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PubMed1993

Does ventricular fibrillation cause myocardial stunning during defibrillator implantation?

Induction of ventricular fibrillation (VF) is an important part of the process of inserting implantable cardioverter defibrillators (ICDs), allowing the measurement of defibrillation thresholds. However, animal studies have revealed that repeated cycles of VF and defibrillation result in depressed left ventricular (LV) function and reduced cardiac output. Short intervals of VF do not affect myocardial contractility but longer periods produce heart failure. Induced VF was used in a canine model to study profound myocardial stunning leading to heart failure, as well as the therapeutic potential of the phosphodiesterase inhibitor, amrinone (combined with epinephrine and norepinephrine). Amrinone was found to significantly (p < 0.05) increase contractility when added to a stable preparation supported by epinephrine and norepinephrine infusion; amrinone or catecholamines alone had no effect. In the clinical setting, the following factors may affect LV contractility during ICD surgery: catecholamines released as a result of hypotension; negative VF; ischemia; antiarrhythmic drugs; anesthetics; and bradycardia after device testing. Patients (n = 125) have tolerated ICD insertion well. Early data reveals no significant changes in ejection fraction. Though rare, death due to myocardial stunning and LV power failure can occur during ICD insertion. It may be possible to use arterial pressure monitoring to predict this event in vulnerable patients.

Animals↗

PubMed1984

Ventricular fibrillation: the importance of being coarse?

Ventricular fibrillation (VF) has been classified electrocardiographically as "fine amplitude" or "coarse amplitude" VF. It has been suggested that coarse VF represents increased "synchronization" of myocardial activation which could result in lower thresholds for defibrillation. To test the "synchronization" differences between coarse VF and fine VF, we induced VF in ten normal anaesthetized dogs. Standard limb lead and His bundle electrograms were recorded simultaneously with 12 bipolar epicardial electrograms (eight dogs) and six lead ECG (two dogs). Activation "synchronization" was assessed by calculating the standard deviations (SD) of electrogram activation times during one coarse VF and one fine VF cycle. Less synchronization during VF was indicated by a 50% larger SD (CVF: 29.3 +/- 1.1 msec, FVF: 32.6 +/- 1.6 msec) compared to ventricular pacing (21.2 +/- 1.6 msec) and 500% larger than sinus rhythm (6.5 +/- 0.5 msec). Coarse VF and fine VF did not differ. In addition, the 6-lead ECG recorded during early VF had episodes of coarse VF and fine VF occurring simultaneously. The amplitude of all electrograms diminished over 15 minutes until only fine VF could be recorded. We conclude that coarse VF does not reflect greater synchronization of activity than fine VF early in fibrillation (five minutes). Rather, differences are due to lead orientation. Later in the fibrillation bout, fine VF probably reflects metabolically induced degeneration of cellular excitability.

Animals↗

PubMed1995

Change in opioid peptide level in the heart and blood plasma during acute myocardial ischaemia complicated by ventricular fibrillation.

1. The influence of acute myocardial ischaemia (AMI) complicated by ventricular fibrillation (VF) on opioid peptide level in myocardium and blood plasma of rats has been studied. 2. Leu-enkephalin level in myocardium of rats with AMI and VF has been found to be significantly lower than in animals with AMI but without VF. 3. Met-enkephalin level has been found to be significantly increased in both animals with VF and without it. We have not found a significant difference in met-enkephalin level in myocardium of animals with VF and without it. 4. AMI was induced to increase the enkephalin and beta-endorphin level in blood plasma of all the animals, whether VF had occurred or not. 5. Preliminary administration of D-Ala2,Leu5,Arg6-enkephalin, a synthetic analogue of leu-enkephalin, has prevented a decrease of ventricular fibrillation threshold in experimental coronary occlusion. 6. The obtained results allow us to conclude that enkephalins of myocardium but not opioid peptides of blood plasma play an important role in VF occurrence.

Animals↗

PubMed2000

[Epicardial mapping of reentrant activation during ventricular fibrillation. An experimental study].

INTRODUCTION AND OBJECTIVES: High-resolution epicardial mapping was used in an experimental model to analyze reentrant activation during ventricular fibrillation. METHODS: In 30 isolated Langendorff-perfused rabbit hearts, recordings were made of ventricular fibrillation activity using an epicardial multiple electrode. In the activation maps with reentrant activation patterns, determinations were made of the number of consecutive rotations, the maximum length of the central core, the area encompassed by the core and two electrodes surrounding it, and the cycle defined by reentrant activation. RESULTS: Most of the activation maps analyzed showed complex patterns with two or more wave fronts that either collided or remained separated by functional block lines (514 maps, 86%). In 112 maps (19%) activation patterns compatible with epicardial breakthrough of the depolarization process were observed. Reentrant activity was recorded in 42 maps (7%) - the maximum number of consecutive rotations being 3 (mean = 1.3 +/- 0.5). The maximum length of the central core ranged from 3 to 7 mm (mean = 5 +/- 1 mm), while the area encompassed by the central core plus two electrodes surrounding it ranged from 35 to 55 mm2 (mean = 45 +/- 6 mm2). The reentrant cycle length (mean = 47 +/- 8 ms) showed a linear relation to the maximum length of the central core reentry (cycle = 4.52 x length + 24.6; r = 0.7; p < 0.0001). CONCLUSIONS: a) Epicardial mapping allowed the identification of reentrant activation patterns during ventricular fibrillation in the experimental model used; b) the reentrant activity detected is infrequent and unstable, and c) a linear relation exists between the duration of the cycles defined by reentrant activity and the maximum length of central core reentry.

Animals↗

PubMed2006

Comparison of nifekalant and lidocaine for the treatment of shock-refractory ventricular fibrillation.

BACKGROUND: Although nifekalant is a class III antiarrhythmic agent without negative inotropic activity, its effect in patients with shock-refractory ventricular fibrillation remains unclear. METHODS AND RESULTS: Patients who had an out-of-hospital cardiac arrest with ventricular fibrillation that persisted after 3 shocks from an external defibrillator, intravenous epinephrine, and another shock were retrospectively studied. The patients received lidocaine from January 1997 through June 2001 and nifekalant from July 2001 through December 2004. Short-term survival rates (survival to hospital admission and 24-h survival) were compared between the groups. The study group comprised 120 patients (mean age: 62+/-16 years): 55 received nifekalant and 65 received lidocaine. Age, sex, history of ischemic heart disease, whether arrest was witnessed or not and time to arrival at the hospital did not differ significantly between the groups. As compared with lidocaine, nifekalant was associated with significantly higher rates of survival to hospital admission (67% vs 37%, p<0.001) and 24-h survival (53% vs 31%, p=0.01). Multivariate analysis showed that treatment with nifekalant and early initiation of cardiopulmonary resuscitation were independent predictors of 24-h survival. CONCLUSIONS: As compared with lidocaine, nifekalant may improve short-term survival in patients with out-of-hospital cardiac arrest due to shock-refractory ventricular fibrillation.

Aged↗

PubMed2000

Lidocaine for prevention of reperfusion ventricular fibrillation after release of aortic cross-clamping.

OBJECTIVE: 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. DESIGN: Prospective, randomized study. SETTING: University hospital. PARTICIPANTS: Patients undergoing coronary artery bypass graft surgery (n = 34). INTERVENTIONS: 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. MEASUREMENTS AND MAIN RESULTS: 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. CONCLUSIONS: 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.

Adult↗

PubMed1998

[Reproducibility of the effectiveness of defibrillation for terminating induced ventricular fibrillation using intraoperatively measured defibrillation threshold energy in patients with implanted cardioverter-defibrillator].

The aim of the present study was to assess the long-term reproducibility of the defibrillation efficacy of energies set at the intraoperatively measured defibrillation threshold using a modified testing protocol. Between December 1993 and January 1996, 83 patients receiving an implantable cardioverter-defibrillator (ICD) in combination with a non-thoracotomy lead system and having an intraoperatively measured defibrillation threshold (DFT) < or = 15 J were enrolled in a substudy of a prospective, randomized multicenter trial ("Low Energy Endotak Trial" (LEET)). Step-down DFT testing was performed intraoperatively (15, 10, 8, 5 J). It was mandatory to reproduce a successful conversion of ventricular fibrillation at the DFT energy during implantation (DFT+). At the end of implantation, at predischarge, and after one year, assessment of the defibrillation efficacy of DFT+ energy was repeated (first shock: DFT+, second shock: 2 x DFT+). Mean DFT+ at implant was 9.6 + 3.3 J. Immediately after implantation, successful conversion of induced ventricular fibrillation was achieved in 70/79 (89%) patients using DFT+ energies. In 7/8 (89%) patients only the second shock set at 2 x DFT+ and in one patient only the third shock set at maximum energy (34 J) was successful. At predischarge, defibrillation efficacy of DFT+ was reproducible in 61/77 (79%) patients. The remaining 16 patients were successfully converted using a second shock set at 2 x DFT+. One year after implantation, conversion of ventricular fibrillation was achieved at energies set at DFT+ in 52/62 (84%) patients and in the remaining 10 patients at energies set at 2 x DFT+. A total of 183/218 (84%) episodes of induced ventricular fibrillation were terminated successfully using DFT+ energies. There was no correlation between the intraoperatively determined DFT+ or the underlying cardiac disease and the defibrillation efficacy. These results demonstrate that the defibrillation efficacy for termination of induced ventricular fibrillation using DFT+ energies is reproducible at implantation, at predischarge, and one year after ICD insertion. Energies set at twice DFT+ seems to allow for reliable defibrillation within the first year after ICD implantation.

Adult↗

PubMed1988

Cocaine-induced ventricular fibrillation: protection afforded by the calcium antagonist verapamil.

There is increasing evidence that the use of cocaine can trigger lethal cardiac events, including ventricular fibrillation. The mechanism responsible for these lethal cardiac arrhythmias remains to be determined. Therefore, 13 mongrel dogs were instrumented so that heart rate, left ventricular pressure (LVP), and d(LVP)/dt could be measured. After a 3- to 4-wk recovery period, the left circumflex coronary artery was occluded for 2 min, beginning with the last minute of an exercise stress test and continuing for 1 min after the cessation of exercise. None of the dogs developed cardiac arrhythmias during the control exercise plus ischemia test. On a subsequent day, the test was repeated after the injection of cocaine HCl (1.0 mg/kg). Cocaine significantly (P less than 0.01) elevated heart rate, systolic LVP, and d(LVP)/dt, and it elicited cardiac arrhythmias in 12 of the 13 animals during the exercise plus test. In fact, 11 animals developed ventricular fibrillation. Verapamil, a calcium channel antagonist (250 micrograms/kg), attenuated the hemodynamic effects of cocaine and prevented the development of ventricular arrhythmias. These data suggest that cocaine can induce ventricular fibrillation during myocardial ischemia and that these lethal arrhythmias may be prevented by a calcium channel antagonist.

Animals↗

PubMed2000

[Recurrent ventricular fibrillation during a febrile illness in a patient with the Brugada syndrome].

Different situations have been involved in the origin of ventricular arrhythmic events in patients with the Brugada syndrome such as bradycardia, alcohol consumption and mental stress. We present a 30 year old male with recurrent ventricular fibrillation due to a febrile illness with intense sweating. He had been previously studied at our Unit in 1995 because of an episode of resuscitated cardiac arrest due to ventricular fibrillation. The twelve-lead electrocardiogram showed the typical characteristics of a patient with the Brugada syndrome. Different invasive and non-invasive tests performed were normal. He received a defibrillator and had no recurrences during 4 years of follow up. In March,1999, after an upper respiratory tract infection he had high fever treated with paracetamol but at down he had sweating and chills, followed by 3 defibrillator shocks. Late interrogation showed 5 episodes of ventricular fibrillation, two of them non-sustained, and the rest adequately treated by the defibrillator. Activation and inactivation kinetics for early INa are twofold faster at higher temperature, and shift activation and steady-state inactivation. This may explain the role of the temperature as a trigger for ventricular arrhythmias in our patient.

Adult↗

PubMed2001

The incidence of out-of-hospital ventricular fibrillation in Helsinki, Finland, from 1994 to 1999.

Early defibrillation by emergency medical services has been a success story in the treatment of ventricular fibrillation. This success has been followed by recommendations to allow public access to defibrillation equipment. We tracked the changes in incidence of ventricular fibrillation from prospectively collected data from the Helsinki Cardiac Arrest Register. We found that the incidence of out-of-hospital ventricular fibrillation of cardiac origin fell by 48% from 1994 to 1999 (p=0.0036). The primary and secondary prevention of coronary artery disease may not be the only reasons for this change and so new public-access defibrillation programmes should be delayed until our findings are confirmed.

Aged↗

PubMed1979

Platelet survival in patients previously resuscitated from out-of-hospital ventricular fibrillation.

Platelet survival times were measured in 11 ambulatory patients within 5 to 21 months of out-of-hospital ventricular fibrillation unassociated with acute myocardial infarction. The mean platelet survival time of 7.7 +/- 2.1 days was shortened when compared with 28 normal controls of similar age (9.0 +/- 1.0 days, p less than 0.03) but not different from 56 other patients with stable angina pectoris (6.85 +/- 1.81 days, p less than 0.2). One patient with a near normal survival time of 7.5 days experienced recurrent ventricular fibrillation without associated acute myocardial infarction 1 month following the platelet survival study. Although one platelet inhibitory agent, sulfinpyrazone, may lower the incidence of sudden cardiac death following acute myocardial infarction, the shortened platelet survival time in the group of patients experiencing out-of-hospital ventricular fibrillation did not distinguish them from others with coronary artery disease.

Aged↗

PubMed1993

[Coronary revascularization using profound hypothermia with elective ventricular fibrillation and total circulatory arrest].

Profound hypothermia with elective ventricular fibrillation and total circulatory arrest was used in a patient undergoing coronary artery bypass grafting (CABG) with severe calcification of the ascending aorta. A 76-year-old woman with unstable angina was referred for coronary revascularization. Ascending aorta was severely calcified with the exception of limited region of proximal ascending aorta, and the coronary arteriography showed high-grade obstruction of the left anterior descending (LAD) and dominant right coronary artery (RCA). The left internal thoracic artery was anastomosed to the LAD, and the saphenous vein graft to the RCA under systemic moderate hypothermia and elective ventricular fibrillation. During the proximal anastomosis of the saphenous vein graft to the non-calcified ascending aorta, profound hypothermia and circulatory arrest was instituted for 11 minutes. The wean from extracorporeal circulation was successful, and the postoperative course was uneventful.

Aged↗

PubMed1983

Effect of molsidomine on spontaneous ventricular fibrillation following myocardial ischemia and reperfusion in the dog.

The effect of the novel antianginal agent molsidomine on the incidence of spontaneous ventricular fibrillation during myocardial ischemia and reperfusion was investigated in the anesthetized dog. Molsidomine was administered as an intravenous bolus at the dose of 0.05 mg/kg. Twenty minutes later, the left anterior descending coronary artery was occluded for 90 min. During the occlusion period, molsidomine was given as a continuous intravenous infusion at the dose of 0.5 micrograms/kg per ml per min. After release of the occlusion, the animals that survived were monitored for another 30 min. Control animals received saline. In the control animals, coronary occlusion was accompanied by an increase in heart rate, heart contractility, left ventricular end-diastolic pressure, and blood pressure as well as by ventricular arrhythmias. Molsidomine either abolished or reduced both hemodynamic and electrical changes. During the reperfusion period, 10 out of 12 control animals died, and the deaths were from ventricular fibrillation; one out of eight molsidomine-treated animals also died of ventricular fibrillation. It is postulated that the protective effect of molsidomine rests on its hemodynamic effects resulting in a shift in blood flow toward the ischemic zones and, consequently, in an increase in ventricular electrical stability.

Animals↗

PubMed1982

A possible role of the specialized conduction system in the conversion of ventricular tachycardia to ventricular fibrillation.

Electrode recordings from the right bundle branch, His bundle, and right atrium in a canine preparation enabled us to observe the activation of the ventricular myocardium and the specialized conduction system during the conversion of ventricular tachycardia to ventricular fibrillation. At times when ventricular tachycardia degenerated to ventricular fibrillation, asynchronous activation of the right bundle branch and the ventricular myocardium was frequently noted. Such asynchrony of activation was not seen during the spontaneous conversion of ventricular tachycardia to sinus rhythm. We suggest that this asynchronous activity produces increasing fractionation of ventricular activation fronts, which in turn yields fibrillation.

Animals↗

PubMedDate not supplied

Ventricular fibrillation in two infants treated with amiodarone hydrochloride.

Antiarrhythmic agents may induce ventricular arrhythmias. Whereas amiodarone is a reported cause of ventricular fibrillation in children, there are no reported cases in infants. We observed two patients with atrial flutter and congestive heart failure who were treated with amiodarone. Both had anatomic heart defects and had failed conventional therapy. Ventricular fibrillation occurred 3 and 12 days after the initial dose. Q-T interval, electrolytes, digoxin level, and amiodarone level (one patient) were normal. Amiodarone may provoke life-threatening ventricular tachyarrhythmias during the convalescent period. Consideration should be given to monitoring in a hospital setting for at least 2 weeks following initiation of amiodarone therapy.

Amiodarone↗

PubMed2002

Estimated global epicardial distribution of activation rate and conduction block during porcine ventricular fibrillation.

INTRODUCTION: A proposed mechanism of the maintenance of ventricular fibrillation (VF) determined by studying small hearts or segments of large hearts is that a single stable rotor exists at the site of maximal activation rate, which gives rise to activation fronts that propagate into slower activating regions where they frequently block. We wished to determine if two predictions of this hypothesized mechanism are true during VF in large hearts: (1) there is a single maximum in the distribution of activation rates with the activation rate decreasing with distance away from this maximum; and (2) the incidence of block is greater outside than inside the fastest activating region. METHODS AND RESULTS: Six 25-second episodes of VF from each of six pigs were recorded from 504 electrodes over the entire ventricular epicardium. The electrodes were divided into four zones: left ventricular base and apex (LVB and LVA) and right ventricular base and apex (RVB and RVA). A fast Fourier transform was performed on each electrogram, and the mean activation rate was estimated from the dominant (peak) frequency (DF) and block was estimated to be present during those time intervals when double peaks (DPs) were present in the power spectrum. The zones had statistically significant distributions of DF (LVB>LVA>RVA>RVB) and DP incidence (RVA>RVB>LVA>LVB). CONCLUSION: During VF, the LV base has the highest estimated activation rate and the lowest estimated block incidence, and the RV has the slowest rate but the highest block incidence. This is consistent with the concept of VF being maintained by activation fronts originating from the LV base.

Animals↗

PubMed1992

Ro 40-5967, a novel calcium channel antagonist, protects against ventricular fibrillation.

Ro 40-5967 is a new calcium channel antagonist that binds at the same membrane sites as verapamil, yet has minimal negative inotropic effects. The effects of Ro 40-5967 on the susceptibility to ventricular fibrillation were investigated and compared to diltiazem. Ventricular fibrillation (VF) was induced in 40 mongrel dogs with healed myocardial infarctions by a 2-min coronary occlusion during exercise. Twenty-four animals were found to be susceptible to VF and were given the treatments described below. Pretreatment with Ro 40-5967 (n = 17, 1000 micrograms/kg i.v.) significantly (P < 0.001) reduced the incidence of VF (13 of 17 protected) during the exercise plus ischemia test. Diltiazem (n = 8, 1000 micrograms/kg) completely suppressed VF. Lower doses of diltiazem and Ro 40-5967 did not prevent VF. The hemodynamic effects of Ro 40-5967 were also compared to diltiazem and verapamil. Diltiazem and verapamil, but not Ro 40-5967, increased P-R interval in a dose-dependent manner. Even when reflex tachycardia was controlled by beta-adrenoceptor blockade, Ro 40-5967 still exerted only minimal effects on P-R interval. Verapamil, but neither Ro 40-5967 nor diltiazem, provoked a dose-dependent negative inotropic response. All three drugs elicited large increases in coronary blood flow. These data support the hypothesis that calcium entry may play a critical role in the development of malignant arrhythmias during ischemia. Further, Ro 40-5967 can protect against ventricular fibrillation without significant negative inotropic or dromotropic effects.

Animals↗

PubMed1986

The influence of verapamil and its isomers on vulnerability to ventricular fibrillation during acute myocardial ischemia and adrenergic stimulation in isolated rat heart.

In isolated heart preparations, dl-verapamil inhibits the increased vulnerability to ventricular fibrillation and reduces myocardial tissue levels of cyclic 3'5'-adenosine monophosphate (cyclic AMP), a proposed arrhythmogenic agent. The ventricular antiarrhythmic effect of dl-verapamil may not be mediated by selective slow channel inhibition since both d(+) and l(-) isomers display equipotent activity. Three different mechanisms may contribute to the antiarrhythmic properties of dl-verapamil: calcium channel antagonism (l(-) isomer), sodium channel inhibition (d(+) isomer) and reduced cyclic AMP accumulation. In the intact animal model, coronary artery ligation is associated with increased levels of circulating catecholamines and sympathetic neural overactivity. In isolated heart preparations, it is therefore appropriate to evaluate the influence of dl-verapamil and isomers on vulnerability to ventricular fibrillation and cyclic AMP accumulation during acute myocardial ischemia with added adrenergic stimulation. We found that dl and l(-) but not d(+)-verapamil (all 1.5 X 10(-7) M) inhibited the fall in ventricular fibrillation threshold through a mechanism not involving cyclic AMP. L(-) but not d(+) verapamil inhibited Ca2+ dependent slow responses and decreased action potential duration at 90% repolarization. We propose that the ventricular antiarrhythmic property of dl and l(-) verapamil during acute regional myocardial ischemia with added adrenergic stimulation is due to inhibition of transsarcolemmal calcium influx.

Animals↗