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PubMed1988

Use of temporary pacemakers during coronary angioplasty: an evolving experience with ventricular fibrillation in 400 cases.

Because of a perceived high frequency of ventricular fibrillation when a pacemaker catheter was placed in the right ventricular apex during PTCA, we reviewed our first 400 cases for this complication. The incidence of ventricular fibrillation in the entire group was 10 of 400 cases (2.5%) compared with 17 of 3,806 (0.4%) diagnostic coronary arteriograms performed in our laboratory during the same time period (P less than .001). Ventricular fibrillation occurred more frequently during PTCA when the pacemaker catheter tip was placed in the right ventricular apex (8 of 63 cases, 12.6%) than when it was positioned in either the pulmonary artery, vena cava, or when a pacemaker catheter was not used (2 of 337 cases, 0.6%, P less than .001). Based on these data we have developed a policy of inserting temporary pacemakers prophylactically during PTCA only for patients undergoing dilation of dominant right or dominant left circumflex coronary arteries and in patients with acute myocardial infarction.

Angioplasty, Balloon↗

PubMed1993

Duration of asystolic reperfusion and reperfusate electrolyte composition influence postcardioplegia ventricular fibrillation.

The conditions of postcardioplegia reperfusion that influence cardiac electrophysiologic recovery have not yet been fully elucidated. Studies of postcardioplegia electrophysiologic recovery and reperfusion-induced arrhythmias, particularly reperfusion-induced ventricular fibrillation, are useful for improving our understanding of reperfusion injury since reperfusion-induced arrhythmias are sensitive indicators for reperfusion injury. The purpose of this study was to determine the effects of asystolic reperfusion and reperfusate electrolyte composition on postcardioplegia electrophysiologic recovery of the heart. The hypothesis tested is that the duration of asystolic reperfusion produced by a hyperkalemic reperfusate is a primary determinant for the return of cardiac electrical activity without reperfusion-induced ventricular fibrillation and that reperfusion with a hypocalcemic-hyperkalemic solution further reduces the prevalence of reperfusion-induced ventricular fibrillation by limiting myocyte calcium exposure during initial postischemic recovery. Fifty-six pigs were supported by cardiopulmonary bypass and subjected to identical conditions of hypothermic cardioplegic arrest. Reperfusion was initiated with unmodified pump blood, a hypocalcemic-normokalemic cardioplegic solution, a hyperkalemic-normocalcemic cardioplegic solution, or a hyperkalemic-hypocalcemic cardioplegic solution. The hyperkalemic-normocalcemic solution was administered at a dose of 500 ml/m2 or 1500 ml/m2. The hyperkalemic-hypocalcemic and hypocalcemic-normokalemic solutions were given only at a dose of 500 ml/m2. All cardioplegic reperfusion solutions were followed by infusion of unmodified pump blood for the remainder of the 15-minute period of controlled reperfusion. Reperfusion-induced ventricular fibrillation was less prevalent in the high-dose hyperkalemic solution group (4/12) than in the low-dose hyperkalemic solution (9/10) or unmodified pump blood (12/12) groups (p < 0.05). The transmyocardial lactate gradient at the time of initial postreperfusion electrical activity was positive (0.21 +/- 0.04 mmol/L) in the high-dose hyperkalemic group and negative (-0.05 +/- 0.09 mmol/L) in the low-dose hyperkalemic group (p < 0.05). Fibrillation was less prevalent in the hypocalcemic-hyperkalemic group (8/12) than in the other groups reperfused with cardioplegic solution at a dose of 500 ml/m2 (hypocalcemic-normokalemic, 10/10; hyperkalemic-normocalcemic, 9/10) or in the group reperfused with unmodified pump blood (12/12) (p < 0.05, hypocalcemic-hyperkalemic group versus other reperfusate groups). Reperfusion-induced ventricular fibrillation is an indicator of reperfusion injury, and in this study the conditions of reperfusion influenced the prevalence of reperfusion-induced ventricular fibrillation. Recovery of aerobic metabolism during hyperkalemia-induced asystolic reperfusion was associated with a lower prevalence of reperfusion-induced ventricular fibrillation. Combining hypocalcemia with hyperkalemia decreased the prevalence of reperfusion-induced ventricular fibrillation.

Animals↗

PubMed2004

Radiofrequency ablation of idiopathic ventricular fibrillation guided by noncontact mapping.

A 32-year-old man with idiopathic ventricular fibrillation and an implantable cardioverter defibrillator presented during a ventricular fibrillation storm. Frequent monomorphic ventricular ectopics with left bundle branch block morphology were documented, some of which initiated fibrillation. He underwent noncontact mapping of the right ventricle, during which the ventricular ectopics were mapped to a site in the free wall displaying a diastolic potential 80 ms before ectopic QRS onset. Following three radiofrequency energy applications, the ectopics were abolished. After 11-month follow-up, he has experienced no further arrhythmias. Noncontact mapping may identify ablatable triggers of ventricular fibrillation and lead to successful outcomes even when only single ectopics are present.

Adult↗

PubMed2006

Enhanced expression of platelet CD40-ligand by in vitro lipopolysaccharide-challenge in patients with ventricular fibrillation complicating acute myocardial infarction.

BACKGROUND: Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet. METHODS AND RESULTS: Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS). As a control group, we studied 19 patients without VF during AMI. CD40-ligand and CD62P expression on platelets and tissue factor binding on monocytes were measured by flow cytometry. Platelet-monocyte aggregates were measured by CD41 expression on platelets adherent to monocytes. Soluble CD40-ligand plasma levels were measured with an ELISA. Without LPS, no significant difference between the patient groups concerning CD40L expression on platelets was observed, but plasma levels of soluble CD40L were significantly higher in patients with a history of AMI with VF. After LPS stimulation, patients with a history of VF showed a significantly increased expression of CD40L in comparison to the patients without ventricular fibrillation, based on a significantly higher increase of CD40L expression. CD62P expression on platelets was significantly increased in patients with a history of VF. CONCLUSIONS: Patients with a history of VF complicating AMI show an enhanced expression of CD40L on platelets after in vitro lipopolysaccharide-challenge with an enhanced platelet activation.

Biomarkers↗

PubMedDate not supplied

Electromechanical dissociation after ventricular fibrillation: prevention with calcium-entry blockers.

Calcium-entry blockers were administered in an attempt to protect myocardium during cardiac arrest due to ventricular fibrillation in mechanically ventilated dogs. An intravenous injection of verapamil, nifedipine, or lidoflazine was administered prior to successively prolonged episodes of ventricular fibrillation, during which no thoracic compression was performed. It is of interest that ventricular defibrillation was more easily obtained after treatment with the three drugs. As previously observed in this model, nine control dogs developed electromechanical dissociation (EMD) after 120 seconds of ventricular fibrillation. In contrast, six of the 11 dogs treated with 0.3 mg/kg of verapamil recovered mechanical systole after 120 seconds of ventricular fibrillation (p less than 0.05). Nifedipine administration also postponed the onset of EMD in three of four dogs. However, lidoflazine postponed the onset of EMD in only one of the eight dogs. The later onset of EMD after administration of verapamil or nifedipine in this model was attributed to myocardial protection by calcium-entry blockers during ventricular fibrillation. Decreased energy utilization during cardiac arrest was considered to be the principal protective mechanism. These observations indicate calcium-entry blockers, and especially verapamil and nifedipine, can be valuable drugs during cardiac resuscitation for ventricular fibrillation.

Animals↗

PubMed1957

Ventricular fibrillation in the isolated rabbit heart.

Ventricular fibrillation has been produced in the isolated and perfused rabbit heart by stimulating electrically at a rate from 500 to 700/min. When the perfusion fluid contained normal amounts of sodium, potassium and calcium, the fibrillation persisted after the stimulation was stopped in about 40% of hearts. When the sodium was reduced to half, tonicity being maintained by sucrose or by choline chloride, persistent fibrillation was observed in 100% of hearts. The addition of eserine or of atropine or of carbachol did not alter the percentage of hearts in which fibrillation persisted. The antimalarial compounds chloroquine, mepacrine, and pyrimethamine arrested persistent fibrillation, restoring a normal rhythm.

Animals↗

PubMed1981

Relation of the endocardial and epicardial ventricular fibrillation thresholds of the right and left ventricle.

Ventricular fibrillation thresholds were measured on the endocardium and epicardium of the right or left ventricle, or both, in 13 dogs. The electrodes, introduced through a right or left atriotomy to avoid injury to the ventricles, were aligned opposite and parallel to each other on the endocardium and epicardium. The ventricular fibrillation threshold was measured during atrial pacing by delivering a train of impulses to the ventricle during the vulnerable period after every 12th paced complex in 1 milliampere (mA) increments of current until fibrillation ensued. The mean (+/- standard deviation) right ventricular epicardial and endocardial fibrillation thresholds were 18.3 +/- 5.3 and 17.6 +/- 5.3 mA, respectively, (values not significantly different). However, the fibrillation threshold of 36.1 +/- 9.5 mA in the left ventricular epicardium was significantly higher than the value of 20.7 +/- 9.4 mA on the left ventricular endocardium. These data suggest that the proximity of the fibrillating electrodes and Purkinje network may be a factor in the measurement of ventricular vulnerability.

Animals↗

PubMed2001

Ischemia-induced ventricular fibrillation in isolated perfused rat heart: role of alpha1A-adrenoceptor mediated activation of protein kinase C.

It previously has been reported in ischemic rat hearts that local release of noradrenaline triggers ventricular fibrillation via alpha1A-adrenoceptor stimulation. In order to elucidate the intracellular pathway mediating ventricular fibrillation in this setting, we used inhibitors or activators of protein kinase C in the absence or presence of the alpha1A-adrenoceptor antagonist WB 4101. Regional ischemia was induced in isolated perfused rat heart byligature of the left coronary artery. Pharmacological interventions were tested by addition of drugs to the perfusate 10 min prior to ligature and throughout 30 min of ischemia while the epicardial electrocardiogram was continuously monitored. Blockade of protein kinase C by polymyxin B (1 micromol/l) significantly reduced ventricular fibrillation to 40% (from 87% in controls). Similar effects were seen with the protein kinase C inhibitors staurosporine 10 nmol/l (46% vs. 91%) and cremophor RH 40 100 micromol/l (33% vs. 77%). Activation of protein kinase C by 1,2-dioctanoyl-sn-glycerol (DOG, 10 micromol/l) or phorbol 12-myristate 13-acetate (PMA, 10 nmol/l) did not affect ventricular fibrillation. In the presence of the alpha1A-adrenoceptor antagonist WB 4101 (0.1 micromol/l), which per se suppressed ventricular fibrillation to 17%, both DOG and PMA increased the occurrence of ventricular fibrillation to 73% and 75%, respectively, whereas the inactive phorbol ester 4alpha-phorbol 12,13-didecanoate (4alpha-PDD, 10 nmol/l) revealed no proarrhythmic effect. In summary, during regional ischemia in the isolated perfused rat heart, alpha1A-adrenoceptor stimulation induces ventricular fibrillation mainly by activating protein kinase C.

Adrenergic alpha-Antagonists↗

PubMed1978

Superiority of practolol versus propranolol in protection against ventricular fibrillation induced by coronary occlusion.

The ability of practolol and propranolol of prevent ventricular fibrillation in experimental anterior myocardial infarction was compared in dogs subjected to ligation of the left anterior descending and first septal coronary arteries. This procedure, which causes ventricular fibrillation in 90 percent of animals within 30 minutes, was performed in control dogs and in dogs pretreated with propranolol (0.5 mg/kg body weight) or with practolol (1.5 to 2.5 mg/kg). These doses produced nearly equivalent shifts in isoproterenol-induced chronotropic dose-response curves, indicating equivalent degrees of beta adrenergic blockade. In 21 dogs with confirmed ligation, cardiogenic shock did not develop. Six of seven control dogs died with ventricular fibrillation. Six of seven dogs pretreated with propranolol also had fibrillation, whereas only one of the seven dogs pretreated with practolol manifested ventricular fibrillation during the 45 minute postligation observation period. Practolol afforded significant protection compared with no treatment or treatment with propranolol (P less than 0.05).

Animals↗

PubMed2001

Catheter ablation of a monofocal premature ventricular complex triggering idiopathic ventricular fibrillation.

A 62 year old man was admitted for evaluation of recurrent episodes of syncope. A surface ECG showed frequent repetitive premature ventricular complexes of right ventricular outflow tract origin. Ventricular fibrillation was inducible by programmed electrical stimulation but otherwise cardiac evaluation was unremarkable. A diagnosis of idiopathic ventricular fibrillation was made and an implantable cardioverter-defibrillator (ICD) was installed. However, spontaneous ventricular fibrillation recurred, requiring repeated ICD discharges. The ventricular fibrillation was reproducibly triggered by a single premature ventricular complex with a specific QRS morphology. Radiofrequency catheter ablation was carried out to eradicate this complex. No ventricular fibrillation has developed after this procedure, and the patient does not require drug treatment.

Catheter Ablation↗

PubMed1979

Disopyramide-induced ventricular fibrillation.

Three cases are described with documented ventricular fibrillation shortly after the patients received disopyramide in moderate dosage. Electrocardiograms showed markedly prolonged Q-T intervals in two patients and a prominent U wave with a prolonged Q-U interval in one patient, but no change in QRS width. Disopyramide-induced ventricular fibrillation appears to be similar to that caused by quinidine and is an indication to discontinue the drug.

Administration, Oral↗

PubMed1993

Innovative emergency defibrillation methods for refractory ventricular fibrillation in a variety of hospital settings.

This article reviews the ability of innovative rescue defibrillation techniques for the treatment of refractory ventricular fibrillation. These data were obtained in a variety of hospital settings at the University of California, San Francisco, from 1986 to 1992. Innovative rescue defibrillation techniques were applied to 15 patients with refractory ventricular fibrillation having failed > or = 2 high-energy transthoracic shocks in a variety of hospital settings. Intracardiac defibrillation was performed from a right ventricular catheter to a posterior patch in nine patients who had refractory ventricular fibrillation in the course of invasive electrophysiologic testing. Emergency simultaneous transthoracic and epicardial defibrillation was successfully performed with standard paddles placed over the thorax in contact with epicardial patch or pacing lead connectors in two patients in the operating room who underwent implantable cardioverter-defibrillator insertion and failed standard rescue defibrillations. Transesophageal defibrillation was performed in four patients in the emergency department who had a refractory ventricular fibrillation in the field. Intracardiac defibrillation successfully terminated refractory ventricular fibrillation in 9 of 9 patients in the electrophysiology laboratory. Similarly, emergency simultaneous transthoracic and epicardial defibrillation restored sinus rhythm in two patients in the operating room. Transesophageal defibrillation performed after 50 minutes of cardiac arrest successfully terminated ventricular fibrillation in each patient. Thus alternative methods now exist that permit rescue defibrillation in a variety of hospital emergency settings. These techniques are performed with simple-to-use equipment that is compatible with standard defibrillators.

Defibrillators, Implantable↗

PubMed1998

Telemetry-documented, pace-terminable ventricular tachycardia in patients with ventricular fibrillation.

The follow-up prevalence of electrogram-confirmed spontaneous ventricular tachycardia with a cycle length of >280 ms (53%) exceeds the prevalence of ventricular fibrillation (23%) in patients whose only spontaneous arrhythmia before implantable cardioverter defibrillator implantation was ventricular fibrillation. Antitachycardia pacing therapy safely terminates most (89%) of these slower ventricular tachycardia episodes, recommending the use of tiered-therapy devices and anticipatory activation of ventricular tachycardia detection and treatment algorithms for ventricular fibrillation patients who receive an implantable cardioverter defibrillator.

Electrocardiography↗

PubMed1990

Long-term outcome in patients who survive out of hospital ventricular fibrillation and undergo electrophysiologic studies: evaluation by electrophysiologic subgroups.

The long-term outcome of 241 survivors of out of hospital ventricular fibrillation who underwent programmed electrical stimulation was evaluated. Patients were categorized according to the rhythm induced at baseline drug-free electrophysiologic testing. Ventricular fibrillation was induced in 39 patients (16%) (Group 1), sustained ventricular tachycardia in 66 patients (27%) (Group 2) and nonsustained ventricular tachycardia in 34 patients (14%) (Group 3); 102 patients (42%) (Group 4) did not have an arrhythmia inducible at baseline electrophysiologic testing. Antiarrhythmic drugs were administered over the long term to 92% of patients in Group 2, 91% of patients in Group 1 and 47% of patients in Group 4. At a mean follow-up time of 30 +/- 15 months, recurrent sudden cardiac death or nonfatal ventricular fibrillation occurred in 11 (28%) of 39 patients with inducible ventricular fibrillation (Group 1), 14 (21%) of 66 patients with inducible sustained ventricular tachycardia (Group 2), 4 (12%) of 34 patients with inducible nonsustained ventricular tachycardia (Group 3) and 16 (16%) of 102 patients without inducible arrhythmias (Group 4). Actuarial analysis revealed a 2 year cumulative arrhythmia-free survival rate of 65% for patients in Group 2, 71% for patients in Group 1, 79% for patients in Group 3 and 81% for patients in Group 4 (p = 0.02). Actuarial survival of patients with inducible sustained ventricular tachycardia or ventricular fibrillation suppressed by electrophysiologically guided drug therapy was not significantly different from that in patients whose arrhythmia was not suppressed. Multivariate regression analysis revealed that only the presence of congestive heart failure was an independent predictor of outcome in these patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

PubMedDate not supplied

[Ventricular extrasystole in comparison with manifestations of ventricular tachycardia and ventricular fibrillation in acute myocardial infarct]].

We studied 76 patients with first recent myocardial infarction being not older than 12 hours. The patients included 58 men and 18 women. Their mean age was 62 years. We recorded continuously during the first three days following infarction the heart rate, all forms of ventricular premature beats, ventricular tachycardia, ventricular fibrillation, clinical status and activity of creatinine-phosphokinase and its isoenzyme MB. The results showed that ventricular premature beats (coupled and multiform) as well as ventricular tachycardia were more frequent in the first day of illness, while ventricular premature beats (except bigeminy, for which there is no explanation) were infrequent in the second and the third day after development of an infarct. The incidence of ventricular tachycardia during the follow-up period did not differ significantly. Ventricular fibrillation developed in 7 patients (9.2%). A comparison of the relation between ventricular premature beats and malignant ventricular tachycardia, i.e. ventricular tachycardia and ventricular fibrillation, revealed that the patients with more frequent ventricular tachycardia usually had frequent ventricular premature beats, particularly more often bigeminy, trigeminy, polymorphous ventricular premature and coupled ventricular premature beats, but not ventricular premature beats with R-on-T phenomenon. Ventricular tachycardia, however, was also found in patients with an evidence of more rare ventricular premature beats. This suggests that the occurrence of aforementioned forms of ventricular premature beats denotes only a somewhat greater probability that ventricular tachycardia will occur. The fact that there is a lack of correlation between ventricular tachycardia and R-on-T phenomenon indicates that this probability is not so significant. In conclusion, the authors believe that the patients with recent myocardial infarction and ventricular premature beats should be adequately followed up, and that prophylactic antiarrhythmic therapy is not required in most cases, as it was previously widely accepted concept. It should be administered only when ventricular tachycardia develops. Patients with ventricular fibrillation had more frequent ventricular premature beats, although ventricular premature beats in these patients were not statistically more frequent from those found in the patients in whom ventricular fibrillation was not verified. The presence or absence of ventricular tachycardia and ventricular fibrillation, respectively, had no influence on the other followed up parameters.

Female↗

PubMed1994

Effects of amiodarone on refractory ventricular fibrillation in acute myocardial infarction: experimental study.

OBJECTIVES: The aim of this study was to evaluate the efficacy of a single dose of intravenous amiodarone in facilitating defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks in experimental acute myocardial infarction. BACKGROUND: Amiodarone has been hailed as the most effective single antiarrhythmic drug for the treatment of ventricular arrhythmias. However, intravenous amiodarone has only sporadically been used in the defibrillation of ventricular fibrillation in acute myocardial infarction. METHODS: Acute myocardial infarction was induced in 60 dogs by ligation of the proximal left anterior descending coronary artery for 2 h. Animals that developed spontaneous ventricular fibrillation were treated with lidocaine and epinephrine plus five direct-current countershocks. Dogs with ventricular fibrillation refractory to this regimen were randomized to further treatment with additional intravenous administration of epinephrine and bolus lidocaine plus < or = 15 direct-current countershocks (group I) or administration of amiodarone, 10 mg/kg body weight intravenously, followed by defibrillation with direct-current counter-shock (group II). RESULTS: Sixteen (27%) of the 60 dogs in which the protocol was attempted developed spontaneous ventricular fibrillation 21 min after ligation and were included in the study. Lidocaine and epinephrine plus five direct-current countershocks succeeded in converting ventricular fibrillation in one dog (6%). The other 15 dogs were randomized to group I (8 dogs) or group II (7 dogs). Defibrillation was achieved in one of the eight dogs in group I and in six of the seven dogs in group II (p < 0.005). CONCLUSIONS: In an experimental model of acute ischemia, intravenous amiodarone (10 mg/kg) influences positively the response to defibrillation of ventricular fibrillation refractory to lidocaine and epinephrine plus direct current countershocks.

Amiodarone↗

PubMed1993

A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion.

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.

Cardiomyopathies↗

PubMed1980

Late ventricular fibrillation following successful resuscitation from postinfarction cardiogenic shock with intraaortic balloon pumping.

Early ventricular fibrillation occurs in approximately 5% of patients admitted for acute myocardial infarction. Although late ventricular fibrillation (> 48 hours postinfarction) may occur in stable patients, it occurs more commonly when severe left ventricular power failure is present. We have encountered late ventricular fibrillation in three of 42 (7%) patients treated with intraaortic balloon pumping (IABP) for profound cardiogenic shock secondary to myocardial infarction. These patients progressed to our hemodynamic Class A prior to weaning, and were thought to be stable prior to IABP removal. They were the only ones who expired after achieving Class A status. The episodes of late ventricular fibrillation occurred after the patients had been successfully weaned from IABP and were free of arrhythmias. This experience suggests that prolonged antiarrhythmic therapy may be indicated for postinfarction patients who have had ventricular dysrhythmias during IABP support.

Journal Article↗