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PubMed1998

Vulnerability to ventricular fibrillation.

One of the factors that favors the development of ventricular fibrillation is an increase in the dispersion of refractoriness. Experiments will be described in which an increase in dispersion in the recovery of excitability was determined during brief episodes of enhanced sympathetic nerve activity, known to increase the risk of fibrillation. Whereas in the normal heart ventricular fibrillation can be induced by a strong electrical shock, a premature stimulus of moderate intensity only induces fibrillation in the presence of regional ischemia, which greatly increases the dispersion of refractoriness. One factor that is of importance for the transition of reentrant ventricular tachycardia to ventricular fibrillation during acute regional ischemia is the subendocardial Purkinje system. After selective destruction of the Purkinje network by lugol, reentrant tachycardias still develop in the ischemic region, but they do not degenerate into fibrillation. Finally, attempts were made to determine the minimal mass of thin ventricular myocardium required to sustain fibrillation induced by burst pacing. This was done by freezing of subendocardial and midmural layers. The rim of surviving epicardial muscle had to be larger than 20 g. Extracellular electrograms during fibrillation in both the intact and the "frozen" left ventricle were indistinguishable, but activation patterns were markedly different. In the intact ventricle epicardial activation was compatible with multiple wavelet reentry, in the "frozen" heart a single, or at most two wandering reentrant waves were seen. (c) 1998 American Institute of Physics.

Journal Article↗
PubMed1980

Comparison of the effects of left ventricular distention during cardioplegic-induced ischemic arrest and ventricular fibrillation.

To evaluate the role of left ventricular distention in the pathophysiology of myocardial injury during cardiac surgery, 40 isolated, perfused feline hearts were subjected to 1 hour of either hypothermic potassium arrest (groups 1, 2 and 3) or 1 hour of hypothermic ventricular fibrilation (groups 4 and 5). During this period, intracavitary left ventricular pressure was maintained at 0 mm Hg in groups 1 and 4, at 30 mm Hg in groups 2 and 5 and 45 mm Hg in group 3. After either reperfusion of defibrillation, myocardial gas tensions, left ventricular function, coronary blood flow, the ration of endocardial to epicardial blood flow, and myocardial water content were measured to evaluate the degree of myocardial injury incurred. In addition, structural changes in the myocardium were assessed using light and electron microscopy. No differences in these parameters were seen in hearts that underwent ischemic arrest, regardless of the presence or absence of significant left ventricular distention. In fibrillating hearts, however, dilatation decreased ventricular performance, impaired subendocaridal blood flow and elevated myocardial CO2 tensions. These results suggest that left ventricular distention per se is not harmful during periods of ischemia. During periods of ventricular fibrillation, howevr, distention produces impaired subendocardial blood flow, resulting increased ischemia and decreased recovery of ventricular performance.

Animals↗
PubMed1984

Antiarrhythmic and electrophysiologic actions of bethanidine sulfate in primary ventricular fibrillation or life-threatening ventricular tachycardia.

Antiarrhythmic and electrophysiologic actions of bethanidine sulfate, a chemical analog of bretylium tosylate, were studied using programmed cardiac electrical stimulation in 14 survivors of out-of-hospital cardiac arrest unassociated with acute myocardial infarction. Before bethanidine sulfate was administered sustained ventricular tachyarrhythmias (VT) were inducible in 11 patients and reproducible nonsustained VT was induced in 3 patients. Bethanidine sulfate shortened sinus cycle length and absolute and relative ventricular refractory periods measured during sinus rhythm, but did not alter ventricular effective refractory period measured during ventricular pacing. Bethanidine sulfate prevented inducible VT in 8 patients (57%), increased the number of extrastimuli needed to induce VT in 2 patients, and was ineffective in 4 patients. In contrast, in only 1 of 26 trials with other conventional and investigational antiarrhythmic drugs in these patients was VT prevented. Orthostatic hypotension was a prominent side effect of bethanidine sulfate therapy, but could be reversed in most patients by concomitant administration of protriptyline. Five patients in whom bethanidine sulfate was effective in the laboratory have been treated chronically (400 to 600 mg 4 times daily), and all are alive at 3 to 40 months. In the remaining 9 patients, 8 were treated empirically because no drug was effective in the laboratory and 1 was treated with quinidine, which appeared to be protective during testing. Four of these 9 patients, including the patient treated with quinidine, died suddenly during follow-up. Thus, although bethanidine sulfate therapy is difficult to initiate because of orthostatic hypotensive side effects, it may be useful in treating patients at high risk of recurrent cardiac arrest.

Adult↗
PubMed1983

Detailed analysis of 24 hour ambulatory electrocardiographic recordings during ventricular fibrillation or torsade de pointes.

Although the terminal cardiac rhythm is often well documented in many cases of sudden cardiac death, the antecedent or premonitory arrhythmias are usually not retrievable. The ambulatory electrocardiographic recordings of 12 patients who sustained ventricular fibrillation or torsade de pointes while wearing a long-term electrocardiographic monitor were analyzed in detail. A printout of the entire electrocardiographic recording was made and hand counts of ventricular arrhythmias were correlated with heart rate, QTc interval, RR interval preceding ventricular fibrillation or torsade de pointes and (RR')/QT initiating ventricular fibrillation or torsade de pointes. Common ambulatory electrocardiographic features in these 12 patients experiencing ventricular fibrillation or torsade de pointes included: 1) a period of high density of increasingly frequent or complex ventricular arrhythmias, or both, preceding ventricular fibrillation or torsade de pointes (11 patients); 2) R on T beats frequently initiating ventricular fibrillation or torsade de pointes (9 patients); and 3) repolarization abnormalities present for several hours before ventricular fibrillation or torsade de pointes (7 patients). No consistent relation between the RR and RR' interval initiating ventricular fibrillation or torsade de pointes was found; no consistent alteration in heart rate occurred before ventricular fibrillation or torsade de pointes. Thus, ventricular arrhythmias leading to sudden death in an ambulatory population do not occur in isolation but are preceded by a period of increased ventricular ectopic activity. Future guidelines for assessment of antiarrhythmic drug efficacy should include an evaluation of a drug's impact not only on ectopic beat frequency but also on arrhythmia density.

Adult↗
PubMed1980

Protective effect of verapamil on vulnerability to ventricular fibrillation during myocardial ischaemia and reperfusion.

The effects of verapamil on vulnerability to ventricular fibrillation were studied in 55 chloralose-anaesthetised dogs. Ventricular fibrillation threshold was measured before and during a 10 min period of left anterior descending coronary artery occlusion and following abrupt release of occlusion. The action of intravenous verapamil (0.01 mg.kg-1.min-1, following a 0.1 mg.kg-1 bolus) on vulnerability to fibrillation was examined before and during coronary artery occlusion and reperfusion. While the infusion of verapamil did not alter the ventricular fibrillation threshold in the nonischaemic myocardium, the vulnerable period threshold was raised and the incidence of spontaneous ventricular fibrillation was reduced both after coronary artery occlusion and release. Since cardiocardiac sympathetic reflexes are elicited in response to coronary artery occlusion, the effect of verapamil on vulnerability during left stellate ganglion stimulation and during noradrenaline infusion was investigated. Verapamil completely prevented the reduction in vulnerable period threshold during sympathetic nerve stimulation or noradrenaline infusion. This study suggests that the antifibrillatory action of verapamil during coronary artery occlusion may be, in part, related to antagonism of enhanced adrenergic input to the heart, while the mechanism of protection during reperfusion is as yet uncertain.

Adrenergic Fibers↗
PubMed1977

Ventricular fibrillation in a medically supervised cardiac exercise program. Clinical, angiographic, and surgical correlations.

Five patients with ischemic heart disease were resuscitated after experiencing ventricular fibrillation in a medically supervised exercise program. Four subsequently had successful myocardial revascularization (three prior to hospital discharge), and three have returned to an exercise prescription of reduced intensity. Multivessel operative coronary disease is common in patients experiencing ventricular fibrillation. Ventricular fibrillation may occur unpredictably (two to 48 months) in duration of exercise. Exercise fitness centers for such patients should be medically supervised and equipped with a defibrillator and appropriate drugs.

Adult↗
PubMed2004

Recurrent ventricular fibrillation secondary to aortic valve tumor.

The case of a patient with recurrent ventricular fibrillation secondary to an aortic tumor is reported. Ventricular fibrillation occurs secondary to ischemia, arrhythmia, or congenital disease, or it may be an idiopathic event. Irreversible and recurrent situations require placement of an implantable cardioverter defibrillator (ICD). A patient with recurrent syncope secondary to documented ventricular fibrillation without a clear mechanism and a negative electrophysiologic study underwent ICD placement. A cardiac papillary fibroelastoma at the aortic valve subsequently was found. Cardiac tumors in the aortic valve can obstruct the coronary arteries, secondarily causing ischemia and ventricular fibrillation. Such a mechanism must be considered in the differential diagnosis of sudden death.

Aortic Valve↗
PubMed1997

Changes in the QT interval and its adaptation to rate, assessed with continuous electrocardiographic recordings in patients with ventricular fibrillation, as compared to normal individuals without arrhythmias.

Various QT interval variables and heart rate variability parameters were studied in six patients with ventricular fibrillation but without heart disease and compared with findings in 21 normal persons. QT and QT dispersion (QTd) were measured from conventional 12 lead ECGs: for dynamic QT analysis, QT intervals were automatically measured to the end of the T wave (QTe) on a 24 h ECG recording. The adaptation of the QT interval to changes in heart rate was expressed as the slope of the linear regression lines relating QTc to the RR interval (Sc). The complete 24 h ECG recording and four 6 h segments were studied (morning, day, evening, and night). Ventricular fibrillation patients had slightly prolonged QTmax intervals on the 12 lead ECG, QT dispersion was longer in ventricular fibrillation patients than in normal persons (88 +/- 29 ms vs 59 +/- 26 ms. P < 0.05), and on the 24 h ECG recording, normal persons and ventricular fibrillation patients had a comparable RR. In addition, parameters for long-term (SD, standard deviation of normal RR intervals) and short-term (RMSSD, the root-mean-square successive differences of normal RR intervals heart rate variability were not different. Automatic measurement of the QT interval and the QTc/RR slopes was possible over 24 h and in the 6 h intervals in a large majority of patients (25/27 and 88/108 readings). The mean 24 h QT and the mean 6 h QT interval were comparable in normal subjects and ventricular fibrillation patients except for the day segment. The 24 h Se was significantly lower in ventricular fibrillation patients, compared to normal individuals. Furthermore, Se in the morning and night segment was also significantly lower in ventricular fibrillation patients (both P < 0.05). In conclusion, patients with ventricular fibrillation but without underlying structural heart disease have normal heart rate variability parameters. However, abnormal repolarization behaviour, characterized by an increased QTd and a depressed adaptation of QT to variations in RR (especially during the night and the morning), is present. These findings may help to understand and treat arrhythmias in this patient group.

Adult↗
PubMed1990

Noninvasive detection of patients with ischemic and nonischemic heart disease prone to ventricular fibrillation.

Abnormalities in the fast Fourier transforms of signal-averaged electrocardiograms (ECGs) obtained during sinus rhythm appear to distinguish patients with ischemic heart disease and sustained monomorphic ventricular tachycardia from those without ventricular tachycardia. This study was performed to determine the power of frequency analysis to detect patients with a history of ventricular fibrillation, to determine the extent to which spectra of signal-averaged ECGs from patients with ischemic and nonischemic heart disease are comparable and to compare results of signal-averaged ECG analysis in patients with ventricular fibrillation with results of programmed ventricular stimulation. Signal-averaged ECGs were obtained during sinus rhythm from 60 patients with sustained ventricular tachycardia (Group I) and 34 patients with ventricular fibrillation (Group II). Results of signal-averaged ECG analysis were abnormal in 92% of patients with ventricular tachycardia and 85% of patients with ventricular fibrillation (p = NS). Abnormal spectra were detected in the signal-averaged ECGs from 90% of patients with ischemic and from 86% of patients with nonischemic heart disease (p = NS). In contrast, the results of programmed stimulation differed markedly between the two patient groups. Sustained ventricular arrhythmias were induced in 91% of the patients with ventricular tachycardia compared with only 46% of those with ventricular fibrillation (p less than 0.0001). Moreover, ventricular tachycardia was inducible in 81% of patients with ischemic heart disease compared with only 50% of those with nonischemic heart disease (p less than 0.02). Thus, abnormalities in the spectra of signal-averaged ECGs were found in the majority of patients with ventricular fibrillation and were detectable even in those whose arrhythmia was not inducible by programmed stimulation. These results broaden the potential clinical application of noninvasive interrogation of signal-averaged ECGs to include the prospective identification of patients with ischemic or nonischemic heart disease prone to ventricular tachycardia or ventricular fibrillation.

Cardiac Pacing, Artificial↗
PubMed1991

Long-term survival after resuscitation from ventricular fibrillation occurring before hospital admission.

Factors related to long-term (post-discharge) outcome following successful resuscitation from pre-hospital ventricular fibrillation by a physician-manned mobile coronary care unit were studied. Between 1 January 1966 and 31 December 1987, 190 patients were resuscitated from pre-hospital ventricular fibrillation (158 male; mean age 56 years). The aetiology of ventricular fibrillation was acute myocardial infarction in 131 patients (69 per cent), ischaemic heart disease without infarction in 48 (25 per cent) and other or unknown in 11 (6 per cent). Predicted actuarial survival rates at 1, 2, 5, 10 and 20 years were 76 per cent, 66 per cent, 41 per cent, 27 per cent and 12 per cent respectively. Of 128 recorded deaths over 20 years, 85 per cent were cardiac and 48 per cent were defined as sudden death outside hospital. Factors significantly associated with increased long-term mortality (p less than 0.05), based on analysis of 10 year actuarial life tables using the Lee-Desu statistic were ventricular fibrillation due to ischaemic heart disease without infarction rather than acute myocardial infarction, a history of previous myocardial infarction, a history of hypertension, digoxin and diuretic therapy before ventricular fibrillation and digoxin as discharge medication, and failure to stop smoking after discharge from hospital by patients who had been smoking prior to ventricular fibrillation. In addition, Cox's regression analysis showed that patient age greater than or equal to 60 years was significantly associated with increased long-term mortality. On multivariate analysis, factors independently associated with increased long-term mortality were ventricular fibrillation occurring before 1977, previous myocardial infarction or hypertension and digoxin as discharge medication.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Heart rate variability and dispersion of QT interval in patients with vulnerability to ventricular tachycardia and ventricular fibrillation after previous myocardial infarction.

OBJECTIVES: This study was designed to compare QT dispersion measured from the standard 12-lead electrocardiogram and 24-h heart rate variability in patients with vulnerability to either ventricular tachycardia or ventricular fibrillation after a previous myocardial infarction. BACKGROUND: Increased QT interval dispersion and reduced heart rate variability have been shown to be associated with vulnerability to ventricular tachyarrhythmias, but the data have mainly been pooled from patients with presentation of stable ventricular tachycardia and ventricular fibrillation. METHODS: QT dispersion and time domain and two-dimensional vector analysis of heart rate variability were studied in 30 survivors of ventricular fibrillation with a previous myocardial infarction and with inducible unstable ventricular tachyarrhythmia by programmed electrical stimulation and in 30 postinfarction patients with clinical and inducible stable monomorphic sustained ventricular tachycardia. Both of these patient groups were matched, with respect to age, gender and left ventricular ejection fraction, with an equal number of postinfarction control patients without a history of arrhythmic events or inducible ventricular tachyarrhythmia and arrhythmia-free survival during a follow-up period of 2 years. Forty-five age-matched healthy subjects served as normal control subjects. RESULTS: Standard deviation of all sinus intervals and long-term continuous RR interval variability analyzed from Poincaré plots were reduced in patients with vulnerability to ventricular fibrillation (p < 0.001 for both), but not in patients with ventricular tachycardia (p = NS for both), compared with postinfarction control subjects. Corrected QT (QTc) dispersion was significantly broader both in patients with ventricular fibrillation (p < 0.001) and in those with ventricular tachycardia (p < 0.05) than in matched postinfarction control subjects. Heart rate variability performed better than QTc dispersion in predicting vulnerability to ventricular fibrillation. CONCLUSIONS: Increased QT dispersion is associated with vulnerability to both ventricular tachycardia and ventricular fibrillation. Low heart rate variability is specifically related to susceptibility to ventricular fibrillation but not to stable monomorphic ventricular tachycardia, suggesting that the autonomic nervous system modifies the presentation of life-threatening ventricular arrhythmias.

Aged↗
PubMed2004

Precountershock cardiopulmonary resuscitation improves initial response to defibrillation from prolonged ventricular fibrillation: a randomized, controlled swine study.

OBJECTIVES: To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF). DESIGN: Randomized, controlled trial. SETTING: University animal laboratory. SUBJECTS: Thirty swine (27 +/- 1 kg). INTERVENTIONS: After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks. MEASUREMENTS AND MAIN RESULTS: After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p <.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p <.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation. The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p <.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p <.0001) CONCLUSIONS: Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.

Animals↗
PubMed1982

Onset of atrial fibrillation during antidromic tachycardia: association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome.

Electrophysiologic evaluation in an 18 year old youth with the Wolff-Parkinson-White syndrome who had a sudden cardiac arrest while playing racquetball revealed two types of paroxysmal reciprocating tachycardia: (1) A normal QRS tachycardia with a short ventriculoatrial (V-A) interval fulfilled the criteria for reentry within the atrioventricular (A-V) node; and (2) a wide QRS tachycardia with a QRS configuration of maximal preexcitation was demonstrated to be the result of an antidromic mechanism. During laboratory study, the wide QRS tachycardia spontaneously degenerated into atrial fibrillation. In the basal state, the shortest R-R interval between preexcited QRS complexes was 270 ms, but after infusion of isoproterenol (1.6 microgram/min intravenously), the shortest R-R interval became 180 ms. Consequently, this electrophysiologic study suggested that evolution of antidromic reciprocating tachycardia into atrial fibrillation with a rapid ventricular response during exercise-induced catecholamine release may have been the mechanism for ventricular fibrillation in this patient.

Adolescent↗
PubMed1995

Selective right ventricular angiography in apparently idiopathic ventricular fibrillation.

The definition of underlying heart disease in apparently idiopathic ventricular fibrillation seems to be important in regard to prognosis and choice of therapy. From October 1989, until August 1993, cardiac arrest due to the documented ventricular fibrillation occurred in eight consecutive patients with normal results on clinical examination, normal echocardiography, and normal or apparently nonspecific electrocardiogram (ECG) findings. Complete invasive investigations, including selective right ventricular angiography, were done; regional hypokinesia and segmental bulging of the right ventricle were found in seven patients (88%). Arrhythmogenic right ventricular dysplasia was suspected in these patients, although endomyocardial biopsy was not performed. After the finding of localized right precordial QRS prolongation of more than 110 ms in November 1993 in five patients, a retrospective, a more precise approach to QRS duration in standard ECG supported this diagnosis. Selective right ventricular angiography is of great help in identifying underlying heart disease in patients with apparently idiopathic ventricular fibrillation, and confirms ECG findings.

Adolescent↗
PubMed1996

Ventricular fibrillation following administration of thrombolytic treatment. The EMIP experience. European Myocardial Infarction Project.

Reperfusion-induced ventricular fibrillation has been demonstrated in animal models of myocardial ischaemia, but no evidence exists for this in humans. The European Myocardial Infarction Project compared the efficacy and safety of pre-hospital thrombolytic therapy with that of hospital therapy. The objective of this study was to investigate the occurrence of reperfusion-induced ventricular fibrillation in acute myocardial infarction patients following thrombolytic therapy. In a double-blind multicentre trial, eligible patients were randomized to receive anistreplase at home followed by placebo in the hospital (A/P group), or placebo followed by anistreplase (P/A group). The occurrence of ventricular fibrillation, and other adverse events were recorded on specific study forms and could be attributed to defined time intervals. The incidence of ventricular fibrillation in the A/P group was significantly higher following the pre-hospital injection than in the P/A group (2.5% vs 1.6%; P = 0.021); the situation was reversed following the hospital injection (3.6% vs 5.3%; P = 0.002). No relationship was found between this excess of ventricular fibrillation and the patients' condition, with the exception of the site of the infarct. These results suggest the existence of reperfusion-induced ventricular fibrillation in patients developing myocardial infarction who receive thrombolytic treatment.

Anistreplase↗
PubMedDate not supplied

Depletion of myocardial high energy phosphates by induction of ventricular fibrillation prior to cardioplegic arrest.

The effects of a short period of ventricular fibrillation on myocardial high energy phosphates were assessed in two groups of rats. Group 1 underwent hypothermic crystalloid cardioplegia infusion and aortic cross-clamping. In Group 2, cardioplegia and cross-clamping were preceded by ten seconds of induced ventricular fibrillation. In rat hearts that had undergone ventricular fibrillation, adenosine triphosphate levels averaged only 70% (p less than .0001) and creatine phosphate levels averaged only 60% (p less than .0005) of levels measured following standard cardioplegic arrest without ventricular fibrillation. These findings are of potential importance in both routine cardiac surgical procedures and in organ procurement.

Adenosine Triphosphate↗