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PubMed2000

Recurrent ventricular fibrillation in a marathon runner during exercise testing.

We report a case of a marathon runner who presented with chest tightness, ST-segment depression, and ventricular fibrillation following treadmill exercise testing. At cardiac catheterization, the patient was found to have an isolated lesion in the left anterior descending (LAD) artery that was hemodynamically insignificant by accepted angiographic and coronary flow reserve standards. Ventricular fibrillation was thought to be idiopathic, and an implantable cardioverter defibrillator was placed. Chest pain and ST-segment depression followed by ventricular fibrillation was reproduced during follow-up treadmill testing, prompting reconsideration of the original diagnostic hypothesis. A coronary stent was deployed in the LAD artery. The patient has been asymptomatic and arrhythmia free during follow-up treadmill testing and recreational running.

Angioplasty, Balloon, Coronary↗

PubMed2002

The role of heme oxygenase-related carbon monoxide and ventricular fibrillation in ischemic/reperfused hearts.

Reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO)-related carbon monoxide (CO) production in isolated ischemic/reperfused rat hearts were studied by gas chromatography. Hearts were subjected to 30 min ischemia followed by 2 h reperfusion, and the expression of HO-1 mRNA (about 4-fold) was observed in ischemic/reperfused-nonfibrillated hearts. In fibrillated hearts, the reduction (about 75%) in HO-1 mRNA expression was detected. These changes in HO-1 mRNA expression were reflected in tissue CO production. Thus, in the absence of VF, CO production was increased about 3.5-fold, while in the presence of VF, CO production was under the detectable level in comparison with the control group. Our results suggest that the stimulation of HO-1 mRNA expression may lead to the prevention of reperfusion VF via an increase in endogenous CO production. To prove this, hearts were treated with 1 microM of N-tert-butyl-alpha-phenylnitrone (PBN) as an inducer of HO-1. PBN treatment resulted in about 20 times increase in HO-1 mRNA expression, and even a higher production rate in endogenous CO. HO protein level and enzyme activity followed the same pattern, as it was observed in HO-1 mRNA expression, in fibrillated and nonfibrillated myocardium. Five mM/l of zinc-protoporphyrin IX (ZnPPIX) significantly blocked HO enzyme activity and increased the incidence of VF, therefore the application of ZnPPIX led to a significant reduction in HO-1 mRNA and protein expression. Our data provide direct evidence of an inverse relationship between the development of reperfusion-induced VF and endogenous CO production. Thus, interventions that are able to increase tissue CO content may prevent the development of reperfusion-induced VF.

Animals↗

PubMed1989

Ventricular fibrillation in coronary angiography: what is the role of contrast medium?

A retrospective review of patients with coronary angiography was undertaken to establish the incidence of ventricular fibrillation and other serious arrhythmias and to identify possible causative factors, in particular whether the use of non-ionic contrast medium increased the risk of a serious arrhythmia. Out of 3660 patients reviewed there were 10 cases of ventricular fibrillation. In all cases, there were identifiable technical factors thought to have accounted for the arrhythmia. There were no cases of ventricular fibrillation complicating a technically satisfactory injection of ionic or non-ionic contrast medium. There was no significant difference in the incidence of serious arrhythmias between patients given ionic and those given non-ionic contrast medium.

Angiocardiography↗

PubMed2003

Automated external defibrillation versus manual defibrillation for prolonged ventricular fibrillation: lethal delays of chest compressions before and after countershocks.

STUDY OBJECTIVE: We sought to determine whether the delays in chest compressions and defibrillation associated with an automated external defibrillator would adversely affect outcome compared with manual defibrillation in a swine model of out-of-hospital prolonged ventricular fibrillation. METHODS: After 8 minutes of untreated ventricular fibrillation, 16 swine (33+/-4 kg) were randomly assigned to automated external defibrillator defibrillation or manual defibrillation with the same biphasic truncated exponential waveform 150-J shock through the same type of pads. Defibrillation with the automated external defibrillator was performed as recommended by the manufacturer, and manual defibrillation was provided per American Heart Association Guidelines. The primary outcome measure was 24-hour survival with good neurologic outcome. Data are described as means+/-SD. RESULTS: None of 8 animals in the automated external defibrillator group survived for 24 hours, whereas 5 of 8 animals in the manual defibrillation group survived 24 hours, all with good neurologic outcome (P=.027). The time interval from simulated defibrillator arrival to first compressions was 98+/-18 seconds in the automated external defibrillator group versus 68+/-15 seconds in the manual defibrillation group. In particular, the interval from first shock to first chest compressions was 46+/-18 seconds versus 22+/-16 seconds, respectively. The mean percentage of time that chest compressions were performed in the first minute after the first countershock was 15%+/-13% versus 40%+/-15%, respectively. As a result, return of spontaneous circulation within 5 minutes of simulated defibrillator arrival occurred in only 1 of 8 animals in the automated external defibrillator group versus 6 of 8 animals in the manual defibrillation group. CONCLUSION: The longer delays in chest compressions with automated external defibrillator defibrillation versus manual defibrillation can worsen the outcome from prolonged ventricular fibrillation.

Animals↗

PubMed1993

A quantitative measurement of spatial order in ventricular fibrillation.

INTRODUCTION: The degree of organization in ventricular fibrillation (VF) is not known. As an objective measurement of spatial order, spatial correlation functions and their characteristic lengths were estimated from epicardial electrograms of pigs in VF. METHODS AND RESULTS: VF was induced by premature stimulation in five pigs. Electrograms were simultaneously recorded with a 22 x 23 array of unipolar electrodes spaced 1.12 mm apart. Data were obtained by sampling the signals at 2000 Hz for 20 minutes immediately after the initiation of FV. Correlations between all pairs of signals were computed at various times. Correlation lengths were estimated from the decay of average correlation as a function of electrode separation. The correlation length of the VF in pigs was found to be approximately 4 to 10 mm, varying as fibrillation progressed. The degree of correlation decreased in the first 4 seconds after fibrillation then increased over the next minute. CONCLUSION: The correlation length is much smaller than the scale of the heart, suggesting that many independent regions of activity exist on the epicardium at any one time. On the other hand, the correlation length is 4 to 10 times the interelectrode spacing, indicating that some coherence is present. These results imply that the heart behaves during VF as a high dimensional, but not random, system involving many spatial degrees of freedom, which may explain the lack of convergence of fractal dimension estimates reported in the literature. Changes in the correlation length also suggest that VF reorganizes slightly in the first minute after an initial breakdown in structure.

Animals↗

PubMed1992

Effects of calcium channel agonism by Bay-K-8644 on ventricular fibrillation threshold of isolated heart.

The hypothesis tested was that enhanced entry of calcium into cardiac cells would increase the susceptibility to ventricular fibrillation as measured by the ventricular fibrillation threshold (VFT) of the isolated perfused rat heart. Bay-K-8644 was used as a calcium-channel agonist. There was a biphasic effect with a maximal increase in left ventricular systolic pressure and oxygen uptake at a concentration of 10(-7) M. The same concentration caused a major reduction in the VFT. The bell-shaped pattern of fall of the VFT was inversely related to the effect on LV developed pressure. The changes in VFT could be dissociated from those on myocardial metabolites. Although Bay-K-8644 increased the heart rate, reduction of the VFT could also be obtained in paced hearts. The addition of ryanodine, an agent known to interrupt intracellular recycling of calcium through the sarcoplasmic reticulum, was able to abolish approximately half the effect of Bay-K-8644 on the VFT. Therefore, increased entry of calcium via the calcium channel is able to reduce VFT, acting in part through enhanced recycling of calcium through the sarcoplasmic reticulum.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

PubMed1996

Ventricular fibrillation in the neonate: elusive or illusive?

Ventricular fibrillation (VF) in mature large mammals is usually a terminal event. It constitutes the most common mode of exitus and the main cause of sudden cardiac death in humans. In neonates, VF is of particular interest because it often reverse spontaneously and promptly to potentially become a non-lethal event. Accordingly, the study of VF and spontaneous defibrillation (SDF) in the neonate is key for the understanding of the developmental anatomical and functional characteristics enabling mammalian myocardium to initiate and sustain this lethal arrhythmia. Such characteristics may include age-related changes of myocardial tissue properties, mass and geometry, autonomic cardiac innervation and myocardial perfusion/hydration. In the human neonate, VF/SDF could provide a plausible framework for explaining and directing the search for the elusive evidence underlying the mechanism and age distribution of the sudden infant death syndrome.

Animals↗

PubMed1982

Increased ventricular fibrillation threshold with severe myocardial ischemia.

The ventricular fibrillation threshold (VFT) is a measure of myocardial electrical vulnerability to exogenous electrical stimulation. Previous studies have shown that the VFT is inversely related to ischemia. We studied the relation of the VFT to myocardial blood flow (MBF) during ischemia produced by interruption of blood flow to the left anterior descending coronary artery, and severe ischemia produced by retrograde bleeding an ischemic segment of myocardium. The VFT with severe ischemia (8.6 +/- 1.3 mA; MBF 0.024 +/- 0.01 ml/min/gm tissue), although lower than nonischemic control values (14.2 +/- 2.0 mA; 0.76 +/- 0.05; both p less than 0.05), was higher than that obtained with moderate ischemia (4.6 +/- 0.9 mA; 0.15 +/- 0.02 ml/min/gm; both, p less than 0.05). Thus the relationship between the VFT and MBF is nonlinear. Interventions which cause the VFT to rise may do so by worsening rather than improving regional MBF.

Animals↗

PubMed1986

Failure of sodium bicarbonate to improve resuscitation from ventricular fibrillation in dogs.

To determine the value of sodium bicarbonate in resuscitation from ventricular fibrillation and the prevention of spontaneous refibrillation, sodium bicarbonate (1 meq/kg) or placebo was administered on a random basis to 16 pentobarbital-anesthetized dogs 18 min after the induction of ventricular fibrillation and cardiopulmonary resuscitation. Defibrillation was attempted 2 min after the administration of bicarbonate or placebo. All animals were successfully defibrillated, but three of eight bicarbonate-treated and two of eight control animals died in electromechanical dissociation (p = NS). Spontaneous refibrillation occurred in three animals in each group (p = NS). Successful resuscitation was not dependent on treatment, arterial or mixed venous Pco2, or arterial or mixed venous pH but correlated strongly with coronary perfusion pressure (p less than .003). Spontaneous refibrillation occurred without relation to any identifiable variable. The gradient between diastolic aortic and right atrial pressures was 24 +/- 2 mm Hg in controls and 23 +/- 2 mm Hg in treated animals over the entire 20 min of cardiopulmonary resuscitation (p = NS). However, among animals successfully resuscitated, mean diastolic coronary perfusion pressure averaged 27 +/- 2 mm Hg compared with 20 +/- 1 mm Hg among those dying in electromechanical dissociation (p less than .02). For the final 2 min of resuscitation, after drug administration, these gradients were 31 +/- 2 and 23 +/- 2 mm Hg, respectively (p less than .01). Microsphere determined myocardial perfusion correlated with the diastolic aortic-right atrial perfusion pressure gradient (r = .86) and was 0.43 +/- 0.03 ml/min/g in survivors and 0.22 +/- 0.01 ml/min/g in nonsurvivors (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Prognostic significance of field response in out-of-hospital ventricular fibrillation.

We reviewed 94 cases of prehospital ventricular fibrillation (VF) to determine aspects of field response that predicted outcome. Only one of 37 patients (3 percent) failing to achieve rhythms other than VF or asystole after the first two defibrillations survived to hospital discharge compared to nine of 57 (16 percent) achieving organized rhythms by this point (p less than 0.05). None of 56 patients failing to achieve pulses prior to transport survived to hospital discharge compared to ten of 38 achieving field pulses (p less than 0.01). However, survival to discharge was not significantly different between patients who developed pulses immediately with their rhythms (5 of 17, 29 percent) and those who were defibrillated into pulseless rhythms but later developed pulses in the field (five of 21, 24 percent). Thus, for prehospital VF, the best field response identifies potential survivors prior to hospital arrival. In addition, the frequent occurrence and potentially favorable outcome of an initially pulseless rhythm necessitates reevaluation of current therapy.

Ambulatory Care↗

PubMed1995

Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms.

The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.

Adenosine↗

PubMed2001

Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart.

Reentrant ventricular tachycardia (VT) is the most common sustained arrhythmia leading to ventricular fibrillation (VF). However, despite more than a century of research, the mechanism(s) of the conversion from reentrant VT to VF have not been elucidated. Based on their different electrocardiographic appearance, reentrant VT and VF have traditionally been thought of as resulting from two widely different mechanisms. Whereas VT is seen as a rapid but well organized process whereby the excitation wave rotates about a single well-defined circuit, fibrillation has been described as turbulent cardiac electrical activity, resulting from the random and aperiodic propagation of multiple independent wavelets throughout the cardiac muscle. Recently, the application of concepts derived from the theory of non-linear dynamics to the problem of wave propagation in the heart and the advent of modern high-resolution mapping techniques, have led some investigators to view VT and VF in terms of a single mechanism, whereby the self-organization of electrical waves forms 'rotors' that give rise to rapidly rotating spiral waves and results in either VT or VF, depending on the frequency of rotation and on the interaction of wave fronts with the cardiac muscle. As such, monomorphic VT is thought to result from a stationary rotor, whose frequency of rotation is within a range that allows 1:1 excitation of both ventricles. On the other hand, VF is thought to result from either a single rapidly drifting rotor, or a stationary rotor whose frequency of excitation is exceedingly high, thus resulting in multiple areas of intermittent block and giving rise to complex patterns of propagation with both deterministic and stochastic components. This article reviews the prevailing theories for the maintenance of VF, and discusses recently proposed mechanisms underlying transitions between VT and VF.

Death, Sudden, Cardiac↗

PubMed1980

Left stellectomy in the prevention of ventricular fibrillation caused by acute myocardial ischemia in conscious dogs with anterior myocardial infarction.

The potential of left stellectomy in reducing the incidence of ventricular fibrillation associated with acute myocardial ischemia was investigated in a new animal model for sudden death. Thirty-two dogs had an anterior myocardial infarction produced by ligation of the left descending coronary artery. One week later they were randomly allocated to a control or to an experimental group that underwent left stellectomy. One month after ligation while the dogs were conscious, a balloon occluder previously positioned around the circumflex coronary artery was inflated and the ensuing coronary occlusion was maintained for 10 minutes. Ventricular fibrillation occurred in 11 of 17 (65%) control dogs, compared with five of 15 (33%) (p < 0.05) in the experimental group. Among the survivors the incidence of arrhythmias was less in the experimental group compared with the control group. Infarct size (21 +/- 2% vs 20 +/- 2%), resting heart rate (143 beats/min vs 127 beats/min) and QTc (347 +/- 11 msec vs 349 +/- 13 msec) were similar between control and experimental groups. The dogs that died had a greater increase in heart rate at 1 minute postocclusion than survivors and also had significantly longer QT intervals. Our study indicates that left stellectomy exerts a major protective effect in reducing the incidence of ventricular fibrillation when conscious dogs with a previous anterior myocardial infarction undergo acute myocardial ischemia. This simple and safe surgical procedure may be considered for a clinical trial in subgroups of patients with ischemic heart disease at very high risk for sudden death.

Animals↗

PubMed1986

Neurochemical approaches to the prevention of ventricular fibrillation.

Current evidence indicates that susceptibility to ventricular fibrillation (VF) can be reduced by decreasing cardiac sympathetic activity and by increasing vagal tone. Pharmacological agents that favor such a pattern of autonomic outflow protect the heart against fibrillation. These include morphine sulfate, clonidine, digitalis drugs, and bromocriptine. An intriguing new approach involves changing the serum concentration of amino acid precursors of the central neurotransmitters that modulate autonomic traffic. Considerable evidence indicates that accumulation of serotonin in the brain reduces sympathetic neural activity. When L-tryptophan or 5-hydroxytryptophan is administered with phenelzine (a monoamine oxidase inhibitor) and carbidopa (a selective peripheral L-amino acid decarboxylase inhibitor) to raise brain serotonin, a significant increase in myocardial electrical stability is observed. This effect results from a decrease in cardiac sympathetic tone as indicated by selective denervation and nerve recording studies. Enhancing serotoninergic neurotransmission can also significantly reduce vulnerability to VF during acute coronary artery occlusion. The effect of augmenting serotoninergic activity without the use of enzyme inhibitors has been investigated by administering agents such as melatonin, 5-methoxytryptophol, and 6-chloro-2-(1-piperazinyl) pyrazine (MK-212). Each of these substances increases cardiac electrical stability. The protective influence is unaffected by bilateral vagotomy but is blocked by the specific serotonin antagonist methergoline. Diminution of cardiac sympathetic drive appears to be the main mechanism of action. Thus, neurochemical interventions can exert a profound effect on cardiac electrical stability. Recent advances in neurochemistry and psychopharmacology promise new insights into the problem of sudden death and suggest a fresh approach for the management of life-threatening arrhythmias.

Animals↗

PubMedDate not supplied

Effects of encainide (MJ9067) on the ventricular fibrillation threshold in anesthetized dogs.

The right ventricular epicardial ventricular fibrillation threshold (VFT) was determined during paced supraventricular rhythm using 100 Hz trains of stimuli at 15 min intervals in dogs before and during the intravenous administration of encainide, a new antiarrhythmic drug. With each VFT determination, simultaneous blood samples were obtained for determination of drug concentration. In 6 control dogs, VFT determined every 15 min during a 210 administered as a 90 min intravenous infusion at three successive rates (0.01, 0.02 and 0.04 mg/kg/min) for 30 min each. VFT measured at 5 and 20 min of each infusion increased from a mean control of 11.5 +/- 1.5 (+/-SE) to 20.2 +/- 2.2 mA (p less than 0.01) after 20 min of the third infusion. The maximal effect occurred during the second infusion with plasma concentration of 594 +/- 46 ng/ml and then reached a plateau. In group II (n = 6), encainide was administered in four successive sequences, each one including a bolus loading intravenous dose followed by a 45 min intravenous infusion. VFT measured at 30 and 45 min of each infusion when the encainide plasma concentration was close to a steady state increased significantly (p less than 0.01) after the second infusion from 11.8 +/- 2 to 27.3 +/- 4 mA. Two dogs in group II developed transient complete atrioventricular block at an encainide plasma concentration of greater than 800 ng/ml. These results show that the new antiarrhythmic drug encainide increases the VFT in anesthetized dogs.

Anesthesia↗

PubMed1988

Relation of cardiac surface QRST distributions to ventricular fibrillation threshold in dogs.

The relation between ventricular fibrillation threshold (VFT) and cardiac surface QRST area distributions was studied in eight pentobarbital-anesthetized dogs. Unipolar epicardial electrograms were recorded from 64 sites evenly distributed on the right and left ventricles. Localized areas of short repolarization properties were produced by directing five intensities of light onto the surface of the anterior right ventricle through apertures of three sizes. VFT, measured at the center of the lesion, decreased during warming and had a high negative correlation to the change (warming-control) in QRST area (delta QRST1) in the electrogram recorded from the center of the lesion. This correlation was independent of lesion size. For the six experiments, the correlation coefficients for 400-, 800-, and 1,600-mm2 lesions averaged -0.95, -0.94, and -0.96, respectively. The correlation between VFT and delta QRST1 without regard to lesion size averaged -0.88. VFT also had a negative correlation to root mean square (RMS)delta QRST because of warming. RMS delta QRST was calculated from the change in QRST areas (warming-control) in all 64 electrograms. The correlation between VFT and RMS delta QRST was dependent on lesion size. For all experiments, the correlation between VFT and RMS delta QRST averaged -0.97, -0.93, and -0.93 for 400-, 800-, and 1,600-mm2 lesions, respectively. The correlation between VFT and RMS delta QRST without regard to lesion size, however, was considerably lower, -0.59. The results of this study provide the first direct evidence that VFT is correlated with cardiac surface QRST area distributions.

Animals↗

PubMed2001

The distribution of refractory periods influences the dynamics of ventricular fibrillation.

The spatial and dynamic properties of ventricular fibrillation (VF) may be random or related to cellular electrical properties of the normal heart. Local activation intervals (AIs) in VF may depend on the local refractory period (RP), and sustained VF may require a steep action potential (AP) restitution curve. In guinea pig hearts, AP durations (APDs) and RPs on the epicardium are shorter at the apex and progressively longer toward the base, producing gradients of RPs that may influence the spatial organization of VF. In the present study, the influence of APDs on VF dynamics is investigated in perfused guinea pig hearts stained with a voltage-sensitive dye by comparing APD gradients to the dynamics of VF elicited by burst pacing. In VF, AIs had no clear periodicity, but average AIs were shorter at the apex (57.5+/-8.1 ms) than the base (76.1+/-1.5 ms, n=6, P<0.05) and had gradients similar to APD gradients (correlation coefficient 0.71+/-0.04). Analysis of local velocity vectors showed no preferential directions, and fast Fourier transform (FFT) power spectra were broad (10 to 24 Hz) with multiple peaks (n=6). However, the selective inhibition of delayed K(+) rectifying currents, I(Kr) (E4031; 0.5 micromol/L, n=3), shifted FFT spectra from complex to a lower dominant frequency (10 Hz) and altered repolarization but retained the correlation between mean AIs and RPs. Thus, VF dynamics are consistent with a multiple wave-make and wave-break mechanism, and the local RP influences VF dynamics by limiting the range of VF frequencies and AIs at each site. The full text of this article is available at http://www.circresaha.org.

Action Potentials↗

PubMed1999

Relation between cellular repolarization characteristics and critical mass for human ventricular fibrillation.

INTRODUCTION: The critical mass for human ventricular fibrillation (VF) and its electrical determinants are unclear. The goal of this study was to evaluate the relationship between repolarization characteristics and critical mass for VF in diseased human cardiac tissues. METHODS AND RESULTS: Eight native hearts from transplant recipients were studied. The right ventricle was immediately excised, then perfused (n = 6) or superfused (n = 2) with Tyrode's solution at 36 degrees C. The action potential duration (APD) restitution curve was determined by an S1-S2 method. Programmed stimulation and burst pacing were used to induce VF. In 3 of 8 tissues, 10 microM cromakalim, an ATP-sensitive potassium channel opener, was added to the perfusate and the stimulation protocol repeated. Results show that, at baseline, VF did not occur either spontaneously or during rewarming, and it could not be induced by aggressive electrical stimulation in any tissue. The mean APD at 90% depolarization (APD90) at a cycle length of 600 msec was 227+/-49 msec, and the mean slope of the APD restitution curve was 0.22+/-0.08. Among the six tissues perfused, five were not treated with any antiarrhythmic agent. The weight of these five heart samples averaged 111+/-23 g (range 85 to 138). However, after cromakalim infusion, sustained VF (> 30 min in duration) was consistently induced. As compared with baseline in the same tissues, cromakalim shortened the APD90 from 243+/-32 msec to 55+/-18 msec (P < 0.001) and increased the maximum slope of the APD restitution curve from 0.24+/-0.11 to 1.43+/-0.10 (P < 0.01). CONCLUSION: At baseline, the critical mass for VF in diseased human hearts in vitro is > 111 g. However, the critical mass for VF can vary, as it can be reduced by shortening APD and increasing the slope of the APD restitution curve.

Action Potentials↗