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PubMed2004

Is idiopathic ventricular fibrillation a short QT syndrome? Comparison of QT intervals of patients with idiopathic ventricular fibrillation and healthy controls.

OBJECTIVE: The purpose of this study was to determine if patients with idiopathic ventricular fibrillation (VF) have shorter QT intervals than comparable healthy controls. BACKGROUND: The upper limit of the normal QT is well defined. Less is known about the lower limit of the normal QT. Patients with the recently described "short QT syndrome" have characteristics resembling those of patients with idiopathic VF. METHODS: The ECGs of 28 consecutive patients with idiopathic VF (17 men and 11 women, age 31 +/- 17 years) were compared to those of 270 age- and gender- matched healthy controls. Based on published literature, we defined "short QT" as QTc < or = 360 ms for males and < or = 370 ms for females. RESULTS: Despite significant overlapping, the QTc of males with idiopathic VF was shorter than the QTc of healthy males (371 +/- 22 ms vs 385 +/- 19 ms, P = .034). Short QT intervals were found more frequently among males with idiopathic VF (35% vs 10%, P = .003). No such differences were apparent among women. Short QTc intervals were more commonly seen during bradycardia. However, the correlation between short QT and a history of VF was independent of heart rate. CONCLUSIONS: "Short" QTc values are commonly seen in male patients with idiopathic VF. However, "short" QTc values are not rare among healthy adults, especially at slow heart rates. Further studies are needed to define when a given QT is really "too short."

Adult↗
PubMed2005

Electrophysiological mechanisms of ventricular fibrillation induction.

Ventricular fibrillation (VF) is known as a main responsible cause of sudden cardiac death which claims thousands of lives each year. Although the mechanism of VF induction has been investigated for over a century, its definite mechanism is still unclear. In the past few decades, the development of new advance technologies has helped investigators to understand how the strong stimulus or the shock induces VF. New hypotheses have been proposed to explain the mechanism of VF induction. This article reviews most commonly proposed hypotheses that are believed to be the mechanism of VF induction.

Journal Article↗
PubMed1995

Emergency intracardiac defibrillation for refractory ventricular fibrillation.

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life-saving capabilities of intracardiac defibrillation.

Aged↗
PubMed2005

Magnetic resonance imaging during untreated ventricular fibrillation reveals prompt right ventricular overdistention without left ventricular volume loss.

BACKGROUND: Most out-of-hospital ventricular fibrillation (VF) is prolonged (>5 minutes), and defibrillation from prolonged VF typically results in asystole or pulseless electrical activity. Recent visual epicardial observations in an open-chest, open-pericardium model of swine VF indicate that blood flows from the high-pressure arterial system to the lower-pressure venous system during untreated VF, thereby overdistending the right ventricle and apparently decreasing left ventricular size. Therefore, inadequate left ventricular stroke volume after defibrillation from prolonged VF has been postulated as a major contributor to the development of pulseless rhythms. METHODS AND RESULTS: Ventricular dimensions were determined by MRI for 30 minutes of untreated VF in a closed-chest, closed-pericardium model in 6 swine. Within 1 minute of untreated VF, mean right ventricular volume increased by 29% but did not increase thereafter. During the first 5 minutes of untreated VF, mean left ventricular volume increased by 34%. Between 20 and 30 minutes of VF, stone heart occurred as manifested by dramatic thickening of the myocardium and concomitant substantial decreases in left ventricular volume. CONCLUSIONS: In this closed-chest swine model of VF, substantial right ventricular volume changes occurred early and did not result in smaller left ventricular volumes. The changes in ventricular volumes before the late development of stone heart do not explain why defibrillation from brief duration VF (<5 minutes) typically results in a pulsatile rhythm with return of spontaneous circulation, whereas defibrillation from prolonged VF (5 to 15 minutes) does not.

Animals↗
PubMed1989

The effect of beta-adrenergic blockade on vulnerability to ventricular fibrillation and inducibility of ventricular arrhythmia in short- and long-term feline infarction models.

Previous investigation, predominantly in the short-term canine model, has documented a potent antifibrillatory effect of beta-adrenergic blockade. To determine whether the protection afforded by beta blockade is species- and model-specific, we studied 23 chloralose-anesthetized cats. Eight animals were studied over a short term and underwent serial determinations of the ventricular fibrillation (VF) threshold prior to and 1 minute after occlusion of the left anterior descending coronary artery (LAD) and immediately following reperfusion of a 10-minute occlusion. Beta-blocking doses of intravenous propranolol (P) (0.5 mg/kg) attenuated the fall in VF threshold during acute ischemia. Increasing the dose of P to 1 mg/kg did not provide further protection, nor did P protect against reperfusion VF. The other 15 animals underwent a preliminary surgical procedure during which the LAD was completely and irreversibly occluded (nine animals) or in which a sham procedure was performed (six animals). Two weeks later, we measured ventricular refractoriness at several left ventricular sites, ventricular inducibility using programmed electrical stimulation, and VF thresholds both before and after administration of intravenous P (1 mg/kg). Ventricular refractory periods in the infarcted zones were significantly increased compared with normal sites and with values obtained in sham-operated animals. In addition, VF thresholds in the infarcted animals were lower than those obtained in the sham-operated group. Before treatment, a reproducible sustained ventricular tachyarrhythmia was induced by means of programmed stimulation in seven of the nine chronically infarcted animals but in none of the sham-operated animals (p less the 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Importance of calcium for the vulnerability to ventricular fibrillation detected by premature ventricular stimulation: single pulse versus sequential pulse methods.

Vulnerability to ventricular fibrillation (VF) is frequently evaluated by VF threshold, a variable which may not be free of confounding factors and which may not be sensitive to all factors contributing to vulnerability. Therefore, we tested whether VF threshold determination affects intracellular free Ca2+ ([Ca2+]i) and whether VF thresholds are sensitive to changes in [Ca2+]i. For this purpose, we analysed [Ca2+]i by surface fluorometry and indo-1 in intact perfused rat hearts undergoing VF threshold determination by a single pulse method and tested whether such thresholds are lowered by increased [Ca2+]i. Additionally, we sought to determine the importance of Ca2+ for the vulnerability to VF under nonischemic conditions. For this purpose, we measured VF thresholds by a new pulse number method which scanned the vulnerable period by an increasing number of sequential pulses at increasing prematurity but constant intensity. We found that VF threshold determination by a single pulse method led to a rise in systolic [Ca2+]i. However, this rise does not perturb VF threshold interpretation because such thresholds were insensitive to changes in [Ca2+]i. Nevertheless, [Ca2+]i is of importance for the vulnerability to VF under nonischemic conditions because the number of VF-free tolerated premature pulses was dependent on [Ca2+]i. This relationship may only be detectable if evaluated by sequential pulse methods. These findings suggest that the method of VF threshold determination may be crucial for the result of studies testing Ca2+ antagonists or situations of altered [Ca2+]i and could explain controversial results of VF threshold studies testing Ca2+ antagonists by varying methods.

Animals↗
PubMed2000

Induction of atrial fibrillation with rapid high voltage ventricular pacing for ventricular fibrillation conversion testing. The Ventak AV II DR Study.

OBJECTIVE: To assess whether rapid high voltage ventricular pacing can also induce atrial fibrillation, and whether the induction of atrial fibrillation during ventricular fibrillation conversion testing is related to the patient's heart disease. DESIGN: Prospective study of 50 patients who received the dual chamber implantable cardioverter-defibrillator (ICD) Ventak AV II DR (Guidant) as a first implant. This device can record atrial activity even during a ventricular fibrillation episode and can induce atrial fibrillation by rapid atrial bursts. MAIN OUTCOME MEASURES: Frequency of atrial fibrillation after induction of ventricular fibrillation; clinical characteristics of patients with and without induced atrial fibrillation; frequency of atrial fibrillation induced by rapid atrial bursts during predischarge testing. RESULTS: Atrial fibrillation was observed in 40 of the 217 ventricular fibrillation episodes (18%) that could be detected immediately after delivery of high voltage pacing. The biphasic ICD shock for termination of ventricular fibrillation also terminated the atrial fibrillation in all cases. The 40 episodes of simultaneous atrial and ventricular fibrillation occurred in 18 patients (36%). The distribution of the clinical characteristics of the patients and the inducibility of atrial fibrillation during predischarge testing were similar in those with and without induced atrial fibrillation. CONCLUSIONS: Rapid high voltage ventricular pacing frequently induces atrial fibrillation, which was terminated by the subsequent biphasic ICD shock. The induction of atrial fibrillation seems to be a non-specific phenomenon, unrelated to the clinical status of the patient.

Adult↗
PubMed2004

Current concepts on ventricular fibrillation: a vicious circle of cardiomyocyte calcium overload in the initiation, maintenance, and termination of ventricular fibrillation.

Based on recent experimental studies, this review article introduces the novel concept that cardiomyocyte Ca2+ and ventricular fibrillation (VF) are mutually related, forming a self-maintaining vicious circle in the initiation, maintenance, and termination of VF. On the one hand, elevated myocyte Ca2+ can cause delayed afterdepolarizations, triggered activity, and consequently life-threatening ventricular tachyarrhythmias in various pathological conditions such as digitalis toxicity, myocardial ischemia, or heart failure. On the other hand, VF itself directly and rapidly causes progressive myocyte Ca2+ overload that maintains VF and renders termination of VF increasingly difficult. Accordingly, energy levels for successful electrical defibrillation (defibrillation thresholds) increase as both VF and Ca2+ overload progress. Furthermore, VF-induced myocyte Ca2+ overload can promote re-induction of VF after defibrillation and/or postfibrillatory myocardial dysfunction (postresuscitation stunning) due to reduced myofilament Ca2+ responsiveness. The probability of these adverse events is best reduced by early detection and rapid termination of VF to prevent or limit Ca2+ overload. Early additional therapy targeting transsarcolemmal Ca2+ entry, particularly during the first 2 min of VF, may partially prevent myocyte Ca2+ overload and thus, increase the likelihood of successful defibrillation as well as prevent postfibrillatory myocardial dysfunction.

Journal Article↗
PubMed1997

Regression of left ventricular hypertrophy with captopril restores normal ventricular action potential duration, dispersion of refractoriness, and vulnerability to inducible ventricular fibrillation.

BACKGROUND: Left ventricular hypertrophy (LVH) is associated with multiple cellular electrophysiological abnormalities, susceptibility to ventricular arrhythmias, and an increased risk of sudden death. Several pharmacological therapies have been shown to produce regression of hypertrophy, but the value of regression is unclear. The present study examines whether pharmacological regression of LVH has effects on the susceptibility to ventricular arrhythmia or the cellular electrophysiological abnormalities of LVH. METHODS AND RESULTS: Rabbits underwent unilateral renal artery banding and contralateral nephrectomy to induce LVH or were placed in the control group. Both groups were studied 3 months later by in vivo and in vitro electrophysiological techniques. Banded rabbits had increased mean arterial pressure, increased left ventricular weight and wall thickness, increased dispersion of refractoriness, and lower ventricular fibrillation thresholds than control rabbits. Action potential duration and cell capacitance were also greater in the banded group. Additional rabbits were treated beginning 3 months after banding with either captopril (5 mg x kg(-1) x d(-1)) or vehicle added to their diet for an additional 3 months. These rabbits and age-matched controls were then studied by in vivo and in vitro electrophysiological techniques. In banded rabbits that received vehicle and were studied 6 months after banding, increased dispersion of refractoriness, a lower ventricular fibrillation threshold, and action potential prolongation persisted and were unchanged from animals studied 3 months after banding. Captopril, started 3 months after banding, caused regression of hypertrophy and normalization of the in vivo and in vitro electrophysiological abnormalities. Addition of captopril to the tissue bath during in vitro electrophysiological study showed no effect on cells from control or banded rabbits. CONCLUSIONS: Pharmacological regression of LVH with captopril normalizes the in vivo and in vitro electrophysiological abnormalities of ventricular hypertrophy and reduces the vulnerability to ventricular fibrillation in a renovascular model of LVH.

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