[Research on the mechanism and treatment of induced ventricular fibrillation].
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Humans↗
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Results for “VENTRICULAR FIBRILLATION”
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Spectral and correlation analyses of the verapamil-induced conversion of ventricular fibrillation to tachycardia in isolated rat hearts.
Ventricular tachycardia (VT) is considered to be the most common precursor of ventricular fibrillation (VF). However, the mechanisms underlying the transition from VT to VF remain unclear. Here, we investigated whether and how perfusion of the heart with verapamil, a blocker of L-type calcium channels, changed the macro-dynamics of the heart between VT and VF. The experiments were performed with Langendorff perfused isolated rat hearts, in which left ventricular pressure and left ventricular cardiomyogram were measured. Sustained VT or VF was induced by burst pacing of the left ventricular muscles. During sustained VF, verapamil perfusion resulted in the conversion of VF to VT. A cross-correlation analysis between left ventricular cardiomyogram and left ventricular pressure revealed that the correlation coefficient was small during VF, but became larger during VT. This study showed that inactivation of L-type Ca(2+) channels occurred during verapamil-induced conversion of pacing-induced sustained VF to VT, and characterized the changes in macro-dynamics of the heart associated with the transition.
Animals↗
Amiodarone in the management of patients with ventricular tachycardia and ventricular fibrillation.
Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximum-tolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800-1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 +/- 1.7 months (mean +/- S.D.) of treatment with amiodarone at a mean daily dose of 588 +/- 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5-9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 +/- 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF over a follow-up period of 21.5 +/- 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600-800 mg per day of amiodarone.
Amiodarone↗
Electrophysiology of ventricular fibrillation and defibrillation.
The survival rate from ventricular fibrillation is very high for short-duration fibrillation (<30 secs) but decreases to approximately 3% to 30% in out-of-hospital conditions. During short-duration fibrillation, action potentials occur rapidly with no intervening period of electrical diastole; a shock defibrillates by interacting with the fibrillation action potential to produce a uniformly long postshock extension of refractoriness. In contrast, during long-duration fibrillation, ischemia-induced degradation of cellular electrophysiology occurs, which causes intervening periods of electrical diastole between fibrillation action potentials and, thus, slowing of fibrillation frequency. A successful defibrillation shock must now not only prolong refractoriness when delivered during the action potential but must also excite cells during the periods of depolarized diastole. Biphasic waveforms enhance both effects by causing premature membrane repolarization with the first pulse, thereby allowing sodium channel recovery from inactivation so that the second pulse produces better-formed responses both during the cellular action potential and during the depolarized diastole. Therefore, biphasic waveforms remain superior to monophasic waveforms for treatment of long-duration fibrillation. Improved understanding of the ischemia-induced changes in cellular electrophysiology will suggest further improvements in both defibrillator waveforms and resuscitation techniques.
Animals↗
Appropriate sensing of ventricular fibrillation after failed shocks in a transvenous cardioverter-defibrillator system.
BACKGROUND: Reduction in R-wave amplitude immediately after defibrillation shocks in an integrated shock/sense transvenous cardioverter-defibrillator (TCD) lead system has prompted concerns regarding adequate sensing after failed shocks. We therefore studied redetection characteristics for ventricular fibrillation after unsuccessful defibrillation shocks in a TCD system to determine if these observations have clinical relevance. METHODS AND RESULTS: Fifty patients with this shock/sense TCD lead system underwent conversion testing of their TCD at several time intervals. There were a total of 142 failed shocks events recorded, including 10, 15, 70, and 47 events at implantation, predischarge, and 2- and 6-month testing, respectively. Initial detection time (IDT) and redetection time (RDT) for ventricular fibrillation were measured from event markers for all unsuccessful defibrillation shocks. To assess the effect of failed shocks on electrogram quality, 54 failed shock episodes were evaluated in 37 of the 50 patients by measuring electrograms during VF before and after shock. Mean RDT for the entire group was 5.3 +/- 3.5 seconds compared with an IDT of 4.5 +/- 3.3 seconds (P = NS). There were no significant differences between IDT and RDT at implantation or any follow-up testing period, despite a significant decline in R-wave amplitude from 8.1 +/- 3.5 to 6.8 +/- 2.8 mV (P < .0001) measured 3 to 6 seconds after shock delivery. Analysis of 8 individuals with any extended RDT (> or = 10 seconds) showed no significant differences in clinical or implantation characteristics when compared with 42 individuals without extended RDT. CONCLUSIONS: In this integrated shock/sense TCD lead system, unsuccessful shock delivery has no significant effect on redetection of ventricular fibrillation at device implantation or up to 6 months of follow-up, despite an observed reduction in postshock R-wave amplitude. Therefore, the reported reduction in electrogram quality after a shock is of no practical importance because sensing of ventricular fibrillation does not appear to be compromised in this particular TCD system. Whether this applies to other implantable cardioverter-defibrillator pulse generators and lead systems with different sensing characteristics requires further evaluation.
Aged↗
[Heart transplantation in therapy-resistant, recurrent ventricular tachycardias and ventricular fibrillation].
In life-threatening, drug resistant ventricular tachycardia (VT) or ventricular fibrillation (VF), orthotopic heart transplantation should be considered as an alternative to a directed surgical approach or to the implantation of an automatic defibrillator. We report on nine patients with primary VT or VF who underwent transplantation. These comprised eight men and one woman with a mean age of 35 years (range, 19-51 years); dilative cardiomyopathy was present in seven and coronary artery disease in two. Left ventricular ejection fraction was 19% (11-26%), arrhythmia was recurrent VF in five cases, recurrent VT in two, and recurrent VT/VF in two. Two patients died, one due to acute rejection, and the other 8 months postoperatively due to chronic rejection. The seven other patients are all asymptomatic and leading normal lives without arrhythmias or antiarrhythmic drug therapy. Based on our preliminary experience, some advantages and disadvantages of heart transplantation are discussed in comparison with other treatment modalities. Despite limited indications for orthotopic heart transplantation we feel that it should become the therapy of first choice in young patients with progressive, surgically incorrectable cardiac disease complicated by drug resistant VT or VF.
Adult↗
Stratification of sudden death risk in patients receiving long-term amiodarone treatment for sustained ventricular tachycardia or ventricular fibrillation.
One hundred twenty-two patients treated chronically with amiodarone for sustained ventricular tachycardia or ventricular fibrillation after failing conventional antiarrhythmic therapy were analyzed to determine which factors were predictive of sudden cardiac death during follow-up. The mean left ventricular ejection fraction in the study group was 0.32, and 87% of the patients had coronary artery disease with a prior myocardial infarction. During a median follow-up of 19.5 months, 30 patients died suddenly. The only variable that was predictive of sudden death was left ventricular ejection fraction. Twenty-nine of the 84 patients with ejection fractions < 0.40 died suddenly, compared with 1 of 35 patients with ejection fractions > or = 0.40. The actuarial probability of sudden death at 5 years was 49% when the ejection fraction was < 0.40, and 5% when the ejection fraction was > or = 0.40 (p = 0.0004). These results indicate that patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation whose ejection fractions are > or = 0.40 are at low risk for sudden death. Patients with ejection fractions < 0.40 remain at high risk for sudden death, and should be considered for additional or alternative therapy.
Actuarial Analysis↗
Panoramic optical mapping reveals continuous epicardial reentry during ventricular fibrillation in the isolated swine heart.
During ventricular fibrillation (VF), activation waves are fragmented and the heart cannot contract synchronously. It has been proposed that VF waves emanate from stable sources ("mother rotors"). Previously, we used new optical mapping technology to image VF wavefronts from nearly the entire epicardial surface of six isolated swine hearts. We found that VF was not driven by epicardial rotors, but could not exclude the presence of stable rotors hidden within the ventricular walls. Here, we use graph theoretic analysis to show that, in all 17 VF episodes we analyzed, it was always possible to trace sequences of wavefronts through series of fragmentation and collision events from the beginning to the end of the episode. The set of wavefronts that were so related (the dominant component) consisted of 92%+/-1% of epicardial wavefronts. Because each such wavefront sequence constitutes a continuous activation front, this finding shows that complete reentrant pathways were always present on the epicardial surface and therefore, that wavefront infusion from nonepicardial sources was not strictly necessary for VF maintenance. These data suggest that VF in this model is not driven by localized sources; thus, new anti-VF treatments designed to target such sources may be less effective than global interventions.
Action Potentials↗
Intravenous nicorandil can reduce the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in acute myocardial infarction.
BACKGROUND: Because nicorandil, a potassium channel opener, has a cardioprotective effect and attenuates reperfusion injury in patients with acute myocardial infarction (AMI), intravenous nicorandil should reduce arrhythmic mortality and QT dispersion in patients with AMI. OBJECTIVES: The purpose of this study was to evaluate whether intravenous nicorandil reduces the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in AMI. METHODS: A historical cohort study on the effect of nicorandil on ventricular fibrillation and QT dispersion was conducted. Eighty-three patients with AMI who underwent successful percutaneous transluminal coronary angioplasty (PTCA) were enrolled. The patients were divided into two groups: nicorandil (n=46) and control group (n=37). Nicorandil was injected at 4 mg/h continuously from admission to 48 h after PTCA in the nicorandil group. QT dispersion was measured before, immediately after, 24 h after and 48 h after PTCA. RESULTS: Ventricular fibrillation was observed in three patients in the control group, but none was observed in the nicorandil group. QT dispersion in the nicorandil group was shorter than that in the control group 48 h after PTCA (QT dispersion was 23.2+/-16.1 ms and 33.4+/-24.0 ms, respectively, P<0.05). There was a significant difference between the two groups in time course after the onset of AMI (P<0.05). CONCLUSIONS: Because intravenous nicorandil reduces the occurrence of ventricular fibrillation and QT dispersion in patients with successful coronary angioplasty in AMI, it would prevent the occurrence of cardiac events after successful PTCA for AMI.
Angioplasty, Balloon, Coronary↗
Tyrosine administration decreases vulnerability to ventricular fibrillation in the normal canine heart.
Intravenous infusion of tyrosine (1, 2, or 4 milligrams per kilogram) for 20 to 30 minutes caused dose-dependent increases in the ventricular fibrillation threshold in normal dogs. Administration of valine, a neutral amino acid that competes with tyrosine for uptake at the blood-brain barrier, in a dose equimolar to the most effective dose of tyrosine, slightly decreased the ventricular fibrillation threshold when given alone and significantly blocked elevation of the ventricular fibrillation threshold after tyrosine infusion. Hence, tyrosine, presumably acting in the central nervous system, can protect against certain ventricular arrhythmias.
Animals↗
Transmyocardial laser treatment reduces ischemia-induced ventricular fibrillation during the early phase (1a) after coronary artery occlusion in open chest anesthetized pigs.
INTRODUCTION: It has previously been shown that transmyocardial revascularization with laser (TMR) prior to coronary artery occlusion decreases the occurrence of ischemia-induced arrhythmias. The aim of the present study was to determine the effects of TMR on ventricular fibrillation and other arrhythmias during the early (1a) and late phase (1b) of ischemia in pigs. METHODS: In six pigs TMR was performed in the anterior wall of the left ventricle 60 minutes prior to occlusion of the proximal LAD. Six other pigs were subjected to coronary occlusion without preceding TMR and served as controls. RESULTS: During the 30 min period with LAD occlusion ventricular fibrillation occurred 22 times in 5 of 6 control animals (20 episodes in phase la, 2 in phase 1b), whereas none of the animals subjected to TMR prior to the coronary artery occlusion developed ventricular fibrillation (p<0.01). The total number of premature beats per animal was lower during the early phase (la) after LAD occlusion in the TMR group than in the control group (18+/-13 vs 248+/-82, p<0.05). CONCLUSIONS: TMR prior to occlusion of LAD reduced the occurrence of early phase (la) ischemia-induced ventricular fibrillation and premature beats. This anti-fibrillatory effect might explain the improved survival observed in experimental studies after TMR prior to coronary artery occlusion found by others.
Animals↗
Physician interpretation and quantitative measures of electrocardiographic ventricular fibrillation waveform.
OBJECTIVES: The characteristics of the ventricular fibrillation (VF) waveform may influence treatment decisions and the likelihood of therapeutic success. However, assessment of VF as being fine or coarse and the distinction between fine VF and asystole are largely subjective. The authors sought to determine the level of agreement among physicians for interpretation of varying VF waveforms, and to compare these subjective interpretations with quantitative measures. METHODS: Six-second segments of waveform from LIFEPAK 300 units were collected. Fifty segments, including 45 VF and five ventricular tachycardia (VT) distracters, were graphed to simulate rhythm strips. These waveforms were quantitatively described using scaling exponent, root-mean-squared amplitude, and centroid frequency. Thirty-two emergency medicine residents were asked to interpret the arrhythmias as VT, "coarse" VF, "fine" VF, or asystole. Their responses were compared with the qantitative measures. Interphysician agreement was assessed with the kappa statistic. RESULTS: One thousand four hundred forty interpretations were analyzed. There was fair agreement between physicians about the classification of arrhythmias (kappa = 0.39). Mean values associated with coarse VF, fine VF, and asystole differed in all three quantitative measure categories. The decision whether to defibrillate was highly correlated with the distinction between VF and asystole (Pearson chi-square = 1,170.40, df = 1, p[two-sided] < 0.001). CONCLUSIONS: With only fair agreement on the threshold of fine VF and asystole, defibrillation decisions are largely subjective and caregiver-specific. These data suggest that quantitative measures of the VF waveform could augment the current standard of subjective classification of VF by emergency care providers.
Analysis of Variance↗
Protective Effects of Ranolazine on Ventricular Fibrillation Induced by Activation of the ATP-Dependent Potassium Channel in the Rabbit Heart.
BACKGROUND: The authors studied the antifibrillatory effects of the adenosine-triphosphate (ATP)-sparing metabolic modulator ranolazine in a rabbit isolated heart model in which ventricular fibrillation occurs under conditions of hypoxia/reoxygenation in the presence of the ATP-dependent potassium channel opener pinacidil. METHODS AND RESULTS: Ten minutes after ranolazine or vehicle administration, addition of pinacidil (1.25 µM) to the buffer was followed by a 12-minute hypoxic period and 40 minutes of reoxygenation. At a reduced concentration of ranolazine (10 µM), ventricular fibrillation occurred in 60% of the hearts, compared to 89% in the control group (P = NS). In contrast, only three of nine hearts (33%) treated with 20 µM ranolazine developed ventricular fibrillation (P <.05 vs vehicle). Hemodynamic parameters including coronary perfusion pressure, left ventricular developed pressure, and +/-dP/dt were not affected by the presence of ranolazine in the perfusion medium. Ranolazine did not prevent or modify the negative inotropic or coronary vasodilator actions of pinacidil, suggesting a mechanism of action independent of potassium channel antagonism. CONCLUSIONS: Ranolazine significantly reduced the incidence of ventricular fibrillation in the hypoxic/reoxygenated heart exposed to the ATP-dependent potassium channel opener, pinacidil. The reported ability of ranolazine to prevent the decrease in cellular ATP during periods of a reduced oxygen supply may account for its observed antifibrillatory action. By maintaining intracellular ATP, ranolazine may modulate or prevent further opening of the ATP-dependent potassium channel in response to hypoxia and/or pinacidil.
Journal Article↗
Ventricular fibrillation induced by coronary spasm during noncardiac surgery.
We report two cases of ventricular fibrillation during noncardiac surgery. Although an emergency coronary angiogram showed no significant coronary stenosis, coronary artery spasm was induced by the intracoronary injection of acetylcholine. It is possible that ventricular fibrillation is caused by coronary artery spasm during noncardiac surgery in patients without overt coronary artery disease.
Aged↗
Effects of propafenone on pacing-induced ventricular fibrillation and intracellular calcium in rat hearts.
Propafenone is an antiarrhythmic agent with fast sodium channel, calcium channel, and beta-adrenergic receptor blocking properties. The effects of propafenone on arrhythmias, free intracellular calcium and left ventricular performance were studied using perfused rat hearts during (i) pacing-induced ventricular fibrillation and (ii) infusion with 2.65 x 10(-6) M, 5.3 x 10(-6) M and 7.9 x 10(-6) M propafenone hydrochloride (corresponding to approximately 1, 2 and 3 mg kg-1 body weight). A bolus of 1 mg kg-1 propafenone during ventricular fibrillation resulted in a decrease in intracellular calcium, with subsequent conversion to sinus rhythm. In perfused hearts with sinus rhythm propafenone produced a dose-dependent decrease in heart rate and myocardial oxygen consumption together with a rise in left ventricular diastolic pressure, and diastolic [Ca2+]i, indicative of depression of left ventricular function. We conclude that a bolus of propafenone during ventricular fibrillation leads to a decrease in [Ca2+]i preceding conversion to sinus rhythm. In rat hearts with sinus rhythm the depressive effects of propafenone on [Ca2+]i are dose dependent.
Animals↗
Lidocaine to prevent ventricular fibrillation in the prehospital phase of suspected acute myocardial infarction: the North-Norwegian Lidocaine Intervention Trial.
The efficacy of lidocaine to prevent ventricular fibrillation during the prehospital phase of suspected acute myocardial infarction was assessed 3 hours after administration in a randomized controlled trial. A total of 204 patients examined within 6 hours after onset of symptoms were included, and acute myocardial infarction was later confirmed in 63% of these. Lidocaine, administered as a 100 mg intravenous bolus dose followed by a 300 mg intramuscular injection, failed to prevent ventricular fibrillation, which was observed in 2 (2.1%) of 96 patients in the lidocaine group and in 3 (3.0%) of 101 patients in the placebo group (p = 0.95; odds ratio 0.7, 95% confidence interval 0.4 to 1.3). In addition, sudden cardiac collapse with unknown heart rhythm was observed in three patients who received lidocaine (3.1%) compared with none in the placebo group (p = 0.23; odds ratio 7.6, 95% confidence interval 2.8 to 22.1). The results of this small study suggest that lidocaine, even when given in a high dose, is ineffective in preventing ventricular fibrillation when administered before hospitalization for suspected acute myocardial infarction. Prophylactic use of lidocaine in this situation may therefore not be warranted or advisable.
Adult↗
Myocarditis-associated ventricular fibrillation. An unusual cause of syncope in Wolff-Parkinson-White syndrome.
We report the case of a 60-year-old man with long-standing symptomatic Wolff-Parkinson-White syndrome who presented with recurrent syncope and documented spontaneous ventricular fibrillation. This primary ventricular fibrillation, which was not preceded by atrial fibrillation, was associated with lymphocytic myocarditis and not with Wolff-Parkinson-White syndrome. The patient was treated with radiofrequency ablation of the accessory pathway and a drug regimen of prednisone, amiodarone, and metoprolol. At the 6-month follow-up, he was asymptomatic and had returned to work. To our knowledge, the association of acute lymphocytic myocarditis and Wolff-Parkinson-White syndrome has not been previously reported.
Catheter Ablation↗
Analysing the ventricular fibrillation waveform.
The surface electrocardiogram associated with ventricular fibrillation has been of interest to researchers for some time. Over the last few decades, techniques have been developed to analyse this signal in an attempt to obtain more information about the state of the myocardium and the chances of successful defibrillation. This review looks at the implications of analysing the VF waveform and discusses the various techniques that have been used, including fast Fourier transform analysis, wavelet transform analysis and mathematical techniques such as chaos theory.
Electrocardiography↗