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PubMed1998

Ventricular fibrillation: one spiral or many?

Ventricular fibrillation is the major cause of sudden cardiac death, the leading cause of death in the industrialized world; however, the mechanisms for its onset are not well understood. To further understand the dynamics of fibrillation at and near its onset, we compared spatial and temporal variability of mean interactivation intervals in a stable canine model for ventricular fibrillation. Temporal variability was very small, suggesting that the relevant physiological parameters remained constant during our experiments. Spatial variability was usually significantly larger and appeared incompatible with the dynamics of a single, meandering spiral wave. This confirmed recent results that a single spiral wave cannot generate ventricular fibrillation. Thus the onset of fibrillation is a multistage process, with spiral-wave breakdown providing a crucial step in the quasi-periodic route to fibrillation.

Analysis of Variance↗
PubMed1978

[Prevention of ventricular fibrillation in animal experiments].

The precursors of ventricular fibrillation and asystole developing after ligation of a branch of the coronary artery and adrenalin injection were studied in 30 albino rats. The comparative efficacy of antiarrhythmic agents (ajmalin, lidocaine, isoptin, visken) in the prevention of ventricular fibrillation induced by electric current was determined in 40 rats. Ventricular extrasystole and tachysystole as well as the block of the bundle of His branch were the most common precursors of ventricular fibrillation. In some experiments fibrillation was preceded by complete atrioventricular block, cardiac fibrillation, sinus bradycardia, nonparoxysmal ventricular tachycardia, and excaped ventricular contractions. Ventricular asystole was most frequently preceded by complete atrioventricular block and the bundle of His branch block. Among the antiarrhythmic agents studied, ajmalin proved most effective in prevention of ventricular fibrillation; it raised the fibrillation threshold in all animals. Lidocaine, which produced a prophylactic effect in 50% of experiments, was second in effectiveness. Changes in the ventricular fibrillation threshold due to the effect of these agents were statistically significant on the average. Isoptin and visken proved to be less effective.

Ajmaline↗
PubMed1992

Frequency analysis of ventricular fibrillation and resuscitation success.

In 56 patients, frequency analysis of the electrocardiogram of ventricular fibrillation exhibited power spectra with a distinct dominant frequency. The greatest success for resuscitation from ventricular fibrillation is recorded when ventricular fibrillation develops after the patient comes under coronary care. Of the 41 patients in whom the onset and first 8 s of ventricular fibrillation were artefact-free the mean dominant frequency of primary ventricular fibrillation (no cardiogenic shock or cardiac failure) in 21 patients was 6.2 +/- 0.2 Hz, significantly higher than the mean dominant frequency of the first 8 s of secondary ventricular fibrillation (cardiogenic shock or heart failure) (4.0 +/- 0.2 Hz, 20 patients, p = 0.0001). In these patients the peak-to-trough amplitude (ECG) of the first 8 s of ventricular fibrillation was similar in both primary and secondary ventricular fibrillation as was the mean duration of ventricular fibrillation prior to the first DC shock. There was a significantly lower success rate for resuscitation from secondary ventricular fibrillation (6 of 20 patients) compared with resuscitation from primary ventricular fibrillation (18 of 21 patients, chi 2 17.8, p = 0.001). Of the remaining 15 patients who were collapsed between 3 and 20 min before the arrival of the mobile coronary care unit, the dominant frequency of the first 8 s of ventricular fibrillation fell with increased duration of collapse (from 5.5 Hz at 3 min to a mean of 2.1 Hz at 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Ventricular fibrillation does not depress postfibrillatory contractility in blood-perfused dog hearts.

We studied whether ventricular fibrillation depresses ventricular contractility in a blood-perfused heart. In 12 excised, cross-circulated dog hearts, we measured left ventricular pressure and myocardial oxygen consumption at a middle left ventricular volume as control and induced ventricular fibrillation electrically. Six hearts were subjected to 20 minutes of ventricular fibrillation (group A), and the other six hearts were subjected to 40 minutes of ventricular fibrillation (group B). Then we defibrillated the heart with direct current shock and measured left ventricular pressure, left ventricular volume, and myocardial oxygen consumption immediately, 10 minutes, 20 minutes, and 30 minutes after the defibrillation. Coronary perfusion pressure was maintained normal (around 100 mm Hg) by the arterial pressure of the support dog throughout each experiment. Ventricular contractility was quantified by the maximum value for the instantaneous pressure/volume ratio (Emax). Pooled data of both groups A and B showed that Emax immediately after defibrillation increased to 116% +/- 28% (p less than 0.05) of control level and Emax 10 minutes after defibrillation decreased to 84% +/- 17% (p less than 0.05) of control level. Then Emax recovered to the control level: 95% +/- 18% (p greater than 0.05) of control level at 20 minutes and 100% +/- 20% (p greater than 0.05) of control level at 30 minutes after defibrillation. Emax of group A was not different from that of group B at comparable measurement times after defibrillation. Changes in myocardial oxygen consumption per beat were in proportion to the changes in Emax. We conclude that ventricular fibrillation per se for 20 to 40 minutes does not depress postfibrillatory contractility when coronary blood perfusion is maintained normal in the dog left ventricle.

Animals↗
PubMed2001

Case report: adenosine induced ventricular fibrillation in a patient with stable ventricular tachycardia.

Adenosine is frequently used in emergency departments and intensive care units for the termination of narrow complex tachycardias. Recently its utility in terminating wide complex tachycardias has been reported in the literature. Adenosine is generally felt to be a safe medication even though its proarrhythmic effects in the setting of narrow complex or supraventricular tachycardias have been well documented. Herein, we describe the first case to our knowledge of adenosine inducing ventricular fibrillation in a patient with a stable wide complex tachycardia that was subsequently proven to be ventricular tachycardia at electrophysiologic study.

Adenosine↗
PubMed1975

[Recurrent ventricular fibrillation (author's transl)].

106 episodes of ventricular fibrillation were observed in 11 patients, 9 of whom had acute myocardial infarctions. The heart rate before the onset of ventricular fibrillation was below 50 in two episodes, 60 to 100 in 63, and above 100 in 41. 83 attacks of ventricular fibrillation were preceded by fewer than five ventricular premature beats, 23 by more than five, 19 by more than ten. Multifocal ventricular premature beats occurred ten times, runs of ventricular premature beats 11 times, with only three falling into the vulnerable period. Left bundle branch block was present in three patients, right bundle branch block with left anterior hemiblock in two, isolated left anterior hemiblock in two, left posterior hemiblock in one. 85 episodes of ventricular fibrillation occurred during antiarrhythmic treatment, 72 during lidocaine administration. Antiarrhythmic drugs were effective only in reducing the number of ventricular premature beats. The only successful treatment of recurrent episodes of ventricular fibrillation was repeated electrical countershocks.

Aged↗
PubMed1998

Spatiotemporal evolution of ventricular fibrillation.

Sudden cardiac death is the leading cause of death in the industrialized world, with the majority of such tragedies being due to ventricular fibrillation. Ventricular fibrillation is a frenzied and irregular disturbance of the heart rhythm that quickly renders the heart incapable of sustaining life. Rotors, electrophysiological structures that emit rotating spiral waves, occur in several systems that all share with the heart the functional properties of excitability and refractoriness. These re-entrant waves, seen in numerical solutions of simplified models of cardiac tissue, may occur during ventricular tachycardias. It has been difficult to detect such forms of re-entry in fibrillating mammalian ventricles. Here we show that, in isolated perfused dog hearts, high spatial and temporal resolution mapping of optical transmembrane potentials can easily detect transiently erupting rotors during the early phase of ventricular fibrillation. This activity is characterized by a relatively high spatiotemporal cross-correlation. During this early fibrillatory interval, frequent wavefront collisions and wavebreak generation are also dominant features. Interestingly, this spatiotemporal pattern undergoes an evolution to a less highly spatially correlated mechanism that lacks the epicardial manifestations of rotors despite continued myocardial perfusion.

Electric Stimulation↗
PubMed1992

Prediction of hospital discharge in immediate survivors of ventricular fibrillation or asystole.

Survival from ventricular fibrillation and asystole is influenced by variables measured during resuscitation that affect both immediate survival and discharge from hospital. These variables have been used to develop a formula to calculate an individuals chances of immediate survival and hospital discharge. It has allowed this heterogenous group to be subdivided into groups which can be compared both within and between institutions for the purposes of audit and evaluation of resuscitation protocols. This study evaluates the addition of clinical parameters to the prognostic index. One hundred twelve immediate survivors of ventricular fibrillation or asystole were examined immediately after resuscitation and clinical parameters measured and recorded. At the same time parameters previously described were recorded. The increase in the numbers of survivors improved the reliability (area under the receiver operator curve (ROC) improved from 0.79 to 0.83) of the index for predicting hospital discharge. Addition of the clinical variables of conscious state, respiratory state, blood pressure and pulse rate improved the prognostic index further to an ROC area of 0.86. This ensures that the predictive power of the new index is now highly reliable for predicting hospital discharge after successful resuscitation from ventricular fibrillation and asystole.

Aged↗
PubMed1987

Ventricular fibrillation during coronary angiography: the precatheterization QT interval.

Ventricular fibrillation during coronary angiography is associated with contrast-induced changes in repolarization and thus pre-catheterization abnormalities could predispose to this event. We retrospectively examined angiograms, pre-catheterization electrocardiograms and records of 26 consecutive patients who had ventricular fibrillation during coronary angiography, and compared these patients to controls matched for age, sex, and left ventricular function. Diatrizoate meglumine was used as the angiographic contrast agent in all instances. Catheterization findings and the prevalence of prior myocardial infarction were similar in both groups. However, pre-catheterization QT intervals in the ventricular fibrillation group (0.43 +/- 0.05 sec) were significantly longer than in control patients (0.39 +/- 0.04 sec, P less than 0.005) as were their QT intervals corrected for heart rate (QTc) (0.47 +/- 0.04 vs 0.42 +/- 0.03 sec; P less than 0.001). Only seven of the 16 patients (44%) with ventricular fibrillation who had a precatheterization QTc greater than 0.44 sec had the arrhythmia during angiography of a critically stenosed (greater than 75%) coronary artery, whereas VF followed injection of critically stenosed vessels in eight of 10 (80%) of those with a normal QTc (p NS). After a follow-up period of 24 to 54 months (mean 39), two ventricular fibrillation patients have died (one suddenly), as compared to five in the control group (two suddenly) (p NS). Therefore, pre-catheterization QT prolongation was associated with ventricular fibrillation during coronary angiography, but ventricular fibrillation did not necessarily portend a worse long-term prognosis.

Angiography↗
PubMed1986

Incidence and clinical significance of ventricular fibrillation induced with single and double ventricular extrastimuli.

Of 718 patients evaluated for suspected or documented ventricular tachyarrhythmias, ventricular fibrillation (VF) was induced in 28 (incidence 3.9%) by single and double extrastimuli. Nine of the 28 patients had suspected but no clinically documented ventricular tachycardia (VT) or VF (group 1), 11 had documented VT (group 2) and 8 had out of hospital VF (group 3). In group 1, electropharmacologic control was achieved in 8 patients with the initial agent tested; however, symptoms recurred in 6 patients. In 4 patients the drug was discontinued. After a follow-up of 26 +/- 11 months in group 1, no patient had died. In only 2 of 19 patients in groups 2 and 3 were arrhythmias controlled with the initial agent; 15 patients had VT and 2 VF. Control with class I agents was achieved in 9 of 19 patients and none died until the drug regimen was changed empirically in 3 of these 9. Ten patients, all from groups 2 and 3, were treated empirically with amiodarone; 3 died. All patients died either suddenly or in VT. The mortality rate in groups 2 and 3 after a mean follow-up of 24 +/- 9 months was 32% (p less than 0.05). Continued symptoms and no deaths in group 1 suggests a nonclinical nature of induced VF. Control of induced VF on serial drug testing in group 2 and 3 also indicates a false-negative drug efficacy response, as pharmacologic control of emergent VT on subsequent studies appeared essential to their survival despite control of induced VF. Thus, even with single or double premature stimuli, induction of VF can be a nonclinical response, especially in patients without clinical VF.

Adult↗
PubMed1995

Evidence for electrical organization during ventricular fibrillation in the human heart.

INTRODUCTION: Ventricular fibrillation is a most dangerous cardiac arrhythmia that has received considerable attention, yet its pattern of electrical activation remains controversial. The aim of this study was to investigate the degree of organization during the clinical arrhythmia and to examine the phase relationship between deflections in independent ECG leads. METHODS AND RESULTS: Ten recordings of ventricular fibrillation were examined. Each had been provoked during routine electrophysiological study. The mean duration of ventricular fibrillation was 21 seconds (range 11 to 34). Independent and approximately orthogonal ECG leads I, aVF, and V2 were recorded to computer at a sampling rate of 250 Hz. The phase relationship of each ECG lead pair was measured from the lag of peaks in their cross-correlation function (CCF). In 61% of the 1-second ECG epochs analyzed, CCF peak lag changed by < 20 msec compared to the previous epoch. Thus, the overall phase relationship was stable most of the time. Changes in CCF peak lag tended to be either gradual or to punctuate periods of stability. CONCLUSIONS: This study provides evidence of organized myocardial activation during human ventricular fibrillation.

Electrocardiography↗
PubMed1988

Verapamil and tiapamil in prevention of ventricular fibrillation in pigs with coronary ligation. Comparative effects on left ventricular function.

Antiarrhythmic and hemodynamic effects of the calcium channel antagonist verapamil were compared with those of tiapamil, a congener, in open-chest pigs with anterior descending coronary artery ligation. Tiapamil (6 mg/kg i.v.) decreased the incidence of ventricular fibrillation to 4 of 10 versus 22 of 25 in controls (p less than 0.05) and maintained left ventricular dP/dtmax after ligation (predrug value: 2,312 +/- 112 mm Hg/sec; 20 minutes after ligation: 2,139 +/- 229 mm Hg/sec). Tiapamil increased blood flow in the peripheral ischemic zone (24 +/- 3.2% vs. 16.9 +/- 1.6% of preligation value in controls, p less than 0.05) as well as in the peri-ischemic and nonischemic zones (153.9 +/- 12.7% and 186.3 +/- 17.1%, respectively; both p less than 0.0001 vs. 97.9 +/- 5% and 91.3 +/- 4.7% in controls). Verapamil (0.6 mg/kg i.v.) decreased the incidence of ventricular fibrillation to 0 of 7 versus 22 of 25 in controls (p less than 0.005); left ventricular dP/dtmax decreased from 2,062 +/- 144 to 1,060 +/- 168 mm Hg/sec (p less than 0.0001). Verapamil did not change blood flow in the peripheral, peri-ischemic, or nonischemic zones. Thus, tiapamil, and not verapamil, decreased ischemic ventricular fibrillation while maintaining left ventricular mechanical function. Verapamil congeners warrant further evaluation as antiarrhythmic agents in acute myocardial ischemia.

Animals↗
PubMed2000

A prospective randomized-controlled trial of ventricular fibrillation detection time in a DDDR ventricular defibrillator. Ventak AV II DR Study Investigators.

Implantable cardioverter defibrillators (ICDs) with dual chamber and dual chamber rate responsive pacing may offer hemodynamic advantages for some ICD patients. Separate ICDs and DDDR pacemakers can result in device to device interactions, inappropriate shocks, and underdetection of ventricular fibrillation (VF). The objectives of this study were to compare the VF detection times between the Ventak AV II DR and the Ventak AV during high rate DDDR and DDD pacing and to test the safety of dynamic ventricular refractory period shortening. Patients receiving an ICD were randomized in a paired comparison to pacing at 150 beats/min (DDD pacing) or 175 beats/min (DDDR pacing) during ICD threshold testing to create a "worst case scenario" for VF detection. The VF detection rate was set to 180 beats/min, and VF was induced during high rate pacing with alternating current. The device was then allowed to detect and treat VF. The induction was repeated for each patient at each programmed setting so that all patients were tested at both programmed settings. Paired analysis was performed. Patient characteristics were a mean age of 69 +/- 11 years, 78% were men, coronary artery disease was present in 85%, and a mean left ventricular ejection fraction of 0.34 +/- 0.11. Fifty-two episodes of VF were induced in 26 patients. Despite the high pacing rate, all VF episodes were appropriately detected. The mean VF detection time was 2.4 +/- 1.0 seconds during DDD pacing and 2.9 +/- 1.9 seconds during DDDR pacing (P = NS). DDD and DDDR programming resulted in appropriate detection of all episodes of VF with similar detection times despite the "worst case scenario" tested. Delays in detection may be seen with long programmed ventricular refractory periods which shorten the VF sensing window and may be avoided with dynamic ventricular refractory period shortening.

Aged↗
PubMed1995

Primary ventricular fibrillation is associated with increased paced right ventricular electrogram fractionation.

BACKGROUND: The mechanisms of spontaneous ventricular fibrillation (primary VF) in patients without structural heart disease are obscure. A new technique has shown that in patients with hypertrophic cardiomyopathy conduction of fractionated ventricular paced beats, recorded at several right ventricular sites, is prolonged in individuals who have suffered a VF arrest, and this may reveal one component of a reentrant substrate. Patients with primary VF were studied with the same methods to determine whether similar abnormalities are present in this group. METHODS AND RESULTS: Nine patients with primary VF were studied by pacing one right ventricular (RV) site by use of a constant drive train with an extrastimulus inserted every third beat and reducing the extrastimulus coupling interval (S1S2 interval) by 1 ms on each occasion while recording at three other sites. The delay of each fractionated potential in the high-pass-filtered electrograms in response to the extrastimulus was determined and used to form conduction curves of delay versus the S1S2 interval. These curves were repeated by pacing each RV site in turn and recording from the other three sites. The curves were characterized by determining the S1S2 interval at which electrogram components increased in delay by 0.75 ms/20 ms reduction in S1S2 interval and the increase in electrogram duration between a coupling interval of 350 ms and 1 ms above refractoriness. Seven control patients were studied using the same method. The mean increase in electrogram duration in VF patients was 13 ms (range, 3 to 23 ms) compared with 4 ms (range, -2 to 14 ms) in unaffected control patients. The extrastimulus coupling interval at which delay increased was 318 ms (range, 293 to 334 ms) in VF patients and 274 ms (range, 265 to 284 ms) in control patients (P < .01). There was no difference between the number of fractionated potentials in VF patients and control patients. CONCLUSIONS: In primary VF patients, the individual potentials within fractionated electrograms have increased delays when compared with control patients. This may identify one component of a reentrant arrhythmic substrate.

Adolescent↗
PubMed2001

[Ventricular fibrillation secondary to radiofrequency application in ventricular tachycardia ablation].

Radiofrequency catheter ablation has become a first line therapy for several types of tachycardias because of its high efficacy and low complication rate. The development of proarrhythmic complications due to a direct effect of radiofrequency is very unusual. We describe a patient with previous myocardial infarction and well tolerated sustained monomorphic ventricular tachycardia who underwent catheter ablation of the tachycardia substrate. During two of the radiofrequency applications, ventricular fibrillation developed and external defibrillation was required.

Catheter Ablation↗
PubMed1984

Vulnerability to ventricular fibrillation in patients with clinically manifest ventricular tachycardia.

Ventricular vulnerability may be assessed by measuring the threshold current for the induction of ventricular fibrillation (VF). This technique has been widely utilized in animal experimentation and has been safely applied in a small number of clinical studies. We measured the VF threshold (VFT), using the single stimulus technique in 10 patients with coronary artery disease just prior to the institution of cardiopulmonary bypass. There were no adverse effects of VFT measurement. Three patients had nonsustained ventricular tachycardia (VT) on 24-hour ambulatory monitoring and had VFTs of 10, 14, and 16 mA. In this group VF was induced without any preceding repetitive ventricular responses. Seven patients had no repetitive forms on ambulatory monitoring. Their VFTs ranged from 30 to greater than 40 mA (mean greater than 37). Repetitive extrasystoles were regularly observed in this group at current intensities which ranged from 53% to 80% of the VFT. Thus patients with manifest VT appear to have an enhanced vulnerability to VF. Single or multiple responses were not observed in these patients but appeared to be present in patients with coronary disease and no demonstrable rhythm disorder.

Aged↗
PubMed1981

Recurrence of ventricular fibrillation in acute ischemic heart disease.

We assessed factors during an initial episode of ventricular fibrillation that may be predictive of recurrence. Of 141 consecutive patients with acute ischemic heart disease who survived an initial episode of ventricular fibrillation, 41 (29%) had recurrent ventricular fibrillation during hospitalization. The incidence of recurrent ventricular fibrillation was lower among those with an acute myocardial infarction than among those with acute ischemic episode. Recurrent ventricular fibrillation occurred more frequently among patients with secondary ventricular fibrillation complicating an acute myocardial infarction than among those with primary ventricular fibrillation. Primary ventricular fibrillation than occurred within 2 hours of the onset of symptoms was no more likely to be recurrent than when it occurred later. Age, sex, site of infarction, place of arrest, adequacy of initial resuscitation, interval onset of symptoms to the initial episode of ventricular fibrillation, onset of symptoms to intensive care and delay before initial attempted defibrillation were not significantly related to the recurrence of ventricular fibrillation.

Acute Disease↗