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PubMed1998

Dispersions of the QT interval in postmyocardial infarction patients presenting with ventricular tachycardia or with ventricular fibrillation.

Increased QT interval dispersion is associated with ventricular arrhythmias. The aim of this study was to examine if in postmyocardial infarction patients with impaired left ventricular function, increased QT dispersion is associated with ventricular tachycardia (VT) and ventricular fibrillation (VF). Measures of QT dispersion, calculated as maximum-minimum (D) and standard deviation (SD) of QTend, QTapex, JTend, JTapex, and Tend intervals in the 12-lead electrocardiogram, were compared in patients who late after myocardial infarction experienced sustained VT (VT group) only, VF (VF group) only, or had no ventricular arrhythmias (controls). The 25 patients in each group were individually matched for age, gender, number of diseased coronary vessels, location of the previous myocardial infarction, and left ventricular ejection fraction. Dispersion measures of QTend, QTapex, and JTapex intervals separated VT group from controls, but none of the measures separated the VF group from controls. QTendD was 49+/-18 ms in controls, 57+/-18 ms in the VF group (controls vs VF group, p = NS), and 65+/-29 ms in the VT group (controls vs VT group, p <0.05). VT group had increased QTapexSD, JTapexSD, and JTapexD compared with the VF group. The cycle length of induced sustained monomorphic VT, present in 19 VT and 19 VF patients, correlated with several dispersion indexes in the VT group, but not with those in the VF group. Thus, in postmyocardial infarction patients with a severely damaged left ventricle, increased QT dispersion is associated with susceptibility to sustained VT, but not to VF.

Aged↗

PubMed1998

[Implanted automatic defibrillator after ventricular fibrillation treated with semi-automatic defibrillation].

We report two cases of out-of-hospital ventricular fibrillation treated without delay, with basic life support practiced by the witness, followed by a successful defibrillation by paramedics with a semi-automatic defibrillator. In the subsequent month, a cardioverter-defibrillator was implanted. In one patient, a ventricular tachycardia occurring 10 months later and a ventricular fibrillation 9 months later in the other respectively, were successfully reversed by the implanted defibrillator. These two cases illustrate the value of the "survival chain" concept (undelayed alert, basic life support by witness, early defibrillation by paramedics with a semi-automatic defibrillator, advanced life support by a physician) as well as the benefit of the implanted cardioverter-defibrillator.

Adult↗

PubMed2005

Recurrent cardiac events in patients with idiopathic ventricular fibrillation, excluding patients with the Brugada syndrome.

BACKGROUND: The recurrence of cardiac events in patients with idiopathic ventricular fibrillation (VF) excluding patients with the Brugada syndrome is unclear since this entity remains present in previous studies. METHODS: Since 1992, 18 patients (72% male) with idiopathic VF out of 455 ICD implants were treated with an implantable cardioverter defibrillator (ICD). The mean age at first ICD implantation was 42 +/- 14 years. Brugada syndrome, as well as other primary electrical diseases (e.g. long QT), were systematically excluded in all patients by the absence of the typical electrocardiogram (ST elevation in the right precordial leads) at rest and/or after pharmacological tests (ajmaline, flecainide, or procainamide). Recurrence of cardiac events was prospectively assessed. RESULTS: During a mean follow-up period of 41 +/- 27 months, VF recurrence with appropriate shock occurred in 7 patients (39%) covering a total of 27 shocks. The median time to first appropriate shock was 12 +/- 9 months. There were no deaths. In the electrophysiological study, 39% of patients were inducible, but inducibility failed to predict subsequent arrhythmic events. Forty-four percent of patients suffered 21 inappropriate shocks, which were caused by sinus tachycardia, atrial arrhythmias or lead malfunction. CONCLUSION: Idiopathic ventricular fibrillation patients have a high recurrence rate of potentially fatal ventricular arrhythmias, excluding patients with the Brugada syndrome or other known causes. ICD prevents sudden cardiac death but inappropriate shocks remained a major issue in this young and active population.

Adult↗

PubMed1990

Electrophysiologic testing after aortic valve replacement in two patients with aortic stenosis and preoperative ventricular fibrillation.

In two patients with severe aortic stenosis successful resuscitation from ventricular fibrillation was documented by Holter recording/ECG monitoring. After aortic valve replacement programmed ventricular stimulation was performed in both patients, but ventricular tachycardia/ventricular fibrillation was not inducible. The patients were left without antiarrhythmic therapy and have been free from cardiac events for 18 and 20 months, respectively. The prognostic value of postoperative electrophysiologic testing after aortic valve replacement in patients with severe aortic stenosis and preoperative resuscitation is discussed.

Aortic Valve Stenosis↗

PubMed1994

Effects of glibenclamide on ventricular fibrillation in non-insulin-dependent diabetics with acute myocardial infarction.

BACKGROUND: Glibenclamide, a hypoglycemic sulfonylurea, has shown antiarrhythmic effects in acutely ischemic myocardium. The aim of the present study was to evaluate the effectiveness of the drug in preventing ventricular fibrillation in diabetic patients with acute myocardial infarction. METHODS: We studied 232 patients with non-insulin-dependent diabetes mellitus (106 on glibenclamide, group A1; 126 treated with another hypoglycemic drug or with diet only, group A2) and 830 non-diabetic people. All the patients were admitted to our coronary care unit with their first myocardial infarction. RESULTS: Ventricular fibrillation occurred in 1.9% of group A1, 7.9% of group A2, and 9.9% of the non-diabetic (A1 versus A2, P < 0.05; A2 versus the non-diabetic group, NS; A1 versus the non-diabetic group, P < 0.01). Sustained ventricular tachycardia was not significantly different among the groups. CONCLUSIONS: The antiarrhythmic effectiveness of glibenclamide might be related to its blocking action on the ATP-dependent potassium channel, with consequent attenuation of the efflux of potassium induced by ischemia. We also observed a higher mortality rate resulting from heart failure in group A2 than in group A1 or the non-diabetic group. Since glibenclamide has never shown significant effects on myocardial contractility, this finding remains to be elucidated. Glibenclamide therefore appears to have an antifibrillatory effect in acute myocardial infarction; with respect to acute coronary events, the drug might be able to prevent ventricular fibrillation, which is most often fatal when it occurs before hospitalization.

Adult↗

PubMed1998

Ventricular fibrillation and defibrillation thresholds in sheep and dogs.

Ventricular defibrillation studies normally use dogs rather than other large species. To investigate the suitability of sheep, which are often cheaper and more readily available, we compared ventricular fibrillation and defibrillation thresholds (VFT, DFT) in sheep and dogs. A total of 12 sheep (31 +/- 5 kg) and six dogs (19 +/- 1 kg) were anesthetised with halothane. Fibrillation was induced via epicardial pacing leads, using a 1 s 50 Hz pulse. Biphasic defibrillation shocks were delivered across epicardial patches. Voltage-response curves for both fibrillation and defibrillation were generated. Logistic regression analysis was used to determine 50 and 90% probability of success for fibrillation induction and defibrillation. VFT was similar in sheep and dogs. DFT at 50% probability of success was significantly higher in sheep (369 +/- 14 V) than in dogs (299 +/- 31 V, P < 0.04) but within each species there was no correlation between heart weight and DFT. After defibrillation sheep took longer to return to sinus rhythm than dogs and electro-mechanical dissociation was observed in sheep, but not in dogs. Thus, sheep may not be an ideal model for ventricular defibrillation research but further studies of the intrinsic differences between sheep and dogs may provide insights into basic mechanisms of defibrillation.

Animals↗

PubMed1992

Effects of drugs on ventricular fibrillation and ischaemic K+ loss in a model of ischaemia in perfused guinea-pig hearts in vitro.

In a perfused guinea-pig heart model of myocardial ischaemia, reducing coronary flow by 95% for four successive 6 min periods caused a reproducible net loss of K+ into the coronary perfusate. This was reduced in a concentration-dependent manner by ATP dependent K+ channel blockers (glibenclamide and glipizide) and calcium channel blockers (verapamil and nifedipine). Other K+ channel blockers (UK-66,914, 4-aminopyridine, R56865 and phentolamine) and beta 1-adrenoceptor and beta 2-adrenoceptor antagonists (betaxolol and ICI118551) did not reduce this loss significantly. A single 30 min low-flow period reliably induced K+ release and ventricular fibrillation in control hearts. Glibenclamide, glipizide and phentolamine suppressed ventricular fibrillation but not ischaemic K+ loss in this model. R56865 and 4-aminopyridine and coadministration of betaxolol and ICI118551 yielded similar results while UK-66,914 suppressed neither. In our model, modulation of ischemic K+ loss and suppression of ventricular fibrillation were not closely associated and appeared to occur via separate mechanisms.

4-Aminopyridine↗

PubMed1980

[Effects of sulfinpyrazone on early ventricular fibrillation and 2d-phase arrhythmias in acute myocardial infarction (author's transl)].

Clinical and experimental studies indicate that ventricular arrhythmias, mainly ventricular fibrillation, are responsible for sudden cardiac death. A recent double-blind multicenter trial ("Anturane Reinfarction Trial") showed that the incidence of sudden cardiac death was reduced in Sulfinpyrazone-treated patients after acute myocardial infarction compared with the placebo group, although the rate of reinfarctions was not diminished. We investigated the efficacy of Sulfinpyrazone on the reduction and prevention of ventricular arrhythmias and primary ventricular fibrillation, utilizing a standardized experimental canine preparation. At normal therapeutic and at high cumulative doses of the drug, a reduction in ventricular arrhythmias within the first 24 hours after coronary occlusion could not be observed. Sulfinpyrazone failed also to alter the ventricular vulnerability to fibrillation in the very early myocardial infarction period. Furthermore, haemodynamics, contractility and oxygen consumption of the heart were not changed. These experimental findings show that the reduction in sudden cardiac deaths in Sulfinpyrazone-treated patients cannot be attributed to antiarrhythmic effects of the drug. Further research is needed to delineate the mechanism of action of Sulfinpyrazone as reported by the Anturane Reinfarction Trial Research Group.

Animals↗

PubMed1975

Effects of bretylium and lidocaine on ventricular fibrillation in the isolated rabbit heart.

We studied the effects of bretylium tosylate and lidocaine on ventricular fibrillation in the isolated, perfused rabbit heart induced by perfusion with potassium-deficient solutions and by premature stimuli. The purpose of the study was to determine if the reported antifibrillatory effects of the drugs could be reproduced in the absence of an intact sympathetic nervous system. Lidocaine in the concentration of 5 mug/ml. prevented ventricular fibrillation induced by both methods while bretylium, in concentrations of 25 to 50 mug/ml. prevented neither type of filbrillation. These results indicate that the antifibrillatory effects of lidocaine can be attributed to drug-induced alterations in cellular electrophysiology, whereas those of bretylium are independent of such changes. Our study suggests that the reported antifibrillatory capability of bretylium is related to the drug's effects at sympathetic nerve terminals and thus is dependent upon an intact sympathetic nervous system.

Animals↗

PubMed1986

Ventricular fibrillation during orotracheal intubation of hypothermic dogs.

Physical manipulation of the hypothermic patient is well known to cause ventricular fibrillation. Careful review of the literature fails to demonstrate a true temporal relationship between orotracheal intubation and ventricular fibrillation (VF) when acceptable temperature-corrected arterial blood gases have been obtained. Eleven mongrel dogs were anesthetized and cooled, with orotracheal intubation and extubation performed every two degrees centrigrade, starting at 27 C. Ventilator setting were adjusted to maintain normal pH according to arterial blood gases drawn every two degrees and corrected for temperature. There was only one episode of VF during 42 intubations performed at temperatures less than 28 C (2.38%). There were eight separate episodes of spontaneous VF unrelated to intubation in five dogs. Four of these five with spontaneous VF were resuscitated with countershock only, further cooled, and reintubated an additional 11 times without a single episode of VF during intubation. Our data suggest that the incidence of VF during intubation in the hypothermic patient is much less than previously described, provided that normal pH is maintained and hypoxemia is corrected.

Animals↗

PubMed1979

[Characteristics of the changes in the intra- and extracellular K+ and Na+ concentrations and the intra- and extracellular pH in the area of cardiac ishemia in experimental myocardial infarct complicated by ventricular fibrillation].

Localized ischemia of the heart complicated by ventricular fibrillation is characterized by a tendency to a higher rate of decrease in intra- and extracellular K+ gradient and intracellular pH in the myocardium as compared to cases without fibrillation. The higher rate of K+ escape from the ischemic cells may be linked with a sharper intracellular oxidation, evidence of which is the correlative dependence between the severity of disorders of K+ balance and decrease in intracellular pH in the myocardium in ischemia.

Animals↗

PubMed1982

Extended endocardial resection for the treatment of ventricular tachycardia and ventricular fibrillation.

A total of 40 patients with drug-refractory, life-threatening cardiac rhythm disturbances--ventricular tachycardia in 23 patients and ventricular fibrillation in 17 patients--underwent extended endocardial resection (EER) of scar tissue. Scarring was due to myocardial infarction in 38 patients, to previous congenital heart operation in 1 patient, and to sarcoidosis of the heart in 1. The EER procedure was directed by epicardial and endocardial mapping data whenever possible, and was usually combined with revascularization, aneurysmectomy, or, in 5 patients, mitral valve replacement. Operative mortality was 10%, incident to poor preoperative ventricular function and hemorrhage secondary to previous cardiac surgical procedures. Thirty-three of the 36 survivors (92%) are free of arrhythmia at follow-up periods ranging from 3 to 36 months (mean, 12.5 months); the arrhythmia in the remaining 3 patients is now drug controlled. Thirty-three patients had postoperative electrophysiological studies, and in 30 (91%), the arrhythmia was no longer inducible. The results of surgical treatment for ventricular tachycardia and ventricular fibrillation were similar. The results also proved satisfactory whether the EER procedure was directed by visual observation or mapping.

Adolescent↗

PubMed1998

[Ventricular fibrillation and myocarditis].

We report a case of ventricular fibrillation with subacute myocarditis as the only underlying pathological abnormality in a 9-year-old child. The patient died suddenly after a follow-up of 13 years, despite the apparent control of the arrhythmia.

Biopsy↗

PubMedDate not supplied

Terminating SVT-mediated recurrent ventricular fibrillation with verapamil.

Verapamil has been established as the drug of choice in the treatment of supraventricular dysrhythmias and is recognized as useful in the treatment of ischemic heart disease and hypertension. However, verapamil has not generally been considered helpful in the treatment of ventricular dysrhythmias. Five cases are reported in which verapamil was used to terminate a cycle of supraventricular tachycardia-mediated recurrent ventricular fibrillation that could not be suppressed by conventional antidysrhythmics such as lidocaine, procainamide, and bretylium, Proposed mechanisms of verapamil's beneficial effect in this usually fatal situation include (1) a reduction in oxygen consumption related to the reduction in heart rate, thereby raising the ventricular fibrillation threshold; (2) direct anti-ischemic effect; and (3) a direct antidysrhythmic effect. These proposed mechanisms are substantiated by clinical studies. On the basis of this observation, it is recommended that in a situation of supraventricular tachycardia-mediated recurrent ventricular fibrillation that cannot be terminated by conventional antidysrhythmics, the administration of verapamil should be considered.

Aged↗

PubMed2000

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.

Animals↗

PubMed1988

Prevention of postischemic ventricular fibrillation late after right or left stellate ganglionectomy in dogs.

To gain insight into the differences in antiarrhythmic potential of right vs left stellate ganglionectomy, 72 dogs were randomized to either unilateral stellectomy or second intercostal space thoracotomy and left circumflex coronary arteriovenous pedicle occlusion was performed, without vagotomy, a mean of 8 weeks later under anesthesia. The type and timing of ventricular ectopic beats, including both nonsustained and sustained ventricular tachycardia and ventricular fibrillation, were investigated. Several covariates, including postischemic electrocardiographic changes, were considered. Both right and left stellate ganglionectomy reduced the incidence of early (0 to 10 min) (p = .004 and p = .001, respectively) and total (0 to 60 min) (p = .009 and p = .008, respectively) ischemia-induced ventricular fibrillation, and improved outcome (p = .0013 and p = .0012, respectively). Early sustained ventricular tachycardia was similarly reduced (p = .02) in both stellectomized groups. By contrast, neither the type nor the time distribution of the other forms of ventricular arrhythmias differed significantly among the randomized groups. The multivariate Cox's regression model showed that ST segment elevation at 3 min postocclusion, unilateral stellate ganglionectomy (either right or left), sex, and weight were significant independent predictors of the incidence of ventricular fibrillation during the occlusion period. Lower ST segment elevation and reduced incidence of sustained ventricular tachycardia in the early postischemic period might explain improved outcome in stellectomized dogs by Cox analysis. The side of intervention (either stellectomy or sham operation) did not influence survival; however, left-sided interventions were more effective than right-sided ones. These results confirm the previously reported antifibrillatory effect of left and indicate like effects of right stellate ganglionectomy in a randomized experimental study.

Animals↗

PubMedDate not supplied

[Myocardial protection of the homograft. III - Evaluation of ventricular fibrillations with hypothermic coronary perfusion (author's transl)].

The homotransplanted heart is in severe failure in the immediate post-operative period, secondary to ischemia inherent to the technic of orthotopic transplantation. The present work was carried out to investigate if ventricular fibrillation followed by cold coronary perfusion could protect the homograft during implantation by evaluating the post-operative cardiac performance. In the control group, 7 hearts were excised, immediately immersed in physiological saline at 5 degrees C, and homotransplanted. In a second group of 4 grafts, ventricular fibrillation was induced and the coronary bed was perfused immediately with cold (5 degrees C) extracellular solution for a period of 10 minutes before orthotopic implantation. All animals were prepared at the end of surgery for hemodynamic studies to be carried out 3, 24 and 48 hours post-operatively in the resting state. In group I, the myocardial temperature dropped to 13.5 degrees C in 14.5 minutes. In group II, the hypothermia by perfusion was more rapid and deeper (11 degrees C within 10 minutes). Three hours post-operatively, cardiac function of group II was superior to that of group I as demonstrated by the increase of cardiac index (39%), stroke volume index (41%) mean systolic ejection rate index (44%), maximum systolic flow index (58%), maximum acceleration index (36%), stroke power index (88%), stroke work index (67%). Twenty-four and forty-eight hours post-operatively the cardio-vascular function improved in both groups but remained superior in group II. These results demonstrate that ventricular fibrillation followed by cold coronary perfusion increases protection of the homograft during the initial period of implantation.

Animals↗

PubMed1982

[Effect of cordaron on the threshold of ventricular fibrillation in cats].

In an experimental study on cats, cordaron administered in a dose of 5 mg/kg significantly increased ventricular fibrillation threshold. Used in a concentration of 1.5 x 10(-6) g/ml, the drug prevented ventricular fibrillation in an isolated heart which had been caused by reduced content of potassium ions and increased content of calcium ions in the perfusate. This action may be due to its influence on myocardial ion transport.

Amiodarone↗