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4,400 | Lidocaine for prevention of reperfusion ventricular fibrillation after release of aortic cross-clamping. | To determine the efficacy of a bolus of lidocaine administered by way of the pump before releasing the aortic cross-clamp (ACC) in preventing the occurrence of reperfusion ventricular fibrillation.</AbstractText>Prospective, randomized study.</AbstractText>University hospital.</AbstractText>Patients undergoing coronary artery bypass graft surgery (n = 34).</AbstractText>Seventeen patients received 100 mg of lidocaine by way of the pump 2 minutes before releasing the ACC, and a control group of 17 patients received 5 mL of normal saline.</AbstractText>In the control group, the incidence of reperfusion ventricular fibrillation was 70%, which was significantly decreased to 11% in the lidocaine group. A higher cardiac output after weaning from cardiopulmonary bypass was observed in the lidocaine group; this may be attributed to the lower incidence of reperfusion ventricular fibrillation and consequently the lower need for defibrillation by electric countershocks.</AbstractText>The results suggest that a bolus of 100 mg of lidocaine administered 2 minutes before release of the ACC can safely decrease the incidence of reperfusion ventricular fibrillation and is associated with better hemodynamics after weaning from cardiopulmonary bypass.</AbstractText> |
4,401 | Ventricular arrhythmias with or without programmed electrical stimulation after incremental overdosage with lidocaine, bupivacaine, levobupivacaine, and ropivacaine. | It is unclear whether the mechanism of death from local anesthetic (LA) intoxication is primarily a consequence of cardiac arrhythmias or myocardial contractile depression, and whether LAs might differ in this susceptibility to these two mechanisms. By using programmable electrical stimulation (PES) protocols in anesthetized, ventilated dogs, we compared the arrhythmogenic potential of bupivacaine (BUP), ropivacaine (ROP), levobupivacaine (LBUP), and lidocaine (LIDO). Open-chest dogs were randomized to receive escalating incremental infusions of the four local anesthetics until cardiovascular collapse. We assumed a concentration relationship of 4:1 for LIDO/BUP, LBUP, and ROP. The effective refractory period did not change significantly until the dose increment corresponding to target concentrations of 8 and 32 microg/mL for BUP, LBUP, ROP, and LIDO, respectively. Thirty percent to 50% increases in effective refractory period occurred in surviving dogs at this dose. The incidence of spontaneous or PES-induced ventricular tachycardia and ventricular fibrillation did not differ among groups. Compared with LIDO, the incidence of PES-induced extrasystoles was more frequent for BUP- and LBUP-treated dogs (P: < 0.05). ROP-treated dogs did not differ from LIDO-treated dogs with respect to PES-induced extrasystoles. At the dose increment preceding cardiovascular collapse, all LAs produced significant increases in heart rate and reductions in blood pressure compared with their respective baseline values. The incidence of programmable electrical stimulation-induced ventricular tachycardia and fibrillation with BUP does not differ from the incidence that occurs with the single S:(-) enantiomers LBUP and ROP, providing further evidence against stereoselective arrhythmogenesis as a primary component of local anesthetic-induced cardiotoxicity.</AbstractText>Progressive bupivacaine intoxication in anesthetized, ventilated dogs does not produce early arrhythmogenic events. The incidence of programmable electrical stimulation-induced ventricular tachycardia and fibrillation with bupivacaine does not differ from the incidence that occurs with the single S:(-) enantiomers levobupivacaine and ropivacaine, providing further evidence against stereoselective arrhythmogenesis as a primary component of local anesthetic-induced cardiotoxicity.</AbstractText> |
4,402 | Commotio cordis: an underappreciated cause of sudden death in athletes. | Over the last few years, the recognised cardiovascular risks of sporting activities have been extended to include cardiac arrest resulting from low-energy precordial chest impact produced by projectiles (e.g. baseball) or bodily contact, in the young, healthy and active athlete [also known as commotio cordis (CC)]. However, case reports of CC in European medical literature can be traced back for at least 130 years. CC accounts for a small, but important, subset of sudden death during sporting activities. It is a devastating electrophysiological event in the young athlete, and one which has generated considerable concern, both in the medical profession as well as in the public. The mechanism of sudden death appears to be caused by ventricular fibrillation, which occurs when the chest impact is delivered within a narrow, electrically vulnerable portion of the cardiac cycle, that is, during repolarisation, just before the peak of the T wave. Resuscitation of these victims is possible with prompt cardiopulmonary resuscitation and defibrillation. Preventive measures, such as the use of age-appropriate safety baseballs and suitably designed chest wall protection, may reduce the risk of sudden death and, thus, make the athletic field a safer place for young athletes. |
4,403 | [High resolution electrocardiography of P-wave signals in clinical cardiology]. | Signal-averaged electrocardiography of the QRS complex detects presence of late potentials which represent significant arrhythmogenic marker responsible for increased risk of life-threatening ventricular arrhythmias especially in post myocardial infarction patients. The P wave signal-averaged electrocardiography has been designed to predict development of atrial fibrillation in different populations of patients. Many P wave signal-averaging methodological procedures have been developed. However their common disadvantages remain lack of standardization, relatively low specificity and sensitivity, low positive predictive value as well as limited number of larger prospective clinical trials. Recent software and technological improvements of the P wave high resolution techniques as well as some new reports about the influence of antiarrhythmic drugs on the parameters of the P wave signal-averaged electrocardiography are creating new possibilities not only for the diagnosis of paroxysmal atrial fibrillation but also for the prediction of antiarrhythmic drug efficiency. |
4,404 | [Ventricular fibrillation in chronic heart disease]. | The objective of the work was to describe in subjects with spontaneous ventricular fibrillation, after elimination of acute cardiac disease, the strategy of antiarrhythmic treatment and to evaluate, based on prospective follow-up, the effectiveness of this treatment. The authors included in the group 36 patients (30 men and 6 women) within the range from 34 to 78 years (mean age 58 +/- 11 years) with spontaneous ventricular fibrillation. They divided the group into a subgroup (15 subjects) without revascularization of the heart muscle, into a subgroup (17 subjects) with revascularization of the myocardium (coronary angioplasty and bypasses) and a subgroup (4 subjects) where ischaemic heart disease was ruled out (mostly cardiomyopathies). In all subgroups they used programmed ventricular stimulation (apparatuses of Quinton Co. USA, Biotronik Co. GFR), in the subgroup with revascularization within 3 months. During the diagnostic procedure of ventricular stimulation they tested antiarrhythmic drugs most frequently amiodarone per os (for 4 weeks). An implantable cardioverter--defibrillator was implanted in 17 patients (8 subjects without revascularization, 6 subjects with revascularization, 3 subjects without ischaemic heart disease). All patients were followed up till death, maximum 24 months. The authors evaluated the rate of cardiac deaths (death on cardiac grounds, incl. sudden arrhythmic death) and sudden arrhythmic deaths (within one hour after the onset of symptoms or the first malignant ventricular tachyarrhythmia recorded after implantation of the defibrillator). In the subgroup without revascularization with electric instability of the ventricles according to programmed stimulation 66.7% they described seven cardiac deaths (46.7%) and 6 sudden "arrhythmic" deaths (40%) incl. 5 subjects with ineffective testing of antiarrhythmic drugs. Conversely in the subgroup with revascularization and with diagnostic programmed stimulation in 47.1% they found 3 cardiac deaths (17.7%), one sudden "arrhythmic" death (5.9%)--a subject with ineffective testing. In the subgroup without ischaemic heart disease they recorded cardiac and sudden "arrhythmic" deaths in half the subjects, in all instances in subjects without inducible ventricular tachyarrhythmia. The authors found in the course of a two-year investigation a relapse of cardiac arrest in 25% of subjects after spontaneous ventricular fibrillation. A third of these subjects (all without a cardioverter-defibrillator) died. They confirm the benefit of implantation of a defibrillator for all subjects regardless of the basic diagnosis and revascularization of the heart muscle. |
4,405 | Short-term forecasting of life-threatening cardiac arrhythmias based on symbolic dynamics and finite-time growth rates. | Ventricular tachycardia or fibrillation (VT-VF) as fatal cardiac arrhythmias are the main factors triggering sudden cardiac death. The objective of this study is to find early signs of sustained VT-VF in patients with an implanted cardioverter-defibrillator (ICD). These devices are able to safeguard patients by returning their hearts to a normal rhythm via strong defibrillatory shocks; additionally, they store the 1000 beat-to-beat intervals immediately before the onset of a life-threatening arrhythmia. We study these 1000 beat-to-beat intervals of 17 chronic heart failure ICD patients before the onset of a life-threatening arrhythmia and at a control time, i.e., without a VT-VF event. To characterize these rather short data sets, we calculate heart rate variability parameters from the time and frequency domain, from symbolic dynamics as well as the finite-time growth rates. We find that neither the time nor the frequency domain parameters show significant differences between the VT-VF and the control time series. However, two parameters from symbolic dynamics as well as the finite-time growth rates discriminate significantly both groups. These findings could be of importance in algorithms for next generation ICD's to improve the diagnostics and therapy of VT-VF. |
4,406 | Isoflurane pretreatment ameliorates postischemic neurologic dysfunction and preserves hippocampal Ca2+/calmodulin-dependent protein kinase in a canine cardiac arrest model. | Inhalational anesthetics are neuroprotective in rat models of global ischemia. To determine whether isoflurane at a clinically relevant concentration is neuroprotective in a canine model of cardiac arrest, we measured neurologic function and hippocampal Ca2+/calmodulin-dependent protein kinase II (CaMKII) content 20 h after cardiac arrest.</AbstractText>We tested the neuroprotective effect of 30 min of 1.5% isoflurane exposure before 8 min of global ischemia induced with ventricular fibrillation. Animals were randomized to four groups: control, isoflurane-control, ischemia, and isoflurane-ischemia. After resuscitation and 20 h of intensive care, each animal's neurologic deficit score was determined by two blinded evaluators. The hippocampal content of CaMKII, determined by immunoblotting, was measured by an individual blinded to the treatment groups. CaMKII activity was measured in samples from the cortex, hippocampus, and striatum of animals in each group.</AbstractText>Isoflurane-ischemic animals had a median neurologic deficit score of 22.6% compared with 43.8% for the ischemic animals (P < 0.05). Hippocampal levels of the beta-subunit of CaMKII (CaMKIIbeta) were relatively preserved in isoflurane-ischemic animals (68 +/- 4% of control) compared with ischemic animals (48 +/- 2% of control; P < 0.001), although both groups were statistically significantly lower than control (P < 0. 001 ischemia vs. control and P < 0.05 isoflurane-ischemia vs. control).</AbstractText>Isoflurane is an effective neuroprotective drug in a canine cardiac arrest model in terms of both functional and biochemical criteria.</AbstractText> |
4,407 | Effects of sodium channel blockade on ibutilide induced prolongation of repolarization in the isolated rabbit ventricle. | Ibutilide fumarate is indicated for the termination of atrial fibrillation and atrial flutter. It's mechanism of action is unclear but may involve activation of a late inward Na(+) current.</AbstractText>Twenty seven experiments were performed using an isolated perfused rabbit right ventricle preparation. In each experiment effective refractory periods (ERP) and transmembrane 90% action potential durations (APD) were measured. In 8 experiments ERP and APD were measured at baseline, in the presence of ibutilide (0. 1[emsp4 ]uM), and in the presence of both ibutilide and tetrodotoxin (TTX, 2[emsp4 ]uM). In 8 experiments lidocaine (10[emsp4 ]uM) was used in place of TTX. Measures were made at 200, 400, and 800[emsp4 ]msec paced cycle lengths under each condition. The baseline values for APD at 200, 400 and 800[emsp4 ]msec cycle lengths for the experiments treated with ibutilide and TTX were 111+/-8, 140+/-14 and 159+/-22[emsp4 ]msec, respectively. In the presence of ibutilide, APD increased to 130+/-19, 192+/-26 and 217+/-35[emsp4 ]msec at 200, 400 and 800[emsp4 ]msec cycle lengths, respectively (all p< or =0.03). After the addition of TTX there was no shortening of APD or ERP compared to treatment with ibutilide alone at any cycle length (all p> or =0.062). Similarly, in the presence of ibutilide and lidocaine there were no changes in APD or ERP compared to treatment with ibutilide alone (all p > or =0.41). In 11 control experiments, there were no changes in APD or ERP on serial measures after placebo and TTX or lidocaine.</AbstractText>Ibutilide induced prolongation of ventricular repolarization is not affected by Na(+) channel blockade with lidocaine or TTX in the isolated rabbit heart. These findings suggest that the effects of ibutilide are not mediated by a Na(+) channel dependent late current or that this mechanism contributes minimally to its action in this model.</AbstractText> |
4,408 | Automated external defibrillators in long-term care facilities are cost-effective. | To assess the cost per life saved of equipping long-term care facilities (LTCFs) with automated external defibrillators (AEDs).</AbstractText>Outcomes for cardiac arrests within LTCFs were retrieved for 1994 to 1997 from a comprehensive out-of-hospital cardiac arrest registry in a mid-sized U.S. city. The total expense for all LTCFs to obtain and maintain AEDs and to educate and maintain staff skill was estimated for a theoretical four-year period. The cost per life saved to the time of hospital discharge was calculated based on an estimated survival rate of 25% of patients found in ventricular fibrillation (VF) with placement of AEDs in LTCFs. A sensitivity analysis that varied survival rates and costs was conducted.</AbstractText>Over four years, there were 160 actual arrests in 43 LTCFs, with a hospital discharge survival rate of 2/160. Twenty of 160 presented to emergency medical services in VF. Training costs for four years were $1,225 per AED. Purchase and maintenance expenses for one AED over four years were $3,941. Placing AEDs in LTCFs would cost $87,837 per life saved if 25% of patients found in VF survived to hospital discharge. Sensitivity analysis using survival rates of 5%, 15%, and 35% established the cost per life saved at $439,184, $146,395, and $62,741, respectively. When costs were calculated at one-half and twice the estimated expense, the cost per life saved was $43,918 and $175,674, respectively.</AbstractText>Placing AEDs in LTCFs is cost-effective at $87,837 per life saved, if a hospital discharge survival rate of 25% of patients in VF can be achieved.</AbstractText> |
4,409 | A comparison of biphasic and monophasic shocks for external defibrillation. Physio-Control Biphasic Investigators. | The ability of a shock to defibrillate the heart depends on its waveform and energy. Past studies of biphasic truncated exponential (BTE) shocks for external defibrillation focused on low energy levels. This prospective, randomized, double-blind clinical trial compared the first-shock efficacies of 200-joule (J) BTE, 130-J BTE, and 200-J monophasic damped sine wave shocks.</AbstractText>Ventricular fibrillation (VF) was induced in 115 patients during evaluation of implantable cardioverter-defibrillator function and 39 patients during electrophysiologic evaluation of ventricular arrhythmias. After 19 +/- 10 seconds of VF, a randomized transthoracic shock was administered. Mean first-shock success rates of the three groups were compared using a "Tukey-like" statistical test, adjusting for multiple comparisons. Blood pressures and arterial oxygen saturations were measured before VF induction and 30, 90, and 150 seconds after successful defibrillation.</AbstractText>First-shock success rates were 61/68 (90%) for 200-J monophasic, 39/39 (100%) for 200-J biphasic, and 39/47 (83%) for 130-J biphasic shocks. The 200-J biphasic shocks were simultaneously superior in first-shock efficacy to both 200-J monophasic and 130-J biphasic shocks (experimentwise error rate, alpha < 0.01). There was no significant difference between the efficacies of 200-J monophasic and 130-J biphasic shocks, nor was there any significant difference between the three groups in hemodynamic parameters after successful shocks.</AbstractText>Biphasic shocks of 200 J provide better first-shock defibrillation efficacy for short-duration VF than 200-J monophasic and 130-J biphasic shocks and thus may allow earlier termination of VF in cardiac arrest patients.</AbstractText> |
4,410 | Effects of dietary n-3 fatty acids on contractility, Na+ and K+ currents in a rat cardiomyocyte model of arrhythmia. | The n-3 polyunsaturated fatty acids (PUFAs) have been reported to prevent ventricular fibrillation in human clinical studies and in studies involving experimental animals and isolated cardiomyocytes. This study aimed to determine whether dietary n-3 PUFAs could prevent isoproterenol and free radical-induced arrhythmic (asynchronous) contractile activity in adult rat cardiomyocytes and whether whole-cell Na(+) and K(+) currents measured by patch-clamp techniques were affected. Dietary supplementation with fish oil for 3 weeks significantly increased the proportion of total n-3 PUFAs in ventricular membrane phospholipids compared with saturated fat supplementation (18.8 +/- 0.6% vs. 8.1 +/- 1.0%, respectively). Cardiomyocytes from the fish oil group were less susceptible to isoproterenol-induced asynchronous contractile activity than were those from the saturated fat group [EC(50) values: 892 +/- 130 nM, n = 6 and 347 +/- 91 nM, n = 6 (P < 0.05), respectively]. Fish oil supplementation also prolonged the time taken to develop asynchronous contractile activity induced by superoxide and hydrogen peroxide. The voltage dependence of inactivation of Na(+) currents were significantly altered (-73.5 +/- 1.2 mV, n = 5 vs. -76.7 +/- 0.7 mV, n = 5, P < 0.05, for saturated fat and fish oil treated groups, respectively). The voltage dependence of activation of Na(+) and K(+) currents was not significantly affected by the dietary fish oil treatment. These results demonstrate the antiarrhythmic effects of dietary fish oil in a cardiomyocyte model of arrhythmia. |
4,411 | Gender differences in state-wide EMS transports. | There are gender differences in emergency medical services (EMS) transports and management based on diagnosis. Data were extracted from the EMS State Ambulance Transport database. This database exists because of a legal requirement that all EMS transports generated by 911 calls and all interhospital transports be reported to the State EMS Bureau. All ambulance transports reported to the State EMS Division during 1995 were evaluated. Cases were excluded if they were aborted, admission or discharge transports, outpatient transports, or cases listed as "other" without a diagnosis. Gender-related treatment differences were determined for problems for which EMTs have specific treatment options. These were cardiac arrest, chest pain, allergic reactions, and extremity fractures. Results were compared using a two-tailed Chi squared or Fischer's Exact with significance at P < .05. Odds Ratios (OR) and 95% confidence intervals (CIs) were calculated. There were a total of 164,595 ambulance transports reported to the State EMS Division. Of these 76,074 (46%) were men and 88,521 (54%) were women. Of these, 50,211 were excluded. This left 52,607 injury transport and 61,777 illnesses transport. Men were significantly more likely than women to have injuries related to all-terrain vehicle accidents, motorcycle accidents, RV accidents, burns, gunshot wounds, and stab wounds. Men were significantly more likely than women to have illnesses related to cardiac arrest, dead on arrivals (DOAs), drowning, and smoke inhalation. For cardiac arrest transports, significantly more male patients presented ventricular fibrillation, more males received defibrillation, lidocaine, and bicarbonate, but more women received atropine. Male chest pain patients were more likely to receive oxygen and morphine and less likely to receive nitroglycerin. Male allergic reaction patients were more likely to receive an i.v. and subcutaneous epinephrine. Male extremity fracture patients were more likely to get an i.v. line, but there was no difference in morphine use or splinting. There are numerous disease-specific gender differences in the demographics of illness and injury transported by EMS. The use of various medications and procedures may also be related to gender. Understanding these differences may help in preparing EMS professionals for patient management. |
4,412 | [Ventricular fibrillation: the current methods for analysing the degree of irregularity of the process]. | Ventricular fibrillation has traditionally been described as "chaotic" and in recent years there has been discussions that fibrillation may be an instance of deterministic chaos in the context of nonlinear dynamical systems theory. The current paper summarizes modern methods of mathematical analysis of the degree of electrical irregularities of the heart during VF. The traditional methods of Fourier analysis of electrocardiographic data as well as concepts of chaos theory--fractal dimension, entropy, reconstruction of attractors and some new methods such as spatial coherence have been considered. The results are discussed in context of mathematical models and hypothesis of mechanisms of VF. |
4,413 | Risk factors for arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot: a multicentre study. | Ventricular arrhythmia and sudden cardiac death late after repair of tetralogy of Fallot are devastating complications in adult survivors of early surgery, but their prediction remains difficult.</AbstractText>We examined surgical, electrocardiographic, and late haemodynamic data, and their relation to clinical arrhythmia and sudden death occurring over 10 years, in a multicentre cohort of patients with repaired tetralogy, who were alive in 1985.</AbstractText>Of 793 patients (mean age at repair 8.2 years [SD 8], mean time from repair 21.1 years [8.7]) who entered the study, 33 patients developed sustained monomorphic ventricular tachycardia, 16 died suddenly, and 29 had new-onset sustained atrial flutter or fibrillation. Electrocardiographic markers (QRS duration, QRS rate of change between 1985 and 1995) were significantly greater in the ventricular tachycardia and sudden-death groups. Older age at repair was associated with a higher risk of sudden death and atrial tachyarrhythmia. Pulmonary regurgitation was the main underlying haemodynamic lesion for patients with ventricular tachycardia and sudden death, whereas tricuspid regurgitation was for those with atrial flutter/fibrillation. Despite adverse haemodynamics, no patient who died suddenly had undergone late reoperation.</AbstractText>Arrhythmia and sudden death are important late sequelae for patients after repair of tetralogy of Fallot. The electrophysiological and haemodynamic substrate of sudden death resembled that of sustained ventricular tachycardia, with pulmonary regurgitation being the predominant haemodynamic lesion. Preservation or restoration of pulmonary valve function may thus reduce the risk of sudden death. Furthermore, electrocardiographic markers can help to identify patients at risk.</AbstractText> |
4,414 | Two years' clinical experience with a quadrileaflet stentless bioprosthesis in the mitral position. | Currently available bioprosthetic mitral valves do not provide sufficient durability. A new stentless pericardial prosthesis was designed for better hemodynamic performance and reduction of stress load compared with current stented bioprostheses.</AbstractText>Between September 1997 and August 1999, the Quadrileaflet mitral valve (QMV) was implanted in 17 patients at our institution. Four patients had minimally invasive mitral valve replacement. Mean patient age was 62.2 +/- 16.3 years; preoperative NYHA class was 3.06 +/- 0.2; ejection fraction was 64.1 +/- 14.7%. Echocardiography was performed pre-, intra- and postoperatively, and at 3-6, 12 and 24 months follow up.</AbstractText>Fifteen patients had an uneventful intra- and postoperative course. Two patients died, one from acute left heart failure at 6 h after surgery, and one on the first postoperative day after resuscitation for ventricular fibrillation. A small-sized prosthesis was implanted in four patients, medium-sized in eight and large-sized in five. The mean duration of cardiopulmonary bypass was 138.3 +/- 37.0 min; mean cross-clamp time was 91.3 +/- 26.3 min. Postoperative control echocardiography showed a mean valve orifice area of 2.5 +/- 0.4 cm2, transvalvular velocity (Vmax) was 1.6 +/- 0.4 m/s, and mean pressure gradient 3.6 +/- 2.0 mmHg. Echocardiographic evaluation after 3, 6 and 12 months showed no significant difference compared with the intraoperative data. Three patients had a minor mitral regurgitation (grade I-II). At 12 months all patients were in NYHA class I or II.</AbstractText>The implantation technique of the QMV is more demanding, but the prosthesis is a promising alternative to conventional biological mitral valve replacement. Further follow up is needed to confirm these favorable mid-term results.</AbstractText> |
4,415 | Time dependent variability of QT dispersion after acute myocardial infarction and its relation to ventricular fibrillation: a prospective study. | To show whether increased QT dispersion on admission predicts ventricular fibrillation after acute myocardial infarction, and to determine the nature of time related changes in QT dispersion.</AbstractText>Prospective cohort study.</AbstractText>Coronary care units of three teaching hospitals in Newcastle-upon-Tyne over an eight month period.</AbstractText>All had acute myocardial infarction according to World Health Organization criteria.</AbstractText>For all patients, QT dispersion (QTd) and Bazett rate corrected QTc dispersion (QTcd) were measured from a high quality 12 lead ECG recorded on admission at a paper speed of 50 mm/s. In a subset, serial ECGs were recorded regularly to show time related changes in QTcd following acute myocardial infarction.</AbstractText>Occurrence of ventricular fibrillation within the first 24 hours after myocardial infarction.</AbstractText>Data collected from 201 patients, 12 of whom (6%) developed ventricular fibrillation within 24 hours. Neither QTd nor QTcd differed between those developing ventricular fibrillation and those who did not: QTd mean (SD), 74 (24) ms (95% confidence interval (CI) 59 to 89) v 66 (24) ms (95% CI 62 to 70), respectively; QTcd, 86 (26) ms(0.5) (95% CI 70 to 102) v 77 (29) ms(0.5) (95% CI 72 to 82), respectively. Significant QTcd changes occurred early after myocardial infarction.</AbstractText>Admission QTd and QTcd do not predict ventricular fibrillation after acute myocardial infarction. There are significant changes in QTcd with time, which may account for this measured lack of correlation.</AbstractText> |
4,416 | [Recurrent syncope in a 34-year-old woman triathlete]. | Some weeks previously a 34-year old athlete, specializing in the triathlon, had 6 syncopes in one day. They had caused abrasions and contusions resulting from the falls. At another hospital paroxysmal atrial fibrillation had been diagnosed and treatment with disopyramide (2 x 200 mg) initiated, but she had about 15 further syncopes within 2 weeks. She was admitted for establishing their cause.</AbstractText>Initial ECGs and neurological examination failed to provide a diagnosis and she was discharged with an "event recorder".</AbstractText><AbstractText Label="DIAGNOSIS, TREATMENT AND COURSE" NlmCategory="METHODS">Three weeks after discharge she had another syncope. The event recorder was activated by the patient's partner and revealed polymorphous ventricular tachycardia. She underwent extensive invasive cardiological tests, including a right ventricular biopsy, but no abnormality was demonstrated. However, a provocation test with ajmaline produced ST segment elevations in V1 and V2 typical of the syndrome previously described by the Brugadas (right bundle branch block, precordial ST elevations in V1-V3 and sudden cardiac death). A cardioverter-defibrillator was implanted. During the subsequent observation period of 2 month the ICD delivered one countershock, triggered by the onset of polymorphous ventricular tachycardia with syncope.</AbstractText>In patients with serious ventricular arrhythmias but no diagnostic findings, including a normal resting ECG, a drug provocation test should be performed to exclude a Brugada syndrome.</AbstractText> |
4,417 | Effects of cardiac glycosides on atrial contractile dysfunction after short-term atrial fibrillation. | Despite a long history of use in the treatment of paroxysmal atrial fibrillation (AF), the efficacy of cardiac glycosides has not been established. If such drugs are beneficial in this condition, the general view is that the benefit must be related to their inotropic actions.</AbstractText>To assess the effects of the rapid-acting cardiac glycoside, acetylstrophanthidin (AS), on AF and AF-induced right atrial (RA) "stunning," RA wall motion (with ultrasonic crystals), RA pressure, and peak first derivative of pressure (dp/dt) (with microtip transducers) were measured before and after 5 min of high-intensity rapid atrial stimulation (10 Hz; 10 mA; 1 ms) and after the cessation of poststimulation AF. Measurements were made in neurally intact and autonomically blockaded dogs both before and after the administration of AS (0.01 mg/kg IV bolus and 0.015 mg/kg/h IV infusion). AS prevented the post-AF reduction in RA peak dp/dt under neurally intact and autonomically blockaded conditions, and it prevented the post-AF increase in the RA end-systolic dimension and the decrease in the percentage of RA systolic shortening with autonomic blockade. AS was beneficial whether or not baseline inotropy was enhanced by AS. The duration of AF following atrial stimulation was the same before and after AS, but when compared to controls, AS treatment appeared to prolong AF.</AbstractText>Cardiac glycosides exert a favorable effect on AF-induced RA stunning, but this action is unrelated to its effects on the duration of AF.</AbstractText> |
4,418 | Admission serum potassium in patients with acute myocardial infarction: its correlates and value as a determinant of in-hospital outcome. | Although controversial, hypokalemia (LK) in patients with acute myocardial infarction (MI) is thought to predict increased in-hospital morbidity, particularly cardiac arrhythmias, and mortality. Also, the mechanism of low serum potassium in the setting of MI has not been delineated. We evaluated the frequency, attributes, and outcome, and speculated on the mechanism of LK in patients with MI.</AbstractText>This was a prospective cross-sectional study of 517 consecutive patients with MI admitted to the coronary care unit (CCU). Serum potassium was measured in the emergency department and repeatedly thereafter throughout hospitalization, and was used in the analysis, along with a large array of clinical and laboratory variables.</AbstractText>The patients were allocated to a LK and a normokalemic (NK) cohort, based on the emergency department serum potassium measurement. The 41 patients with LK (3.16+/-0.24 mEq/L; 7.9% of total) were comparable on admission in their baseline assessment to the 476 patients with normal serum potassium (4.28+/-0.56 mEq/L), except for lower emergency department magnesium (1.48+/-0.15 mg/dL vs. 1.96+/-0.26 mg/dL; p = 0.0005) and earlier presentation after onset of symptoms (3.0+/-4.1 h vs. 4.4+/- 6.2 h; p = 0.05). There was a poor correlation between serum potassium and magnesium on admission (r = 0.14). Peak creatine kinase (CK) and myocardial isomer of CK were higher in the LK patients (3,870+/-3, 840 IU/L vs. 2,359+/-2,653 IU/L [p = 0.018] and 358+/-312 IU/L vs. 228 +/- 258 IU/L [p = 0.013], respectively). Management of the two cohorts was the same, except for a higher rate of use of magnesium (14.6% vs. 4.6%; p = 0.007), serum potassium supplements (90.2% vs 43. 1%; p = 0.000005), and antiarrhythmic drugs (78.0% vs 50.4%; p = 0. 0007) in the LK patients. No difference was detected between the LK and NK patients in total mortality (24.4% vs. 18.3%; p = 0.34), cardiac mortality (17.1% vs. 15.3%; p = 0.52), atrial fibrillation (14.6% vs 13.9%; p = 0.89), and ventricular tachycardia (22.0% vs. 16.0%; p = 0.32), but ventricular fibrillation (VF) occurred more often (24.4% vs 13.0%; p = 0.04) in the LK patients. However, proportions of VF occurring in the emergency department, CCU, or wards in the two cohorts were not different, but they were higher during the time interval prior to emergency department admission in LK patients (17.1% vs 2.1%; p = 0.00001).</AbstractText>LK is seen in approximately 8% of patients with MI in the emergency department; LK is associated with low emergency department magnesium, and low serum potassium levels in the CCU and throughout hospitalization. LK has no relationship to preadmission use of diuretics, it is associated with early presentation to the emergency department, and it is not a predictor of increased morbidity or mortality.</AbstractText> |
4,419 | beta(2)-Adrenoceptors and ventricular fibrillation. | beta-Adrenoceptor antagonists significantly reduce the incidence of sudden cardiac death in patients with contractile dysfunction. Contractile dysfunction is associated with a decline in beta(1)-adrenoceptors, no change in the number of beta(2)-adrenoceptors, and an increased responsiveness to beta(2)-adrenoceptor stimulation. Selective beta(2)-adrenoceptor blockade prevents ventricular fibrillation in a canine model of sudden cardiac death. Cardiac beta(2)-adrenoceptor stimulation increases L-type Ca(2+) currents, but unlike beta(1)-adrenoceptor stimulation, it fails to elicit phospholamban phosphorylation. Restoration of resting diastolic [Ca(2+)] following beta(2)-adrenoceptor-mediated increases in Ca(2+) influx is more dependent on Na(+)/Ca(2+) exchange, which generates an arrhythmogenic transient inward current that can trigger ventricular fibrillation. |
4,420 | Effects of ICI 118.551, a selective beta-2 adrenergic blocking agent on the guinea pig cardiac excitability and ventricular fibrillation threshold. | In isolated guinea pig perfused hearts ICI 118.551, a selective beta 2 adrenoceptor antagonist, induced transient ventricular extrasystoles. Following the termination of the perfusion, a very significant increase of both the ventricular fibrillation threshold and the refractory periods were measured. In guanethidine pretreated hearts, ICI 118.551 failed to induce premature beats. At the same time the fibrillation threshold and refractory periods exhibited a very significant decrease. The perfusion of equimolecular concentration of metoprolol, a beta-1-adrenoceptor antagonist, and (+) propranolol, a quinidine-like compound, induced, in most experimental settings, similar results as ICI 118.551. Thus, besides its beta-2-adrenoceptor antagonist properties, ICI 118.551 presented other pharmacological actions. |
4,421 | [Plasma cardiac natriuretic peptide as a biological marker of recurrence of atrial fibrillation in elderly people]. | We designed this study to evaluate the relationship between plasma atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels and recurrence of atrial fibrillation (AF) after direct current cardioversion (DC) and the differences with aging. Fifty patients with mild congestive heart failure (CHF) undergoing elective DC of AF were included in this study (New York Heart Association (NYHA) functional class II: n = 42, III = 8). Patients who failed to show restoration of sinus rhythm or those with mitral valve stenosis were excluded. Before successful DC, we measured plasma levels of ANP and BNP and evaluated left atrial dimension (LAD), left ventricular end-diastolic dimension (LVDd), and left ventricular ejection fraction (EF) by echocardiography. Twenty-one patients had recurrence of AF within 2 months after DC (average 9.05 days). We followed up the other 29 patients for 580.5 days. By Cox stepwise multivariate analysis, history of AF (p = 0.007), low plasma levels of ANP (p = 0.003), and high plasma levels of BNP (p = 0.0003) were found to be independent predictors of recurrent AF. High plasma BNP levels indicating ventricular dysfunction and low plasma ANP levels may be due to atrial histological change such as fibrosis. In these patients, plasma ratios of ANP and BNP (ANP/BNP) less than 0.43 were predictive factors for AF recurrence (sensitivity 70%, specificity 62%), especially in patients who were older than 70 years (sensitivity 100%, specificity 80%). Relatively low plasma ANP level compared to BNP is an independent risk factor of AF recurrence in patients with CHF, especially in elderly patients, suggesting that plasma cardiac natriuretic peptides are important biochemical markers of AF recurrence in elderly patients with CHF. |
4,422 | Pharmacokinetics of milrinone in patients with congestive heart failure during continuous venovenous hemofiltration. | To evaluate the pharmocokinetics of intravenous milrinone in patients with severe congestive heart failure during continuous venovenous hemofiltration (CVVH).</AbstractText>Prospective study of patients with congestive heart failure admitted to the intensive care unit (ICU).</AbstractText>ICU between September 1997 and August 1999.</AbstractText>Six patients with severe congestive heart failure during CVVH: all patients received a continuous infusion of milrinone of 0.25 microg x kg(-1) min(-1). The hemodynamics and plasma concentration of milrinone were measured before and after the infusion. Pharmacokinetics were analyzed with one-compartment model featuring constant rate infusion.</AbstractText>The steady-state concentration (Css) was 845 +/- 135 (mean +/- SD) ng/ml, and the half-life time (t1/2) was 20.1 +/- 3.3 h. Cardiac index and stroke volume index after the infusion of milrinone increased significantly compared with pre-infusion levels. Other hemodynamic parameters did not change significantly. All patients died within 1 month after the injection of milrinone because of severe forms of arrhythmia, such as ventricular tachycardia and ventricular fibrillation.</AbstractText>We found that the mean Css and the mean t1/2 of milrinone in subjects during CVVH were much higher and longer than those previously reported for subjects with normal renal function. It is therefore essential to adjust the dose or modify the dosing interval of milrinone during renal replacement therapy for patients with severe congestive heart failure. However, further studies are needed to determine the details of pharmacokinetics of milrinone and therapeutic procedures for patients with severe heart failure during CVVH.</AbstractText> |
4,423 | Enhanced Na(+) channel intermediate inactivation in Brugada syndrome. | Brugada syndrome is an inherited cardiac disease that causes sudden death related to idiopathic ventricular fibrillation in a structurally normal heart. The disease is characterized by ST-segment elevation in the right precordial ECG leads and is frequently accompanied by an apparent right bundle-branch block. The biophysical properties of the SCN5A mutation T1620M associated with Brugada syndrome were examined for defects in intermediate inactivation (I:(M)), a gating process in Na(+) channels with kinetic features intermediate between fast and slow inactivation. Cultured mammalian cells expressing T1620M Na(+) channels in the presence of the human beta(1) subunit exhibit enhanced intermediate inactivation at both 22 degrees C and 32 degrees C compared with wild-type recombinant human heart Na(+) channels (WT-hH1). Our findings support the hypothesis that Brugada syndrome is caused, in part, by functionally reduced Na(+) current in the myocardium due to an increased proportion of Na(+) channels that enter the I:(M) state. This phenomenon may contribute significantly to arrhythmogenesis in patients with Brugada syndrome. The full text of this article is available at http://www.circresaha.org. |
4,424 | [Recurrent ventricular fibrillation after defibrillation in a patient with pacemaker]. | A 62-year-old patient was admitted for an operation of a hernia of the right groin in the surgical department. He had a dual chamber pacemaker because of a binodal disease. Pre-operatively the patient was reanimated because of ventricular fibrillation in dilated cardiomyopathy and was defibrillated 12 times, unexpectedly often.</AbstractText>The reason of the repeated ventricular fibrillation was a spike-on-T-phenomenon due to loss of the sensing function of the pacemaker (entrance bloc).</AbstractText>Therefore, the pacemaker was explanted, and the ventricular fibrillation came to an end. The patient recovered.</AbstractText>The repeated defibrillations with the electrodes over the basis and the apex of the heart damaged the pacemaker. The following fibrillation episodes were founded on a spike-on-T-phenomenon. In order to prevent such damage of pacemakers, pacemaker patients should be defibrillated and cardioverted in anterior-posterior position of the electrodes.</AbstractText> |
4,425 | Chest impedance: characteristics of local patients. | The Pre-hospital Defibrillation Program in Singapore has in some cases demonstrated a lower amplitude of Ventricular Fibrillation (VF) than considered the norm. The Electrode Skin Impedance (ESI) refers to the skin impedance determined between two electrodes placed at specific positions on the body surface. The objective of this prospective study was to measure the ESI of patients at 5 Hz and 2 kHz frequencies, and assess its change with time from the application of electrodes, the difference between the ESI at two different sets of electrode placement positions and correlation with patient factors. Patients who were 25 years or older and not critically ill had their ESI measured with a modified Heart-Save 911 defibrillator, using signal frequencies at 5 Hz and 2 kHz, at 10 seconds, 1 and 2 minutes after electrodes application. Two sets of positions were used; Position 1 where an electrode is placed in the right infra-clavicular region and another just lateral to the apex beat on the left and Position 2, which represents the mirror image of Position 1. 36 each of male and female patients were studied. The mean age and weight were 59.9 +/- 13.5 years and 56.8 +/- 24.1 kg respectively. There was no significant correlation between the ESI and patients' body weight or sex. However, there was a significant decrease in the ESI with time from application of electrodes at both Positions (p < 0.05) with the two different frequencies. The ESI was lower when measured at lower frequencies and higher when taken at higher frequencies, but there was no statistically significant difference between the two mirror-image positions used. Thus, with lower frequency, the ECG amplitude of VF recorded on the automated external defibrillator could be enhanced. |
4,426 | Inappropriate pacing due to autoperpetuation of the ventricular rate stabilization algorithm: a manifestation of T wave oversensing by ICDs. | Preventive pacing algorithms designed to eliminate the pause that follows a premature ventricular depolarization have been incorporated in current implantable defibrillators. We report a patient in whom intermittent T wave oversensing frequently invoked the ventricular rate stabilization algorithm and resulted in periods of inappropriate VVI pacing. The problem was solved by decreasing the maximum sensitivity from 0.3 mV to 0.45 mV. Implant testing had revealed adequate sensing of ventricular fibrillation with a maximum sensitivity of 1.2 mV. |
4,427 | Ventricular pacing failure after a single oral dose of pilsicainide in a patient with a permanent pacemaker and paroxysmal atrial fibrillation. | A single oral dose of pilsicainide, a Class Ic antiarrhythmic drug, is a widely used and highly effective therapy for termination of recent onset atrial fibrillation. We report on a patient in which ventricular pacing failure occurred immediately after a single oral dose of pilsicainide. It did not exhibit a parallel relationship between the change in the pacing threshold and plasma concentration of pilsicainide, and the recovery period for the ventricular pacing threshold was longer than that of the plasma concentration of pilsicainide in this patient. Careful attention should be paid when a single oral dose of pilsicainide for termination of recent onset atrial fibrillation is used in patients with permanent pacemakers. |
4,428 | Aortocoronary bypass grafting: a comparison of HTK cardioplegia vs. intermittent aortic cross-clamping. | Intermittend, hypothermic aortic cross-clamping (IAC) with myocardial fibrillation and cardioplegic arrest (CA) have been established both as effective methods for coronary artery bypass surgery (CABG). Nevertheless, there exists controversy about the more beneficial cardioprotective effect of one of these procedures in CABG-patients.</AbstractText>In this prospective study we compared the clinical outcome, ischemic serum-markers (CK, CK-MB, Troponin I), electrocardiogram (ECG)-changes, and hemodynamic data of 103 patients. Randomization in group I (IAC; n=52) or group II (CA; n=51) was done consecutively, all data were compared by Student's t-test or chi(2)-test and P<0.05 was regarded as significant. The Bretschneider-HTK solution was used for cardioplegic arrest. Data were collected before operation, before ischemic arrest, after 5 and 60 min of reperfusion, 1 and 6 h after operation, 1, 2 and 10 days postoperatively.</AbstractText>There were no significant differences between both groups regarding general patient data: age (IAC: 64. 8+/-9.2 vs. CA: 63.8+/-9.0 years), left ventricular function (ejection fraction: IAC: 62+/-14 vs. CA: 64+/-13%), the amount of bypassed vessels (IAC: 3.4+/-0.5 vs. CA: 3.6+/-0.5), total bypass time (IAC: 113+/-31 vs. CA 108+/-20 min). The total time of ischemia was significantly less in the IAC group with 37+/-10 vs. 48+/-10 min in the CA group. In the IAC-group, a higher mortality was noticed (7. 7 vs. 3.9%; N.S.). This was combined with a significantly higher amount of patients with peak serum-values of CK-MB (>40 U/l) and troponin I (>50 ng/ml), 17 in the IAC-group (33%) vs. eight in CA-group (16%). Cerebral strokes were seen in two IAC-patients and none in CA-patients (NS). ECG-changes occurred in 22 IAC patients (42%) vs. 16 CA patients (31%); persistent ischemia related ECG-changes in six IAC (11.5%) vs. five CA-patients (9.8%).</AbstractText>Both cardioprotective methods, IAC and HTK-cardioplegia, seem to offer sufficient myocardial protection in normal CABG-procedures. Although neurologic disorders and mortality rates were higher in patients with intermittent aortic cross-clamping, the differences to the cardioplegia group were not significant. According to the analysis of increased ECG-changes, higher CK-MB and troponin I values, which occurred especially in patients with myocardial ischemia time longer than 40 min, we conclude that cardioplegic arrest with HTK seems to offer more beneficial effects in procedures with prolonged ischemia.</AbstractText> |
4,429 | Multicenter, randomized, controlled trial of 150-J biphasic shocks compared with 200- to 360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Optimized Response to Cardiac Arrest (ORCA) Investigators. | In the present study, we compared an automatic external defibrillator (AED) that delivers 150-J biphasic shocks with traditional high-energy (200- to 360-J) monophasic AEDs.</AbstractText>AEDs were prospectively randomized according to defibrillation waveform on a daily basis in 4 emergency medical services systems. Defibrillation efficacy, survival to hospital admission and discharge, return of spontaneous circulation, and neurological status at discharge (cerebral performance category) were compared. Of 338 patients with out-of-hospital cardiac arrest, 115 had a cardiac etiology, presented with ventricular fibrillation, and were shocked with an AED. The time from the emergency call to the first shock was 8.9+/-3.0 (mean+/-SD) minutes.</AbstractText>The 150-J biphasic waveform defibrillated at higher rates, resulting in more patients who achieved a return of spontaneous circulation. Although survival rates to hospital admission and discharge did not differ, discharged patients who had been resuscitated with biphasic shocks were more likely to have good cerebral performance.</AbstractText> |
4,430 | Pacing following shocks stronger than the defibrillation threshold: impact on defibrillation outcome. | A recent study of shocks near defibrillation threshold (DFT) strength demonstrated that at least three rapid cycles always occur after failed shocks but not after successful shocks, suggesting that the number and rapidity of postshock cycles are important in determining defibrillation success. To test this hypothesis, rapid pacing was performed following a shock stronger than the DFT that by itself did not induce rapid cycles and ventricular fibrillation (VF).</AbstractText>Epicardial activation was mapped in six pigs using a 504-electrode sock. The DFT was determined by an up/down protocol with S1 shocks (right ventricle-superior vena cava, biphasic). Ten shocks that were 100 to 200 V above the DFT (aDFT) were delivered after 10 seconds of VF to confirm they always defibrillated. Then, S2, S3, etc., pacing at 5 to 10 times diastolic threshold was performed from the left ventricular apex after aDFT shocks during VF. First, the postshock interval after aDFT shocks was scanned with an S2 stimulus to find the shortest S1-S2 coupling interval (CI) that captured. This was repeated for S3, S4, etc., until VF was induced. To induce VF after aDFT shocks, three pacing stimuli (S2, S3, S4) with progressively shorter CIs were always required; S2 or S2,S3 never induced VF. For the S2-S4 cycles, the intercycle interval was shorter (P < 0.01), and the wavefront conduction time was longer (P < 0.01) for episodes in which VF was induced (n = 57) than for episodes in which it was not (n = 60). Following the S4 cycle that induced VF, two types of spontaneous activation patterns appeared: focal (88%) and reentrant (12%).</AbstractText>VF induction after aDFT shocks always required at least three rapid successive paced-induced cycles. Thus, the number and rapidity of the first several postshock cycles rather than just the first postshock cycle may be determining factors for defibrillation outcome.</AbstractText> |
4,431 | Prediction of defibrillation outcome by epicardial activation patterns following shocks near the defibrillation threshold. | Ventricular defibrillation is probabilistic and shock strength dependent. We investigated the relationship between defibrillation outcome and postshock activation patterns for shocks of the same strength (approximately 50% probability of success for defibrillation [ED50] to yield an equal number of successful and failed shocks).</AbstractText>In five pigs, 10 shocks of approximately ED50 strength (right ventricle-superior vena cava, biphasic, 6/4 msec) were delivered after 10 seconds of ventricular fibrillation (VF). Epicardial activation sequences following shocks were mapped with a 504-electrode shock and analyzed by animating dV/dt of the electrograms. Intercycle interval (ICI, time between the onset of successive postshock cycles), wavefront conduction time (WCT, time between the earliest and latest activation of a cycle), and overlapping index (WCT of cycle[n]/ICI of cycle[n+1]) were determined for the first five postshock cycles. An overlapping index >1 indicates overlap between successive cycles. Of 50 defibrillation attempts, 25 were successes. There was no difference between successful and failed episodes for both ICI (68 +/- 9 msec vs 62 +/- 10 msec) and WCT (97 +/- 24 msec vs 100 +/- 14 msec) of cycle 1. However, starting at cycle 2, the ICI was longer, and the WCT was shorter for successful than failed episodes (P < 0.01). Overlapping cycles (index > 1) were found during the transition from cycles 2 through 5 in all failed (index >1) and in no successful episodes.</AbstractText>(1) Defibrillation outcome cannot be determined during the first postshock cycle. (2) At least three rapid successive cycles with overlap of cycles 2 and 3 are present in all failed and in no successful episodes. (3) The overlapping index is a marker to predict defibrillation outcome.</AbstractText> |
4,432 | Predictive factors of ventricular fibrillation triggered by pause-dependent torsades de pointes associated with acquired long QT interval: role of QT dispersion and left ventricular function. | Death due to acquired torsades de pointes usually is caused by ventricular fibrillation (VF), but the contributing factors to VF triggered by pause-dependent torsades de pointes are not understood.</AbstractText>We evaluated 91 patients who fulfilled four criteria: (1) pause-dependent torsades de pointes; (2) prolonged QT interval and/or corrected QT (QTc) (>0.44 sec); (3) long-short initiation sequence; and (4) conditions known to induce pause-dependent torsades de pointes. There were 38 patients with a documented VF (group I) and 53 without VF (group II). Absolute and relative dispersions of QT and QTc were calculated based on the 12-lead standard ECG. Group I differed from group II with regard to myocardial infarction history (32% vs 13%; P = 0.035), left ventricular ejection fraction (44% +/- 14% vs 65% +/- 9%; P < 0.0001), presence of structural heart disease (100% vs 20.8%; P < 0.0001), QT mean (591 +/- 73 msec vs 514 +/- 78 msec; P < 0.0001), QTc mean (563 +/- 76 msec vs 508 +/- 90 msec; P = 0.002), absolute QT dispersion (166 +/- 56 msec vs 84 +/- 49 msec; P < 0.0001), relative QT dispersion (9.9% +/- 3.5% vs 6.3% +/- 3.2%; P < 0.0001), absolute QTc dispersion (158 +/- 57 msec vs 81 +/- 44 msec; P < 0.0001), and relative QTc dispersion (9.9% +/- 3.6% vs 6.2% +/- 3%; P < 0.0001). Multiple regression analysis showed that ejection fraction (P = 0.0001), presence of structural heart disease (P < 0.0001), and relative QTc dispersion (P = 0.038) were the only independent predictors of VF.</AbstractText>Left ventricular function, presence of structural heart disease, and QTc relative dispersion should be evaluated carefully in patients with conditions susceptible to inducing torsades de pointes.</AbstractText> |
4,433 | The incidence of pulmonary embolism in unexplained sudden cardiac arrest with pulseless electrical activity. | The cause of many cases of sudden cardiac arrest from pulseless electrical activity is unknown. We hypothesized that pulmonary embolism was responsible for a substantial proportion of these cases and used transesophageal echocardiography to identify pulmonary embolism among patients with sudden cardiac arrest.</AbstractText>We performed a prospective study at a tertiary care, university-operated county hospital, with a level 1 trauma center. Consecutive patients (n = 36) who were admitted with (n = 20) or unexpectedly developed (n = 16) sudden cardiac arrest of unknown cause were studied with transesophageal echocardiography during cardiopulmonary resuscitation. We determined the presence of central pulmonary embolism, right ventricular enlargement, and other causes of sudden cardiac arrest (such as myocardial infarction and aortic dissection) using prospectively defined criteria.</AbstractText>Of the 25 patients with pulseless electrical activity as the initial event, 9 (36%) had pulmonary emboli (8 seen with transesophageal echocardiography and 1 diagnosed at autopsy) compared with none of the 11 patients with other rhythms, such as asystole or ventricular tachycardia or fibrillation (P = 0.02). Of the 8 patients who had pulmonary embolism diagnosed by transesophageal echocardiography, 2 survived to hospital discharge.</AbstractText>Mortality from massive pulmonary embolism is high, particularly if patients present with sudden cardiac arrest. Earlier diagnosis of pulmonary embolus may permit wider use of thrombolytic agents or other interventions and may potentially increase survival.</AbstractText> |
4,434 | Electrophysiological instability in the acute phase: prognostic significance of early ventricular fibrillation in acute myocardial infarction. | In the prognostic stratification of patients affected by AMI is important to evaluate, besides the assessment of left ventricular function and residual ischemia, the presence of electrophysiological instability.</AbstractText>We have analysed 15 patients all affected by AMI complicated by early ventricular fibrillation. During the hospital phase we evaluated the E.F.% (ECHO) and the presence of late ventricular potentials (SAECG). After hospital discharge we followed up the patients for 6 months.</AbstractText>None of the patients died during the hospital phase while the posthospital cardiac mortality was 20%. The three patients dead during the follow-up had an AMI localized in the anterolateral wall of the left ventricle, an E.F.% less than 40% and LVP positive in the hospital phase. Besides the clinical course was complicated by cardiac failure.</AbstractText>We conclude that these three patients are a "high risk profile subgroup" and should be submitted to extensive evaluation with cardiac catheterization, coronary arteriography and programmed ventricular stimulation.</AbstractText> |
4,435 | Origins of spiral wave meander and breakup in a two-dimensional cardiac tissue model. | We studied the stability of spiral waves in homogeneous two-dimensional cardiac tissue using phase I of the Luo-Rudy ventricular action potential model. By changing the conductance and the relaxation time constants of the ion channels, various spiral wave phenotypes, including stable, quasiperiodically meandering, chaotically meandering, and breakup were observed. Stable and quasiperiodically meandering spiral waves occurred when the slope of action potential duration (APD) restitution was < 1 over all diastolic intervals visited during reentry; chaotic meander and spiral wave breakup occurred when the slope of APD restitution exceeded 1. Curvature of the wave changes both conduction velocity and APD, and their restitution properties, thereby modulating local stability in a spiral wave, resulting in distinct spiral wave phenotypes. In the LRI model, quasiperiodic meander is most sensitive to the Na+ current, whereas chaotic meander and breakup are more dependent on the Ca2+ and K+ currents. |
4,436 | Dramatic improvement of LV function after coronary sinus thromboembolectomy. | We present the case of a 79-year-old man suffering from chronic atrial fibrillation, severe left ventricular dysfunction, massive right atrial thrombosis, and pulmonary hypertension. Complete coronary sinus thrombosis was found incidentally during preoperative screening. Successful coronary sinus, right atrial, and pulmonary operative embolectomy was followed soon after by a dramatic improvement of cardiac performance; the patient's left ventricular function recovery, in particular, suggests that cardiac venous system played an important role in the genesis of myocardial impairment. |
4,437 | [Improved survival after in-hospital cardiac arrest]. | Internationally, survival among patients suffering in-hospital cardiac arrest is relatively low and unchanged at about 15%. Our experience at Sahlgrenska Hospital in Göteborg indicates a higher rate. We found survival to be related to the type of arrhythmia initially encountered, the highest rate having been observed among patients in ventricular fibrillation. We also found survival among patients suffering cardiac arrest to be higher in monitored as opposed to non-monitored wards. Whether the improved survival rate observed at Sahlgrenska as compared with international observations among patients suffering cardiac arrest is due to improvements in the organization or to patient selection is not clear. In order to achieve a higher survival rate after in-hospital cardiac arrest an efficient organization in which health care providers are given regular training and feed back is most likely of the utmost importance. |
4,438 | The involvement of cytokines in the second window of ischaemic preconditioning. | We utilized a rat model of myocardial infarction to investigate whether manganese superoxide dismutase (Mn-SOD), an intrinsic radical scavenger, and tumour necrosis factor- alpha (TNF-alpha) and/or interleukin-1beta (IL-1beta) are involved in the late phase of ischaemic preconditioning (IP). IP was induced in anaesthetized rats by four 3-min left coronary artery (LCA) occlusions, each separated by 10 min of reperfusion. Twenty-four hours after the repetitive brief ischaemia, the LCA was occluded for 20 min followed by reperfusion for 48 h. IP reduced the infarct size by approximately 46% as determined after 48 h of reperfusion. Antisense oligodeoxynucleotides to Mn-SOD inhibited the increases in Mn-SOD content and activity, and abolished the expected decrease in myocardial infarct size. Sense or scrambled oligodeoxynucleotides did not abolish either Mn-SOD induction or tolerance to ischaemia/reperfusion. The simultaneous administration of the antibodies to TNF-alpha (0.5 ml) and IL-1beta (0.5 mg) prior to IP abolished the cardioprotection and the increase in Mn-SOD activity induced by IP. We conclude that the induction and activation of Mn-SOD, mediated by TNF-alpha and IL-1beta after IP, plays an important role in the acquisition of late-phase cardioprotection against ischaemia/reperfusion injury in rats. |
4,439 | RSD1019 suppresses ischaemia-induced monophasic action potential shortening and arrhythmias in anaesthetized rabbits. | The electrophysiological actions of lidocaine, tedisamil and RSD1019 were assessed on normal and ischaemic cardiac tissue using monophasic action potentials (MAPs) recorded from the epicardium of anaesthetized rabbits. Drug effects on ischaemia-induced arrhythmias were assessed simultaneously in the same rabbits. Lidocaine, infused at 2.5, 5 and 10 micromol kg(-1) min(-1) i.v., accelerated and worsened the electrophysiological derangement caused by ischaemia, had profibrillatory actions and reduced the time to the occurrence of ventricular fibrillation (VF) relative to controls. Tedisamil, infused at 0.063, 0.125 and 0.25 micromol kg(-1) min(-1) i.v., prolonged MAP duration at 90% repolarization (MAPD(90%)) before induction of ischaemia in a dose-related manner; however, this effect was not maintained 5 min after induction of ischaemia. Tedisamil had no significant antiarrhythmic actions over the dose-range tested. RSD1019, infused at 2, 4 and 8 micromol kg(-1) min(-1) i.v., produced a small increase in MAPD(90%) before induction of ischaemia and only at the highest dose tested. In contrast to tedisamil, RSD1019 suppressed ischaemia-induced MAP shortening assessed 5 min after induction of ischaemia. This effect was dose-related. RSD1019 completely prevented ischaemia-induced tachyarrhythmias at the mid and highest infusion levels tested. The results of this study illustrate a pathologically targeted approach for preventing ischaemia-induced arrhythmias. Suppression of ischaemia-induced MAP shortening, demonstrated herein for RSD1019, represents a novel antifibrillatory approach. |
4,440 | Calcium and digoxin vs. calcium alone for severe verapamil toxicity. | Calcium chloride (CaCl(2)) is ineffective in severe calcium channel antagonist overdoses. Digoxin increases intracellular calcium by inhibiting the sodium-potassium adenosine triphosphatase enzymes.</AbstractText>To examine the effect of calcium and digoxin on the treatment of verapamil toxicity.</AbstractText>Sixteen dogs were instrumented to monitor hemodynamics. Verapamil toxicity (50% decrease in mean arterial pressure) was induced with verapamil (VER) at 6 mg/kg/hr and maintained for 30 minutes by titrating the VER rate. Following toxicity, the dogs received either digoxin (0.018 mg/kg) (DIG) (n = 8) or saline (No-DIG) (n = 8). Both groups received VER at three sequential rates (1 mg/kg/hr from 0 to 90 min, 6 mg/kg/hr from 90 to 130 min, and 18 mg/kg/hr from 130 to 170 min). Calcium boluses were given (500 mg at 0 and 15 min; 1 g at 140, 150, and 160 min). Data were analyzed using a repeated-measures analysis of covariance comparing DIG vs No-DIG across the infusion rates and time. Animal weight, does of VER administered during the toxicity phase, and baseline values were included as covariates. Mortality rates were compared at 230 minutes following a total dose of 500 mg of VER.</AbstractText>The DIG group had a higher systolic blood pressure (SBP) than the No-DIG group during the 1-mg/kg/hr (early p = 0.028, late p = 0.01), 6-mg/kg/hr (p = 0.051), and 18-mg/kg/hr (p = 0.038) VER infusion rates. There were no deaths in the DIG group and four deaths in the No-DIG group (Fisher = 0.08). Neither ventricular tachycardia nor ventricular fibrillation developed in either group. Other hemodynamic parameters did not show significant changes.</AbstractText>In a model of severe verapamil toxicity, digoxin plus calcium raised SBP and did not result in ventricular arrhythmias when compared with calcium alone.</AbstractText> |
4,441 | Functional suppression of sodium channels by beta(1)-subunits as a molecular mechanism of idiopathic ventricular fibrillation. | Ventricular fibrillation leading to sudden cardiac death can occur even in the absence of structural heart disease. One form of this so-called idiopathic ventricular fibrillation (IVF) is characterized by ST segment elevation (STE) in the electrocardiogram. Recently we found that IVF with STE is linked to mutations of SCN5A, the gene encoding the cardiac sodium channel alpha -subunit. Two types of defects were identified: loss-of-function mutations that severely truncate channel proteins and missense mutations (e.g. a double mutation, R1232W and T1620M) that cause only minor changes in channel gating. Here we show that co-expression of the R1232W+T1620M missense mutant alpha -subunits in a mammalian cell line stably transfected with human sodium channel beta(1)-subunits results in a phenotype similar to that of the truncation mutants. In the presence of beta(1)subunits the expression of both ionic currents and alpha -subunit-specific, immunoreactive protein was markedly suppressed after transfection of mutant, but not wild-type alpha -subunits when cells were incubated at physiological temperature. Expression was partially restored by incubation at reduced temperatures. Our results reconcile two classes of IVF mutations and support the notion that a reduction in the amplitude of voltage-gated sodium conductance is the primary cause of IVF. |
4,442 | Incidence of left atrial thrombi in patients in sinus rhythm and with a recent neurologic deficit. | We sought to determine the incidence of left atrial (LA) thrombi in patients in sinus rhythm (SR) and with a recent neurologic deficit and to analyze the relation between LA thrombi and LA chamber and appendage function in patients in SR.</AbstractText>A prospective study was conducted in 869 consecutive patients. The study group consisted of 583 patients in SR (67%). The remaining 286 patients had atrial fibrillation (AF) and served as controls (33%).</AbstractText>The incidence of LA thrombi was significantly higher in patients with AF (n = 39 [14%]) compared with patients in SR (n = 6 [1%]; P <.001). Three of 6 patients with thrombi in SR had mitral stenosis, 1 patient had aortic stenosis, 1 patient had coronary artery disease, and another patient had a cardiomyopathy. Of the patients with detected thrombi, those in SR did not receive anticoagulation, whereas those with AF did in 18 cases. Patients with thrombi in SR and with AF did not significantly differ in LA diameter (5.1 +/- 0.8 cm vs 4.8 +/- 0.7 cm; 95% confidence interval [CI], -0.78 to 0.45), left ventricular ejection fraction (46% +/- 13% vs 42% +/- 15%; 95% CI, -18.7 to 7.4), LA appendage area (5.8 +/- 2.7 cm(2) vs 6.7 +/- 3.2 cm(2); 95% CI, -1.9 to 3.6), peak emptying velocity of the LA appendage (0.19 +/- 0.08 m/s vs 0.17 +/- 0.07 m/s; 95% CI, -0.08 to 0.04), or LA spontaneous echo contrast (3. 5 +/- 0.6 vs 3.9 +/- 0.5; 95% CI, -0.06 to 0.45).</AbstractText>LA appendage thrombi are an infrequent cause of thromboembolism in patients in SR and are associated either with mitral valve disease or LA chamber and appendage dysfunction. Routine transesophageal echocardiography for the exclusion of LA thrombi is not recommended in patients in SR without underlying heart disease and normal LA function as assessed by transthoracic echocardiography.</AbstractText> |
4,443 | The mode selection trial (MOST) in sinus node dysfunction: design, rationale, and baseline characteristics of the first 1000 patients. | More than 200,000 permanent pacemakers will be implanted in the United States in 2000 at a cost of more than $2 billion. Sick sinus syndrome (SSS) will likely account for approximately half of all cases necessitating implantation. Pacemaker technology permits the selection of ventricular (single-chamber) or dual-chamber devices. However, clinical and outcomes data are inadequate to support a clear recommendation that one or the other type of device be used.</AbstractText>The Mode Selection Trial (MOST) is a single-blind study supported by the National Heart, Lung, and Blood Institute designed to enroll 2000 patients with SSS. All patients will receive a DDDR pacemaker programmed to VVIR or DDDR before implantation. The average time of follow-up will be 3 years. MOST has a >90% power to detect a 25% reduction in the primary end point-nonfatal stroke or total (all cause) mortality-in the DDDR-treated group. Secondary end points will include health-related quality of life and cost effectiveness, atrial fibrillation, and development of pacemaker syndrome. Prespecified subgroups for analysis will include women and the elderly. Enrollment was completed in October 1999, with a total of 2010 patients.</AbstractText>The median age of the first 1000 enrolled patients is 74 years, with 25% of patients 80 years or older. Women comprise 49%, and 17% are nonwhite, predominantly black (13%). Before pacemaker implantation, 22% of patients reported a history of congestive heart failure, 11% coronary angioplasty, and 25% coronary bypass surgery. Supraventricular tachycardia including atrial fibrillation was present in 53% of patients. A prior stroke was reported by 12%. Antiarrhythmic therapy was in use in 18% of patients.</AbstractText>MOST will fill the clinical need for carefully designed prospective studies to define the benefits of dual-chamber versus single-chamber ventricular pacing in patients with SSS. The MOST population is typical of the overall pacemaker population in the United States. Thus the final results of MOST should be clinically generalizable.</AbstractText> |
4,444 | Recent progress in advanced cardiac life support. | The revised guidelines for advanced cardiac life support (ACLS) from the American Heart Association are anticipated in the fall of 2000. Although dramatic changes in the approach to adult basic and ACLS are not anticipated, several controversies and new drugs on the horizon may radically change our approach to emergent cardiac resuscitation. This article features some of the evolving thinking on the emergent treatment of the adult with ventricular fibrillation or ventricular tachycardia, the critical rhythms seen in most cases of acute cardiac distress. Approaches to airway therapy drug administration and new agents also are described. |
4,445 | Endocardial activation during ventricular fibrillation in normal and failing canine hearts. | Because congestive heart failure (CHF) promotes ventricular fibrillation (VF), we compared VF in seven dogs with CHF induced by combined myocardial infarction and rapid ventricular pacing to VF in six normal dogs. A noncontact, multielectrode array balloon catheter provided full-surface real-time left ventricular (LV) endocardial electrograms and a dynamic color-coded display of endocardial activation projected onto a three-dimensional model of the LV. Fast Fourier transform (FFT) analysis of virtual electrograms showed no difference in peak or centroid frequency in CHF dogs compared with normals. The average number of simultaneous noncontiguous wavefronts present during VF was higher in normals (2.4 +/- 1.0 at 10 s of VF) than in CHF dogs (1.3 +/- 1.0, P < 0.005) and decreased in both over time. The wavefront "turnover" rate, estimated using FFT of the noncontiguous wavefront data, did not differ between normals and CHF and did not change over 5 min of VF. Thus the fundamental frequency characteristics of VF are unaltered by CHF, but dilated abnormal ventricles sustain fewer active wavefronts than do normal ventricles. |
4,446 | K(ATP) channel activation reduces the severity of postresuscitation myocardial dysfunction. | Postresuscitation myocardial dysfunction has been recognized as a leading cause of the high postresuscitation mortality rate. We investigated the effects of ischemic preconditioning and activation of ATP-sensitive K(+) (K(ATP)) channels on postresuscitation myocardial function. Ventricular fibrillation (VF) was induced in 25 Sprague-Dawley rats. Cardiopulmonary resuscitation (CPR), including mechanical ventilation and precordial compression, was initiated after 4 min of untreated VF. Defibrillation was attempted after 6 min of CPR. The animals were randomized to five groups treated with 1) ischemic preconditioning, 2) K(ATP) channel opener, 3) ischemic preconditioning with K(ATP) channel blocker administered 1 min after VF, 4) K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning, and 5) placebo. Postresuscitation myocardial function, as measured by the rate of left ventricular pressure increase at 40 mmHg, the rate of left ventricular decline, cardiac index, and duration of survival, was significantly improved in both preconditioned and K(ATP) channel opener-treated animals. K(ATP) channel blocker administered 45 min before induction of ischemic preconditioning completely abolished the myocardial protective effects of preconditioning. We conclude that ischemic preconditioning significantly improved post-CPR myocardial function and survival. These results also provide evidence that the myocardial protective effects of ischemic preconditioning are mediated by K(ATP) channel activation. |
4,447 | Continuous intravenous diltiazem infusion for short-term ventricular rate control in children. | Intravenous diltiazem was administered to 10 pediatric patients with primary atrial tachyarrhythmias with rapid ventricular response. Rapid, consistent, and safe temporary ventricular rate control was obtained in all patients given this medication. |
4,448 | Pentoxifylline improves circulatory and metabolic recovery after cardiopulmonary resuscitation. | To evaluate the effectiveness of a bolus application of pentoxifylline (PTXF) at the beginning of CPR in a standardized resuscitation animal model.</AbstractText>In a laboratory model of cardiac arrest, 12 Wistar rats (382-413 g) were randomized into two groups. Both groups underwent 4 min of cardiopulmonary arrest induced by a transthoracic application of a fibrillating current of 10 mA. At the beginning of CPR, group one (n=6) received a bolus injection of 10 mg kg(-1) body weight PTXF versus sodium chloride in group two (controls: n=6). All animals developed a severe lactate acidosis during and after CPR but in PTXF treated animals acid-base values returned to baseline pattern. During return of spontaneous circulation (ROSC) in the PTXF group lactate concentration decreased from 13.4+/-2.1 to 1.9+/-0.7 mmol l(-1) within 60 min (P<0.01). In control animals, lactate values remained high (10.8+/-3.5 by 60 min, P<0.01). After bolus injection of PTXF pH increased from 6.93+/-0.06 to 7.29+/-0.13 within 60 min of ROSC versus 6.85+/-0.05 to 6.97+/-0.23 in sodium chloride treated animals (P<0.01). Within 5 min of ROSC, PTXF treated animals achieved higher oxygenation values (PTXF P(a)O(2)=216.9+/-62.5 mmHg, control 132. 2+/-15.1 mmHg, P<0.01).</AbstractText>Administration of PTXF at the beginning of CPR improved macrocirculation, acid-base status and arterial oxygenation.</AbstractText> |
4,449 | Effects of endothelin-1 on resuscitation rate during cardiac arrest. | Endothelin-1 (ET-1) is a potent peripheral and coronary artery vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during cardiac arrest. The effect of ET-1 on return of spontaneous circulation (ROSC) following cardiac arrest has not been studied. Our hypothesis was that ET-1 does not improve ROSC from cardiac arrest when compared to placebo.</AbstractText>A total of 11 immature swine were used in this laboratory study. Animals were randomized to receive 300 microg ET-1 and standard dose epinephrine (SDE) or placebo and SDE during arrest. After a 10-min period of no-flow ventricular fibrillation (VF), CPR was performed for 3 min followed by ET-1/SDE or placebo/SDE administration. Following drug administration, standard ACLS was followed with SDE given every 3 min. Aortic pressure was monitored during resuscitation. ROSC was defined as any perfusing rhythm with a systolic pressure greater than 60 mmHg for 60 s. Animals received post-ROSC care as needed for 2 h post-ROSC. CPP and ROSC were analyzed using repeated measures ANOVA and Fischer's exact test respectively. P<0.05 was considered significant.</AbstractText>Pre-arrest variables and CPP prior to ET-1 administration were not different between groups. Following ET-1 administration, CPP was significantly increased at all time points in ET-1/SDE versus placebo/SDE animals. ROSC was achieved in 1/5 (20%) ET-1/SDE versus 1/6 (16.7%) placebo/SDE animals (P>0.05). The resuscitated ET-1/SDE animal survived 6.5 min compared to 120 min for the resuscitated placebo/SDE animal.</AbstractText>In our study, ET-1 administration during cardiac arrest increases CPP but does not improve ROSC.</AbstractText> |
4,450 | Ventricular fibrillation exhibits dynamical properties and self-similarity. | Electrocardiographic recordings of ventricular fibrillation (VF) appear chaotic. Previous attempts to characterize the chaotic nature of VF have relied on peak-to-peak intervals [Witkowski et al., Phys. Rev. Lett. 1995;75(6):1230-3; Garfinkel et al., J. Clin. Investig. 1997;99(2):305-314; Hastings et al., Proc. Natl. Acad. Sci. USA 1996;93:10495-9], the frequency spectrum [Goldberger et al., 1986;19:282-289] or other derived measures [Kaplan and Cohen, Circ. Res. 1990;67:886-92], with results that demonstrate some characteristics of chaos. We have sought to determine whether VF is chaotic rather than random and whether the waveform can be described quantitatively using the tools of fractal geometry. We have constructed an attractor, measured the correlation dimensions, estimated the embedding dimension and measured Lyapunov exponents. When the digitized waveform is analyzed directly, VF exhibits nonrandom, chaotic behavior over a decade of sampling frequency. Within the scaling range we have estimated the Hurst exponent, and the self-similarity dimension of the VF waveform, supporting the presence of chaotic dynamics. Furthermore, these characteristics are measurable in a porcine model of VF under different recording conditions, and in VF recordings taken from human subjects immediately prior to defibrillation. Analyses of the Hurst exponents and self-similarity dimensions are correlated with the duration of VF, which may have clinical applications. |
4,451 | One-year survival after out-of-hospital cardiac arrest in Copenhagen according to the 'Utstein style'. | To determine survival after out-of-hospital cardiac arrest (CA) in Copenhagen, according to the Utstein recommendations, and compare this with other emergency medical services systems.</AbstractText>Register-based cohort study.</AbstractText>Copenhagen, population 465000, area 90 km(2).</AbstractText>Consecutive group of patients with out-of-hospital CA occurring between January 1 1991 and December 31 1993, followed up via the hospital database systems.</AbstractText>Two specially equipped advanced life support (ALS) units, staffed with an anaesthesiologist and a specially trained fireman, operating to support basic life support units.</AbstractText>Of 2225 patients who were unconscious without a pulse or breathing, 1461 were declared dead by the anaesthesiologist. Advanced cardiac life support was initiated in 764, 61 of which were of non-cardiac aetiology. The presumed aetiology was cardiac in 703: in 235 the event was unwitnessed, in 464 witnessed and in four the information was missing. Of 464 witnessed CA the initial rhythm was asystole in 72 cases, in 302 ventricular fibrillation (VF) or ventricular tachycardia (VT), and in 90 were in other rhythms. In these subgroups discharged rates were 5 (7%), 62 (21%) and 1 (1%), and 1-year survival rates were 4 (6%), 49 (16%) and 1 (1%), respectively. The median ALS call-response interval was 6 min.</AbstractText>Survival after CA is more likely if the collapse was witnessed and in patients with VF/VT of cardiac aetiology.</AbstractText> |
4,452 | Outcome after cardiac arrest in adults in UK hospitals: effect of the 1997 guidelines. | To assess the effectiveness of the ILCOR Advisory Statements on Advanced Life Support adopted by the Resuscitation Council (UK), as the standard for resuscitation following cardiac arrest.</AbstractText>Over the period May to November 1997, data on the process and outcome of cardiopulmonary resuscitation following in-hospital cardiac arrest were collected from 49 hospitals throughout the UK.</AbstractText>Of 2074 audit forms submitted, 1368 were included in the final analysis. The initial rhythm monitored was ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) in 429 patients, of whom 181 (42.2%) were discharged alive, compared to 6. 2% when the initial rhythm was non-VF/VT. Overall, 240 (17.6%) patients were discharged alive. At 6 months after discharge 195 (82. 3%) of 237 patients were still alive. Successful initial resuscitation, defined as return of spontaneous circulation lasting longer than 20 min (ROSC>20 min), was significantly associated with VF/VT as the initial arrest rhythm, return of circulation in less than 3 min, age less than 70 years and the use of an advanced airway (P<0.01). There was a significant increased likelihood of survival to discharge when the circulation was restored in less than 3 min and age was less than 70 years (P<0.05). The administration of any adrenaline (epinephrine) was significantly associated with a reduced likelihood of ROSC>20 min or alive discharge (P<0.0001).</AbstractText>Compared to the last major multiple hospital study published in 1992, the results of this study suggest that there appears to have been an improvement in survival of in-hospital patients in the UK who have a VF/VT cardiac arrest. How much of this is directly attributable to the adoption of the latest guidelines is uncertain.</AbstractText> |
4,453 | Ebstein's malformation. surgical treatment and results. | Ebstein's malformation can be defined as an anomaly of the tricuspid valve existing in the setting of a right ventricular dysfunction. The technique introduced by Carpentier in 1980 is based on the concept of mobilization of the restrictive anterosuperior leaflet associated with a longitudinal plication of the inlet component of the right ventricle. From January 1980 to December 1999, 142 patients underwent surgery. The mean age was 25 +/- 15 years (1-65). Cyanosis was present in 48% and associated lesions in 64% of the patients. Patients were classified using a functional approach according to the severity of the lesions. Mild displacement of the septal leaflet, along with small size of the atrialized chamber was seen in 5% (referred to as Type A). Massive displacement of the septal leaflet, but with normal motion of the anterosuperior leaflet and an extensive atrialized chamber, was seen in 35% (Type B). In 51%, the mural (inferior) leaflet was absent, the anterosuperior leaflet was severely restricted by muscular trabeculations and very short tendinous cords, and the anterolateral papillary muscle was incorporated in the right ventricular wall. In these patients (Type C), the atrialized chamber was markedly enlarged and had dyskinetic walls. In such cases, the contractility of the distal (functional) right ventricle was also impaired, and some degree of stenosis of the tricuspid valve was present in one-fifth of them. In the most severe cases (8%), the leaflet tissue of the valve was extremely reduced and the right ventricular walls were thin and contracted poorly. This resulted in the so-called tricuspid sack arrangement (Type D). Valve replacement was needed in only 4 cases, with conservative surgery being achieved in 138 patients by means of mobilization of the anterosuperior leaflet and longitudinal plication of the inlet component of the right ventricle. Additional procedures included the use of a prosthetic ring (94 patients) and partial Glenn anastomosis (30 patients). The hospital mortality was 10%, mainly due to acute postoperative right ventricular failure. Actuarial survival was 75% at 10 years. After operation, 94% of the patients were in functional class I or II of the New York Heart Association, and 88% had no or mild tricuspid valve insufficiency as judged by echocardiography. The rate of reoperation was 9% with a mean delay of 3 years. A second repair was performed in 5 patients. Freedom from reoperation was 87% at 10 years. Sinus rhythm was present in 81%, and 8 pacemaker devices were implanted, 5 for surgically induced atrioventricular block, and 3 because of preoperative conduction disturbances. The use of the partial Glenn anastomosis was introduced recently in cases where the right ventricular contractility was severely impaired, and/or tricuspid valve repair was difficult, and/or permanent atrial fibrillation was present. In those patients with high risk, adding partial Glenn anastomosis reduced the operative mortality from 24% to 6%. Another benefit of the cavo-bipulmonary anastomosis was better functional tolerance of mild residual tricuspid valve incompetence. Those patients with the tricuspid sack arrangement had a high rate of reoperation (2/11) and valve replacement (3/11), but suffered no operative deaths. We conclude that tricuspid valvoplasty associated with longitudinal right ventricular plication is superior to valve replacement. The arrangement producing a tricuspid sack is not suitable for conservative surgery. An associated cavo-pulmonary anastomosis decreases the operative mortality in patients at high risk, and seems to preserve right ventricular function. |
4,454 | Ebstein's anomaly in adults. Arrhythmias: diagnosis and therapeutic approach. | Patients with Ebstein's anomaly (M.E.) are known to have a high potential for developing arrhythmia, in the vast majority, of the tachycardia type. Most of these tachycardias are based on accessory pathways (AP) located along the anomalous atrioventricular valve, found in up to 30% of this patient cohort. Next to this main representative for congenital arrhythmogenic substrates, various types of acquired tachycardia were found in patients with M.E., such as atrial ectopic tachycardia (AET), atrial flutter (A. Flutt.), atrial reentry tachycardia (ART), atrial fibrillation and ventricular tachyarrhythmia. Refractoriness to medical treatment and a higher potential for side effects in these patients resulted in an increasing referral to interventional electrophysiology recent years. A total of 37 patients with M. E. and tachycardia underwent an attempt for radiofrequency current (RFC) treatment at our institution, 30 of whom were adults aged 18 to 61 yrs (33 +/- 12.2. yrs). Just 4 patients under went surgery for reconstruction of the anomalous valve and closure of an ASD (2 patients), in whom a total of 6 cases of atrial tachycardia were found, 3 common A. Flutt. and 3 atriotomy-scar related ART. Of the 26 unoperated patients, one presented with typical AV-nodal reentry tachycardia and the remaining patients with atrioventricular reentry tachycardia, based on a total of 39 APs. 27/39 Aps had bidirectional conduction properties, causing the WPW syndrome in 16 patients, 8 APs were concealed and the remaining 4 were Mahaim fibers. Within 39 sessions, 26 of the 30 patients were successfully treated by RFC ablation of the arrhythmogenic substrates. Mean session duration lasted for 313 +/- 151 min (range 95 to 660 min), and a fluoroscopy time of 56.0 +/- 38.4 min (2.2 to 146.8 min) was required. There were no severe acute complications.</AbstractText>In patients with M. E. not only a high potential for the development of tachycardia, but also a tendency towards multiple arrhythmogenic substrates in the single patient can be ascertained. RFC ablation can be used safely and effectively for treatment for various types of tachycardias in patients with M. E.. Such therapy carries the potential for a definitive treatment and should be taken early into consideration as it meets the requirements this patient cohort.</AbstractText> |
4,455 | Effect of bystander cardiopulmonary resuscitation in out-of-hospital cardiac arrest patients in Sweden. | Information from the Swedish Cardiac Arrest Registry was used to investigate: (a) The proportion of patients suffering an out-of-hospital cardiac arrest who were given bystander cardiopulmonary resuscitation (B-CPR). (b) Where and by whom B-CPR was given. (c) The effect of B-CPR on survival.</AbstractText>a prospective, observational study of cardiac arrests reported to the Swedish Cardiac Arrest Registry. Analyses were based on standardised reports of out-of-hospital cardiac arrests from ambulance organisations in Sweden, serving 60% of the Swedish population. From 1983 to 1995 approximately 15-20% of the population had been trained in CPR.</AbstractText>Of 9877 patients, collected between January 1990 and May 1995, B-CPR was attempted in 36%. In 56% of these cases, the bystanders were lay persons and in 25% they were medical personnel. Most of the arrests took place at home (69%) and only 23% of these patients were given B-CPR in contrast to cardiac arrest in other places where 53% were given CPR. Survival to 1 month was significantly higher in all cases that received B-CPR (8.2 vs. 2.5%). The odds ratio for survival to 1 month with B-CPR was in a logistic regression analysis 2.5 (95% CI 1.9-3.1).</AbstractText>In Sweden, the willingness and ability to perform B-CPR appears to be relatively widespread. More than half of B-CPR was performed by laypersons. B-CPR resulted in a two to threefold increase in survival.</AbstractText> |
4,456 | Transthoracic monophasic and biphasic defibrillation in a swine model: a comparison of efficacy, ST segment changes, and postshock hemodynamics. | Biphasic waveforms for transthoracic defibrillation (DF) have been tested extensively after brief (15 s) episodes of VF in animal models and in patients undergoing electrophysiologic testing. The purpose of this study was to compare the effects mono- and biphasic waveforms for DF on postdefibrillation ST segments and left ventricular pressure, markers of myocardial injury, after more extended periods of VF (30 and 90 s).</AbstractText>21 anesthetized and instrumented swine were randomized to truncated exponential monophasic or biphasic waveform DF. VF was induced electrically and 30 s later, DF with the designated waveform was attempted with a shock dose of 200 J. If unsuccessful, 300 J and then 360 J were administered if necessary. Following return to control hemodynamic values and normalization of the surface ECG, VF was again induced and, after 90 s, DF was attempted as in the 30 s VF period. CPR was not performed during VF and each animal was countershocked with only one waveform for both VF episodes. Waveforms were compared for frequency of first shock defibrillation success, surface ECG indicators of myocardial injury (ST segment changes at 10, 20, and 30 s after countershock) and time to return to pre-VF hemodynamics after successful DF, an indicator of postshock ventricular function.</AbstractText>Successful first shock conversion rates at 30 and 90 s were 60 and 63% for monophasic and 64 and 82% for biphasic (NS). Biphasic DF after 30 s produced ST segment changes (measured 10 s after DF) in 1/10 animals while six of eight animals in the monophasic group showed ST segment changes (P=0.013). After 90 s of VF, ST segment changes were observed in 6/8 in the monophasic group and 2/10 in the biphasic group (P=0.054). Differences in the time to hemodynamic recovery (return to control peak left ventricular pressure) were not observed between biphasic and monophasic waveforms after 30 or 90 s of VF.</AbstractText>Monophasic and biphasic transthoracic defibrillation are equally effective in terminating VF of 30 and 90 s duration and restoring a perfusing rhythm. The biphasic waveform produced less ECG evidence of transient myocardial injury. However, there was no difference in the rate of return to control hemodynamics. ST segment changes following countershock of VF of brief duration are transient and of questionable significance.</AbstractText> |
4,457 | Mechanisms of ventricular fibrillation induction by 60-Hz alternating current in isolated swine right ventricle. | The mechanisms by which 60-Hz alternating current (AC) can induce ventricular fibrillation (VF) are unknown.</AbstractText>We studied 7 isolated perfused swine right ventricles in vitro. The action potential duration restitution curve was determined. Optical mapping techniques were used to determine the patterns of activation on the epicardium during 5-second 60-Hz AC stimulation (10 to 999 microA). AC captured the right ventricles at 100+/-65 microA, which is significantly lower than the direct current pacing threshold (0.77+/-0.45 mA, P:<0.05). AC induced ventricular tachycardia or VF at 477+/-266 microA, when the stimulated responses to AC had (1) short activation CLs (128+/-14 ms), (2) short diastolic intervals (16+/-9 ms), and (3) short diastolic intervals associated with a steep action potential duration restitution curve. Optical mapping studies showed that during rapid ventricular stimulation by AC, a wave front might encounter the refractory tail of an earlier wave front, resulting in the formation of a wave break and VF. Computer simulations reproduced these results.</AbstractText>AC at strengths less than the regular pacing threshold can capture the ventricle at fast rates. Accidental AC leak to the ventricles could precipitate VF and sudden death if AC results in a fast ventricular rate coupled with a steep restitution curve and a nonuniform recovery of excitability of the myocardium.</AbstractText> |
4,458 | Predicting outcome of defibrillation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest. | In 156 patients with out-of-hospital cardiac arrest of cardiac cause, we analyzed the ability of 4 spectral features of ventricular fibrillation before a total of 868 shocks to discriminate or not between segments that correspond to return of spontaneous circulation (ROSC).</AbstractText>Centroid frequency, peak power frequency, spectral flatness, and energy were studied. A second decorrelated feature set was generated with the coefficients of the principal component analysis transformation of the original feature set. Each feature set was split into training and testing sets for improved reliability in the evaluation of nonparametric classifiers for each possible feature combination. The combination of centroid frequency and peak power frequency achieved a mean+/-SD sensitivity of 92+/-2% and specificity of 27+/-2% in testing. The highest performing classifier corresponded to the combination of the 2 dominant decorrelated spectral features with sensitivity and specificity equal to 92+/-2% and 42+/-1% in testing or a positive predictive value of 0.15 and a negative predictive value of 0.98. Using the highest performing classifier, 328 of 781 shocks not leading to ROSC would have been avoided, whereas 7 of 87 shocks leading to ROSC would not have been administered.</AbstractText>The ECG contained information predictive of shock therapy. This could reduce the delivery of unsuccessful shocks and thereby the duration of unnecessary "hands-off" intervals during cardiopulmonary resuscitation. The low specificity and positive predictive value indicate that other features should be added to improve performance.</AbstractText> |
4,459 | The unclampable ascending aorta in coronary artery bypass patients: A surgical challenge of increasing frequency. | The unclampable ascending aorta (UAA) is a condition increasingly encountered during CABG procedures. We report our experience with CABG patients with UAA and place particular emphasis on the preoperative diagnosis and surgical management.</AbstractText>UAA was diagnosed in 211 of 4812 consecutive CABG patients (4.3%). On the basis of the chest radiograph, echocardiogram, and coronary angiograph, a preoperative diagnosis was achieved in only 58 patients (27.4%). An age of >70 years, diabetes, smoking, unstable angina, diffuse coronaropathy, and peripheral vasculopathy were all predictors of UAA. Patients were treated with hypothermic ventricular fibrillation (no-touch technique n=129) or beating heart revascularization (no-pump technique n=82) depending on the possibility of founding an arterial cannulation site. The overall in-hospital mortality rate was 2.8% (6 of 211) with no differences between the 2 surgical strategies. The no-touch technique was associated with a greater incidence of neurological complications (stroke and transient ischemic attack), renal insufficiency, and stay in the intensive care unit and hospital. However, at midterm follow-up, more patients of the no-pump group had ischemia recurrence.</AbstractText>A preoperative diagnosis of UAA is achievable only in a minority of patients, which highlights the necessity revising the current diagnostic protocols. The use of the no-touch technique is associated with an high perioperative risk but a superior possibility of complete revascularization, whereas adoption of the no-pump strategy ensures a smoother postoperative course at the expense of an higher incidence of ischemia recurrence.</AbstractText> |
4,460 | Comparison of echocardiographic markers of embolism in atrial flutter and fibrillation: frequency of protruding atherosclerotic plaques in the thoracic aorta. | The potential additional embolic risk of protruding aortic plaques > or = 4 mm and left atrial abnormalities such as thrombus, spontaneous echocardiographic contrast (SEC), low left atrial appendage velocity, recently has been shown in patients with atrial fibrillation (AF). However, the presence and potential role of transesophageal echocardiographic (TEE)-detected protruding aortic plaques > or = 4 mm have not been systematically evaluated in patients with atrial flutter. Among 2493 patients evaluated by TEE, 271 consecutive patients with atrial flutter (n = 41) and AF (n = 230) > or = 2 days duration were included in the study. Clinical and echocardiographic characteristics in consecutive patients with atrial flutter were compared to those in patients with AF, especially atrial morphology and function and atherosclerotic disease of the thoracic aorta. Clinical characteristics of patients with atrial flutter and AF were similar with regard to age (68 +/- 13 and 67 +/- 12, P = 0.628), sex ratio (men, 66% and 54%, P = 0.212), and previous embolic events (5% and 15%, P = 0.126), respectively. The frequency of protruding atherosclerotic plaques > or = 4 mm (12% and 11%, P = 0.919) and SEC (15% and 14%, P = 0.847) in the thoracic aorta was similar in patients with atrial flutter and AF. Left atrial appendage area was smaller (3.1 +/- 0.7 and 6.0 +/- 3.0 cm(2), P = 0.001), left atrial appendage SEC was less frequent (17% and 37%, P = 0.024), and left atrial appendage emptying velocity was higher (47 +/- 10 and 30 +/- 10 cm/s, P = 0.030) in patients with atrial flutter as compared to those with AF. There was no difference between the two groups regarding left ventricular fractional shortening (30 +/- 10% and 33 +/- 13%, P = 0.630), rheumatic valvular disease (5% and 12%, P = 0. 301), left atrial diameter (43 +/- 7 and 45 +/- 8 mm, P = 0.134), right atrial area (16 +/- 4 and 17 +/- 6 cm(2), P = 0.384), left atrial SEC (39% and 53%, P = 0.124), or atrial thrombus ( 2% and 3%, P = 0.888) respectively. Our results point to the high prevalence of protruding atherosclerotic plaques in the thoracic aorta in patients with atrial flutter. |
4,461 | [Anesthetic management of a patient with Brugada syndrome]. | Brugada syndrome is characterized by right bundle-branch block, ST elevation in leads V 1 through V 3 and normal QT interval. Ventricular fibrillation frequently occurs in patients with Brugada syndrome. There have been few reports of anesthetic management of Brugada patients. We managed a 47-year-old man with Brugada syndrome, who underwent hemilaminectomy under general anesthesia, without untoward cardiovascular events. Potential problems in anesthetic management of patients with Brugada syndrome are also discussed. |
4,462 | A multifilamented electrode in the middle cardiac vein reduces energy requirements for defibrillation in the pig. | To compare the defibrillation efficacy of a novel lead system placed in the middle cardiac vein with a conventional non-thoracotomy lead system.</AbstractText>In eight pigs (weighing 35-71 kg), an electrode was advanced transvenously to the right ventricular apex (RV), with the proximal electrode in the superior caval vein (SCV). Middle cardiac vein (MCV) angiography was used to delineate the anatomy before a three electrode system (length 2 x 25 mm + 1 x 50 mm) was positioned in the vein. An active housing (AH) electrode was implanted in the left pectoral region. Ventricular fibrillation was induced and biphasic shocks were delivered by an external defibrillator. The defibrillation threshold was measured and the electrode configurations randomised to: RV-->AH, RV+MCV-->AH, MCV-->AH, and RV-->SCV+AH.</AbstractText>For these configurations, mean (SD) defibrillation thresholds were 27.3 (9.6) J, 11.9 (2.9) J, 15.2 (4.3) J, and 21.8 (9.3) J, respectively. Both electrode configurations incorporating the MCV had defibrillation thresholds that were significantly less than those observed with the RV-->AH (p < 0.001) and RV-->SCV+AH (p < 0.05) configurations. Necropsy dissection showed that the MCV drained into the coronary sinus at a location close to its orifice (mean distance = 2.7 (2.2) mm). The MCV bifurcated into two main branches that drained the right and left ventricles, the left branch being the dominant vessel in the majority (6/7) of cases.</AbstractText>Placement of specialised defibrillation electrodes within the middle cardiac vein provides more effective defibrillation than a conventional tight ventricular lead.</AbstractText> |
4,463 | Late arrhythmia in adults with the mustard procedure for transposition of great arteries: a surrogate marker for right ventricular dysfunction? | To examine the relation between ventricular dysfunction and late clinical arrhythmia in adults who underwent the Mustard procedure for transposition of the great arteries.</AbstractText>Observational study based on periodic outpatient assessment of biventricular function.</AbstractText>Tertiary referral centre.</AbstractText>Analysis of data from 12 lead ECGs, echocardiography, exercise radionuclide ventriculography, and magnetic resonance imaging.</AbstractText>Clinical outcome and late onset clinical arrhythmia during follow up. ECG and ventricular function indices obtained before arrhythmia onset were used for analysis.</AbstractText>51 patients (mean (SD) age 25.7 (5.0) years) fulfilled entry criteria at a mean of 23.4 (4.0) years after the Mustard procedure. Late arrhythmia occurred in 11 (22%): sustained atrial flutter/fibrillation in 10, ventricular tachycardia in one. Compared with patients who remained arrhythmia free, patients with arrhythmia had longer QRS (129 (26) v 112 (16) ms, p = 0.01), greater QT dispersion (107 (28) v 51 (24) ms, p < 0.001), and increased ratio of right to left ventricular end diastolic diameter (2.4 (0.9) v 1.7 (0.7), p = 0.02), but no difference in wall thickness. Systemic ejection fraction was also reduced in the arrhythmia subgroup (at rest: 34.1 (13)% v 47 (16)%, p = 0.04; during exercise: 37.8 (12)% v 52 (17)%, p = 0.03). QRS duration correlated with right ventricular end diastolic diameter (r = 0.59, p < 0.001), suggesting a possible mechano-electric relation after the Mustard procedure. QT dispersion was the only predictor of clinical arrhythmia in multivariate analysis.</AbstractText>Impaired ventricular function in adults with the Mustard procedure for transposition of the great arteries relates to clinical arrhythmia. Late atrial flutter/fibrillation may be a surrogate marker for ventricular dysfunction, and these patients may also be at risk of ventricular tachycardia.</AbstractText> |
4,464 | Circadian variation in witnessed out of hospital cardiac arrest. | To examine the effect on circadian variation of out of hospital cardiac arrest according to the underlying aetiology and presenting rhythm of arrest, and to explore strategies that might help to improve survival outcome using circadian variation.</AbstractText>Population based retrospective study.</AbstractText>County of Nottinghamshire with a total population of 993 914 and an area of 2183 km(2).</AbstractText>Between 1 January 1991 and 3 December 1994, all witnessed cardiac arrests attended by the Nottinghamshire Ambulance Service, of which 1196 patients had a cardiac cause for their arrest (ICD, 9th revision, codes 390-414 and 420-429) and 339 had a non-cardiac cause.</AbstractText>The circadian variation of the cardiac cases was not significantly different from that of non-cardiac cases (p = 0.587), even when adjusted for age, sex, or presenting rhythm of arrest. For cardiac cases, the circadian variation of those who presented with ventricular fibrillation was significantly different from those presenting with a rhythm other than ventricular fibrillation (p = 0.005), but was similar to the circadian variation of bystander cardiopulmonary resuscitation (p = 0.306) and survivors (p = 0.542). Ambulance response time was also found to have a circadian variation.</AbstractText>There is a common circadian variation of out of hospital cardiac arrest, irrespective of underlying aetiology, where the presenting rhythm is other than ventricular fibrillation. This is different from the circadian variation of cases of cardiac aetiology presenting with ventricular fibrillation. The circadian variation of ventricular fibrillation, and consequently survival, may be affected by the availability of bystander cardiopulmonary resuscitation and the speed of ambulance response.</AbstractText> |
4,465 | Initial clinical experience with ambulatory use of an implantable atrial defibrillator for conversion of atrial fibrillation. Metrix Investigators. | A recent study has shown that the implantable atrial defibrillator can restore sinus rhythm in patients with recurrent atrial fibrillation when therapy was delivered under physician observation. The objective of this study was to evaluate the safety and efficacy of ambulatory use of the implantable atrial defibrillator.</AbstractText>An atrial defibrillator was implanted in 105 patients (75 men; mean age, 59+/-12 years) with recurrent, symptomatic, drug-refractory atrial fibrillation. After successful 3-month testing, patients could transition to ambulatory delivery of shock therapy. Patients completed questionnaires regarding shock therapy discomfort and therapy satisfaction using a 10-point visual-analog scale (1 represented "not at all," 10 represented "extremely") after each treated episode of atrial fibrillation. During a mean follow-up of 11.7 months, 48 of 105 patients satisfied criteria for transition and received therapy for 275 episodes of atrial fibrillation. Overall shock therapy efficacy was 90% with 1.6+/-1.2 shocks delivered per episode (median, 1). Patients rated shock discomfort as 5.2+/-2.4 for successful therapy and 4.2+/-2.2 for unsuccessful therapy (P:>0.05). The satisfaction score was higher for successful versus unsuccessful therapy (3.4+/-3. 3 versus 8.7+/-1.3, P:<0.05). There was no ventricular proarrhythmia observed throughout the course of this study.</AbstractText>Ambulatory use of an implantable atrial defibrillator can safely and successfully convert most episodes of atrial fibrillation, often requiring only a single shock. Successful therapy is associated with high satisfaction and only moderate discomfort.</AbstractText> |
4,466 | [Long QT interval and malignant ventricular arrhythmia during treatment with cisapride. Report of a clinical case]. | Cisapride is largely used in the treatment of secondary symptoms due to gastroesophageal reflux, as a prokinetic drug that increases and coordinates gastrointestinal motility and gastroesophageal sphincteric tone. Potential proarrhythmic effects of the drug have been demonstrated in several clinical studies and reported by the drug manufacturers. These effects are increased in the presence of risk factors such as renal insufficiency, electrolytic disorders, coronary artery disease and positive history for arrhythmias including atrial fibrillation and bradyarrhythmia. Therefore in such cases a careful cardiac evaluation, both clinical and electrocardiographic, is recommended. This is still not routinely performed. The following case report shows an example in which diagnosis of increased QT interval due to cisapride was missed. This caused hospitalization for malignant ventricular arrhythmias and recurrent syncope. |
4,467 | [Heart failure with conserved systolic function. Therapeutic potential with beta blocking agents]. | It is increasingly recognized that the syndrome of congestive heart failure may occur in the absence of any abnormality of left ventricular systolic function. In this situation, the clinical picture of heart failure, particularly the presence of symptoms and/or signs of pulmonary congestion, is usually considered a consequence of an abnormal diastolic function of the left ventricle (diastolic heart failure). However, in the individual patient, several other potential causes should be taken into account before attributing to an isolated diastolic dysfunction of the left ventricle the pathogenetic role of clinical presentation. In fact, due to the current lack of validated criteria for diagnosis of diastolic heart failure, it still represents an exclusion diagnosis in the clinical setting. Prevalence of heart failure with preserved left ventricular systolic function is widely variable among the different studies, from 13% to over 70%, with most reports showing a prevalence of 30-40%. These differences depend on several factors, such as the criteria used for diagnosis of heart failure, as well as those used for recognizing a normal systolic function or the clinical setting considered (for example hospital versus community). According to an analysis of the studies published, heart failure with preserved left ventricular systolic function seems to be more common in the female sex and in elderly patients, and it is associated with hypertension and electrocardiographic or echocardiographic evidence of left ventricular hypertrophy. Atrial fibrillation, either paroxysmal or chronic, is common and may represent a precipitating factor of clinical deterioration. According to most studies, patients with preserved left ventricular systolic function show, compared to patients with reduced left ventricular systolic function, a better prognosis, as indicated by a lower mortality and hospital readmission rates. Regarding the therapy of these patients, it is known that there are virtually no well-controlled studies of the effect of pharmacological treatment on outcome. Accordingly, the therapeutic approach of heart failure with preserved systolic function is currently based on a careful pathophysiological interpretation of clinical picture in the individual patient. |
4,468 | [The new German resuscitation guidelines in the context of international recommendations]. | The German Guidelines for Cardiopulmonary Resuscitation were adapted to match the revised International Guidelines. The revised German edition was based both on the guidelines issued by the American Heart Association (AHA) in 1992 and on those of the European Resuscitation Council (ERC) of 1998, as well as on those released by the International Liaison Committee on Resuscitation (ILCOR) in 1997. Due to the diverging instructions for action the emergency physicians felt considerably unsafe as to what they should really do to achieve maximum results. Only 10.3 per cent of the german emergency physicians followed the recommendations given by the German Federal Chamber of Physicians. Innovations in respect of the basic checkup concern the time for controlling the respiration and circulation (ten seconds). Contrary to the international recommendations the "diagnostic block" is performed in Germany without interspersing basic reanimation. In artificial respiration the tidal volume has been reduced to 600 ml in accordance to the ERC and ILCOR guidelines. The search for the pressure point for cardiac pressure massage has also been adapted to the international recommendations. Also in accordance with the international recommendations defibrillation in case of ventricular fibrillation is now being performed only thrice in series without interspersed basic reanimation. There is some uncertainty with regard to choosing the requisite energy: 16.6% of the emergency physicians opt for less than 200 joule in primary defibrillation whereas 13% are in favour of more than 200 joule. Contrary to the international recommendations which prescribe peripheral venous access as application site for reanimation by drugs, the german guidelines favour the endobronchial path, which is already being practised by 57.4% of the emergency physicians. Hence, emergency medication can be effected in Germany 4 minutes earlier than in other countries. After three unsuccessful applications of 1 mg each of adrenalin the dosage is increased to 5 mg, and in agreement with the AHA guidelines escalating doses are also possible. Sodium bicarbonate is recommended only after more than 20 minutes of reanimation and if so, only in a reduced dose of 0.5 mval/kg body weight. In accordance with the international recommendations there is now a universal algorithm that decides on application only between ventricular fibrillation and nonfibrillation. The new german recommendations have adapted the reanimation procedure in agreement with ERC to national usage without abandoning any principles of the international guidelines. |
4,469 | Fatal "crack" cocaine ingestion in an infant. | This report describes a 10-month-old infant girl who died of cocaine poisoning. The infant was found apneic and in ventricular fibrillation after the parents summoned rescue personnel and claimed she had ingested rat poison. The parents later admitted that 2 hours before calling for assistance, the infant's 2-year-old brother was found eating "crack" cocaine and also feeding it to the infant. Investigators found "crack" cocaine throughout the house and in the infant's crib. At autopsy, the infant had two pieces of "crack" cocaine in the duodenum. The brain exhibited a markedly thinned corpus callosum. Toxicologic examination showed high concentrations of cocaine in the blood and in other specimens. The manner of death was classified as homicide because the infant was willfully placed in a hazardous environment with an easily accessible toxic substance, medical attention was deliberately delayed for 2 hours, and medical personnel were deceived when they were falsely told she had ingested rat poison. These features were thought to constitute neglect. The toxicologic characteristics of this case are unique. There are numerous reports of passive cocaine inhalation in infants and children less than 5 years of age, but ingestion of cocaine in this age group has rarely been documented. This age group also has no reported deaths due to cocaine ingestion and no cases of "crack" cocaine ingestion. The high concentrations of cocaine seen in this case, combined with the "crack" cocaine found in the duodenum, indicate ingestion as the route of exposure. The thinned corpus callosum in this case may be a consequence of intrauterine cocaine exposure. |
4,470 | Ionic remodeling in the heart: pathophysiological significance and new therapeutic opportunities for atrial fibrillation. | Heart disease has long been recognized to alter cardiac electrical function. Detailed studies of disease-induced remodeling of ionic transport processes that underlie ventricular electrophysiological alterations have been performed over the past 10 years, but our knowledge of atrial ionic remodeling is more limited and has emerged much more recently. The present review focuses on recent findings regarding ionic remodeling at the atrial level, particularly with respect to two conditions that promote atrial fibrillation (AF) in well-developed clinically relevant animal models: (1) sustained atrial tachycardia and (2) ventricular tachypacing-induced congestive heart failure. Complementary data from experimental models and from observations in atrial tissue samples from patients are examined critically and integrated. Consideration is also given to potential molecular mechanisms underlying remodeling, the relationship between atrial and ventricular ionic remodeling in response to similar stimuli, and the potential relevance of insights into ionic remodeling for understanding the pathophysiology of AF and developing improved therapeutic approaches. |
4,471 | Cardiac rhythm disturbances in the obstructive sleep apnea syndrome: effects of nasal continuous positive airway pressure therapy. | A high incidence of nocturnal cardiac rhythm disturbances among patients with obstructive sleep apnea (OSA) syndrome has been described in some reports, but not in others. We wished to examine the prevalence of significant cardiac rhythm disturbance in patients with established moderate to severe OSA syndrome and, in particular, to assess the impact of nasal continuous positive airway pressure (nCPAP) therapy.</AbstractText>A prospective study of consecutive eligible patients in a dedicated sleep disorders unit of a university teaching hospital.</AbstractText>Holter monitoring was performed for 18 h in 45 patients with previously diagnosed OSA syndrome (mean [SD] apnea/hypopnea frequency [AHI] of 50 [23]/h) and repeated within 2 to 3 days after institution of nCPAP therapy. Investigators were blinded to the patients' treatments during data analysis. Thirty-five patients were found to have some cardiac rhythm disturbance, but only 8 had pathologically significant disturbances (ventricular tachycardia or fibrillation, complex ventricular ectopy, new-onset supraventricular tachycardia other than sinus tachycardia, pauses of > 2 s, and second- or third-degree heart block). Significant rhythm disturbances occurred only during the nighttime, and there was a significant correlation between OSA severity and the severity of rhythm disturbance (p = 0.04, r = 0.301). No significant correlation was found between OSA severity and any other anthropometric parameter measured. nCPAP therapy resulted in abolition of rhythm disturbance in seven of these eight patients; the eighth patient was found to have coexisting severe aortic valve disease requiring valve replacement.</AbstractText>The data indicate that OSA syndrome predisposes to clinically significant cardiac rhythm disturbances that can be successfully controlled by nCPAP therapy.</AbstractText> |
4,472 | Monophasic versus biphasic transthoracic countershock after prolonged ventricular fibrillation in a swine model. | We sought to compare the defibrillation efficacy of a low-energy biphasic truncated exponential (BTE) waveform and a conventional higher-energy monophasic truncated exponential (MTE) waveform after prolonged ventricular fibrillation (VF).</AbstractText>Low energy biphasic countershocks have been shown to be effective after brief episodes of VF (15 to 30 s) and to produce few postshock electrocardiogram abnormalities.</AbstractText>Swine were randomized to MTE (n = 18) or BTE (n = 20) after 5 min of VF. The first MTE shock dose was 200 J, and first BTE dose 150 J. If required, up to two additional shocks were administered (300, 360 J MTE; 150, 150 J BTE). If VF persisted manual cardiopulmonary resuscitation (CPR) was begun, and shocks were administered until VF was terminated. Successful defibrillation was defined as termination of VF regardless of postshock rhythm. If countershock terminated VF but was followed by a nonperfusing rhythm, CPR was performed until a perfusing rhythm developed. Arterial pressure, left ventricular (LV) pressure, first derivative of LV pressure and cardiac output were measured at intervals for 60 min postresuscitation.</AbstractText>The odds ratio of first-shock success with BTE versus MTE was 0.67 (p = 0.55). The rate of termination of VF with the second or third shocks was similar between groups, as was the incidence of postshock pulseless electrical activity (15/18 MTE, 18/20 BTE) and CPR time for those animals that were resuscitated. Hemodynamic variables were not significantly different between groups at 15, 30 and 60 min after resuscitation.</AbstractText>Monophasic and biphasic waveforms were equally effective in terminating prolonged VF with the first shock, and there was no apparent clinical disadvantage of subsequent low-energy biphasic shocks compared with progressive energy monophasic shocks. Lower-energy shocks were not associated with less postresuscitation myocardial dysfunction.</AbstractText> |
4,473 | Lipid lowering drugs and recurrences of life-threatening ventricular arrhythmias in high-risk patients. | To evaluate a possible effect of lipid lowering drugs on recurrences of ventricular arrhythmias (VA) after implantable cardioverter defibrillator (ICD) implantation.</AbstractText>In patients with coronary artery disease (CAD), lipid lowering drugs reduce total and sudden cardiac death. Because the mechanism is not completely understood, we studied whether these drugs have a favorable influence on the occurrence of life-threatening VA in patients with CAD and ICD implants.</AbstractText>We conducted an observational study in 78 patients with CAD and life-threatening VA, treated with an ICD. After ICD implantation, 27 patients were on treatment with lipid lowering drugs (group I) and 51 were not (group II). Patients were studied for the following end points: recurrences of VA requiring ICD intervention, cardiac death and hospitalization.</AbstractText>After a mean follow-up of 490 +/- 319 days, 35 patients (45%) had recurrences of VA requiring ICD intervention. In multivariate analysis, the use of lipid lowering drugs (chi-square 6.33, p = 0.012) and poorly tolerated sustained monomorphic ventricular tachycardia as initial presentation (chi-square 4.84, p = 0.028) remained as independent predictors of recurrences of VA. Patients in groups I and II had similar baseline clinical characteristics, but patients in group I had a lower incidence of recurrences of VA (6/27 or 22% vs. 29/51 or 57%, p = 0.004) and of the combined end points of cardiac death and hospitalization (4/27 or 15% vs. 23/51 or 45%, p = 0.015) compared with patients in group II.</AbstractText>This is the first observation that the use of lipid lowering drugs is associated with a reduction of recurrences of VA in patients with CAD and ICD implants. These data require confirmation in a prospective randomized trial.</AbstractText> |
4,474 | A case of sinus pause due to the proarrhythmia of pilsicainide. | A 74-year-old man received oral administration of pilsicainide, a pure sodium channel blocker with slow recovery kinetics, to convert paroxysmal atrial fibrillation to sinus rhythm and developed loss of consciousness two days later. The ECG monitoring revealed sinus pause with markedly prolonged PQ interval and QRS width. Two days after the drug was discontinued, the duration of the QRS complex was normalized. This drug is rapidly absorbed from the gastrointestinal tract, most of which is excreted from the kidney. The plasma concentration of pilsicainide, although not measured, must have been very high, since his renal function was impaired. When pilsicainide is prescribed in patients with coronary artery disease or renal dysfunction, close attention must be paid to avoid life-threatening arrhythmias due to high plasma concentrations of the drug. This is an interesting case because the proarrhthmia of the drug was not tachyarrhythmia, such as ventricular tachycardia or torsades de pointes, but sinus pause. |
4,475 | Unsolved problems in diastole. | It is now recognized that a sizable portion of patients who exhibit symptoms of congestive heart failure have relatively well-preserved systolic function, but have significantly elevated LV filling pressures. This syndrome, termed "diastolic heart failure," is associated with various conditions such as aging, anatomic abnormalities, hypertension, ischemic disease, tachycardia, and atrial fibrillation. Advances in the proper medical and surgical management of these patients will depend on the continued delineation of the basic physiologic mechanisms that account for normal and pathologic cardiac diastolic function. This goal can only be achieved by the integration of information acquired from basic science investigations conducted in vitro and in vivo, mathematic modeling simulation studies, and prospective, community-based investigations that characterize the incidence, prevalence, and natural history of the disease. In addition, randomized clinical trials will be needed to determine the optimal treatment strategies for this group of patients--strategy choices undoubtably complicated by a disease whose treatment is influenced to a large extent by its origin. The future therapies evaluated in these randomized clinical trials will most likely range from medical therapies that target either the heart directly or the peripheral vascular system, to surgical interventions such as direct myocardial revascularization, to gene therapy. Finally, it is worth mentioning one more unresolved issue that is of general practical concern not only to the physiologist studying diastolic function, but also to the clinician: whether or not it is even feasible to develop a single, sensitive, specific, clinically relevant index of diastolic function that is free from the contaminating influences of rate, contractility, and load. As observed by Glantz 20 years ago, developing indexes with the hope that one might fully delineate the left ventricle's diastolic properties, rather than concentrating on discovering the physiologic significance of such indexes, is probably counterproductive. More recently, in a related article, Slinker implied that an operational definition of any aspect of cardiac function must allow for the measurement of that function over an adequate range of essential variables. Therefore, as previously mentioned, the physiologist studying cardiac function has the daunting task of trying to understand, in a precise way, how the processes and mechanisms of the various phases of the cardiac cycle couple together to produce either a normal or abnormal functioning heart. It seems clear that because of the complex weave of factors that control overall cardiac diastolic function, the derivation of any single index that adequately describes LV diastolic function in vivo may not be possible. |
4,476 | Predictive value of clinical and electrophysiological variables in patients with chronic chagasic cardiomyopathy and nonsustained ventricular tachycardia. | Risk stratification of patients with nonsustained ventricular tachycardia (NSVT) and chronic chagasic cardiomyopathy (CCC).</AbstractText>Seventy eight patients with CCC and NSVT were consecutively and prospectively studied. All patients underwent to 24-hour Holter monitoring, radioisotopic ventriculography, left ventricular angiography, and electrophysiologic study. With programmed ventricular stimulation.</AbstractText>Sustained monomorphic ventricular tachycardia (SMVT) was induced in 25 patients (32%), NSVT in 20 (25.6%) and ventricular fibrillation in 4 (5.1%). In 29 patients (37.2%) no arrhythmia was inducible. During a 55. 7-month-follow-up, 22 (28.2%) patients died, 16 due to sudden death, 2 due to nonsudden cardiac death and 4 due to noncardiac death. Logistic regression analysis showed that induction was the independent and main variable that predicted the occurrence of subsequent events and cardiac death (probability of 2.56 and 2.17, respectively). The Mantel-Haenszel chi-square test showed that survival probability was significantly lower in the inducible group than in the noninducible group. The percentage of patients free of events was significantly higher in the noninducible group.</AbstractText>Induction of SMVT during programmed ventricular stimulation was a predictor of arrhythmia occurrence cardiac death and general mortality in patients with CCC and NSVT.</AbstractText> |
4,477 | Anisotropic effects of sodium channel blockers on the wavelength for ventricular excitation in dogs. | The purpose of this study was to determine the anisotropic effects of sodium channel blockers on wavelength (WL) and proarrhythmia. In 18 anesthetized, open chest dogs, a 64-electrode array was placed on the left ventricle and the ventricle was constantly paced. Disopyramide, lidocaine or flecainide was intracoronarily administered. Conduction velocity (theta) and activation-recovery interval (ARI) were measured in the longitudinal (L) and transverse (T) directions. Flecainide markedly decreased thetaL, but did not alter thetaT or ARIs in either direction. As a result, the wavelength was significantly shortened only in the L direction. Disopyramide or lidocaine did not show direction-dependent effects on theta or WL. In 3 of 6 dogs with flecainide exposure, ventricular fibrillation (VF) developed. However, no VF occurred with disopyramide or lidocaine. Accordingly, the WL is dependent on the fiber orientation of myocardium. The anisotropic shortening of the WL may explain the character of the proarrhythmia observed with flecainide. |
4,478 | Propafenone-induced ataxia: report of three cases. | Propafenone is an effective antiarrhythmic drug used widely for the treatment of supraventricular and ventricular arrhythmias. Although it is generally well tolerated, 30 to 45% of patients may experience adverse cardiac effects. In 15 to 20% of patients, adverse effects may involve other organ systems. A wide variety of adverse central nervous system effects have been reported in association with propafenone; dizziness is the most common. Ataxia caused by propafenone has been reported to the pharmaceutical companies and drug monitoring agencies, but has not been well described or emphasized in the medical literature. We describe 3 elderly patients with moderate to severe ataxia that occurred while they were taking propafenone. |
4,479 | [Anticoagulant treatment in pericardial effusion--a therapeutic dilemma]. | Anticoagulant treatment for acute myocardial infarction (AMI) and pericardial effusion is controversial, since the treatment might cause hemopericardium and tamponade. On the other hand, anticoagulants are strongly indicated in many situations in AMI, including: left ventricular thrombus, unstable angina, severe heart failure, deep vein thrombophlebitis, pulmonary embolism, atrial fibrillation, as part of thrombolytic treatment, and during cardiac catheterization. We describe a 70-year-old man who presented with both pericardial effusion and a left ventricular thrombus 3 weeks after an extensive, anterior wall AMI. Anticoagulants and corticosteroids were administered simultaneously under hemodynamic and echocardiographic monitoring without complications. It is our impression that anticoagulant treatment is safe in patients with pericardial effusion. |
4,480 | [Thrombolytic therapy or primary coronary angioplasty in acute myocardial infarction? Israel Thrombolytic Survey Group]. | There has been continuous debate over the superiority of primary percutaneous, transluminal, coronary angioplasty (PTCA) over thrombolysis for acute myocardial infarction (AMI). It was questioned whether this advantage of primary PTCA reported in selected populations by experienced centers can be replicated in our clinical practice. We compared demographic and clinical variables, therapies and outcome in AMI treated with primary PTCA vs thrombolytic therapy. Clinical and demographic variables of 1,678 unselected AMI patients (admitted January/February and May/July 1996) were analyzed in 16 cardiac care units with on-site catheterization facilities and ability to perform PTCA. Of these 803 (48%) were treated by thrombolysis and 99 (6%) by primary PTCA. The prevalence of adverse prognostic variables, such as anterior wall MI, heart failure on admission or during hospital stay, pulmonary edema, and ventricular tachycardia or fibrillation, was higher in the PTCA group. The 7-day, 30-day and 1-year mortality rates were similar in the 2 groups: 4%, 7.2% and 12.8%, respectively, in the PTCA group and 5%, 7.2% and 11.1% in the thrombolysis group. There was a trend toward lower mortality in subgroups of high-risk patients: those with heart failure on admission (Killip class > 1), the elderly (> 65 years), and those with previous MI treated with PTCA. After adjusting for confounders, treatment with primary PTCA was not found to be associated with lower mortality. Only a small proportion of AMI patients in Israel were treated with primary PTCA in 1996. The frequency of adverse prognostic factors among them was higher but their short and long term outcomes were similar to those of high risk patients treated with thrombolysis. |
4,481 | Role of transthoracic echocardiography in atrial fibrillation. | Atrial fibrillation is a major clinical problem that is predicted to be encountered more frequently as the population ages. The clinical management of atrial fibrillation has become increasingly complex as new therapies and strategies have become available for ventricular rate control, conversion to sinus rhythm, maintenance of sinus rhythm, and prevention of thromboembolism. Clinical and transthoracic echocardiographic features are important in determining etiology and directing therapy for atrial fibrillation. Left atrial size, left ventricular wall thickness, and left ventricular function have independent predictive value for determining the risk of developing atrial fibrillation. Left atrial size may have predictive value in determining the success of cardioversion and maintaining sinus rhythm in selected clinical settings but has less value in the most frequently encountered group, patients with nonvalvular atrial fibrillation, in whom the duration of atrial fibrillation is the most important feature. When selecting pharmacological agents to control ventricular rate, convert to sinus rhythm, and maintain normal sinus rhythm, transthoracic echocardiography (TTE) allows noninvasive evaluation of left ventricular function and hence guides management. The combination of clinical and transthoracic echocardiographic features also allows risk stratification for thromboembolism and hemorrhagic complications in atrial fibrillation. High-risk clinical features for thromboembolism supported by epidemiological observations, results of randomized clinical trials, and meta-analyses include rheumatic valvular heart disease, prior thromboembolism, congestive heart failure, hypertension, older (> 75 years old) women, and diabetes. Small series of cases also suggest those with hyperthyroidism and hypertrophic cardiomyopathy are at high risk. TTE plays a unique role in confirming or discovering high-risk features such as rheumatic valvular disease, hypertrophic cardiomyopathy, and decreased left ventricular function. Validation of the risk stratification scheme used in the Stroke Prevention in Atrial Fibrillation-III trial is welcomed by clinicians who are faced daily with balancing the benefit and risks of anticoagulation to prevent thromboembolism in patients with atrial fibrillation. |
4,482 | Peculiarities of ischemic cardiac arrhythmias in cats against the background of stimulation of sensorimotor cortex and administration of selective opiate receptor agonists. | In acute experiments on Nembutal-anesthetized cats, the effect of opiate receptor agonists DAGO, DSLET, and dinorphin A(1-13) on the incidence of idioventricular rhythm disturbances, including ventricular tachycardia and fibrillation, was studied under conditions of occlusion of circumflex branch of the left coronary artery and stimulation of the sensorimotor cortex. The most pronounced effects were observed with DSLET and dinorphin A(1-13). These preparations completely prevented ventricular fibrillation. DAGO produced a less pronounced protective effect probably because of parallel increase in plasma catecholamine concentration. |
4,483 | Clinical overview of antihypertensive classes--clinically relevant differences: myths or facts? Based on a presentation by Alan H. Gradman, MD. | The goals of antihypertensive therapy are to lower blood pressure and prevent end-organ damage without side effects, which affect quality of life. The antihypertensive drugs, regardless of class, all lower blood pressure, but they vary in their mechanisms of action, side-effect profiles, suitability for patients with other comorbid conditions, and ability to protect against the long-term sequelae of hypertension. The Sixth Report of the Joint National Committee on Prevention, Evaluation, and Treatment of High Blood Pressure (JNC-VI) recommends diuretics and beta-blockers as first-line therapy for uncomplicated hypertension, with diuretics also being strongly preferred for patients with isolated systolic hypertension or hypertension and heart failure and beta-blockers being strongly preferred for patients who have had a myocardial infarction (MI) and those with hypertension and angina, atrial tachycardia, or atrial fibrillation. Because angiotensin-converting enzyme (ACE) inhibitors have been shown to be cardioprotective and renoprotective in patients with diabetes or impaired left ventricular (LV) function, the JNC-VI recommends them as first-line therapy in patients with diabetes with proteinuria, heart failure, and MI complicated by LV dysfunction. It recommends calcium channel blockers for hypertensive patients with angina, long-acting dihydropyridines for those with isolated systolic hypertension, and the nondihydropyridines for those with atrial tachycardia or fibrillation, diabetes, and proteinuria. The angiotensin II receptor blockers (ARBs) share many of the organ-protective effects of ACE inhibitors when studied in animal models. They are effective in lowering blood pressure and have a very benign side-effect profile; however, these agents have not been available long enough to ascertain their efficacy in protecting against long-term complications. |
4,484 | Acute diabetes modulates response to ischemia in isolated rat heart. | Diabetic hearts are suggested to exhibit either increased or lower sensitivity to ischemia. Detrimental effects of prolonged ischemia can be attenuated by preconditioning, however, relatively little is known about its effects in the diseased myocardium. This study was designed to test the susceptibility to ischemia-induced arrhythmias and the effect of preconditioning in the diabetic heart. Rats were made diabetic with streptozotocin (45 mg/kg, i.v.). After 1 week, isolated Langendorff-perfused hearts were subjected to 30 min occlusion of LAD coronary artery without or with preceding preconditioning induced by one cycle of 5 min ischemia and 10 min reperfusion. Glycogen and lactate contents were estimated in the preconditioned and non-preconditioned hearts before and after ischemia. Diabetic hearts were more resistant to ischemia-induced arrhythmias: incidence of ventricular tachycardia (VT) decreased to 42% and only transient ventricular fibrillation (VF) occurred in 17% of the hearts as compared to the non-diabetic controls (VT 100% and VF 70% including sustained VF 36%; p < 0.05). Preconditioning effectively suppressed the incidence and severity of arrhythmias (VT 33%, VF 0%) in the normal hearts. However, this intervention did not confer any additional protection in the diabetic hearts. Despite higher glycogen content in the diabetic myocardium and greater glycogenolysis during ischemia, production of lactate in these hearts was significantly lower than in the controls. Preconditioning caused a substantial decrease in the accumulation of lactate in the normal hearts, whereby in the diabetic hearts, this intervention did not cause any further reduction in the level of lactate. In conclusion, diabetic rat hearts exhibit lower susceptibility to ischemic injury and show no additional response to preconditioning. Reduced production of glycolytic metabolites during ischemia can account for the enhanced resistance of diabetic hearts to ischemia as well as for the lack of further protection by preconditioning. |
4,485 | Pharmacokinetics of landiolol hydrochloride, a new ultra-short-acting beta-blocker, in patients with cardiac arrhythmias. | To elucidate pharmacokinetics and pharmacodynamics of landiolol hydrochloride, newer developed ultra-short-acting beta-blocker, in patients with various cardiac tachyarrhythmias.</AbstractText>The short duration of action and titratability of landiolol hydrochloride make it ideal for use in patients with a clinical need for beta-blockers.</AbstractText>In a total of 31 examinations we infused the drug in 19 patients (mean age, 55 +/- 14 years). After the persistence of the tachyarrhythmias was confirmed, continuous infusion was started at rates of 0.005, 0.01, 0.02, 0.04, and 0.08 mg/kg/min for 5 minutes (for paroxysmal atrial fibrillation, paroxysmal supraventricular tachycardia, and ventricular tachycardia) or 15 minutes (for ventricular premature complex). We analyzed the pharmacokinetics of 16 examinations. A one-compartment model provided a close fit for each blood concentration-time curve.</AbstractText>The maximum blood concentrations obtained clearly showed the dose dependency and revealed very short half-lives (range, 2.3 to 4.0 minutes). Area under the blood concentration-time curves also increased, showing dose dependency. In paroxysmal atrial fibrillation, landiolol hydrochloride reduced the heart rate from 111 +/- 20 to 90 +/- 10/min. Sinus rhythm was restored, without any adverse effects, in three of five patients with paroxysmal supraventricular tachycardia and one patient with ventricular tachycardia. There was no significant change in peripheral blood pressure.</AbstractText>Landiolol hydrochloride has a shorter elimination half-life than any other beta-blocker, and it can be administered safely to patients with various tachyarrhythmias.</AbstractText> |
4,486 | Effects of amphetamine on calcium and potassium currents in rat heart. | We used the patch-clamp technique to study the effects of amphetamine on the membrane currents responsible for rat cardiac action-potential duration. Amphetamine has no effect on the slow inward Ca2+ current (I(Ca)-L), the inwardly rectifying K+ current (I(K1) and the outward K+ delayed rectifier (I(K)) and sustained (I(SS)) currents. Amphetamine blocks the transient outward K+ current (I(to)) both in the open and in the rested state. The transient outward K+ current is largely responsible for action-potential repolarization and for the regional differences in action-potential duration in rat ventricle. Therefore, the reduction of the transient outward K+ current (I(to)) caused by amphetamine may facilitate the appearance of ventricular tachycardia and fibrillation, a reported cause of death in amphetamine users. |
4,487 | [Electrophysiological remodeling induced by atrial fibrillation. An experimental curiosity or major factor in atrial fibrillation in man?]. | Atrial fibrillation usually progresses from a paroxysmal to a permanent arrhythmia, even in the absence of underlying cardiac disease. The treatment is more difficult when the arrhythmia is chronic. This progression may be explained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural changes of the atrial tissues (remodelling) which promote the perpetuation of the arrhythmia and which make treatment less effective. Although the electrophysiological changes predisposing to atrial fibrillation have been known for over 15 years, it was only in 1995 that experimental studies showed the presence of atrial electrophysiological remodelling induced by the arrhythmia. This process of long term adaptation of the atrial myocytes to the tachycardia comprises marked changes of the parameters which sustain the arrhythmia: changes in refractory period (decreased duration, inadaptation to the heart rate, increased dispersion), reduced conduction speed and sinus dysfunction. Atrial remodelling also affects the contractile function by the structural changes. The calcium currents play a major role in its development. This mechanism has not yet been completely defined in the clinical setting and its importance in sustaining the arrhythmia has not been clearly evaluated. Atrial fibrillation remains one of the most difficult arrhythmias to treat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia with progression to chronicity and structural changes responsible for the degradation of atrial contractility. |
4,488 | Atrial high energy phosphate content and mitochondrial enzyme activity during chronic atrial fibrillation. | Prolonged atrial fibrillation (AF) results in (ultra)structural remodelling of atrial cardiomyocytes resembling alterations seen in ischemia-induced ventricular hibernation. The mechanisms underlying these changes are incompletely understood. In the present study we explored the hypothesis that a profound imbalance in energy status during chronic AF acts as a stimulus for structural remodelling.</AbstractText>The content of high energy-phosphates and related compounds together with a selected number of mitochondrial enzymes, known to be altered under ischemic conditions, were determined in tissue samples taken from atria of goats in sinus rhythm (SR) and after 1, 2, 4, 8 and 16 weeks of AF maintained by burst pacing. Atrial remodelling was quantified by counting the percentage of cells with >10% myolysis. During AF structural remodelling developed progressively, after 8 weeks about 40% of the atrial myocytes were affected. The concentration of adenine nucleotides and their degradation products did not change significantly during AF. Also the activity of mitochondrial cytochrome c oxidase activity was similar during AF and SR. Mitochondrial NADH-oxidase and proton-translocating ATPase activities were not induced by AF. The tissue content of phosphocreatine decreased during the first week by 60%, but completely recovered between 8 and 16 weeks of AF.</AbstractText>The analysis of adenine nucleotides during AF provided no indication for the development of severe atrial ischemia. This notion is supported by enzyme cytochemical findings. However, AF-induced atrial remodelling was associated with a transient lowering of phosphocreatine content, suggesting an increase in energy demand during the early phase of AF. The subsequent recovery of the phosphocreatine pool indicates restoration of the balance between energy demand and supply in chronically fibrillating atria.</AbstractText> |
4,489 | Prevention of ventricular fibrillation by pacing in a man with Brugada syndrome. | The unique ECG appearance of Brugada syndrome is caused by failure of the dome of the action potential to develop. It occurs when the outward currents (mainly Ito) overwhelm the inward currents (mainly Ica) at the end of phase 1 of the action potential. Because Ito becomes less prominent at a faster rate, increased heart rate is associated with decreased ST segment elevation on ECG and probably decreased incidence of ventricular arrhythmia. We present the first report on prevention of ventricular fibrillation in a man with Brugada syndrome by overdrive pacing from his dual chamber implantable cardioverter defibrillator. |
4,490 | New approach to biphasic waveforms for internal defibrillation: fully discharging capacitors. | The use of two independent, fully discharging capacitors for each phase of a biphasic defibrillation waveform may lead to the design of a simpler, smaller, internal defibrillator. The goal of this study was to determine the optimal combination of capacitor sizes for such a waveform.</AbstractText>Eight full-discharge (95/95% tilt), biphasic waveforms produced by several combinations of phase-1 capacitors (30, 60, and 90 microF) and phase-2 capacitors (1/3, 2/3, and 1.0 times the phase-1 capacitor) were tested and compared to a single-capacitor waveform (120 microF, 65/65% tilt) in a pig ventricular fibrillation model (n = 12, 23+/-2 kg). In the full-discharge waveforms, phase-2 peak voltage was equal to phase-1 peak voltage. Shocks were delivered between a right ventricular lead and a left pectoral can electrode. E50s and V50s were determined using a ten-step Bayesian process. Full-discharge waveforms with phase-2 capacitors of < or =40 microF had the same E50 (6.7+/-1.7 J to 7.3+/-3.9 J) as the single-capacitor truncated waveform (7.3+/-3.7 J), whereas waveforms with phase-2 capacitors of > or =60 microF had an extremely high E50 (14.5+/-10.8 J or greater, P < 0.05). Moreover, of the former set of energy-efficient waveforms, those with phase-1 capacitors of > or =60 microF additionally exhibited V50s that were equivalent to the V50 of the single-capacitor waveform (344+/-65 V to 407+/-50 V vs 339+/-83 V).</AbstractText>Defibrillation efficacy can be maintained in a full-discharge, two-capacitor waveform with the proper choice of capacitors.</AbstractText> |
4,491 | Marked reduction of ventricular defibrillation threshold by application of an auxiliary shock to a catheter electrode in the left posterior coronary vein of dogs. | For endocardial shocks near the defibrillation threshold (DFT), postshock activity originates from the lateral left ventricular apex, where the shock field is weak. This study tested the hypothesis that an auxiliary shock (AS) delivered between an electrode at this site and a superior vena cava (SVC) electrode before the primary endocardial shock (PS) would reduce the DFT.</AbstractText>In six pentobarbital-anesthetized dogs (26 to 36 kg), catheter electrodes were placed in the right ventricular (RV) apex and the SVC. To simulate transvenous introduction, a small electrode was inserted into the posterior cardiac vein using an epicardial approach. For dual shock treatments, AS (2-msec monophasic) was applied to the coronary vein electrode at different time intervals before a biphasic PS (4 msec/3 msec) to the RV-SVC electrodes. The mean DFT energy for dual shocks treatments were significantly reduced (P < 0.05) in comparison to the control treatment (no AS, 26.5+/-8.8 J). Mean DFT energy after 10 seconds of electrically induced ventricular fibrillation for dual shocks, in which AS and PS were separated by 1, 5, 10, and 20 msec, were 10.2+/-4.1 J, 10.9+/-5.5 J, 11.3+/-6.3 J, and 15.4+/-7.2 J, respectively. These values were all significantly lower than the PS alone (26.5+/-8.8 J).</AbstractText>Addition of an AS from the posterior cardiac vein before an endocardial PS reduces DFT energy by more than 50%. Such DFT reduction could improve therapeutic safety margin or permit reduction in volume of implantable cardioverter defibrillators.</AbstractText> |
4,492 | Clinical characteristics of patients with spontaneous or inducible ventricular fibrillation without apparent heart disease presenting with J wave and ST segment elevation in inferior leads. | The clinical characteristics of three patients with spontaneous or inducible ventricular fibrillation (VF) without apparent heart disease, who presented with J wave and ST segment elevation in inferior leads, are described.</AbstractText>All patients were male and experienced syncope. Their symptoms occurred at night or early in the morning. Holter ECG revealed infrequent premature ventricular complexes. Injection with disopyramide 2 mg/kg augmented ST segment elevation.</AbstractText>These characteristics were very similar to those of patients with Brugada syndrome. These three patients with these specific features might have a variant of Brugada syndrome.</AbstractText> |
4,493 | Amrinone preconditioning in the isolated perfused rabbit heart. | Ischemic preconditioning (IPC) reduces infarct size in experimental preparations. IPC, however, is not without detrimental effects. We studied amrinone as a possible alternative to IPC.</AbstractText>Isolated perfused rabbit hearts were given a 5-minute infusion of 10 micromol/L amrinone followed by a 5-minute washout (n = 6). The anterior descending artery was then occluded for 1 hour and reperfused for 1 hour. Six hearts underwent IPC, with two episodes of 5-minute global ischemia followed by 5-minute reperfusion before LAD occlusion; eight control hearts received no preconditioning. Left ventricular pressure and ischemic zone epicardial monophasic action potentials were continuously monitored.</AbstractText>IPC but not amrinone reduced peak pressure before anterior descending artery occlusion. Peak pressure fell significantly during ischemia and reperfusion in all hearts. End diastolic pressure rose significantly during reperfusion in control and IPC hearts but not in amrinone hearts. Action potentials shortened during ischemia in all hearts. They returned to preocclusion values in control hearts but lasted beyond preocclusion values in IPC and amrinone hearts. Both the incidences of ventricular fibrillation and infarct size were significantly reduced in amrinone hearts but not in IPC hearts.</AbstractText>Amrinone is not only a useful inotropic agent but is also a superior preconditioning agent when compared to IPC.</AbstractText> |
4,494 | Pharmacological preconditioning with the adenosine triphosphate-sensitive potassium channel opener pinacidil. | Ischemic preconditioning (IPC) decreases infarct size after global or regional ischemia. Potassium channel openers also precondition but are subject to dose-limiting vasodilation. We compared the mechanical and electrophysiological effects of ischemic and pharmacological preconditioning in an isolated rabbit heart model.</AbstractText>Rabbit hearts were preconditioned with either 10 micromol/L pinacidil alone (P-), 10 micromol/L pinacidil with 10 micromol/L phenylephrine (P+), or two cycles of global ischemia and reperfusion (IPC) before 1 hour of LAD occlusion. Left ventricular pressure, epicardial monophasic action potential duration (APD) and coronary flow were monitored throughout. Infarct size was determined at the end of reperfusion.</AbstractText>Regional ischemia uniformly decreased APD (p<0.05). During reperfusion, APDs were prolonged beyond preischemic values in all preconditioned groups (p<0.05). P- and P+ reduced the incidence of fibrillation. P- significantly increased coronary flow (+15%, p = 0.001), whereas IPC and P+ did not. However, IPC and P- significantly decreased systolic function (p<0.05) but P+ did not. In addition, IPC depressed diastolic function (p<0.05) but P- and P+ did not. Infarct size was reduced by all methods (p<0.05).</AbstractText>Pinacidil presents a safe and effective alternative to IPC for preserving the heart during regional ischemia. Its coronary vasodilatory effects are safely and effectively reversed by the addition of phenylephrine.</AbstractText> |
4,495 | Intercalated clear cells or pale cells in the sinus node of canine hearts? An ultrastructural study. | Two types of sinus nodal cells were responsible for the main differences in the literature concerning the ultrastructure of the sinuatrial node: the intercalated clear cells and pale cells. Canine hearts were arrested by (1) aortic cross clamping, (2) coronary perfusion with the cardioplegic solution St. Thomas, and (3) coronary perfusion with the cardioplegic solution HTK (Custodiol(R)). After fixation by immersion or perfusion the sinus node tissue was prepared for electron microscopy. Following cardioplegic arrest and perfusion fixation, three nodal cell types in the non-ischemic sinuatrial node were observed: typical nodal cells, transitional cells, and intercalated clear cells. Less than 1% of the non-ischemic sinuatrial cells were intercalated clear cells, surrounded by typical nodal cells or transitional cells. The contractile apparatus of the intercalated clear cells was extremely poorly developed. Great structural variations in the mitochondria were observed in intercalated clear cells, variations that would not appear under conditions of ischemia. In contrast, after 15-25 min of ischemia at 25 degrees C the appearance of the sinus nodal cells was strikingly different from that of the non-ischemic sinuatrial cells. More than 10% of the nodal cells showed typical ischemic alterations, e.g., mitochondrial swelling, clumping of nuclear chromatin, loss of glycogen particles, and cell swelling in varying degrees. Because they look very pale, these nodal cells have been described as pale cells in the literature. Intercalated clear cells appear mainly in non-ischemic nodal tissue. Pale cells are ischemically damaged sinus nodal cells. |
4,496 | Safety of intracoronary Doppler flow measurement. | With the introduction of Doppler-tipped guide wires, intracoronary Doppler flow measurement has been increasingly accepted as an additional diagnostic approach in the catheterization laboratory. However, the safety of intracoronary Doppler flow measurement has not been well-investigated. The purpose of our study was to evaluate the safety of intracoronary Doppler flow measurement using the Doppler FloWire (Cardiometrics, Mountain View, Calif).</AbstractText>A total of 906 patients were examined by intracoronary Doppler with a 0.014-inch or an 0.018-inch Doppler FloWire. For coronary flow reserve measurement, intracoronary injection of adenosine or papaverine was used. Of the patients studied, 77 were cardiac transplant recipients and 829 were patients who had not received a transplant, of whom 617 had undergone diagnostic coronary procedures and 212 had coronary interventions. In 27 (2.98%) of 906 patients adverse cardiac events were observed. Fifteen (1.66%) of 906 patients had severe transient bradycardia develop (asystole or second- to third-degree atrioventricular block) after intracoronary administration of adenosine, 14 of which occurred in the right coronary artery and 1 in the left anterior descending artery. Nine (0.99%) of 906 patients had coronary spasm during the passage of the Doppler wire (5 in the right coronary artery, 4 in the left anterior descending artery). Two (0.22%) of 906 patients had ventricular fibrillation during the procedure. Hypotension with bradycardia and ventricular extrasystole each occurred in 1 (0.11%) of 906 patients. The incidence of complication was significantly higher in transplant recipients than in patients who underwent either diagnostic or interventional procedures (12.99% vs 2.43% vs 0.94%, P <.001). The Doppler measurements in the right coronary artery were associated with a higher incidence of complications, especially bradycardia, compared with the left anterior descending and the left circumflex arteries (right coronary, 5.87% vs left anterior descending, 1.05% vs left circumflex, 0.17%; P <.001). All complications were cured medically.</AbstractText>Intracoronary Doppler flow measurement with Doppler wires and intracoronary administration of adenosine is a safe method. However, severe complications such as bradycardia and coronary spasm can occur. Attention should be paid to the examination of the right coronary artery, especially in heart transplant recipients.</AbstractText> |
4,497 | Decreasing the number of leads required for an implantable atrial defibrillator: use of a new 2-lead system. | The purpose of this study was to evaluate the use of a new 2-lead system for detection of atrial fibrillation (AF) and atrial defibrillation.</AbstractText>In 16 patients undergoing elective cardioversion of AF, a 2-lead system was compared with the conventional 3-lead system in a randomized trial. The new 2-lead system consisted of a catheter with a distal bipolar right ventricular electrode pair and a proximal right atrial shock electrode coil and a separate decapolar defibrillation catheter in the coronary sinus. For the 3-lead system, an additional decapolar catheter was placed in the right atrium. AF and sinus rhythm signal amplitude detection and atrial defibrillation threshold (ADFT) were compared in each patient with both systems.</AbstractText>Successful defibrillation was obtained in all patients. ADFT for the 2-lead system was significantly higher compared with the 3-lead system (370 +/- 112 vs 316 +/- 100 V, P < .05; 9.3 +/- 5.2 vs 6.8 +/- 4.2 J, P < .05). In contrast, there was an increase in impedance for the 3-lead system (77 +/- 16 ohms vs 68 +/- 13 ohms; P < .05). AF had a lower signal amplitude compared with sinus rhythm for both systems (P < .05), and the 2-lead system had a lower signal amplitude compared with the 3-lead system for both rhythms (P < .05).</AbstractText>The use of a 2-lead system with this configuration is not superior to the 3-lead system regarding AF signal amplitude detection and ADFT. Further study is needed with implantable-quality leads in place of the temporary catheters used in this study.</AbstractText> |
4,498 | Myocardial effects of repeated electrical defibrillations in the isolated fibrillating rat heart. | Although substantial myocardial cell injury has been reported after high-energy electrical defibrillation, only minimal injury with transient functional defects seems to develop at energy levels not exceeding those required to reverse ventricular fibrillation. Because multiple electrical shocks are often delivered in clinical settings during attempts to reverse ventricular fibrillation, we investigated the effects of repetitive shocks on postresuscitation myocardial dysfunction by using an isolated rat heart model of ventricular fibrillation.</AbstractText>Prospective and randomized.</AbstractText>Cardiopulmonary resuscitation research laboratory.</AbstractText>Twenty-seven Sprague-Dawley rats.</AbstractText>Hearts were harvested and perfused at a constant flow of 10 mL/min by using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. Ventricular fibrillation (VF) was induced by a 0.05-mA current delivered to the right ventricular endocardium and the perfusate flow was stopped. After 10 mins, the perfusate flow was resumed at 20% of baseline flow and maintained for 15 additional minutes before returning to baseline flow after 25 mins of VF (VF25 mins). Twenty-seven hearts were randomized to receive from VF22 mins to VF25 mins either 0 epicardial shocks, 6 epicardial shocks, or 12 epicardial shocks.</AbstractText>Isovolumic indices of left ventricular function were obtained by using a latex balloon advanced through the mitral valve into the ventricular cavity. After defibrillation, indices of contractile function rapidly returned to baseline without differences among groups. The isovolumic end-diastolic pressure, however, remained elevated throughout the postresuscitation interval. A left shift of the diastolic pressure-volume curves without changes in their slope was observed at 10 mins after resuscitation with partial return to baseline by 30 mins postresuscitation. The shifts were significantly greater in hearts that received 12 shocks.</AbstractText>These findings indicate that repetitive low-energy electrical shocks do not accentuate postischemic systolic dysfunction in the isolated fibrillating rat heart but adversely affect postischemic diastolic dysfunction by reducing the unstressed left ventricular end-diastolic volume.</AbstractText> |
4,499 | Effects of intravenous azimilide on cardiac performance, fibrillation threshold, and hemodynamics in anesthetized dogs. | The class III antiarrhythmic azimilide (E-1-[[[5-(4-chlorophenyl)-2-furanyl]methylene]-amino]-3-[4-(4-methyl-1- piperazinyl)butyl]-2,4-imidazolidinedione dihydrochloride; WHO No. 7299, CAS 149888-94-8), by slow infusion or stepwise bolus doses, was evaluated for effects on heart rate, blood pressure, and cardiac pump function, excitability, and refractoriness in anesthetized dogs. Infusion (0.6 mg/kg/min) in male beagles (n = 5) to a maximum dose of 54 mg/kg increased QTc more than 20 ms at 2.0 mg/kg. At a dose of 8.9 mg/kg i.v., QTc increased 34% above baseline and remained elevated throughout the subsequent infusion and for at least 60 min postinfusion. At this maximum class III dose, azimilide increased heart contractile force (HCF) 10% and +dP/dt 34% and decreased heart rate (HR) 12%, without significantly changing mean blood pressure (MBP), left ventricular end diastolic pressure, -dP/dt, stroke volume (SV), or cardiac output (CO). At the mean maximum 47 mg/kg i.v. dose, QTc remained elevated, but decreases were observed in HCF (-27%), +dP/dt (-24%), -dP/dt (-35%), SV (-16%), and CO (-52%). Cumulative intravenous bolus injections of azimilide (0.3, 1, 3, 10, and 30 mg/kg) in male mongrels (n = 5) increased effective refractory period (ERP) and +dP/dt (18% and 16%, respectively, at 10 mg/kg) as a function of dose and significantly decreased HR (-22% at 10 mg/kg). MBP decreased significantly (-23%) only at the highest dose. Ventricular fibrillation threshold (VFT) was unchanged at 30 mg/kg. Effects of dl- (n = 3) and d-sotalol (n = 4) on ERP and HR were similar to azimilide's, but both compounds caused a greater MBP depression and VFT elevation. These results suggest that azimilide is well tolerated by the cardiovascular system, providing an increase in contractility and a slight decrease in HR at intravenous doses that produced a large or maximum increase in cardiac refractoriness. |
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