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At least 991 records · Page 55Linked to original sources
PubMed1985

Prevention of ventricular fibrillation by dextrorotatory sotalol in a conscious canine model of sudden coronary death.

The antiarrhythmic and antifibrillatory actions of the dextrorotatory isomer of sotalol, administered in a multiple-dose regimen, were evaluated in conscious dogs 3 to 5 days after anterior myocardial infarction. The intravenous administration of d-sotalol, four 8 mg/kg doses over a 24-hour treatment period, suppressed the induction of ventricular tachycardia by programmed electrical stimulation in six of nine dogs tested, slowed the rate of the induced tachyarrhythmia in two of the remaining three dogs, and provided significant protection (5 of 8 d-sotalol vs 0 of 8 vehicle control) against the development of ventricular fibrillation in response to ischemia at a site distant to a previous myocardial infarction. Increases in ventricular myocardial refractoriness and in QTc and paced QT intervals suggest that class III electrophysiologic actions contribute to the antiarrhythmic properties of dextrorotatory sotalol in this animal model. The degree of beta-adrenergic receptor blockade produced by d-sotalol in this dose regimen was negligible. These findings suggest the potential utility of d-sotalol in the prevention of ventricular tachycardia and ventricular fibrillation in the setting of myocardial infarction, particularly when beta-adrenergic receptor blockade is undesirable or contraindicated.

Animals↗
PubMed1992

[Accidental ventricular fibrillation during transesophageal atrial overdrive].

Transesophageal atrial overdrive stimulation is a widely used technique for the interruption of atrial flutter and supraventricular tachyarrhythmias. We describe a case of 60 year old man with a previous myocardial infarction, suffering from angina during effort after aortocoronary bypass who presented several episodes of atrial flutter treated with success by transesophageal atrial overdrive stimulation using swallowing electrodes. During the treatment of the last episode of atrial flutter, after a 5 s burst at 300 b/min ventricular fibrillation occurred and was promptly interrupted by DC shock. This is the first case in our experience and probably the first report of ventricular fibrillation induced by swallowing electrodes. Possible mechanisms as pharmacological interactions, accidental ventricular stimulation, etc, are discussed. In conclusion, even though the risk of dangerous arrhythmias is very low, transesophageal atrial overdrive stimulation should be performed by experts in an equipped room.

Angina Pectoris↗
PubMed2000

Experimental study of the effects of multi-site sequential ventricular pacing on the prophylaxis of ventricular fibrillation.

Previous studies report a significant prophylactic effect on the occurrence of atrial fibrillation by simultaneous multi-site atrial pacing. We investigated the effects of multi-site sequential ventricular pacing (MSVP), which may be preferable to simultaneous multi-site pacing in terms of the prophylaxis of the occurrence of ventricular fibrillation (VF). Needle electrodes were inserted at ten different epicardial sites on both ventricles for MSVP in 12 adult beagle dogs. Four premature ventricular extrastimuli (PVE) were introduced to provoke VF reproducibly from a separate electrode in the left ventricle. The 4 PVE were applied to try to provoke VF during MSVP in a comparable fashion to the activation sequence during sinus rhythm. We compared the prophylactic effects of MSVP on the inducibility of VF by changing the number of stimulation sites to either 1, 3, 5, or 10 epicardial sites. We performed a total of 363 trials of induction and suppression of VF. The occurrence rates of VF by the 4 PVE for the various number of epicardial stimulation sites of MSVP, i.e., at 1, 3, 5, and 10 sites, were 0.8263, 0.4286, 0.4450, and 0.2857, respectively (p < 0.05). There was a significant prophylactic effect of MSVP on the inducibility of VF, and this effect became stronger as the number of MSVP sites was increased from 3 to 10. The hemodynamic state was relatively stable during MSVP. MSVP seems to be a promising method with which to reduce the occurrence of VF, and a larger number of stimulation sites would be more effective in terms of the prophylaxis of VF.

Animals↗
PubMed1996

Influence of ventricular fibrillation on sympathetic nerve activity under biventricular bypass circulation.

Autonomic nerves play an important role in circulatory control. The characteristics of sympathetic nerve activity (SNA) during artificial circulation, however, are not well understood. In this study, we examined the influence of natural heart beating on the renal SNA (RSNA) using pulsatile 100% biventricular assistance and electrically induced ventricular fibrillation in anesthetized goats, whose heart rate and size are similar to the human heart's. Following induction of the ventricular fibrillation, the pulse-synchronous discharges in the RSNA did not change their periodicity and quantity significantly. It was concluded that the beating of the heart had little influence on the RSNA and was presumably not essential for maintaining nervous control of circulation as long as the circulation was maintained by an artificial heart.

Animals↗
PubMed1983

Ventricular fibrillation and initial plasma potassium in acute myocardial infarction.

In a retrospective review of patients admitted to a coronary care unit, 809 patients had a definite myocardial infarction and plasma potassium was measured within 48 hr. The mean (+/- s.d.) plasma potassium was 4.04 (+/- 0.56) mmol/litre. A potassium concentration of less than 4.0 mmol/litre was found in 383 patients, of whom 14 had ventricular fibrillation. A potassium concentration of 4.0 mmol/litre or greater was found in 426 patients, of whom 3 had ventricular fibrillation, a difference significant at the 0.4% level (chi 2 test). Preceding diuretic therapy did not appear to be relevant and there appeared to be no other difference between the two groups. The maintenance of a high-normal plasma potassium, or the prevention of its reduction, in patients with an acute myocardial infarction may be important.

Humans↗
PubMed1989

Ventricular fibrillation detection by autocorrelation function peak analysis.

UNLABELLED: The use of reliable automatic ventricular fibrillation (VF) recognition techniques is critical in performing external automatic defibrillation. The authors' objective was to develop a method to detect VF and life-threatening arrhythmias, based on direct and simple peak analysis of the autocorrelation function (ACF). This method may differentiate between fibrillating and nonfibrillating rhythms, and in the first case between "course" and "fine" VF. ECG records during ventricular tachycardia (VT) and VF were obtained from patients during cardiac surgery. Segments 4 sec long were selected from tapes and digitized at 200 Hz, then split into three groups (VT, VF regular waveform, and VF irregular waveform). The positive peak P(j) of the ACF was defined as the maximum value between two function zeros, and RPL(j) represents the relation between P(j) and twice their own standard error. Parameter TR(1) was defined as the relation between P(1) width and the time of occurrence. ACFs were computed for the entire sample; RPL(j), D(j) = RPL(j) - RPL(j + 1), and TR(1) were calculated for every record. The results indicate that: (A) If RPL(1) greater than 1.2 and (1.6 greater than or equal to RPL(2) greater than 1) and (RPL(3) greater than 0.6 and D(1) greater than 0), then consider VT; (B) If (1.2 greater than or equal to RPL(1) greater than or equal to 1) and (1 greater than or equal to RPL(2) greater than or equal to 0.9) and D(1) greater than 9, then consider VT or VF with very regular waveform; (C) If (RPL(1) less than or equal to 1.8 and RPL(2) less than 0.9) or (RPL(2) less than 1.5 and D(1) less than 0) or RPL(3) less than 0.6, then consider VF. When 0.3 less than TR(1) less than 0.8, the underlying arrhythmia is VF or VT, and when it is outside this range, it is likely to be a supraventricular rhythm. CONCLUSIONS: (A) RPL(j) parameters have a high specificity for discriminating between VT and VF. The method is reliable and simple. (B) The TR(1) parameter together with RPL(j) allow discrimination between supraventricular tachycardias and ventricular originated tachyarrhythmias. (C) Further analysis must be done using problem-oriented arrhythmias data bases.

Data Interpretation, Statistical↗
PubMed2001

Ventricular fibrillation sensing and detection by implantable defibrillators: is one better than the others? A prospective, comparative study.

INTRODUCTION: We prospectively compared the performance of the sensing and detection systems of three leading defibrillator manufacturers: Medtronic, Guidant, and Ventritex. METHODS AND RESULTS: Ventricular fibrillation signal was digitally recorded during defibrillator implantation and subsequently played back sequentially to a Medtronic Micro Jewel II 7223Cx, a Guidant MINI II 1762, and a Ventritex Cadet V-115C. The devices were programmed for single-zone detection, at nominal settings. Rate cutoff was set at 320 msec (185/min for the MINI). We analyzed 253 episodes from 47 patients. Median undersensing was 0%, 2.1%, and 5.3% for the Jewel, MINI, and Cadet, respectively (P < 0.001 for each paired comparison). Detection time was 4.1 +/- 1.6 seconds, 3.4 +/- 1.6 seconds, and 4.3 +/- 2.2 seconds for the Jewel, MINI, and Cadet, respectively (P < 0.001 between MINI-Jewel and MINI-Cadet; P < 0.01 between Jewel-Cadet). Delayed detection (detection time longer than the mean of all observations + 2 SD) occurred in 3 (1.2%), 7 (2.8%), and 18 (7.1%) episodes for the Jewel, MINI, and Cadet, respectively. Performance for all devices was worse when the short-separation integrated bipolar lead was used and when the episode followed a failed high-energy shock. CONCLUSION: Statistically significant differences were seen in sensing and detection performance among the devices and device/lead combinations during ventricular fibrillation. These differences are related to specific features of the respective devices and should be taken into account during clinical practice, as well as in future device development.

Adult↗
PubMed1997

[Ventricular fibrillation after radiofrequency ablation of the atrioventricular node].

The authors report the case of a 77 year old patient who underwent radiofrequency ablation of the atrioventricular node for chronic. Invalidating atrial fibrillation, refractory to pharmacological therapy. A single chamber ventricular pacemaker was implanted one week before interruption of AV conduction. Eleven applications (7 on the right and 4 on the left side of the interventricular septum) were required for successful ablation. Four hours later, the patient developed episodes of non-sustained polymorphic ventricular tachycardia and torsades de pointe. These arrhythmias were initiated by long cycle-short cycle sequences and preceded by changes of ventricular repolarisation (prolongation of the spontaneous and paced QTc and JTc intervals). Eight days after ablation, the patient had an episode of ventricular fibrillation reduced by external DC shock. This arrhythmia was also preceded by changes in ventricular repolarisation. This case demonstrates the potential proarrhythmogenic effect of radiofrequency ablation of the AV node with changes in ventricular repolarisation which induces malignant ventricular arrhythmias. The authors suggest an appropriate preventive attitude. The progression in two distinct phases (immediate and late) imposes prolonged arrhythmia monitoring.

Aged↗
PubMed2001

Electrophysiologic basis by which epinephrine facilitates defibrillation after prolonged episodes of ventricular fibrillation.

STUDY OBJECTIVE: Even though epinephrine has been shown to decrease the electrical stability of the heart, it is used extensively in cardiac resuscitation. The objective of this study is to document electrophysiologic parameters of epinephrine, which would facilitate defibrillation. METHODS: In 20 swine, electrically induced ventricular fibrillation was allowed to continue for 10 minutes. Animals were then randomly assigned to receive either intracardiac injection of 1 mg of epinephrine or 10 mL of normal saline solution. Synchronization and dispersion of the repolarization of fibrillatory waves and cycle length were measured. RESULTS: As the ventricular fibrillation continued, cycle length was prolonged, and synchronization and dispersion deteriorated. With epinephrine, cycle length shortened from 416+/-21 to 204+/-23 ms (P<.005), synchronization improved from 114+/-13 to 61+/-10 ms (P<.05), and dispersion narrowed from 84+/-10 to 49+/-8 ms (P<.005). Normal saline solution had no effect. Successful resuscitation was achieved in all 10 animals administered epinephrine and only 1 animal in the saline solution group. CONCLUSION: Epinephrine's effect on cycle length, synchronization, and dispersion of repolarization of fibrillatory waves may be the mechanism with which it facilitates defibrillation.

Animals↗
PubMed1999

Electrophysiologic properties and ventricular fibrillation in normal and myopathic hearts.

This study tests the hypothesis that moderate myocardial dysfunction is associated with altered myocardial anisotropic properties and structurally altered ventricular fibrillation (VF). Mongrel dogs were randomized to either a control group or a group that was rapidly paced at 250 beats/min until the left ventricular ejection fraction was < or = 40%. Changes in anisotropic properties and the electrical characteristics of VF associated with the development of moderate myocardial dysfunction were assessed by microminiature epicardial mapping studies. In vivo conduction, refractory periods, and repolarization times were prolonged in both longitudinal and transverse directions in myopathic animals versus controls. VF was different in myopathic versus control animals. There were significantly more conducted deflections during VF in normal hearts compared with myopathic hearts. Propagated deflection-to-deflection intervals during VF were significantly longer in myopathic hearts compared with controls (125.5 +/- 49.06 versus 103.4 +/- 32.9 ms, p = 0.009). There were no abnormalities in cell size, cell shape, or the number of intercellular gap junctions and there was no detectable change in the expression of the gap junction proteins Cx43 and Cx45. Moderate myocardial dysfunction is associated with significant electrophysiological abnormalities in the absence of changes in myocardial cell morphology or intercellular connections, suggesting a functional abnormality in cell-to-cell communication.

Animals↗
PubMed2005

Mechanisms of ventricular fibrillation in canine models of congestive heart failure and ischemia assessed by in vivo noncontact mapping.

BACKGROUND: Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF. METHODS AND RESULTS: Three groups of dogs were studied: (1) control (n=8), (2) pacing-induced congestive heart failure (n=7), and (3) acute ischemia produced by 30 minutes of mid left anterior descending artery ligation (n=5). A noncontact mapping catheter (Ensite 3000, ESI) was placed via transseptal into the left ventricle (LV), along with an electrophysiology catheter. A multielectrode basket catheter (EP Technologies) was placed in the right ventricle, along with an electrophysiology catheter. Several episodes of VF were recorded in each animal. In addition to constructing isopotential and isochronal maps of the VF episodes, signals underwent frequency domain analysis as a fast Fourier transform was performed over a 2-second window every 1 second. From the fast Fourier transform, the dominant frequency was determined, and the organization was calculated. In control dogs, meandering, reentrant spiral wave activity was the main feature of the VF. The congestive heart failure group showed evidence of a stable rotor (n=3), evidence of a focal source (n=3), or no evidence of a driver in the LV (n=1). The ischemic group showed evidence of an initial focal mechanism that transitioned into reentry. In the control and ischemic groups, the LV always had higher dominant frequencies than the right ventricle. CONCLUSIONS: Different ventricular substrates produced by the different animal models altered the characteristics of VF. Thus, different mechanisms of VF may be present in the LV, depending on the animal model.

Animals↗
PubMed1994

Bradycardia dependent QT prolongation and ventricular fibrillation following catheter ablation of the atrioventricular junction with radiofrequency energy.

Recurrent ventricular fibrillation was observed in a 67-year-old woman following catheter ablation of the AV junction using radiofrequency energy. This serious complication has been reported following direct current energy ablation of the AV junction, but not after using radiofrequency energy. This life-threatening arrhythmia seemed pause and bradycardia dependent. It was followed by QTc prolongation of the QRS escape rhythm 1 day after the procedure. Ventricular arrhythmias were suppressed by rapid ventricular pacing.

Aged↗
PubMed1984

Ventricular fibrillation causes sudden death in Southeast Asian immigrants.

Young, male, Southeast Asian immigrants living in the United States have a high incidence of unexplained, sudden, nocturnal death. We report the cases of three patients, two Laotians and one Filipino, who were resuscitated and subsequently studied extensively. Each patient was having ventricular fibrillation when first examined by paramedics outside the hospital, and episodes of fibrillation recurred in the early hospital course. Clinical evaluation found no significant coronary atherosclerosis or structural cardiac disease. One patient is asymptomatic after 2 years; the second patient died suddenly at 4 months; and the third is asymptomatic but had inducible ventricular tachycardia on electrophysiologic testing 6 months after resuscitation. The mechanism of sudden death in young Southeast Asian men appears to be ventricular fibrillation. The cause of the arrhythmia is unclear, although in our patients the arrhythmia was not an isolated event; underlying predispositions to further cardiac arrest persisted.

Adult↗
PubMed2002

Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators.

OBJECTIVES: In cellular studies, ventricular refractoriness (ERP) is prolonged in heart failure (CHF), but clinical evidence is lacking. The average ventricular fibrillation cycle length (VFCL) has been shown to correlate with local ERP. We hypothesized that the VFCL increases with left ventricular (LV) dysfunction. Therefore, we evaluated intracardiac VFCL recorded by implantable defibrillators (ICD) in patients with and without LV dysfunction. METHODS: We analyzed intracardiac VFCL recorded by sensing leads of Ventak MINI (Guidant) ICD in 49 patients (35 men; age 54 +/- 13 years; 25 (51%) with coronary artery disease; mean LV ejection fraction (EF) 41 +/- 17%, range 76-10) from the European Ventak MINI Investigator Group. No patients were receiving antiarrhythmic drugs, including beta-blockers. Mean and median VFCL were obtained at predischarge testing during first charge time (4.5 +/- 2.7 s, range 1.4-11). RESULTS: Mean median VFCL was 186 +/- 21ms (range 150-230 ms). Patients with LVEF >/= 50% (n = 14) had shorter median VFCL than patients with LVEF < 50% (n = 35), (171 +/- 14 vs. 191 +/- 20 ms; p = 0.002). Median VFCL correlated with LVEF (r = -0.41; p = 0.003) and age (r = 0.28, p = 0.04), but was not significantly associated with charge time and defibrillation threshold at implant. Similar results occurred with mean VFCL. In multiple linear regression and correlation models, only LVEF% was a significant predictor (p < 0.05 for all models) of median VFCL. CONCLUSIONS: LV dysfunction prolongs averaged VFCL in patients at risk for malignant ventricular arrhythmias who have implantable cardioverter defibrillators. This phenomenon might be related to alterations in the ventricular refractory period.

Analysis of Variance↗
PubMed2004

Mechanism of pacing-induced ventricular fibrillation in the infarcted human heart.

BACKGROUND: The mechanisms by which ventricular fibrillation (VF) is initiated in the infarcted human heart have not been defined. METHODS AND RESULTS: Left ventricular noncontact mapping of 8 episodes of pacing-induced VF in 6 patients (age 64.8+/-7.9 years, with previous myocardial infraction and left ventricular ejection fraction of 36+/-4%) undergoing ventricular tachycardia (VT) ablation revealed a consistent mechanism of VF induction. Whether during VT or sinus rhythm, the first of a train of paced extrastimuli to capture the LV produced an arc or arcs of functional block at regions bordering scar. With subsequent extrastimuli, the arcs elongated to circumscribe an enlarging area of increasingly late activation, with reentry through part of this functional (unidirectional) block leading to wavefront fragmentation and VF. These regions had longer fibrillation intervals (263+/-63 ms) than remote LV regions (209+/-23.4 ms; P<0.0001), implying longer refractory periods, and in 6 of the 8 VF episodes, these regions correlated with VT exit sites. In each of the 2 patients with 2 episodes of VF, both episodes formed arcs of functional block in the same location, despite pacing from different sites. CONCLUSIONS: Pacing-induced VF in the infarcted human heart is initiated by the development of functional lines of block dictated by the properties of a particular region of myocardium characterized by longer refractory periods, at or near VT circuit exit sites. Identification of these characteristic properties may help stratify risk of arrhythmic death and explain the potential for VT ablation to modify risk of VF in the infarcted heart.

Aged↗
PubMed2007

Wave similarity of human ventricular fibrillation from bipolar electrograms.

AIMS: The aim of this report was to review existing techniques for assessment of directionality in fibrillation and to describe the concept of wave similarity analysis in human VF. METHODS: We applied a technique called wave similarity analysis to bipolar electrograms to study directionality during various rhythms (sinus rhythm, ventricular tachycardia and ventricular fibrillation) in humans. This technique uses the barycentre to determine the activation time and a similarity index is calculated using a technique described previously for AF studies. RESULTS: We show here that using the wave similarity concept it is possible to recognize myocardial regions that are activated from multiple directions and differentiate those areas from regions that are activated by wave fronts in similar direction or at the exact mirror angle in ventricular fibrillation. CONCLUSIONS: Wave similarity analysis provides a tool for assessing directional organization in human VF. This analysis of directional organization may have implications for the study of mechanisms of VF in the clinical arena.

Electrocardiography↗