from the effects of either alone, with important potential implications for understanding the pathophysiology of arrhythmias in the diseased heart.</AbstractText> |
1,327 | Mechanism of pacing-induced ventricular fibrillation in the infarcted human heart. | The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined.</AbstractText>Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites.</AbstractText>Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.</AbstractText> |
1,328 | Health system costs of out-of-hospital cardiac arrest in relation to time to shock. | Early defibrillation results in higher admission rates and healthcare costs. This study determined the healthcare resources used and related medical costs after out-of-hospital cardiac arrest (OHCA) in relation to time to shock. We assessed the incremental healthcare costs per life gained from reduction in time to shock of 2, 4, and 6 minutes.</AbstractText>Clinical and costs data of patients in witnessed OHCA with ventricular fibrillation as initial rhythm were collected. Each patient's time to shock was estimated and assigned to 1 of 3 categories: < or =7 minutes (early), 7 to 12 minutes (intermediate), and >12 minutes (late). Incremental cost-effectiveness analysis and Monte Carlo simulation compared scenarios of reduction in time to shock of 2, 4, and 6 minutes. Six-month survival was 22%. Mean prehospital, in-hospital, and posthospital costs in the first half-year after OHCA were 559 Euros, 6869 Euros and 666 Euros. Mean costs were 28,636 Euros per survivor and 2384 Euros per nonsurvivor. Among patients shocked early (n=24), 46% survived, with costs averaging 20,253 Euros. Of the intermediate group (n=149), 26% survived, with costs averaging 31,467 Euros. Among patients shocked late (n=135), 13% survived, with costs averaging 27,781 Euros. The point estimates of the incremental cost-effectiveness ratios of reduction of time to shock of 2, 4, and 6 minutes compared with baseline were 17,508 Euros, 14,303 Euros, and 12,708 Euros per life saved, respectively.</AbstractText>Costs per survivor were lowest with the shortest time to shock because of shorter stay in the intensive care unit. Reducing the time to defibrillation increases the healthcare costs by an acceptable amount according to current standards and is economically attractive.</AbstractText> |
1,329 | Efficacy of quinidine in high-risk patients with Brugada syndrome. | Automatic implantable cardioverter-defibrillator therapy is considered the only effective treatment for high-risk patients with Brugada syndrome. Quinidine depresses I(to) current, which may play an important role in the arrhythmogenesis of this disease.</AbstractText>The effects of quinidine bisulfate (mean dose, 1483+/-240 mg) on the prevention of inducible and spontaneous ventricular fibrillation (VF) were prospectively evaluated in 25 patients (24 men, 1 woman; age, 19 to 80 years) with Brugada syndrome. There were 15 symptomatic patients (including 7 cardiac arrest survivors and 7 patients with unexplained syncope) and 10 asymptomatic patients. All 25 patients had inducible VF at baseline electrophysiological study. Quinidine prevented VF induction in 22 of the 25 patients (88%). After a follow-up period of 6 months to 22.2 years, all patients are alive. Nineteen patients were treated with quinidine for 6 to 219 months (mean+/-SD, 56+/-67 months). None had an arrhythmic event, although 2 had non-arrhythmia-related syncope. Administration of quinidine was associated with a 36% incidence of side effects that resolved after drug discontinuation.</AbstractText>Quinidine effectively prevents VF induction in patients with Brugada syndrome. Our data suggest that quinidine also suppresses spontaneous arrhythmias and could prove to be a safe alternative to automatic implantable cardioverter-defibrillator therapy for a substantial proportion of patients with Brugada syndrome. Randomized studies comparing these two therapies seem warranted.</AbstractText> |
1,330 | Ximelagatran: a new antithrombotic option in atrial fibrillation. | Treatment strategies in patients with atrial fibrillation typically involve pharmacologic or interventional invasive therapies to suppress the rhythm, control ventricular contraction rates, or prevent thromboembolic complications. Current therapies used for rhythm conversion in atrial fibrillation may have undesirable risks or side effects that limit this approach. Lifelong anticoagulation may be necessary to prevent the formation of thrombus in the left atrial chamber that can travel into the cerebral circulation to cause a stroke. Currently, warfarin is the most commonly prescribed anticoagulant for this purpose. Unfortunately, many patients with atrial fibrillation may not receive warfarin because of the difficulties in dosing and maintaining desirable target goals. The oral direct thrombin inhibitor ximelagatran has several pharmacologic properties that provide a unique and potentially desirable treatment option. Clinical studies have demonstrated that ximelagatran, administered in twice-daily doses of 36 mg, is non-inferior to warfarin for thromboprophylaxis against stroke or systemic embolism in atrial fibrillation. The pharmacology of ximelagatran and clinical trials with its use in atrial fibrillation is reviewed. |
1,331 | Antiarrhythmic and proarrhythmic properties of QT-prolonging antianginal drugs. | In recent years there has been a major reorientation of drug therapy for cardiac arrhythmias, its changing role, and above all, a radical change in the class of arrhythmia drugs because of their impact on mortality. The decline in the use of sodium-channel blockers has led to an ex panding use of beta-blockers and simple or complex class III agents for controlling cardiac arrhythmias. Success with these agents in the context of their side effects has spurred the development of compounds with simpler ion-channel blocking properties that have less complex adverse reactions. The resulting so-called pure class III agents, such as dofetilide or ibutilide, were found to have antifibrillatory effects in atrial fibrillation and flutter and in ventricular tachyarrhythmias. Such agents are effective and have diversity, but they have come into therapeutics with a price: the sometimes-fatal torsades de pointes. The drug amiodarone, a complex compound that was synthesized as an antianginal agent, has been an exception in this regard. Its therapeutic use is associated with a negligibly low incidence of torsades de pointes, even though the drug produces significant bradycardia and QT lengthening to 500 to 700 msec. Recent electrophysiologic studies suggest that this paradox is likely due to the differential block of ion channels in endocardium, epicardium, midmyocardial (M) cells, and Purkinje fibers in the ventricular myocardium. There is also clinical evidence suggesting that amiodarone reduces the "torsadogenic" effects of pure class III agents. Ranolazine was also synthesized for the development of antianginal properties that stem from a partial inhibition of fatty acid oxidation; it too has been found to have electrophysioloigic properties. These are somewhat similar to those of amiodarone on ion channels in endocardium, epicardium, M cells, and Purkinje fibers in the ventricular myocardium, but the drug does not prolong the QT interval to the same extent as amiodarone does. Thus, the drug produces modest increases in repolarization as judged by its effects on the action potential duration (APD) without the potential for the development of torsades de pointes. By virtue of its suppressant action on early afterdepolarizations and triggered activity in Purkinje fibers and M cells, the drug appears to have a powerful potential for reducing the torsadogenic proclivity of conventional class III antiarrhythmic compounds. The rationale for the therapeutic niche for amiodarone, and especially in the case of ranolazine, in the prevention of drug-induced torsades de pointes is discussed. |
1,332 | Right ventricular pacing via left superior vena cava. | Negotiating the pacing lead into the right ventricle via left superior vena cava, at times, can be difficult. We report two such cases in which pacing leads were introduced into the right ventricle via left superior vena cava, with the help of stylet tip shaped into a large pigtail loop. |
1,333 | Effect of smoking on QT interval, QT dispersion and rate pressure product. | Smoking may predispose to ventricular fibrillation and sudden cardiac death by altering ventricular recovery time dispersion indices. However, effect of acute smoking on QT interval and QT dispersion in chronic smokers has not been studied so far.</AbstractText>Effect of cigarette smoking on ventricular recovery time dispersion indices and rate pressure product (product of heart rate and systolic blood pressure) was investigated in 25 chronic smokers and compared with 25 age- and sex-matched non-smoker controls. There was increase in R-R interval (p<0.05). corrected QT interval, QT dispersion (p<0.001) and rate pressure product (p<0.05) in chronic smokers at baseline (before smoking) compared to non-smoker controls. On cigarette smoking, there was further increase in heart rate, blood pressure, QT dispersion and rate pressure product (p<0.001) with reduction in R-R interval (p<0.05) in chronic smokers compared to non-smoker controls.</AbstractText>Our observations indicate that there may be some relationship between prolonged ventricular recovery time dispersion indices and ventricular fibrillation and sudden cardiac death associated with smoking.</AbstractText> |
1,334 | Control of rate versus rhythm in rheumatic atrial fibrillation: a randomized study. | Patients with rheumatic heart disease and atrial fibrillation incur significant morbidity and mortality. It is not known which approach, rate control or maintenance of sinus rhythm might be most appropriate. The present study was undertaken to compare the strategy of ventricular rate control versus maintenance of sinus rhythm in rheumatic atrial fibrillation, and to evaluate the role of amiodarone in this patient population.</AbstractText>We prospectively studied 144 patients with chronic rheumatic atrial fibrillation in a double-blind protocol-rhythm control (group I: 48 patients each with amiodarone -group Ia; and placebo -group Ib) and compared the effects with the ventricular rate control (group II) by diltiazem (n=48, open-label). Direct current cardioversion was attempted in group I. The mean age of the study population was 38.6+/-10.3 years, left atrial size was 4.7+/-0.6 cm, atrial fibrillation duration was 6.1+/-5.4 years, and 72.9% patients had undergone valvular interventions. At 1 year, 45 patients with sinus rhythm in group I compared to 48 patients in group II demonstrated significant increase in exercise to sinus rhythm time, had improvement in functional class and quality of life score. There was no difference in hospitalization rates, systemic bleeds or incidence of thromboembolism. Five patients died in group II but none in group I (p=0.02). In group I, 73/87 (83.9%) patients converted, and 45/86 (52.3%) patients maintained sinus rhythm at 1 year. Conversion rates were 38/43 (88.4%) with amiodarone versus 34/44 (77.3%) with placebo (p=0.49): corresponding rate for maintaining sinus rhythm was 29/42 (69.1%) versus 16/44 (36.4%), p=0.008 respectively.</AbstractText>Maintenance of sinus rhythm appeared to be superior to ventricular rate control in patients with rheumatic atrial fibrillation in terms of an effect on mortality and morbidity. Sinus rhythm could be restored in the majority and amiodarone was superior to placebo in this regard.</AbstractText> |
1,335 | Characterization of QT interval adaptation to RR interval changes and its use as a risk-stratifier of arrhythmic mortality in amiodarone-treated survivors of acute myocardial infarction. | A new method is proposed to evaluate the dynamics of QT interval adaptation in response to heart rate (HR) changes. The method considers weighted averages of RR intervals (RR) preceding each cardiac beat to express RR interval history accounting for the influence on repolarization duration. A global optimization algorithm is used to determine the weight distribution leading to the lowest regression residual when curve fitting the [QT, RR1 data using a patient-specific regression model. From the optimum weight distribution, a memory lag L90 is estimated, expressing the delay in the QT adaptation to HR changes. On average, RR intervals of the past 150 beats (approximately 2.5 min) are required to model the QT response accurately. From a clinical point of view, the interval of the initial tens of seconds to one minute seems to be most important in the majority of cases. A measure of the optimum regression residual (r(opt)) has been calculated, discriminating between post-myocardial infarction patients at high and low risk of arrhythmic death while on treatment with amiodarone. A similar discrimination has been achieved with a variable expressing the character of QT lag behind the RR interval dynamics. |
1,336 | Surgical treatment of atrial fibrillation through isolation of the left atrial posterior wall in patients with chronic rheumatic mitral valve disease. A randomized study with control group. | To determine the effectiveness of surgical isolation of the left atrial posterior wall encompassing the ostia of the pulmonary veins for the treatment of atrial fibrillation of rheumatic etiology.</AbstractText>Prospective and randomized study of patients with rheumatic mitral valve disease, persistent atrial fibrillation for 6 months or longer, age < or = 60 years, and left atrial diameter < or = 65 mm. The patients were randomly distributed into 2 groups as follows: surgical valvular treatment (control group) and surgical valvular treatment associated with isolation of the left atrial posterior wall according to the "cut-and-sew" technique (treated group).</AbstractText>Twenty-nine individuals were operated upon, 27 of whom (13 in the control group and 14 in the treated group) were regularly followed up. The patients of both groups did not differ in regard to their basal characteristics. The mean follow-up time was 11.5 months in the control group and 10.3 months in the treated group. The cumulative frequencies of the patients without atrial fibrillation were significantly greater in the treated group both in the perioperative (P = 0.0035) and late (P = 0.0430) phases.</AbstractText>Surgical isolation of the left atrial posterior wall encompassing the ostia of the pulmonary veins is an effective form of treating atrial fibrillation in rheumatic mitral valve disease.</AbstractText> |
1,337 | [Assessment of regional wall motion using strain Doppler imaging during right ventricular bifocal pacing in a patient with severe congestive heart failure: a case report]. | A 79-year-old man presented with dilated cardiomyopathy and chronic atrial fibrillation. A DDD pacemaker was implanted due to sick sinus syndrome. His left ventricular ejection fraction was 23%. He was repeatedly admitted with congestive heart failure. Although cardiac resynchronization therapy was attempted, insertion of a pacing lead into the coronary sinus failed. Right ventricular bifocal pacing was done. The QRS width was shortened to 155 msec during bifocal pacing and 157 msec during right ventricular outflow pacing from 221 msec during right ventricular apical pacing. Heart failure was improved from New York Heart Association class III to II. Regional wall motion was assessed by strain of the myocardium. Bifocal pacing increased stroke volume due to improvement of longitudinal dyssynchrony of the septal and lateral walls. Bifocal pacing is effective for patients with severe congestive heart failure in whom biventricular pacing therapy has failed. Strain Doppler imaging is useful for the assessment of regional wall motion during cardiac pacing. |
1,338 | Radiofrequency ablation in children with asymptomatic Wolff-Parkinson-White syndrome. | Ventricular fibrillation can be the presenting arrhythmia in children with asymptomatic Wolff-Parkinson-White syndrome. Deaths due to this arrhythmia are potentially preventable.</AbstractText>We performed a randomized study in which prophylactic radiofrequency catheter ablation of accessory pathways was compared with no ablation in asymptomatic children (age range, 5 to 12 years) with the Wolff-Parkinson-White syndrome who were at high risk for arrhythmias. The primary end point was the occurrence of arrhythmic events during follow-up.</AbstractText>Of the 165 eligible children, 60 were determined to be at high risk for arrhythmias. After randomization, but before any ablation had been performed, the parents withdrew 13 children from the study. Of the remaining children, 20 underwent prophylactic ablation and 27 had no treatment. The characteristics of the two groups were similar. There were three ablation-related complications, one of which led to hospitalization. During follow-up, 1 child in the ablation group (5 percent) and 12 in the control group (44 percent) had arrhythmic events. Two children in the control group had ventricular fibrillation, and one died suddenly. The cumulative rate of arrhythmic events was lower among children at high risk who underwent ablation than among those at high risk who did not. The reduction in risk associated with ablation remained significant after adjustment in a Cox regression analysis. In both the ablation and the control groups, the independent predictors of arrhythmic events were the absence of prophylactic ablation and the presence of multiple accessory pathways.</AbstractText>In asymptomatic, high-risk children with the Wolff-Parkinson-White syndrome, prophylactic catheter ablation performed by an experienced operator reduces the risk of life-threatening arrhythmias.</AbstractText>Copyright 2004 Massachusetts Medical Society</CopyrightInformation> |
1,339 | Tissue Doppler echocardiography and biventricular pacing in heart failure: patient selection, procedural guidance, follow-up, quantification of success. | Asynchronous myocardial contraction in heart failure is associated with poor prognosis. Resynchronization can be achieved by biventricular pacing (BVP), which leads to clinical improvement and reverse remodeling. However, there is a substantial subset of patients with wide QRS complexes in the electrocardiogram that does not improve despite BVP. QRS width does not predict benefit of BVP and only correlates weakly with echocardiographically determined myocardial asynchrony. Determination of asynchrony by Tissue Doppler echocardiography seems to be the best predictor for improvement after BVP, although no consensus on the optimal method to assess asynchrony has been achieved yet. Our own preliminary results show the usefulness of Tissue Doppler Imaging and Tissue Synchronization Imaging to document acute and sustained improvement after BVP. To date, all studies evaluating Tissue Doppler in BVP were performed retrospectively and no prospective studies with patient selection for BVP according to echocardiographic criteria of asynchrony were published yet. We believe that these new echocardiographic tools will help to prospectively select patients for BVP, help to guide implantation and to optimize device programming. |
1,340 | Intrapericardial ibutilide administration fails to terminate pacing-induced sustained atrial fibrillation in dogs. | The hypothesis that intrapericardial (ip.) ibutilide administration would terminate pacing-induced sustained atrial fibrillation (AF) and ibutilide distribution were tested.</AbstractText>Sustained (> or =24 hours) AF was induced by 59 +/- 20 day rapid atrial pacing in 19 dogs. After sustained AF was present, the atrial pacemaker was turned off and 9 open chest dogs received 0.015 mg/kg ibutilide (37 degrees C) in 30 ml saline into the pericardial sac. Ten control dogs received 30 ml saline (37 degrees C) ip. QT intervals, right ventricular monophasic action potential duration at 90% of repolarization (RV-MAPD(90)), AF mean cycle length (AFCL(m)), systolic- and diastolic intraarterial blood pressures, intrapericardial-, right atrial- and ventricular pressures, cardiac output and ibutilide concentrations were measured. If AF persisted after the 1st drug infusion, dual site rapid atrial pacing (DRAP) simultaneously from the high right atrium and coronary sinus was performed to terminate AF. If it was ineffective, a 2nd ip. drug infusion in the same fashion as the 1st one, was attempted. There was no significant difference in AF termination [5/9 (56%) in ibutilide treated and 3/10 (30%) in control dogs] between the two groups. DRAP never terminated AF. The AF duration did not differ between the two groups. Compared with control, ibutilide treatment prolonged significantly AFCL(m) (p < 0.001) and non-significantly QT, RV-MAPD(90). No significant difference was found in systolic and diastolic blood pressure and cardiac output between the two groups. The two orders of magnitude greater ibutilide concentration in the pericardial fluid than that in the femoral vein decreased rapidly over time, drug concentration was greatest in the atria, smaller in the ventricular myocardium, with a trend decreasing from the epi- to endocardium.</AbstractText>Despite a significant atrial electrophysiological effect, ip. delivery of ibutilide did not result in higher AF termination rate compared with control.</AbstractText> |
1,341 | Perioperative enoximone infusion improves cardiac enzyme release after CABG. | To assess whether routine postoperative enoximone infusion compared with dobutamine improved clinical and biochemical results after coronary artery bypass grafting with cardiopulmonary bypass.</AbstractText>Prospective nonrandomized study. Data collection was blinded to the choice of inotrope.</AbstractText>Double-institutional clinical investigation.</AbstractText>Two hundred sixteen consecutive patients undergoing myocardial revascularization between May 2000 and December 2002.</AbstractText>Seventy-two patients underwent myocardial revascularization and were treated with enoximone, 5 microg/kg/min (group A). They were compared in a ratio of 1:2 to 144 patients treated with dobutamine at the same dose (group B) after aortic cross-clamp removal. The groups proved to be homogenous in preoperative and intraoperative characteristics.</AbstractText>Hospital outcome, electrocardiogram, echocardiography, further inotropic support, and biochemical markers of ischemia were compared. Subsets of patients with comorbidities and total arterial revascularization were analyzed. Perioperative myocardial infarction, postoperative low-output syndrome, intra-aortic balloon pump, atrial fibrillation, ST-segment changes, postoperative echocardiographic findings, and intensive care and hospital durations were similar between groups. In the postoperative course, more patients belonging to group A maintained low-dose inotropic support, whereas more patients belonging to group B required higher doses. Troponin I and creatine kinase-MB values were higher in patients of group B, especially when subgroups with diabetes, left ventricular hypertrophy, or total arterial revascularization were included.</AbstractText>Postoperative enoximone reduced troponin I release and need for inotropic support in patients undergoing on-pump myocardial revascularization. Subgroup data were confirmed in diabetes, left ventricular hypertrophy, and total arterial revascularization.</AbstractText> |
1,342 | Mode of death after admission to an intensive care unit following cardiac arrest. | To determine the mode of death in patients admitted to an intensive care unit (ICU) after cardiac arrest who died before hospital discharge.</AbstractText>Prospectively defined retrospective review of a database and individual patient medical records and ICU charts.</AbstractText>Eleven-bed multidisciplinary intensive care unit in a general hospital in the United Kingdom.</AbstractText>All patients admitted to ICU between February 1998 and July 2003 after a cardiac arrest in the previous 24 h.</AbstractText>The outcome at hospital discharge and mode of death in non-survivors were recorded. Based on the mode of death, non-survivors were placed in one of three groups: multiple organ failure death, neurological death or cardiovascular death. Two hundred and five patients were admitted to ICU after a cardiac arrest; 113 (55.1%) after out-of-hospital cardiac arrest and 92 (44.9%) after in-hospital cardiac arrest. One hundred and twenty-six (61.5%) patients died before hospital discharge and of these 58 (46.0%) died due to neurological injury. After cardiac arrest, 22.9% of the in-hospital patients and 67.7% of the out-of-hospital patients died due to neurological injury, irrespective of the primary cardiac arrest arrhythmia.</AbstractText>Two-thirds of the patients dying after out-of-hospital cardiac arrest died due to neurological injury and this proportion was approximately the same for ventricular fibrillation/ventricular tachycardia and pulseless electrical activity/asystole. Approximately a quarter of the patients dying after in-hospital cardiac arrest died due to neurological injury.</AbstractText> |
1,343 | "Early" class III drugs for the treatment of atrial fibrillation: efficacy and atrial selectivity of AVE0118 in remodeled atria of the goat. | Currently available antiarrhythmic drugs are only moderately effective against atrial fibrillation (AF) and may cause ventricular proarrhythmia. AVE0118 is a blocker of atrium-specific early K+ currents (I(Kur)/I(to)).</AbstractText>Effects of intravenous AVE0118 and dofetilide on atrial effective refractory period (AERP) and inducibility of AF were measured before and after 48-hours of AF-induced electrical remodeling in the goat. During persistent AF (53+/-19 days), the cardioversion efficacy and effects on atrial wavelength of AVE0118, dofetilide, and ibutilide were evaluated. QT durations were measured during atrial pacing and persistent AF. After 48 hours of AF, the effect of dofetilide on AERP was reduced, and induction of AF was not prevented. In contrast, the class III action of AVE0118 was enhanced, and AF inducibility decreased from 100% to 32% (P<0.001). At 1, 3, and 10 mg x kg(-1) x h(-1), AVE0118 terminated persistent AF in 1 of 8, 3 of 8, and 5 of 8 goats, respectively. Dofetilide and ibutilide terminated AF in 1 of 5 and 2 of 7 goats. AVE0118 0.5, 1.5, and 5 mg/kg prolonged the AERP during AF and increased the fibrillation wavelength from 6.7+/-0.6 to 8.5+/-0.5, 9.7+/-0.5, and 11.2+/-0.9 cm (P<0.01). Whereas dofetilide and ibutilide prolonged QT duration, AVE0118 had no appreciable effect.</AbstractText>AVE0118 markedly prolongs the AERP during AF without affecting QT duration. Cardioversion of AF was due to an approximately 2-fold increase in fibrillation wavelength. Atrium-selective class III drugs like AVE0118 may be a promising new option for safe and effective cardioversion of AF.</AbstractText> |
1,344 | Giving IV and oral amiodarone perioperatively for the prevention of postoperative atrial fibrillation in patients undergoing coronary artery bypass surgery: the GAP study. | We studied the use of perioperative IV and oral administration of amiodarone for the prevention of postoperative atrial fibrillation in patients undergoing coronary artery bypass graft surgery (CABG).</AbstractText>In the United States, > 500,000 patients undergo CABG each year. Numerous studies to date have suggested that postoperative atrial fibrillation occurs in 30 to 50% of patients, leading to significant morbidity, including hypotension, heart failure, thromboembolic complications, prolonged hospital stay, and increased hospital costs. The objective of this study was to assess the use of IV amiodarone in combination with oral amiodarone to reduce the incidence of postoperative atrial fibrillation.</AbstractText>From January 1999 to October 1999, 51 patients scheduled for CABG were randomly selected for participation in the amiodarone administration trial. IV amiodarone, 0.73 mg/min, was administered on call to the operating room for 48 h, followed by oral amiodarone, 400 mg q12h, for the next 3 days. The amiodarone group was case-control matched to the incidence of postoperative atrial fibrillation in 92 patients undergoing CABG using conventional medical therapy during the same period. The primary end point of this study was the incidence of postoperative atrial fibrillation, length of hospital stay, and hospital costs, compared to the control group undergoing CABG during the same time.</AbstractText>Atrial fibrillation occurred in 3 of 51 patients (5.88%) in the amiodarone group, compared to 24 of 92 patients (26.08%) in the control group. Length of hospital stay in the amiodarone group was less than in the control group (5.3 days vs 6.7 days), with a trend toward decrease in hospital costs.</AbstractText>The administration of IV amiodarone in conjunction with oral amiodarone for a total dose of 4,500 mg over 5 days appears to be a hemodynamically well-tolerated, safe, and effective treatment in decreasing the incidence of postoperative atrial fibrillation, shortening length of stay, and a trend toward lowering hospital costs, even in patients with significantly reduced left ventricular function (< 30%). A large multicenter study using IV and oral amiodarone should be pursued prior to deciding whether its use should become standard therapy in all patients undergoing CABG in order to decrease the incidence of postoperative atrial fibrillation.</AbstractText> |
1,345 | Risk of proarrhythmic events in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: a multivariate analysis. | This study examined the risk of proarrhythmic events in patients receiving antiarrhythmic drugs for treatment of atrial fibrillation (AF) according to present-day safety guidelines.</AbstractText>Advances in understanding the proarrhythmic risk of antiarrhythmic drugs has led to development of safety guidelines for these agents. Such guidelines were used in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study.</AbstractText>This study was an analysis of the risk of arrhythmic events (arrhythmic death, resuscitated cardiac arrest, sustained ventricular tachycardia (VT), and torsade de pointes VT) in the antiarrhythmic drug arm of the AFFIRM study. Each time an antiarrhythmic drug was begun, it was counted as an exposure to that drug and the risk of an arrhythmic event was calculated.</AbstractText>A total of 2,033 patients received 3,030 exposures to antiarrhythmic drugs. Ninety-six arrhythmic events occurred by six years. Patients with a left ventricular ejection fraction <40% had more arrhythmic events. Twelve documented cases of torsade de pointes VT were noted. The incidence of torsade de pointes was 0.6% at five years (95% confidence interval 0.32 to 1.07).</AbstractText>The overall risk of adverse arrhythmic events upon exposure to antiarrhythmic drugs in the AFFIRM study was reasonably low. Strict criteria for the safe use of antiarrhythmic drugs were successful in minimizing proarrhythmic events.</AbstractText> |
1,346 | Increased incidence of life-threatening ventricular arrhythmias in implantable defibrillator patients after the World Trade Center attack. | This study was designed to evaluate whether the destruction of the World Trade Center (WTC) on September 11, 2001 (9/11), led to an increased frequency of ventricular arrhythmias among patients fitted with an implantable cardioverter-defibrillator (ICD).</AbstractText>The WTC attack induced psychological distress. Because ICDs store all serious arrhythmias for months, the attack provided a unique opportunity to compare pre- and post-9/11 frequencies of potentially lethal arrhythmias among ICD patients.</AbstractText>Two hundred consecutive ICD patients who presented for regularly scheduled follow-up to six affiliated clinics were recruited into this observational study. The electrograms stored in the ICDs for the three months before 9/11 and 13 months thereafter were scrutinized in a blinded manner (relative to date) for all ventricular tachyarrhythmias (tachycardia or fibrillation) triggering ICD therapy.</AbstractText>The frequency of tachyarrhythmias increased significantly for the 30 days post-9/11 (p = 0.004) relative to all other months between May 2001 and October 2002. In the 30 days post-9/11, 16 patients (8%) demonstrated tachyarrhythmias, compared with only seven (3.5%) in the preceding 30 days, representing a 2.3-fold increase in risk (95% confidence interval 1.1 to 4.9; p = 0.03). The first arrhythmic event did not occur for three days following 9/11, with events accumulating in a progressive non-clustered pattern.</AbstractText>Ventricular arrhythmias increased by more than twofold among ICD patients following the WTC attack. The delay in onset and the non-clustered pattern of these events differ sharply from effects following other disasters, suggesting that subacute stress may have served to promote this arrhythmogenesis.</AbstractText> |
1,347 | Cardiac arrhythmias: the quest for a cure: a historical perspective. | During the last 40 years, much progress has been made in our understanding and management of cardiac arrhythmias. A major step in the late 1960s was to combine programmed electrical stimulation of the heart with intracardiac activation recording. This allowed: 1) localization of the site of the block in the atrioventricular conduction system in patients with bradycardia; and 2) identification of the site of origin and the mechanism of supraventricular and ventricular tachycardia. Combining information from intracardiac studies with findings on the 12-lead electrocardiogram (ECG) resulted in much better localization of conduction abnormalities and arrhythmias using the ECG. This new knowledge led to the development of new therapies, such as bradycardia and antitachycardia pacing, and surgery for supraventricular and ventricular tachycardia. A very important development in the treatment of life-threatening arrhythmias was the implantable defibrillator. Growing concern about failure to protect patients at risk for dying suddenly with antiarrhythmic drugs led to a rapid increase in their number. Cure by catheter ablation became possible for patients with different types of arrhythmias. Genetic analysis allowed the identification of different monogenic arrhythmic diseases. Several challenges remain: the epidemic of atrial fibrillation, arrhythmias in heart failure, and sudden death out-of-hospital. One-fifth of all deaths are sudden and unexpected. The important issue is how we are going to prevent these unnecessary deaths from occurring. |
1,348 | Molecular mechanisms and global dynamics of fibrillation: an integrative approach to the underlying basis of vortex-like reentry. | Art Winfree's scientific legacy has been particularly important to our laboratory whose major goal is to understand the mechanisms of ventricular fibrillation (VF). Here, we take an integrative approach to review recent studies on the manner in which nonlinear electrical waves organize to result in VF. We describe the contribution of specific potassium channel proteins and of the myocardial fiber structure to such organization. The discussion centers on data derived from a model of stable VF in the Langendorff-perfused guinea pig heart that demonstrates distinct patterns of organization in the left (LV) and right (RV) ventricles. Analysis of optical mapping data reveals that VF excitation frequencies are distributed throughout the ventricles in clearly demarcated domains. The highest frequency domains are found on the anterior wall of the LV at a location where sustained reentrant activity is present. The optical data suggest that a high frequency rotor that remains stationary in the LV is the mechanism that sustains VF in this model. Computer simulations predict that the inward rectifying potassium current (IK1) is an essential determinant of rotor stability and frequency, and patch-clamp results strongly suggest that the outward component of IK1 of cells in the LV is significantly larger than in the RV. Additional computer simulations and analytical procedures predict that the filaments of the reentrant activity (scroll waves) adopt a non-random configuration depending on fiber organization within the ventricular wall. Using the minimal principle we have concluded that filaments align with the trajectory of least resistance (i.e. the geodesic) between their endpoints. Overall, the data discussed have opened new and potentially exciting avenues of research on the possible role played by inward rectifier channels in the mechanism of VF, as well as the organization of its reentrant sources in three-dimensional cardiac muscle. Such an integrative approach may lead us toward an understanding of the molecular and structural basis of VF and hopefully to new preventative approaches. |
1,349 | [Surgical treatment of secundum atrial septal defects in adults over 30 years old]. | To summarize the experience of surgical treatment of secundum atrial septal defects in adults over 30 years old.</AbstractText>There were 469 patients with secundum atrial septal defects in our study (male 144, female 325; ages 30-68, mean 38.6 years old). There were 105 cases with pulmonary hypertension and 458 cases with arrhythmia in the group. Surgical closure of defects were performed in all patients. Surgical closure of 358 cases were done by patches including 305 autologous pericardial patches. The low dose (6 x 10(-6)) nitric oxide inhalation was used in 25 postoperative patients with pulmonary hypertension. Right sided maze procedures were done in 5 cases with atrial fibrillation.</AbstractText>Surgical mortality was 0.6% (3 cases), the others were healed. In the group, there were 180 cases with arrhythmia, 27 cases with left ventricular function amyoplasia, 28 cases with low cardiac output syndrome, 12 cases in secondary operation for bleeding and 1 case with air-embolism. The level of mean pulmonary artery pressure of 25 postoperative patients with pulmonary hypertension inhaled nitric oxide was down 28.5%. After right sided maze procedures were done in 5 cases with atrial fibrillation, atrial fibrillation disappeared. 352 cases were followed up from 3 months to 20 years (mean 5.6 years). Twenty-nine cases were in class I-II of cardiac function, and the others were better than class I of cardiac function.</AbstractText>Atrial septal defects in adult should be operated as early as possible. When patch is needed, an autologous pericardial patch is the first selection. Inhaled nitric oxide is an effective method to postoperative pulmonary hypertension. The maze operation should be performed for atrial septal defect with atrial fibrillation while the surgical closure of defect was done. During and after operation, much attention should be paid to preventing and curing arrhythmia and protecting and supporting left heart function.</AbstractText> |
1,350 | Clustering of RR intervals predicts effective electrical cardioversion for atrial fibrillation. | Atrial fibrillation (AF) is characterized by an irregularly irregular ("random") heart beat. However, controversy exists whether the ventricular rhythm in AF is truly random. We investigated randomness by constructing three-dimensional RR interval plots (3D plots), allowing identification of "clustering" of RR intervals. It was hypothesized that electrical cardioversion (ECV) would be more effective in AF patients with clustering, because clustering might reflect a higher degree of organization of atrial fibrillatory activity.</AbstractText>The study group consisted of 66 patients (44 men and 22 women; mean age 68 +/- 11 years), who were referred for ECV because of persistent AF. Twenty-four-hour Holter recordings were used to construct 3D plots by plotting each RR interval (x axis) against the previous RR interval (y axis) and the number of occurrences of each of these x,y combinations (z axis). A clustering index was calculated as the percentage of beats within the peaks in the 3D plot. Based on the 3D plots, clustering of RR intervals was present in 31 (47%) of the 66 patients. ECV was effective in restoring sinus rhythm in 29 (94%) of these 31 patients, whereas sinus rhythm was restored in only 25 (71%) of the remaining 35 patients without clustering (P = 0.020). The clustering index ranged from <2% in the 12 patients with failed ECV to >8% in the 32 patients with sinus rhythm at the end of the study (4 weeks after the ECV); the clustering index in the 22 patients with a relapse of AF after effective ECV was intermediate (P = 0.034 and P = 0.042, respectively).</AbstractText>This study indicates that ECV is more effective in restoring sinus rhythm in AF patients with clustering compared to patients in whom no clustering is apparent on 3D plots. In addition, the degree of clustering appears to be predictive of the overall outcome of ECV; the higher the degree of clustering, the higher the likelihood of sinus rhythm at follow-up.</AbstractText> |
1,351 | Differences in tachyarrhythmia detection and implantable cardioverter defibrillator therapy by primary or secondary prevention indication in cardiac resynchronization therapy patients. | Although numerous trials have shown benefit of implantable cardioverter defibrillators (ICDs) for either primary or secondary prevention, no trial has prospectively enrolled patients from both indications and analyzed ICD utilization between groups.</AbstractText>We performed a retrospective review of MIRACLE ICD, a randomized, prospective double-blind trial of cardiac resynchronization therapy (CRT) in the ICD population. Both secondary prevention (N = 563) and primary prevention patients (N = 415) were enrolled. Subgroup analysis for frequency of ventricular tachycardia (VT) and ventricular fibrillation (VF) episodes and detection accuracy revealed that primary prevention patients had a significantly lower frequency of appropriate episodes (0.09 vs 0.43 episodes/month) at significantly faster cycle lengths (303 +/- 54 ms vs 366 +/- 71 ms, P < 0.0001). These episodes were more likely to be classified as VF by the device and thus receive shock therapy (42% by device classification vs 19% in secondary prevention, P < 0.0001). The absolute rate of inappropriate detections in the primary prevention group per month of follow-up was lower but constituted a much higher proportion of all episodes (30% vs 14%, P < 0.0001). Most inappropriate detections in the secondary prevention group were due to rapidly conducted atrial fibrillation; most in the primary prevention patients were due to sinus tachycardia.</AbstractText>Patients receiving an ICD for CRT therapy with primary prevention indications have a different clinical arrhythmia course than patients with a history of spontaneous VT/VF. This has implications for the optimal programming of ICDs. Longer-term, prospective evaluation of these differences is warranted and should be investigated in the broader ICD patient population.</AbstractText> |
1,352 | [Arrhythmias]. | The success of the radiofrequency catheter ablation procedure for most types of supraventricular and ventricular tachycardia largely eliminated the role of surgical therapy of arrhythmias. However, there remains a subset of arrhythmia patients in whom urgent surgical treatments are required. In this review we mention recent developments of the urgent surgical treatment for arrhythmias. In cases with complete atrioventricular (AV) block and ventricular fibrillation which associated with sudden death, temporary cardiac pacing and cardiac defibrillation using direct current (DC) cardioversion must be immediately induced and followed by implantation of permanent cardiac pacemaker or implantable cardioverter defibrillator (ICD), if necessary. In addition to usual cardiac pacing therapy, novel pacing therapy has been developed recently for the patients with symptomatic heart failure. Cardiac resynchronization therapy (CRT) using biventricular pacing is an emerging therapy for improvement of cardiac function in patients with heart failure in association with intraventricular conduction delay. To prevent the sudden death in patients with heart failure, biventricular pacing combined with ICD are also implanted and its efficacy are reported. With the exception of the pacing therapy, curative surgical treatments are limited in drug-refractory atrial fibrillation and ventricular fibrillation/tachycardia after myocardial infarction requiring Dor's type operation. In any case surgical treatment must be performed promptly and suitably with lower invasive methods. |
1,353 | Differences in mechanisms and outcomes of syncope in patients with coronary disease or idiopathic left ventricular dysfunction as assessed by electrophysiologic testing. | This study evaluated the causes of syncope and the significance and differences in left ventricular (LV) dysfunction, coronary disease, and idiopathic dilated cardiomyopathy (DCM).</AbstractText>Risk stratification of and indications for an automated defibrillator could differ according to the cause of LV dysfunction.</AbstractText>Electrophysiologic study, including atrial and ventricular programmed stimulation, was performed in 119 patients with coronary disease (group I) and 61 patients with DCM (group II) with an left ventricular ejection fraction (LVEF) <40% and syncope. Patients were followed from one to six years (mean 4 +/- 2 years).</AbstractText>Sustained monomorphic ventricular tachycardia (VT) was induced in 44 group I patients (37%) and 13 group II patients (21%); ventricular flutter (>270 beats/min) or ventricular fibrillation (VF) was induced in 24 group I patients (19%) and 9 group II patients (15%); and various other arrhythmias were identified. Syncope remained unexplained in 34 group I patients (30%) and 16 group II patients (27%). Prognosis depended on the heart disease: VT or VF induction was a predictive factor of mortality in coronary disease and identified a group with high cardiac mortality (46%), compared with patients with a negative study, who had a lower mortality (6%; p < 0.001) than in other studies. Cardiac mortality was only correlated with LVEF in DCM.</AbstractText>Various causes could explain syncope in 70% of patients with coronary disease and DCM, but differences were noted: VT was frequent in coronary disease with a bad prognosis, and ischemia could explain syncope; in DCM, different causes such as atrial tachycardia could be responsible for syncope, but the prognosis only depended on LVEF.</AbstractText> |
1,354 | Prevention of ventricular fibrillation, acute myocardial infarction (myocardial necrosis), heart failure, and mortality by bretylium: is ischemic heart disease primarily adrenergic cardiovascular disease? | It is widely, but mistakenly, believed that ischemic heart disease (IsHD) and its complications are the sole and direct result of reduced coronary blood flow by obstructive coronary artery disease (CAD). However, cardiac angina, acute myocardial infarction (AMI), and sudden cardiac death (SCD) occur in 15%-20% of patients with anatomically unobstructed and grossly normal coronaries. Moreover, severe obstructive coronary disease often occurs without associated pathologic myocardiopathy or prior symptoms, ie, unexpected sudden death, silent myocardial infarction, or the insidious appearance of congestive heart failure (CHF). The fact that catecholamines explosively augment oxidative metabolism much more than cardiac work is generally underappreciated. Thus, adrenergic actions alone are likely to be more prone to cause cardiac ischemia than reduced coronary blood flow per se. The autonomic etiology of IsHD raises contradictions to the traditional concept of anatomically obstructive CAD as the lone cause of cardiac ischemia and AMI. Actually, all the signs and symptoms of IsHD reflect autonomic nervous system imbalance, particularly adrenergic hyperactivity, which may by itself cause ischemia as in rest angina. Adrenergic activity causing ischemia signals cardiac pain to pain centers via sympathetic efferent pathways and tend to induce arrhythmogenic and necrotizing ischemic actions on the cardiovascular system. This may result in ischemia induced metabolic myocardiopathy not unlike that caused by anatomic or spasmogenic coronary obstruction. The clinical study and review presented herein suggest that adrenergic hyperactivity alone without CAD can be a primary cause of IsHD. Thus, adrenergic heart disease (AdHD), or actually adrenergic cardiovascular heart disease (ACVHD), appears to be a distinct entity, most commonly but not necessarily occurring in parallel with CAD. CAD certainly contributes to vulnerability as well as the progression of IsHD. This vicious cycle, which explains the frequent parallel occurrence of arteriosclerosis and IHD, an association that appears to be linked by the same cause, comprises a common vulnerability to deleterious adrenergic actions on the myocardium, lipid metabolism, and vascular system alike, rather than viewing CAD and IsHD as having a putative cause and effect relationship as commonly thought. Adrenergic actions can also cause the abnormal lipid metabolism that is associated with CAD and IsHD by catecholamine-induced metabolic actions on lipid mobilization by activation of phospholipases. This may also be part of toxic catecholamine hypermetabolic actions by enhancing deleterious cholesterol and lipid actions in damaging coronary vessels by plaque formation as well as inducing obstructive coronary spasm and platelet aggregation. This may also cause direct toxic necrosis on the myocardium as well as atherosclerosis in blood vessels. In fact, drugs that inhibit adrenergic actions like propranolol, reserpine, and guanethidine all inhibit arteriosclerosis induced by hypercholesterolemia in experimental animals and prevent carotid vascular disease (associated with stroke) in humans. The concomitant development of myocardiopathy and coronary vascular lesions or coronary and carotid artery intimal medial thickening by catecholamine toxicity is reflected by the frequent primary presentation of patients with catecholamine-secreting pheochromocytoma with cardiovascular disease, ie, hypertension arrhythmias, AMI, SCD, CHF, and vascular disease, which represents a clear example of the primary deleterious impact of catecholamines on the entire cardiovascular system causing adrenergic cardiovascular disease. Thus, like myocardiopathy, CAD and atherosclerosis in general may be the consequences of or a complication of catecholamine actions rather than its putative cause. This report shows how prophylactic bretylium not only prevents arrhythmias but prevents myocardial necrosis, shock, CHF, maintains or restores normal contractility, and lowers mortality in AMI patients by inducing adrenergic blockade. |
1,355 | Comparison of rate and rhythm control in patients with atrial fibrillation and nonischemic heart failure. | Atrial fibrillation (AF) is a very common cardiac arrhythmia with an increased mortality in patients with heart failure. Whether the best therapeutic approach to these patients is to restore sinus rhythm or to adequately control the ventricular rate is still controversial. The aim of this study was to compare both strategies in patients with AF and nonischemic heart failure. One hundred and fifty-four patients with AF duration greater than 48 hours and nonischemic left ventricular dysfunction were randomized either to a rhythm (n = 84) or rate (n = 74) control group. The composite end points of the study were embolism, death, and exercise capacity. The average age of the patients was 61 +/- 10 years in the rhythm control group and 58 +/- 12 years in the rate control group (P = NS). The average follow-up period was 35 +/- 21 months in the rhythm control group and 37 +/- 19 months in the rate control group (P = NS). In the first year of the study, exercise capacity and left ventricular ejection fraction (LVEF) were improved in the rhythm control group compared to the exercise capacity and LVEF of the rate control group (P < 0.0001 and P = 0.0005, respectively). There were no statistically significant differences in the embolic event rate between the two groups (P = NS). The mortality rate, especially for death due to pump failure, was significantly higher in the rate control group at the end of the study (P < 0.0001). Restoring and maintaining sinus rhythm had a beneficial effect on mortality and exercise capacity in patients with nonischemic heart failure and AF. |
1,356 | Predictors of heart failure among women with coronary disease. | Although heart failure is common among women with coronary disease, the risk factors for developing heart failure have not been well studied. We determined the risk factors for developing heart failure among postmenopausal women with established coronary disease.</AbstractText>This is a prospective cohort study using data from the Heart and Estrogen/progestin Replacement Study (HERS), a randomized, blinded, placebo-controlled trial of 4.1 years' duration, and subsequent open-label observational follow-up for 2.7 years (HERS II), performed at 20 US clinical centers between 1993 and 2000. Of the 2763 postmenopausal women with established coronary disease in the HERS trial, we studied the 2391 women with no heart failure at baseline by self-report and physical examination. The primary outcome of this analysis was incident heart failure defined by hospital admission or death from heart failure. During the 6.3+/-1.4-year follow-up, 237 women (10%) developed heart failure. Nine predictors were identified: diabetes (defined as a self-reported history of diabetes on treatment), atrial fibrillation, myocardial infarction, creatinine clearance <40 mL/min, systolic blood pressure >120 mm Hg, current smoking, body mass index >35 kg/m2, left bundle-branch block, and left ventricular hypertrophy. Randomization to estrogen/progestin was not associated with heart failure (hazard ratio=1.0; 95% CI, 0.7 to 1.3). Diabetes was the strongest risk factor (adjusted hazard ratio=3.1; 95% CI, 2.3 to 4.2). Diabetic women with elevated body mass index or depressed creatinine clearance were at highest risk, with annual incidence rates of 7% and 13%, respectively. Among diabetic women, hyperglycemia was associated with heart failure risk (adjusted hazard ratio=3.0; 95% CI, 1.2 to 7.5 for fasting glucose >300 mg/dL compared with fasting glucose 80 to 150 mg/dL).</AbstractText>We identified 9 predictors of heart failure in postmenopausal women with coronary disease. Diabetes was the strongest risk factor, particularly when poorly controlled or with concomitant renal insufficiency or obesity.</AbstractText> |
1,357 | Transventricular mitral commissurotomy in critical mitral stenosis during pregnancy. | The management of a pregnant patient with mitral stenosis is a subject of debate with regards to the optimal type of treatment and the time of intervention. We performed trans-ventricular mitral commissurotomy (TVMC) either as an isolated procedure in the second trimester, or in combination with Cesarian section at term. We retrospectively analyzed our experience with TVMC during pregnancy and formulated a protocol for its management. Between January 1987 and April 2002, fifty one patients underwent TVMC for critical mitral stenosis during pregnancy. In 38 patients, elective TVMC was performed during the second trimester, while in 12, it was performed as an initial procedure along with Cesarian section at term. One patient had an emergency TVMC in the second trimester when she presented with intractable acute pulmonary edema. There were no maternal mortalities. Three patients who developed post-operative mitral regurgitation were managed conservatively. Another two patients who developed cerebral embolism with hemiplegia recovered completely without any neurological deficit. There was only one fetal death in a patient where TVMC was performed as an emergency procedure for acute pulmonary edema. We conclude that TVMC in pregnancy is a safe, cost effective alternative in critical mitral stenosis complicating pregnancy. |
1,358 | Systematic review: cardiac resynchronization in patients with symptomatic heart failure. | Even with optimal pharmacotherapy, symptomatic heart failure is associated with substantial morbidity and mortality.</AbstractText>To determine the efficacy and safety of cardiac resynchronization therapy in adults with advanced systolic heart failure.</AbstractText>The Cochrane Central Register of Controlled Trials (2002, volume 4), MEDLINE (1980-2003), EMBASE (1980-2003), other electronic databases, and U.S. Food and Drug Administration reports. We contacted primary study authors and device manufacturers, and we hand searched bibliographies of relevant papers and conference proceedings.</AbstractText>Randomized, controlled clinical trials for efficacy and controlled trials plus prospective cohort studies for safety.</AbstractText>Two reviewers chose studies and extracted data independently; random-effects models were used for analyses.</AbstractText>Nine trials were included in the efficacy review (3216 patients). All trial participants had reduced ejection fraction and prolonged QRS duration, and 85% had New York Heart Association (NYHA) class III or IV symptoms. Cardiac resynchronization therapy improved ejection fraction (weighted mean difference, 0.035 [95% CI, 0.015 to 0.055]), quality of life (weighted mean reduction in score on the Minnesota Living with Heart Failure Questionnaire, 7.6 points [CI, 3.8 to 11.5 points]), and function (58% vs. 37% of patients improved by at least 1 NYHA class). Heart failure hospitalizations were reduced by 32% (relative risk [RR], 0.68 [CI, 0.41 to 1.12]), with benefits most marked in patients with NYHA class III or IV symptoms at baseline (RR, 0.65 [CI, 0.48 to 0.88]; number needed to treat for benefit [NNT(B)], 12). All-cause mortality was reduced by 21% (RR, 0.79 [CI, 0.66 to 0.96]; NNT(B), 24), driven largely by reductions in death from progressive heart failure (RR, 0.60 [CI, 0.36 to 1.01]). Eighteen studies (total of 3701 patients with cardiac resynchronization devices) were included in the safety review. Implant success rate was 90% (CI, 89% to 91%), and 0.4% of patients died during implantation (CI, 0.2% to 0.7%). Over a median 6-month follow-up, leads dislodged in 9% of patients (CI, 7% to 10%) and mechanical malfunctions occurred in 7% (CI, 5% to 8%).</AbstractText>These trials enrolled only patients with heart failure with NYHA class III or IV symptoms despite medical therapy, a prolonged QRS duration, and reduced ejection fraction; in addition, experienced providers implanted the devices. Because all but one of these trials randomly assigned patients after device implantation, their results may overestimate the potential benefits of cardiac resynchronization. Finally, since few patients in these trials had bradyarrhythmias or atrial fibrillation, the role of cardiac resynchronization in such patients is uncertain.</AbstractText>In selected patients with heart failure, cardiac resynchronization therapy improves functional and hemodynamic status, reduces heart failure hospitalizations, and reduces all-cause mortality.</AbstractText> |
1,359 | Inhibition of ischemia/reperfusion-induced damage by dexamethasone in isolated working rat hearts: the role of cytochrome c release. | We investigated the contribution of dexamethasone treatment on the recovery of postischemic cardiac function and the development of reperfusion-induced arrhythmias in ischemic/reperfused isolated rat hearts. Rats were treated with 2 mg/kg of intraperitoneal injection of dexamethasone, and 24 hours later, hearts were isolated according to the 'working' mode, perfused, and subjected to 30 min global ischemia followed by 120 min reperfusion. Cardiac function including heart rate, coronary flow, aortic flow, and left ventricular developed pressure were recorded. After 60 min and 120 min reperfusion, 2 mg/kg of dexamethasone significantly improved the postischemic recovery of aortic flow and left ventricular developed pressure from their control values of 10.7 +/- 0.3 ml/min and 10.5 +/- 0.3 kPa to 22.2 +/- 0.3 ml/min (p < 0.05) and 14.3 +/- 0.5 kPa (p < 0.05), 19.3 +/- 0.3 ml/min (p < 0.05) and 12.3 +/- 0.5 kPa (p < 0.05), respectively. Heart rate and coronary flow did not show a significant change in postischemic recovery after 60 or 120 min reperfusion. In rats treated with 0.5 mg/kg of actinomycin D injected i.v., one hour before the dexamethasone injection, suppressed the dexamethasone-induced cardiac protection. Electrocardiograms were monitored to determine the incidence of reperfusion-induced ventricular fibrillation. Dexamethasone pretreatment significantly reduces the occurrence of ventricular fibrillation. Cytochrome c release was also observed in the cytoplasm. The results suggest that the inhibition of cytochrome c release is involved in the dexamethasone-induced cardiac protection. |
1,360 | Cost effectiveness of therapies for atrial fibrillation. A review. | Atrial fibrillation is the most common supraventricular tachyarrhythmia encountered in clinical practice, affecting over 5% of persons over the age of 65 years. A common pathophysiological mechanism for arrhythmia development is atrial distention and fibrosis induced by hypertension, coronary artery disease or ventricular dysfunction. Less frequently, atrial fibrillation is caused by mitral stenosis or other provocative factors such as thyrotoxicosis, pericarditis or alcohol intoxication. Depending on the extent of associated cardiovascular disease, atrial fibrillation may produce haemodynamic compromise, or symptoms such as palpitations, fatigue, chest pain or dyspnoea. Arrhythmia-induced atrial stasis can precipitate clot formation and the potential for subsequent thromboembolism. Comprehensive management of atrial fibrillation requires a multifaceted approach directed at controlling symptoms, protecting the patient from ischaemic stroke or peripheral embolism and possible conversion to or maintenance of sinus rhythm. Numerous randomised trials have demonstrated the efficacy of warfarin--and less so aspirin (acetylsalicylic acid)--in reducing the risk of embolic events. Furthermore, therapeutic strategies exist that can favourably modify symptoms by restoring and maintaining sinus rhythm with cardioversion and antiarrhythmic prophylaxis. However, the risks and benefits of various treatments is highly dependent on patient-specific features, emphasising the need for an individualised approach. This article reviews the findings of cost-effectiveness studies published over the past decade that have evaluated different components of treatment strategies for atrial fibrillation. These studies demonstrate the economic attractiveness of acute management options, long term warfarin prophylaxis, telemetry-guided initiation of antiarrhythmic therapy, approaches to restore and maintain sinus rhythm, and the potential role of transoesophageal echocardiographic screening for atrial thrombus prior to pharmacological or electrical cardioversion. Further, we discuss the merits and limitations of the cost-effectiveness analyses in the context of overall treatment strategies. Finally, we identify areas that will require additional research to achieve the goal of effective and economically efficient management of atrial fibrillation. |
1,361 | [The Brugada syndrome. To be evoked in case of malaise in a young adult]. | A DIAGNOSIS TO BE EVOKED: The Brugada syndrome is a rare but serious inherited disease that causes sudden cardiac death by ventricular tachycardia and fibrillation, especially in younger men. Diagnostic problems are related to the possible absence of symptoms although the electrocardiogram (ECG) reveals the characteristics of a Brugada syndrome and to the variations in the ECG in the same patient over time. THREE ELECTROCARDIOLOGICAL ASPECTS: Type 1 corresponds to the historical description with ST segment elevation at point J of at least 3 mm from its summit and upward convex ST segment followed by a negative T wave. In Type 2, the extent of point I is of 2 mm, the ST segment has a saddle form and remains at least 1 mm above the isoelectric line, the T wave is positive or biphasic. In Type 3, the terminal section of the ST segment never exceeds 1 mm above the isoelectric line. In the case of a Type 1 ECG, a pharmacodynamic test is of no interest. REGARDING TREATMENT: The only treatment to have demonstrated its efficacy is the implantable automatic defibrillator, indicated in symptomatic patients. |
1,362 | Prevention of primary ventricular fibrillation in acute myocardial infarction with prophylactic lidocaine. | Primary ventricular fibrillation (VF) during an acute myocardial infarction (AMI) occurs with a high incidence and mortality rate with or without thrombolysis. The incidence varies from 2% to 19% depending on the definition of "primary." Primary VF in this study refers to fibrillation occurring in the absence of shock or pulmonary edema. Mortality rate, when primary VF occurs, is 2 to 4 times greater than when it does not. Prevention of VF has been impeded by the publication of the 1996 recommendations of the American Heart Association and American College of Cardiology against the use of prophylactic lidocaine based on meta-analysis studies implying toxicity. This observational study of 4,254 patients with AMI reports the incidence and mortality rates of primary VF over 32 years. Of the 4,254 patients, 4,150 received prophylactic lidocaine, and 104 patients did not receive prophylactic lidocaine due to the 1996 guidelines, after which administration of prophylactic lidocaine was governed by physician choice. The incidence of primary VF was 0.5% among the 4,150 who received prophylactic lidocaine and 10% among the 104 who did not (p <0.0001). Among the 4,150 receiving prophylactic lidocaine, sinoatrial block occurred in 0.5% and complete infranodal atrial ventricular block occurred in 0.2%, all secondary to the site of infarction (concurrent serum lidocaine levels were < 4 microg/ml). Asystole was an agonal rhythm in 4%; these patients had been off lidocaine for 48 hours. Mortality rates were 10.5% in patients without primary VF and 25% in patients with VF (p <0.001). Thus, prophylactic lidocaine markedly decreased the incidence of VF in 4,150 patients with AMI to 0.5% compared with trials before and after thrombolysis (2% to 19%) and with the 104 patients in this study who did not receive prophylactic lidocaine (10%). No lidocaine-induced sinoatrial or atrial ventricular block or asystole occurred. |
1,363 | [The effect of K(ATP)-channel activation on the electrical stability of myocardium in rats with postinfarction cardiosclerosis]. | Opening of the ATP-dependent K-channels (K(ATP) channels) upon intravenous administration of the cardioselective activator BMS 180448 (3 mg/kg) decreased the ventricular fibrillation threshold (VFT) in rats with postinfarction cardiosclerosis (PIC). Preliminary injection of the selective K(ATP) channel blocker glibenclamide (0.3 mg/kg, i.v.) completely abolished the profibrillatory effect of BMS 180448. At the same time, the mitochondrial K(ATP) channel blocker 5-hydroxydecanoic acid (5 mg/kg) did not influence the proarrhythmogen activity of BMS 180448. Simultaneous administration of the sarcoK(ATP) channel inhibitor HMR 1098 (3 mg/kg) and BMS 180448 increased the VFT up to a level in intact animals. Administration of the mitoK(ATP) channel activator diazoxide (5 mg/kg) after preliminary treatment with guanethidine (50 mg/kg) increased the VFT in rats with PIC. It is concluded that opening of the mitoK(ATP) channels increases the cardiac electrical stability in rats with PIC. |
1,364 | [Autoantibodies Against beta(1)-Adrenoreceptors in Patients With Cardiac Rhythm Disorders. Prevalence and Possible Role in Development of Arrhythmia]. | To assess prevalence of autoantibodies against beta(1)-adrenoreceptors (beta(1)-AR) in patients with arrhythmias of various etiology.</AbstractText>Patients with arrhythmias (n=110, including 59 patients with primary [idiopathic] electrical abnormalities, 33 - with chronic myocarditis and dilated cardiomyopathy [DCM]; 18 - with ischemic heart disease [IHD]) and healthy control subjects (n=20).</AbstractText>Antibodies against beta(1)-AR were measured in blood serum by direct immunoassay. Synthetic fragment containing 26 amino acids of beta(1)-AR second loop was used as antigen.</AbstractText>Patients with primary electrical abnormalities and chronic myocarditis/DCM had similar prevalence of beta(1)-AR (49.1% and 54.5%, respectively), what was significantly higher than in controls (10%) and in patients with IHD (16.6%). These results provided evidence for the possible presence of an autoimmune process in the genesis of idiopathic arrhythmias. Among patients with idiopathic arrhythmias beta(1)-AR were found in 40% (10 of 25) of patients with ventricular tachycardia (VT), 63.6% (14 of 22) of patients with ventricular extrasystoles (VE), 41.6% (5 of 12) of patients with atrial fibrillation (AF). Among patients with chronic myocarditis and DCM beta(1)-AR were found in 72.2% (13 of 18) of patients with VT, 28.5% (2 of 7) of patients with VE, 37.5% (3 of 8) of patients with AF. Among patients with idiopathic arrhythmias female sex and frequent respiratory viral diseases were more common in beta(1)-AR-positive compared with beta(1)-AR-negative patients. VT and left ventricular ejection fraction <40% were more common in beta(1)-AR-positive than beta(1)-AR-negative patients among those with chronic myocarditis and DCM.</AbstractText> |
1,365 | [Cardiopulmonary stress test in patients with heart failure and atrial fibrillation]. | The cardiopulmonary stress test (CPST) allows the objective assessment of stress capacity in patients (pts) with heart failure (HF). There are a small number of studies concerning CPST in pts with HF and AF.</AbstractText>to assess the influence of AF on CPST parameters in pts with HF.</AbstractText>The study group consisted of 56 males aged 35-65 years (x = 57.3 year) with diagnosed HF lasting at least 3 months, in the II and I NYHA functional class and with l eft ventricular ejection fraction(EF) below 40%. 12 pts had an idiopathic cardiomyopathy and 44--cardiomyopathy of ischemic origin. All study pts were divided into two groups: group I (gr. I) - with persistent AF and group II (gr. II)--with sinus rhythm.</AbstractText>The BNP ad IL-6 levels were measured and transthoracic echocardiography and CPST were performed in all study pts.We have analysed the echocardiographic and CPST parameters in both study groups.</AbstractText>We found no significant differences in age, BMI, ethiology, left ventricular echocardiographic parameter values and NYHA functional class between both groups. In pts with AF (gr. I) we found significantly higher LA diameter (mm) 49.5, SD = 6.7 vs. 44.8, SD = 6.7 (p = 0.01), significantly higher BNP level (pg/ml) 582.75, SD = 179.36 vs. 442.94, SD = 213.75 (p = 0.03) and IL-6 level (pg/ml) 13.55, SD = 10.94 vs. 8.6, SD = 7.83 (p = 0.05). We also found significant differences in: HRmin (bpm) (gr. I--98.45, SD = 21.70, gr. II--80.48, SD = 15.25 p = 0.001), HRmax (bpm) (gr. I--146.82, SD = 16.14, gr. II--123,14, SD = 16.69 p = 0.001), tmax (sec) (gr. I--414.0, SD = 252.33, gr. II--618.11, SD=268,69, p = 0.02), METS (gr. I--2.09 SD = 1.04, gr. II--4.42, SD = 2.15 p = 0.002) and VO2peak (ml/kg/min) (gr. I--11.52, SD = 1.86, gr. II - 15,03, SD = 4.42, p = 0.01).</AbstractText>(1) Persistent atrial fibrillation in pts with HF is associated with 23% lower VO2peak and lower stress tolerance as compared to pts with sinus rhythm. (2) Higher IL-6 level in pts with HF and AF indicates the sympatethic system's overactivation and the presence of inflammatory reaction in these pts.</AbstractText> |
1,366 | [Long-term results of radiofrequency (RF) catheter ablation of cardiac arrhythmias]. | Although the short-term results after radiofrequency (RF) catheter ablation of atrioventricular nodal reentrant tachycardia (AVNRT), accessorry pathway (AP), atrioventricular junction (AVJ) and common atrial flutter (Aflu) have been widely reported, there is insufficient data on long-term outcome.</AbstractText>To evaluate the long-term efficacy of RF ablation of cardiac arrhythmias in a single center.</AbstractText>The study population consisted of 349 consecutive patients (mean age 49.5 years) who underwent RF ablation of AP (136 patients), AVNRT (105 patients), AVJ (86 patients) or Aflu (15 patients). In 4 patients two AP and in 3 patients AP and AVNRT were ablated during the same session. The patients were subsequently followed-up for an average of 44.3 months (12-76 months).</AbstractText>Ablation was successful in 341 patients (97.7%). Major complications occurred in 8 patients (2.3%) and included av block (6 patients), ventricular fibrillation (1 patient) and cardiac tamponade (1 patient). Tachycardia recurrences were observed in 21 patients (6.2%) after successful ablation. All the recurrences occurred within 10 months (mean 2.3 months) after ablation. The recurrence rate was 5.8% (6 patients) in the AVNRT group, 9.2% (12 patients) in the AP group, 1.2% in the AVJ group (1 patient) and 13% (2 patients) in the Aflu group. The differences between groups were insignifficant.</AbstractText>(1) The immediate success rate of RF ablation of AVNRT, AP, AVJ or Aflu was high and there was a low incidence of complications. (2) The recurrence rate during long-term observation is low. (3). All the recurrences occurred within 10 months after successful ablation.</AbstractText> |
1,367 | Genetic analysis of the cardiac sodium channel gene SCN5A in Koreans with Brugada syndrome. | The SCN5A gene encodes the alpha subunit of the human cardiac voltage-gated sodium channel. Mutations in SCN5A are responsible for Brugada syndrome, an inherited cardiac disease that leads to idiopathic ventricular fibrillation (IVF) and sudden death. In this study, we screened nine individuals from a single family and 12 sporadic patients who were clinically diagnosed with Brugada syndrome. Using PCR-SSCP, DHPLC, and DNA sequencing analysis, we identified a novel single missense mutation associated with Brugada syndrome in the family and detected a C5607T polymorphism in Korean subjects. A single nucleotide substitution of G to A at nucleotide position 3934 changed the coding sense of exon 21 of the SCN5A from glycine to serine (G1262S) in segment 2 of domain III (DIII-S2). Four individuals in the family carried the identical mutation in the SCN5A gene, but none of the 12 sporadic patients did. This mutation was not found in 150 unrelated normal individuals. This finding is the first report of a novel mutation in SCN5A associated with Brugada syndrome in Koreans. |
1,368 | [Implantation of an automatic cardioverter-defibrillator in small children--two case reports]. | Implantation of an automatic cardioverter-defibrillator (ICD) in children may be challenging due to the increased risk of periprocedural and long-term complications. ICD was implanted in two boys with hypertrophic cardiomyopathy, aged 6 and 9 years, with of a body weight of 20 and 25 kg, respectively. In one patient an ICD was implanted due to a history of ventricular fibrillation whereas the second patient underwent prophylactic ICD implantation due to a family history of sudden cardiac death. No short- or mid-term complications were recorded. Difficulties and risks of ICD implantation in children are discussed. |
1,369 | Intermittent hypoxic training protects canine myocardium from infarction. | This investigation examined cardiac protective effects of normobaric intermittent hypoxia training. Six dogs underwent intermittent hypoxic training for 20 consecutive days in a normobaric chamber ventilated intermittently with N2 to reduce fraction of inspired oxygen (FiO2) to 9.5%-10%. Hypoxic periods, initially 5 mins and increasing to 10 mins, were followed by 4-min normoxic periods. This hypoxia-normoxia protocol was repeated, initially 5 times and increasing to 8 times. The dogs showed no discomfort during intermittent hypoxic training. After 20 days of hypoxic training, the resistance of ventricular myocardium to infarction was assessed in an acute experiment. The left anterior descending (LAD) coronary artery was occluded for 60 mins and then reperfused for 5 hrs. At 30 mins of LAD occlusion, radioactive microspheres were injected through a left atrial catheter to assess coronary collateral blood flow into the ischemic region. After 5 hrs reperfusion, the heart was dyed to delineate the area at risk (AAR) of infarction and stained with triphenyl tetrazolium chloride to identify infarcted myocardium. During LAD occlusion and reperfusion, systemic hemodynamics and global left ventricular function were stable. Infarction was not detected in 4 hearts and was 1.6% of AAR in the other 2 hearts. In contrast, 6 dogs sham-trained in a chamber ventilated with compressed air and 5 untrained dogs subjected to the same LAD occlusion/reperfusion protocol had infarcts of 36.8% +/- 5.8% and 35.2% +/- 9.5% of the AAR, respectively. The reduction in infarct size of four of the six hypoxia-trained dogs could not be explained by enhanced collateral blood flow to the AAR. Hypoxia-trained dogs had no ventricular tachycardia or ventricular fibrillation. Three sham-trained dogs had ventricular tachycardia and two had ventricular fibrillation. Three untrained dogs had ventricular fibrillation. In conclusion, intermittent hypoxic training protects canine myocardium from infarction and life-threatening arrhythmias during coronary artery occlusion and reperfusion. The mechanism responsible for this potent cardioprotection merits further study. |
1,370 | Predictors of sudden cardiac death after Mustard or Senning repair for transposition of the great arteries. | The goal of this research was to identify predictors for sudden death (SD) in patients with transposition of the great arteries (TGA) who have undergone atrial inflow repair.</AbstractText>Sudden death is the most common cause of late death after atrial inflow repair of TGA. Little is known about the predictors of SD.</AbstractText>This was a retrospective, multicenter, case-controlled study. We identified 47 patients after Mustard's or Senning's operation who experienced an SD event (34 SD, 13 near-miss SD). Each patient was matched with two controls with the same operation, but without an SD event. Information on numerous variables before the event was obtained and compared with controls at the same time frame.</AbstractText>Presence of symptoms of arrhythmia or heart failure at most recent follow-up and history of documented arrhythmia (atrial flutter [AFL]/atrial fibrillation [AF]) were found to increase the risk of SD. Electrocardiogram (ECG), chest X-ray, and Holter ECG findings were not predictive of SD. Neither medication nor pacing was found to be protective. Most SD events (81%) occurred during exercise. Ventricular tachycardia/ventricular fibrillation were the recorded rhythm during SD in 21 of 47 patients.</AbstractText>Presence of symptoms and documented AFL/AF are the best predictors of SD in TGA patients. Patients with these findings should be further evaluated for risk of SD.</AbstractText> |
1,371 | Prognostic implications of atrial fibrillation in patients undergoing myocardial perfusion single-photon emission computed tomography. | The aim of this research was to determine whether presence of atrial fibrillation (AF) provides incremental prognostic information relative to myocardial perfusion single-photon emission computed tomography (MPS) with respect to risk of cardiac death (CD).</AbstractText>The prognostic significance of AF in patients undergoing MPS is not known.</AbstractText>A total of 16,048 consecutive patients undergoing MPS were followed-up for a mean of 2.21 +/- 1.15 years for the development of CD. Of those, 384 patients (2.4%) had AF. Cox proportional hazards method was used to compare clinical and perfusion data for the prediction of CD in patients with and without AF.</AbstractText>Atrial fibrillation was a significant predictor of CD in patients with normal (1.6% per year vs. 0.4% per year in non-AF patients), mildly abnormal (6.3% per year vs. 1.2% per year), and severely abnormal MPS (6.4% per year vs. 3.7% per year) (p < 0.001 for all). By multivariable analysis, AF patients had worse survival (p = 0.001) even after adjustment for the variables most predictive of CD: age, diabetes, shortness of breath, use of vasodilator stress, rest heart rate, and the nuclear variables. In the 4,239 patients with left ventricular ejection fraction evaluated by gated MPS, AF demonstrated incremental prognostic value not only over clinical and nuclear variables, but also over left ventricular ejection in predicting CD (p = 0.014).</AbstractText>The presence of AF independently increases the risk of cardiac events over perfusion and function variables in patients undergoing MPS. Patients with AF have a high risk of CD, even when MPS is only mildly abnormal. Whether patients with AF and mildly abnormal MPS constitute a group more deserving of early referral to cardiac catheterization is a question warranting further study.</AbstractText> |
1,372 | Myocardial protection with postconditioning is not enhanced by ischemic preconditioning. | Ischemic preconditioning (IPC) has been used in off-pump coronary artery bypass surgery (OPCAB) to reduce potential injury secondary to ligation of the target vessel. Previous studies have shown that a brief period of repetitive coronary occlusion applied at the onset of reperfusion, postconditioning (postcon), attenuates myocardial injury. This study tested the hypothesis that coincident application of IPC and postcon would provide more cardioprotection than either intervention alone by inhibiting oxidant-mediated injury after ischemia and reperfusion.</AbstractText>Four groups of open-chest canines endured 60 minutes coronary occlusion followed by 3 hours reperfusion: control (n = 10), no intervention; IPC (n = 9), 5 minutes left anterior descending coronary artery occlusion preceded 10 minutes of reperfusion before prolonged occlusion; postcon (n = 10), 3 cycles of 30 seconds reperfusion-30 seconds reocclusion were imposed immediately upon reperfusion; IPC+postcon (n = 8), IPC and postcon algorithms were combined.</AbstractText>Collateral blood flow during ischemia was similar in all groups. Compared to control (24% +/- 2%), infarct size was comparably reduced in IPC (13% +/- 2%* [* denotes p less than 0.05 compared with control]), and postcon (10% +/- 1%*), consistent with a reduction in plasma creative kinase activity in these groups; infarct size was not further reduced by IPC+postcon (12% +/- 3%*). Tissue water content in ischemic myocardium was comparably reduced in IPC, postcon, and IPC+postcon compared to control. Superoxide anion generation detected by dihydroethidium staining in area at risk myocardium was comparably reduced in all intervention groups relative to control. Plasma malondialdehyde (microM), a lipid peroxidation byproduct of oxidant injury, was less at 1 hour of reperfusion in IPC (2.2 +/- 0.2*), postcon (2.1 +/- 0.2*), and IPC+postcon (2.5 +/- 0.2*) relative to control (3.3 +/- 0.2). Ventricular fibrillation occurred less often in all intervention groups.</AbstractText>No additive cardioprotective effects by IPC and postcon were observed in a canine model of regional ischemia and reperfusion. The potent attenuation of myocardial injury by postcon may suggest a clinically applicable strategy during some surgical revascularization procedures (ie, OPCAB).</AbstractText> |
1,373 | Bedside programmed ventricular stimulation for sudden death risk stratification. | Patients with myocardial infarction and left ventricular dysfunction are at risk for sudden death. This research was conducted to determine the applicability and safety of a bedside programmed stimulation protocol to determine the risk for sudden death in these patients.</AbstractText>Four hundred and twelve patients with acute myocardial infarction were studied. Left ventricular ejection fraction was evaluated by means of an echocardiogram. Ventricular arrhythmia, late potentials and heart rate variability were determined by means of Holter recordings. Fifty patients (60 +/- 14-year-old; 85% male) presented a left ventricular ejection fraction lower than 0.40 (0.36 +/- 0.10) associated with late potentials, low heart rate variability or ventricular arrhythmia greater than Lown I. After a central venous access was placed under fluoroscopy guidance and ECG monitoring, a quadripolar catheter was advanced to the right ventricular apex to perform programmed ventricular stimulation with up to three extrastimuli. The patients were followed-up to determine in-hospital morbidity and/or mortality.</AbstractText>No patient suffered complications. Ventricular tachycardia or ventricular fibrillation was induced in six patients. All of them received amiodarone and in five an automatic cardioverter-defibrillator was implanted. After a 22 +/- 6 month follow-up, five patients had received appropriate discharges from the implanted device and none had suffered from arrhythmic sudden death.</AbstractText>Bedside programmed stimulation is a safe and useful means for sudden death risk stratification in post myocardial infarction patients. It moreover presents the advantage of being cheaper than conventionally used procedures.</AbstractText>Copyright 2003 Elsevier Ireland Ltd.</CopyrightInformation> |
1,374 | Acute ventricular rate control in atrial fibrillation and atrial flutter. | Atrioventricular node blocking agents including beta-adrenergic blockers, non-dihydropyridine calcium channel blockers and digoxin are usually effective in controlling ventricular rate in atrial fibrillation and flutter. Intravenous beta-blockers and non-dihydropyridine calcium channel blockers are equally effective in rapidly controlling the ventricular rate. The addition of digoxin to the regimen causes a favorable outcome but digoxin as a single agent is generally less effective in slowing the ventricular rate in acute setting. Clonidine, magnesium, and amiodarone have also been used for acute ventricular rate control in atrial fibrillation. Limited data suggest that combination regimens provide better ventricular rate control than any agent alone. The agent of first choice is usually individualized depending upon the clinical situation. Beta-blockers are preferable in patients with myocardial ischemia, myocardial infarction and hyperthyroidism and in post-operative state, but should be avoided in patients with bronchial asthma and chronic obstructive pulmonary disease where non-dihydropyridine calcium channel blockers are preferred. Beta-blockers are preferred drugs used for acute ventricular rate control in atrial fibrillation during pregnancy. In atrial fibrillation with Wolff-Parkinson-White syndrome, beta-blockers, calcium channel blockers and digoxin should be avoided, as these drugs are selective atrioventricular node blockers without slowing conduction through the accessory pathway, which can lead to increased transmission of impulses preferentially through the accessory pathway and precipitate ventricular fibrillation. The drug of choice for atrial fibrillation in pre-excitation syndrome is procainamide but propafenone, flecainide and disopyramide have also been used. When clinical condition is unstable or patient is hemodynamically compromised, immediate electrical cardioversion is the treatment of choice, as the best measure to control ventricular rate is by conversion to sinus rhythm. Factors precipitating rapid ventricular rate should be treated as well. |
1,375 | Magnesium prophylaxis for arrhythmias after cardiac surgery: a meta-analysis of randomized controlled trials. | Magnesium supplementation may reduce the incidence of arrhythmias, which often occur after cardiac surgery; however, recent findings of the effectiveness of magnesium prophylaxis have yielded discrepant results.</AbstractText>We searched electronic databases for randomized controlled trials of magnesium for the prevention of arrhythmias after cardiac surgery. The primary outcomes comprised the incidence of supraventricular and ventricular arrhythmias, and the secondary outcomes comprised serum magnesium concentration, length of hospital stay, myocardial infarction, and mortality. Effect sizes were estimated using a random-effects model.</AbstractText>Seventeen trials (n=2069 patients) met the inclusion criteria. Pooled serum magnesium concentration at 24 hours after surgery in the treatment group was significantly higher than that in the control group (weighted mean difference=0.45 mmol/L [1.1 mg/dL]; 95% confidence interval [CI]: 0.30 to 0.59 mmol/L [0.7 to 1.4 mg/dL]; P <0.001). Magnesium supplementation reduced the risk of supraventricular arrhythmias (relative risk [RR]=0.77; 95% CI: 0.63 to 0.93; P=0.002) and ventricular arrhythmias (RR = 0.52; 95% CI: 0.31 to 0.87; P <0.0001), but had no effect on the length of hospital stay (weighted mean difference=-0.28 days; 95% CI: -0.70 to 1.27 days; P=0.48), the incidence of perioperative myocardial infarction (RR=1.03; 95% CI: 0.52 to 2.05; P = 0.99), or mortality (RR=0.97; 95% CI: 0.43 to 2.20; P=0.94).</AbstractText>Administration of prophylactic magnesium reduced the risk of supraventricular arrhythmias after cardiac surgery by 23% (atrial fibrillation by 29%) and of ventricular arrhythmias by 48%. Supplementation had no notable benefit with respect to length of hospitalization, incidence of myocardial infarction, or mortality.</AbstractText> |
1,376 | Influence of paroxysmal atrial fibrillation attack on brain natriuretic peptide secretion. | Plasma brain natriuretic peptide (BNP) concentration is higher during atrial fibrillation (Af) than sinus rhythm, based on studies of electrical defibrillation treatment of patients with chronic Af. However, the change in paroxysmal atrial fibrillation (PAf) is not well known. This study investigated such changes and the relationship between BNP and Af.</AbstractText>BNP levels were successfully measured at three time points: before Af attack, during Af attack, and after (spontaneous or pharmacological) termination of 68 consecutive Af attacks in 35 outpatients with PAf (23 men, 12 women, mean age 70.4 +/- 9.6 years). BNP was measured by immunoradiometric assay.</AbstractText>BNP (median[quartiles]) during PAf was increased by 66[25, 120] pg/ml (2.4-fold) compared to during sinus rhythm (p < 0.0001), and fell to the former level after return to sinus rhythm (before attack = 39[18, 70], during attack = 102[52, 205], after attack = 35[20, 67]). BNP increased in 55 (81%) of 68 attacks, did not change (within +/- 20 pg/ml) in 11 (16%), and decreased in 2 (3%). BNP was already elevated immediately (within 4 hr) after onset of Af, and BNP elevation (delta BNP) showed no significant relationship with the time elapsed after onset. During the Af attack, 41% of PAf patients were asymptomatic although BNP increased significantly.</AbstractText>These results suggest that elevated amounts of BNP during Af are released from secretory granules in the atrium, and BNP elevation of unknown cause may be attributed to the presence of asymptomatic Af. Cardiac function evaluation using BNP during Af requires special consideration, unlike during sinus rhythm, even in patients with PAf or chronic Af, because BNP during Af is the sum of the BNP values from the ventricle (reflecting left ventricular function) and the atrium (due to Af).</AbstractText> |
1,377 | [Rapidly lethal progression of a therapy-resistant status epilepticus]. | We present a case of death after first manifestation of generalised convulsive status epilepticus in a young man. A previously healthy 23-year-old man was admitted to our emergency department by ambulance service with approximately 20 min of generalised convulsive seizures. First line treatment in the emergency ward with benzodiazepines failed. The patient was cardiopulmonary stable until, after more than 30 min of status epilepticus, he developed tachycardia and became bradypnoeic. Intubation and ventilation was performed and anticonvulsive treatment was escalated with thiopental. Fifteen minutes later he developed ventricular fibrillation. CPR was started. The patient became asystolic after 90 min CPR following the ILCOR (International Liaison Committee on Resuscitation) Instructions. CPR was continued for another 30 min without success. The patient died after 120 min of maximal efforts. Autopsy and toxicology were performed, neuropathologic examination showed general brain edema and neuronal cell loss in purkinje cell layers of the cerebellum and olive knots which may be the consequence of generalised convulsive status epilepticus. We conclude: status epilepticus becomes refractory in approximately 30 % of cases. Until now, there are no randomised trials on the optimal treatment of refractory status epilepticus. Better treatment algorithms are urgently needed. |
1,378 | [Polymorphic ventricular tachycardia with a short coupling interval in a patient with normal heart--a case report]. | We describe a case of a 59-year-old female with paroxysmal atrial fibrillation and arterial hypertension who had syncopal attacks due to polymorphic ventricular tachycardia (PMVT) with a short coupling interval of an initiating beat (280 msec). We excluded structural heart disease. In the resting ECG the QTc interval was 420 msec. During Holter monitoring a slight changes of the ST-T segment in V1 were observed (from positive T wave with ST elevation of 1 mm to flat or negative T wave without ST elevation). Additionally, after PMVT a large U-wave (4 mm of amplitude) with the QTU interval of 600 msec and QTUc interval of 662 msec were observed. The U wave disappeared 9 minutes afterwards. The ajmaline test was positive for the Brugada syndrome. The patient received ICD and sotalol, and during 6-month follow-up she remains asymptomatic. |
1,379 | Safety of transvenous temporary cardiac pacing in patients with accidental digoxin overdose and symptomatic bradycardia. | Patients with digoxin intoxication may need transvenous temporary cardiac pacing (TCP) when symptomatic bradyarrhythmias are present. However, it has been reported that TCP might be associated with fatal arrhythmias in patients with acute digitalis intoxication caused by attempted suicide. The aim of this study was to assess the safety of TCP in patients with accidental digoxin-related symptomatic bradyarrhythmias.</AbstractText>Seventy patients (30 men; age 74 +/- 12 years) were enrolled in this retrospective study. Patients were divided into two groups: group 1 with TCP and group 2 without TCP. A digoxin overdose was defined as a serum digoxin level higher than 2.0 ng/ml combined with the presence of digoxin-related symptoms. Detailed clinical characteristics were reviewed on the basis of the medical records.</AbstractText>Group 1 included 24 patients (34.3%, 10 men). The rhythms prior to pacemaker insertion in group 1 included sinus arrest with junctional bradyarrhythmias (n = 9), atrial fibrillation with a slow ventricular rate (n = 11), and high-degree atrioventricular block (n = 4). The mean duration of pacemaker implantation was 5.8 +/- 2.9 days (2-12 days). There was no major arrhythmic event or mortality after TCP in group 1. Two patients in group 2 (4%) died of ventricular tachyarrhythmias. Group 1 had a higher level of blood urea nitrogen (45.1 +/- 26.0 vs. 33.4 +/- 19.3 mg/dl), of left ventricular ejection fraction (68 vs. 56%), and of digoxin (4.4 +/- 2.1 vs. 3.4 +/- 1.3 ng/ml) but a lower serum calcium level (8.7 +/- 0.6 vs. 9.1 +/- 0.8 mg/dl).</AbstractText>TCP was safe for patients with a digoxin overdose complicated by symptomatic bradycardia and should be recommended in such situations. However, this conclusion does not apply to acute digoxin intoxication as a result of attempted suicide.</AbstractText> |
1,380 | Radiofrequency ablation of idiopathic ventricular fibrillation guided by noncontact mapping. | A 32-year-old man with idiopathic ventricular fibrillation and an implantable cardioverter defibrillator presented during a ventricular fibrillation storm. Frequent monomorphic ventricular ectopics with left bundle branch block morphology were documented, some of which initiated fibrillation. He underwent noncontact mapping of the right ventricle, during which the ventricular ectopics were mapped to a site in the free wall displaying a diastolic potential 80 ms before ectopic QRS onset. Following three radiofrequency energy applications, the ectopics were abolished. After 11-month follow-up, he has experienced no further arrhythmias. Noncontact mapping may identify ablatable triggers of ventricular fibrillation and lead to successful outcomes even when only single ectopics are present. |
1,381 | Death due to an implantable cardioverter defibrillator. | Inappropriate therapy due to noise oversensing caused a true ventricular fibrillation (VF) and death of a patient. A 49-year-old patient with a history of dilated cardiomyopathy received a double-chamber implantable cardioverter defibrillator (ICD) in 1991 for a sustained inducible ventricular tachycardia (VT). One appropriate shock delivered in 1994 terminated an episode of VT. The generator was replaced in 1995 and in 2000, and was connected to the initial leads. Three months after the second replacement, the patient received six consecutive shocks related to detection of noise interpreted as VF. Unfortunately, the sixth shock triggered a true VF, which was not treated due to end of the therapeutic sequence, and the patient died. The causes of the dysfunction are discussed. |
1,382 | Canine model of Brugada syndrome using regional epicardial cooling of the right ventricular outflow tract. | Myocardial cooling can induce J point elevation (Osborn wave) as seen on ECG of the Brugada syndrome by activating transient outward current (Ito) and causing a spike-and-dome configuration of the monophasic action potential (MAP) in the ventricular epicardium in isolated canine ventricular wedge preparations. We determined the effect of regional epicardial cooling of the right ventricular outflow tract (RVOT) on surface ECG and ventricular vulnerability in the dog.</AbstractText>In 12 dogs, a cooling device (20-mm diameter) was attached to the RVOT epicardium, and surface ECG, epicardial MAP, and endocardial MAP were recorded. Regional cooling (29.7 degrees C +/- 2.2 degrees C) elevated the J point from 0.05 +/- 0.06 mV to 0.12 +/- 0.11 mV and induced T wave inversion (from 0.02 +/- 0.12 mV to -0.27 +/- 0.20 mV) in lead V1 in association with "spike-and-dome" configuration of the epicardial MAP. Cooling prolonged MAP duration in the RVOT epicardium from 172 +/- 27 ms to 213 +/- 30 ms (P < 0.01) but not in the RV endocardium and increased transmural dispersion of MAP duration from 9 +/- 8 ms to 44 +/- 21 ms (P < 0.01). Cooling also prolonged the QT interval in lead V1 from 191 +/- 19 ms to 212 +/- 23 ms (P < 0.05), but not in lead V5, and increased spatial dispersion of QT interval from 7 +/- 5 ms to 20 +/- 10 ms (P < 0.01). QT interval in lead V1 correlated positively with MAP duration in the RVOT epicardium (r = 0.75). T wave amplitude in lead V1 correlated inversely with transmural dispersion of MAP duration in the RVOT (r =-0.74). Vagal nerve stimulation accentuated the cooling-induced changes. During cooling, ventricular fibrillation was induced by a single extrastimulus in 2 of 4 dogs, and additional vagal nerve stimulation during isoproterenol administration induced spontaneous ventricular fibrillation in one dog.</AbstractText>Localized epicardial cooling of the RVOT could be an in vivo experimental model of Brugada syndrome.</AbstractText> |
1,383 | Impact of biphasic electrical cardioversion of atrial fibrillation on early recurrent atrial fibrillation and shock efficacy. | Early recurrent atrial fibrillation (ERAF) after external cardioversion of atrial fibrillation (AF) occurs in 12% to 26% of patients. Whether biphasic cardioversion has an impact on the incidence of ERAF after cardioversion of AF is unclear.</AbstractText>Consecutive patients (n = 216, mean age 66 years, 71% male, 88% with structural cardiovascular disease or hypertension) underwent cardioversion with a biphasic (Bi) or monophasic (Mo) shock waveform in randomized fashion. Energies used were 120-150-200-200 Ws (Bi) or 200-300-360-360 Ws (Mo). The two study groups (Bi vs Mo) did not differ with regard to age, sex, body mass index, underlying cardiovascular disease, left atrial diameter, left ventricular ejection fraction, duration of AF fibrillation, and antiarrhythmic drug therapy. Mean delivered energy was significantly lower in the Bi group (Bi: 186 +/- 143 Ws vs Mo: 324 +/- 227 Ws; P < 0.001). Overall incidence of ERAF (AF relapse within 1 minute after successful cardioversion) was 8.9% and showed no difference between the two groups (Bi: 8.1% vs Mo: 9.7%, P = NS). Cardioversion was successful in 95.4% of patients. The success rate was comparable in both groups (Bi: 94.3% vs Mo 96.8%; P = NS). First shock efficacy did not differ between Bi and Mo (76.4% vs 67.7%; P = NS). Mean number of shocks were 1.4 shocks per patient in both groups.</AbstractText>Biphasic cardioversion allows comparable success rates with significantly lower energies. However, the incidence of ERAF is not influenced by biphasic cardioversion. With the energies used, biphasic and monophasic shock waveforms are comparable with regard to first shock and cumulative shock efficacy.</AbstractText> |
1,384 | Sotalol reverses remodeled action potential in patients with chronic atrial fibrillation but does not prevent arrhythmia recurrence. | Recurrence of atrial fibrillation (AF) may be related to AF-induced electrical remodeling characterized by shortening of the atrial action potential duration (APD) and loss of its rate adaptation. We investigated the effects of pretreatment with oral d,l-sotalol on rate-dependent changes in atrial monophasic action potential (MAP) duration after cardioversion of chronic AF with reference to the efficacy in preventing the arrhythmia recurrence.</AbstractText>MAPs were recorded from the right atrium at six pacing cycle lengths (CLs) from 300 to 750 ms in 19 chronic AF patients after electrical cardioversion; 9 had been pretreated with oral d,l-sotalol (196 +/- 42 mg/day) for 7 days and 10 were untreated. MAP duration at 90% repolarization (MAPD90) in 11 control patients increased progressively with increases in CLs from 209 +/- 19 ms at CL = 300 ms to 264 +/- 28 ms at CL = 750 ms. In AF patients without sotalol, the CL-MAPD relation was shifted downward and flattened at longer CLs; MAPD90 values were 206 +/- 11 ms and 227 +/- 16 ms at CLs of 300 and 750 ms, respectively. MAPD90 values at CLs > or =500 ms in AF were significantly shorter than controls. In AF patients with sotalol, the normal CL-MAPD relation was preserved; MAPD90 increased from 226 +/- 19 ms to 282 +/- 46 ms in the CL range. AF recurred within 2 weeks after cardioversion in 14 of 24 patients pretreated with d,l-sotalol (216 +/- 51 mg/day) despite of continuation of sotalol treatment.</AbstractText>Sotalol reverses AF-induced decrease in MAPD adaptation to rate in the atria of chronic AF patients, but this effect does not lead to prevention of AF recurrence.</AbstractText> |
1,385 | Relationships between depolarization abnormality and repolarization abnormality in patients with Brugada syndrome: using body surface signal-averaged electrocardiography and body surface maps. | Repolarization and depolarization abnormalities have been reported to be related to Brugada syndrome.</AbstractText>We evaluated the relationships between repolarization abnormality and depolarization abnormality using 48-lead unipolar signal-averaged electrocardiograms and 87-lead unipolar body surface maps in 15 patients with Brugada-type ECGs. Data were compared with those from healthy control subjects (n = 5) and within subgroups of Brugada syndrome with (n = 8) and without (n = 7) ventricular arrhythmias (VA) induced by programmed electrical stimulation (PES). Eighty-seven-lead body surface maps were recorded, and potential maps were constructed to evaluate elevation of the ST segment 20 ms after the J point. Forty-eight-lead signal-averaged ECGs were recorded, and isochronal maps of duration of the delayed potential (dDP) were constructed to evaluate the dDP in each lead. Potential maps showed that patients with Brugada-type ECG, especially those with VA induced by programmed electrical stimulation, had greater elevation of the ST segment in the right ventricular outflow tract, especially at E5. Isochronal maps of dDP in the Brugada-type ECG group showed that maximum dDP was located at E5 and that the area with long dDP was larger than that in the control subjects. The dDPs at E7, E5, F7, and F5 in the VA-inducible group were significantly longer than those in the VA-noninducible group. These results showed that the location of greater elevation in the ST segment coincided with the location of longer dDP.</AbstractText>Repolarization abnormality and depolarization abnormality in the walls of both ventricles, especially in the right ventricular outflow tract, are related to the VA of Brugada syndrome.</AbstractText> |
1,386 | [Cardiac failure in Chilean hospitals: results of the National Registry of Heart Failure, ICARO]. | Heart failure (HF) is a major public health problem. In Chile hospitalized patients due to HF have not been characterized.</AbstractText>To evaluate clinical profile and outcome of patients hospitalized for heart failure in Chilean hospitals.</AbstractText>Prospective registry of 14 centers. Patients hospitalized for HF in functional class III and IV were included. Epidemiological and clinical data, functional class, type of presentation, decompensation cause, electrocardiogram, echocardiogram, treatment and evolution were registered.</AbstractText>Three hundred seventy two patients aged 69 +/- 13 years old, 59% men, were assessed. The main etiologies of HF were ischemic in 31.6%, hypertensive in 35.2%, valvular in 14.9% and idiopathic in 7.4%. There was a history of hypertension 69%, diabetes in 35%, myocardial infarction in 22%, atrial fibrillation (AF) in 28%. The presentation form of HF was chronic decompensated in 86%, acute in 12%, refractory in 2%. The causes of decompensation were non compliance with diet or medical prescriptions in 28%, infections in 22% and AF 17%. ECG showed AF in 36% and left bundle branch block in 16%. Echocardiography was performed in 52% of the patients, 69% had left ventricular ejection fraction <40%. On admission, 39% received angiotensin converting enzyme (ACE) inhibitors, 15% beta-blocker, 25% digoxin, 16% spironolactone and 53% furosemide. The mean hospital stay was 111 +/- 10 days and mortality was 4.5%.</AbstractText>The elderly is the age group most commonly admitted to hospital due to HF. The main etiologies were ischemic and hypertensive. The main causes for decompensations were noncompliance with diet or medical prescriptions and infections. A significant proportion had a relatively well preserved ventricular systolic function.</AbstractText> |
1,387 | Mice with cardiac-restricted angiotensin-converting enzyme (ACE) have atrial enlargement, cardiac arrhythmia, and sudden death. | To investigate the local effects of angiotensin II on the heart, we created a mouse model with 100-fold normal cardiac angiotensin-converting enzyme (ACE), but no ACE expression in kidney or vascular endothelium. This was achieved by placing the endogenous ACE gene under the control of the alpha-myosin heavy chain promoter using targeted homologous recombination. These mice, called ACE 8/8, have cardiac angiotensin II levels that are 4.3-fold those of wild-type mice. Despite near normal blood pressure and a normal renal function, ACE 8/8 mice have a high incidence of sudden death. Both histological analysis and in vivo catheterization of the heart showed normal ventricular size and function. In contrast, both the left and right atria were three times normal size. ECG analysis showed atrial fibrillation and cardiac block. In conclusion, increased local production of angiotensin II in the heart is not sufficient to induce ventricular hypertrophy or fibrosis. Instead, it leads to atrial morphological changes, cardiac arrhythmia, and sudden death. |
1,388 | Automated external defibrillators: safety and efficacy in children and adolescents. | Although children do not suffer from ventricular fibrillation (VF) as frequently as adults, it does occur in 10% to 20% of pediatric cardiac arrests. The technology is available to recognize and treat ventricular fibrillation in children as quickly as we can for adults. This article discusses the evidence to support automated external defibrillator use in young children. As this technology gains increased acceptance, resuscitation rates and outcomes for VF in children should approach those that are seen in adults. |
1,389 | Commotio cordis. | Commotio cordis is ventricular fibrillation that results from blunt chest trauma and is a life threatening condition; early resuscitation and defibrillation are critical. This may occur during sporting events or from child abuse and most patients are boys who are younger than 16 years. Commotio cordis' prognosis depends on the availability of cardiac defibrillation. Automatic defibrillators at convenient locations near sporting events, combined with improved cardiopulmonary resuscitation education, may improve chances of survival after this rare phenomenon. Transient cardiac conduction abnormalities and arrhythmias have been observed in survivors; therefore, cardiac clearance before resumption of sports is indicated. |
1,390 | Ventricular fibrillation: basic concepts. | This brief overview serves as an introduction to the vast array of basic and clinical concepts that are pertinent to the basic understanding of ventricular fibrillation, its genesis, and its clinical management. |
1,391 | Sudden cardiac death in children and adolescents: introduction and overview. | Sudden unexpected cardiac death (SCD) in a child or adolescent is a devastating event with serious impact on the family, the school, and the community. This article reviews the epidemiology of SCD in children and adolescents and includes a discussion of its incidence and etiologies. It also discusses strategies for prevention. |
1,392 | Arrhythmias observed during high-G training: proposed training safety criterion. | Most arrhythmias during centrifuge training are physiological responses to high +Gz stress. However, potentially dangerous arrhythmias occasionally occur during centrifuge training. We reviewed all arrhythmias recorded during the Japan Air Self-Defense Force (JASDF) centrifuge training from April 2001 to March 2003, and developed a criterion for suspending G-training based on observed arrhythmias.</AbstractText>There were 195 male fighter pilots who received high-G centrifuge training monitored with electrocardiographs (ECGs). We evaluated types and occurrences of all arrhythmias during high-G training over a 24-mo period.</AbstractText>Sinus arrhythmia (48.7%), single premature atrial contraction (32.3%), and single (58.5%) or paired (9.7%) premature ventricular contraction were commonly occurring arrhythmias during high-G training. We considered these arrhythmias as variant physiological responses to high-G training (category 1). In addition, we observed ventricular tachycardia (2.6%), paroxysmal supraventricular tachycardia (1.5%), and paroxysmal atrial fibrillation (0.5%). Further investigation of these trainees revealed a significant proportion with cardiac anomalies. As a result, the JASDF currently categorizes these arrhythmias as indicators to suspend G-training and initiate cardiac workup (category 3). Other arrhythmias, such as non-sustained ventricular tachycardia (VT) or Morbitz type I atrioventricular (AV) block, were considered borderline anomalies; whether training was allowed to continue depended on the decision of the physicians monitoring the training (category 2).</AbstractText>Routine ECG monitoring during centrifuge training is recommended to catch the pathology underlying dangerous arrhythmias for flight safety. Our proposed criterion for stopping the centrifuge is intended to differentiate between serious arrhythmias and arrhythmias of physiologic response.</AbstractText> |
1,393 | The association of chronic atrial fibrillation with right atrial dilatation and left ventricular dysfunction in the elderly. | Left atrial dilatation is often considered as one of the important causes for atrial fibrillation. In this study we sought to examine the relationship between right atrial dilatation and left ventricular function in patients with atrial fibrillation, and the association with the documented duration of the dysrrhythmia.</AbstractText><AbstractText Label="MATERIAL/METHODS" NlmCategory="METHODS">56 consecutive patients with atrial fibrillation were investigated by means of clinical history, electrocardiography and echocardiography.</AbstractText>Right atrial dilatation was found in 34, left atrial dilatation in 36 and bi-atrial dilatation in 31 patients. Patients with a dilated right atrium had a larger left atrium, lower left ventricular shortening fraction, and higher transmitral flow velocity than those with a normal right atrium. A history of atrial fibrillation of over 6 months was associated with enlarged atria, reduced left ventricular shortening fraction and increased transmitral flow compared to that of 3 months or less. Functional mitral and tricuspid regurgitation were only found in patients whose atrial fibrillation was over 6 months in duration.</AbstractText>Dilatation of both right and left atria is common in chronic atrial fibrillation, and is associated with impaired left ventricular function. A longer duration of atrial fibrillation predisposes to atrial dilatation, left ventricular dysfunction, and functional atrio-ventricular regurgitation. These findings suggest that atrial fibrillation may have a significant contribution to morphological and functional cardiac changes, and raise the possibilities that early cardioversion or adequate rate control might prevent these changes and may improve prognosis in the elderly.</AbstractText> |
1,394 | Blockers of the Kv1.5 channel for the treatment of atrial arrhythmias. | Atrial arrhythmias are a common problem in cardiological practice. Despite the availability of several antiarrhythmic drugs, there is a medical need for safer and more efficient antiarrhythmic treatment. Compounds that act atrial selectively without prolonging the QTc-time and without negative inotropy to terminate and/or prevent atrial arrhythmias would be of high interest. In this context, the voltage-gated potassium channel Kv1.5 is regarded as a promising target to achieve atrial selectivity, which in turn would be associated with fewer side effects than classical antiarrhythmics. This review summarizes patents and other publications on compounds which show this novel mode of action. The chemistry, selectivity and structure-activity data disclosed in the literature are discussed in light of recent work demonstrating the antiarrhythmic efficacy of Kv1.5 blockers in vivo. Several studies in pig, dog or goat models have confirmed their proposed atrial selective antiarrhythmic effect in vivo. Most of the more intensively characterized Kv1.5 blockers have turned out not to be selective but also block other ion channels. Based on the currently available data it seems that additional inhibition of Kv4.3 and KACh is beneficial for the desired antiarrhythmic effect or at least does not hamper the atrial selectivity of a Kv1.5 blocker. Significant block of IK1, HERG or sodium channels, however, clearly leads to loss of atrial selectivity and increases the risk of lethal ventricular proarrhythmia. |
1,395 | Blockers of the slowly delayed rectifier potassium IKs channel: potential antiarrhythmic agents. | Prolongation of the cardiac action potential and the effective refractory period is a proven principle to prevent cardiac arrhythmias, especially under conditions when the action potential is shortened. Several approaches have been made to achieve this effect selectively and without proarrhythmic side effects. Besides the blockade of the cardiac sodium channel, blockade of the delayed rectifier potassium channel I(K) was attempted to achieve this goal. After the discovery that the delayed rectifier potassium channel I(K) consists of two distinct channels, the rapidly and the slowly delayed rectifier potassium channel I(Kr) and I(Ks) respectively, blockers for these targets were looked for. But most of the described blockers of I(K), like dofetilide and D-sotalol, are highly selective and potent I(Kr) channel blockers or have only a side-activity on the I(Ks) channel, as described for azimilide. These compounds have shown their efficacy in terminating atrial or ventricular fibrillation under certain circumstances, but they also have shown high risk to induce arrhythmias by themselves. It was speculated that I(Ks) channel blockers may be free of this unwanted effect and several companies put effort to find compounds selective for this novel target. The strategies to find potent and selective I(Ks) channel will be reviewed as well as their first results in in-vitro and in-vivo models of arrhythmia. As side effects are a potential danger for this ubiquitous channel, also the safety studies with these compounds will be summarized. |
1,396 | IKr channel blockers: novel antiarrhythmic agents. | There have been extensive efforts to develop I(Kr) channel blockers as a new antiarrhythmic agent for atrial or ventricular fibrillation, since it was demonstrated that selective blockade of the rapidly activating delayed rectifier K+ channel (I(Kr)) in the heart is not deleterious for the total mortality in fatal ventricular arrhythmia patients. Among them, dofetilide and KCB-328 blocks the I(Kr) specifically. Therefore, it increases the action potential duration (APD) selectively. Ibutilide, trecetilide, nifekalant, dronedarone, BRL-32872, H345/52 and ersentilide block the I(Kr). However, they modify also other cardiac channels or receptors. The frequency dependence of the compounds in prolonging the APD varies from the strong reversed tendency of dofetilide to the relatively neutral profile of KCB-328 and BRL-32872. Every compound reported so far has a proarrhythmic potential of torsade de pointes induction under certain conditions, although depending on the structure, the intensity may be somewhat different. In the coming decade, efforts to improve the reverse frequency dependence profile of the I(Kr) blockers by optimizing the onset and recovery time constant of the HERG block (e.g. KCB-328, vesnarinone) or the balance between the block of I(Kr) and Ca++ channels in the heart (e.g. BRL-32872, H 345/52) to eliminate the proarrhythmic potential of the currently known I(Kr) blockers are warranted. Further trials are also needed to discover more favorable compounds with multiple receptors including I(Kr) (e.g. nifekalant, dronedarone) for treating ventricular arrhythmias. |
1,397 | [The practice guideline 'Atrial fibrillation' from the Dutch College of General Practitioners; a response from the perspective of general practice]. | The practice guideline 'Atrial fibrillation' (AF) from the Dutch College of General Practitioners is a clearly written survey on the diagnosis and treatment of AF in general practice. Rapid cardioversion is no longer an indication for acute referral in AF. As AF, heart failure and COPD often occur simultaneously among elderly people, the exact cause of the symptoms can be unclear. In these complicated cases, with the risk of polypharmacy, a single consultation between general practitioner and cardiologist would be more effective. For control of the rate of ventricular contraction during the treatment of AF, lipophilic beta-blockers are preferable to hydrophilic beta-blockers because the pharmacokinetics in elderly people are substantially different. When there is a high risk of thrombo-embolic complications with AF, treatment with coumarin derivatives is advised. However, little research has been done on this subject among elderly people in a general practice setting. In this age group, the risk of complications due to treatment with coumarin derivatives is sometimes higher than the advantages it offers. This is why the GP should always consider carefully whether or not elderly people with AF should be treated with coumarin derivatives. |
1,398 | Echocardiographic evidence of left atrial abnormality in young patients with lone paroxysmal atrial fibrillation. | Usual assessment of left atrial size by 2-dimensional echocardiography in the anteroposterior dimension often underestimates the true atrial size. We compared 15 young patients (< or =50 years old) with lone paroxysmal atrial fibrillation to age-matched controls, and measured atrial size in the inferosuperior and mediolateral dimensions. These additional measurements and atrial volumes were significantly increased compared with control patients, revealing that patients with apparent "lone" paroxysmal atrial fibrillation may have subtle structural abnormalities of the left atrium. |
1,399 | Cardiac Pacing for Bradycardia Support: Evidence-based Approach to Pacemaker Selection and Programming. | The vast majority of pacemakers implanted in the United States for the treatment of symptomatic bradycardia are dual-chamber systems with a complex array of functions, such as rate responsiveness, dynamic atrioventricular delay, and automatic mode switching. Basic hemodynamic studies have convincingly demonstrated the superiority of maintaining atrioventricular synchrony. However, clinical trials have failed to demonstrate the impressive results expected based on physiologic data. The most recent randomized clinical trials have demonstrated that dual-chamber devices, when compared with single-chamber ventricular pacing, do not prevent mortality or stroke, and lead to an unexpectedly small reduction in heart failure hospitalizations. Although improvements in quality of life have not been consistently found when comparing ventricular-based versus atrial-based pacing, a reduction in the incidence of newly diagnosed atrial fibrillation in dual chamber-paced patients has been reported by most trials. Dual-chamber pacing has been reported to reduce pacemaker syndrome in US trials. The addition of rate modulation, in spite of attempting to replicate the normal response to exercise, has not shown a consistently positive impact on quality of life or treadmill time. The use of pacemakers for the treatment of vasovagal syncope is controversial. Adding dual-chamber sensing ability to current implanted defibrillators considerably reduces the number of inappropriate shocks but may increase mortality if not programmed to minimize ventricular stimulation. |
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