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PubMed1975

Primary ventricular fibrillation and resumption of work, sexual activity, and driving after first acute myocardial infarction.

The resumption of work, sexual activity, and driving were studied in 32 patients who had suffered primary ventricular fibrillation after their first myocardial infarction. They were compared with 95 patients whose myocardial infarction was not so complicated. Though initially slowing rehabilitation, primary ventricular fibrillation did not affect ultimately either the return to work or the resumption of normal sexual activity and driving.

Age Factors↗
PubMed2006

Autonomic modulation of electrical restitution, alternans and ventricular fibrillation initiation in the isolated heart.

OBJECTIVE: Abnormal autonomic nerve activity is a strong prognostic marker for ventricular arrhythmias but the mechanisms underlying the autonomic modulation of ventricular fibrillation (VF) initiation are poorly understood. We examined the effects of direct sympathetic (SS) and vagus (VS) nerve stimulation on electrical restitution, alternans and VF threshold (VFT) in a novel isolated rabbit heart preparation with intact dual autonomic innervation. METHODS: Monophasic Action Potentials (MAPs) were recorded from a left ventricular epicardial site on innervated, isolated rabbit hearts (n=16). Standard restitution, effective refractory period (ERP), electrical alternans and VFT were measured at baseline and during SS and VS separately. RESULTS: The restitution curve was shifted downwards and made steeper with SS whilst VS caused an upward shift and a flattening of the curve. The maximum slope of restitution was increased from 1.30+/-0.10 at baseline to 1.86+/-0.17 (by 45+/-12%, P<0.01) with SS and decreased to 0.69+/-0.10 (by 51+/-6%, P<0.001) with VS. ERP was decreased from 127.3+/-2.5 ms to 111.8+/-1.8 ms with SS (by 12+/-2%, P<0.001) and increased to 144.0+/-2.2 ms with VS (by 13+/-2%, P<0.001). VFT was decreased from 4.7+/-0.6 mA to 1.9+/-0.5 mA with SS (by 64+/-5%, P<0.001) and increased to 8.7+/-1.1 mA with VS (by 89+/-14%, P<0.0005). There was a significant inverse relationship between the maximum slope of restitution and VFT (r=-0.63, P<0.0001). When compared with baseline, SS caused electrical alternans at longer pacing cycle lengths (139.0+/-8.4 vs. 123.0+/-7.8 ms, P<0.01) with greater degree of alternans (32.5+/-9.9 vs. 15.4+/-3.2%, P<0.05). It also caused a wider range of cycle lengths where alternans occurred (53.0+/-6.2 vs. 41.0+/-7.0 ms, P<0.05) whilst vagus nerve stimulation shortened this range (33.0+/-7.3 ms, P<0.001). CONCLUSIONS: Sympathetic stimulation increased maximum slope of restitution and electrical alternans but decreased ERP and VF threshold whilst vagus nerve stimulation had opposite effects. The interaction between action potential duration and beat-to-beat interval may play an important role in the autonomic modulation of VF initiation.

Action Potentials↗
PubMed1998

Beat-to-beat variation of the ST segment in a patient with right bundle branch block, persistent ST segment elevation, and ventricular fibrillation: a case report.

The authors describe a patient with ventricular fibrillation associated with right bundle branch block-like QRS morphology and persisting ST segment elevation in the precordial leads, in whom the morphology of the ST segment changed from the coved type to the saddle-back type or vice versa on a beat-to-beat basis. Such an observation has never been reported in the previous literature.

Adult↗
PubMed1975

[Ventricular fibrillation during testing of a demand pacemaker (author's transl)].

Ventricular fibrillation was precipitated in a patient with an implanted unipolar demand pacemaker while its function was being tested by switching over to a fixed-rate output by means of a magnet. There was no evidence of either myocardial infarction, abnormal electrolyte state, or digitalis intoxication. This, probably unique, case indicates that non-synchronized stimulation, even during brief switching over of a demand pacemaker to a fixed-rate one, may endanger the patient.

Aged↗
PubMed1976

[Prevention of ventricular fibrillation during the acute phase of experimentally induced myocardial infarction by affecting the ion and acid-base balance of the heart].

For the purpose of prevention of ventricular fibrillation in acute coronary insufficiency a multi-component solution was developed that produces a normalizing effect on the acid-base and ion balance disorders in the heart under ischaemia. The injection of this solution into the left atrium sharply elevated the ventricular fibrillation threshold in cats with an occluded coronary artery. The administration of the solution into the left atrium of dogs following an occlusion of the descending left coronary artery prevented the development of fibrillation in all the experiments, while in the control series of experiments it developed in 62% of cases (p less than 0.001). The solution was decided to posses a high antifibrillation activity that manifests itself when the solution is introduced into the left atrium, and the mechanisms of the beneficial effects of the solution are discussed

Animals↗
PubMed1977

Primary ventricular fibrillation. Some unusual features.

A 47-year-old man experienced ventricular fibrillation three times during a 3 1/2-year period. Each episode was preceded by an auditory aura, and no ventricular irritability was identified between episodes. The results of coronary arteriographic, hemodynamic, and intracardiac electrophysiologic studies were all normal. Hypokalemia and abnormal oxyhemoglobin dissociation were present. The possible relationships of these unusual features to the patient's disturbances in rhythm are discussed.

Diphosphoglyceric Acids↗
PubMed1985

Ventricular fibrillation in myocardial sarcoidosis.

A 35 year old male with intractable ventricular fibrillation due to myocardial sarcoidosis is described. Myocardial involvement in patients with sarcoidosis is not uncommon. Since severe ventricular arrhythmias due to myocardial sarcoidosis are often refractory to conventional antiarrhythmic treatment, steroids should be tried.

Adult↗
PubMed1993

[Two cases of idiopathic ventricular fibrillation with interesting electrocardiographic findings].

We encountered two cases of ventricular fibrillation (VF) without overt heart disease. The first case we report is that of a 47-year-old man, and the second case is a 39-year-old man. VF occurred in the night unrelated to myocardial ischemia or myocarditis. Their basic ECGs showed normal sinus rhythm, but neither QT prolongation nor abnormal Q wave was seen. But we could see IRBBB and ST segment elevation in the V1-2 lead not only in the acute phase, but also in the chronic phase. Abnormal findings were not found in noninvasive cardiac examinations, nor in cardiac catheterization and histological examinations. In the second case, VF was induced by electrical stimulation, and Disopyramide was found to be effective for the prevention of VF. The patient in the first case died suddenly two years after his first attack. Both cases have interesting ECG findings, and it may be that they play on important role in discovering the etiology of sudden cardiac death.

Adult↗
PubMed2004

Catheter ablation of frequently recurring ventricular fibrillation in a patient after aortic valve repair.

It has been demonstrated that idiopathic ventricular fibrillation (VF) can be triggered by ventricular premature beats (VPBs) arising from the Purkinje fibers. Eliminating these VPBs by radiofrequency catheter ablation prevented VF recurrences. Whether the same pathophysiology and the same treatment option exist in patients with structural heart disease is unknown. Recurrent VF was observed in a 17-year-old patient after aortic valve repair of a perforated noncoronary cusp with resulting severe aortic regurgitation. VF recurred despite therapy with various antiarrhythmic drugs. A maximum of 14 external defibrillations was necessary during a 24-hour period to stabilize the patient. Due to increasing hemodynamic instability as a result of this electrical storm, the patient was referred for invasive diagnostics. During electrophysiologic study, frequent short runs of VF initiated by VPB with a narrow QRS complex were observed. After extensive mapping of the right and left ventricles, two distinct sources of VPBs originating from anteroseptal and inferoseptal areas of the left ventricle could be successfully ablated. VPBs were preceded by distinct Purkinje potentials with intervals from the Purkinje potential to QRS onset of VPB of 68 ms and 30 ms at effective sites, respectively. During short-term follow-up of 2 months, there was no VF recurrence. VPB originating from the Purkinje system may be one possibility for VF initiation in patients with structural heart disease. Eliminating these sources of VPBs by catheter ablation can prevent recurrent VF in such patients.

Adolescent↗
PubMed1982

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode.

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was less than or equal to 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks less than or equal to 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.

Aged↗
PubMed1994

Circadian rhythm of the ventricular fibrillation threshold in female Wistar rats.

The circadian rhythm of ventricular fibrillation threshold (VFT) and its relation to the heart rate (HR) and the rectal temperature (RT) was studied in female Wistar rats. The animals were exposed to daily light-dark cycles of 12 h of light alternating with 12 h of darkness and were under pentobarbital anaesthesia (40 mg/kg i.p.). The experiments were performed on open chest animals and VFT was measured by direct stimulation of the myocardium. VFT in female rats showed a circadian rhythm with the acrophase -338 degrees (at 22.53 h), with the mesor 2.58 mA and the amplitude 0.33 mA. HR was not significantly changed during the experiments and no dependence was found between VFT and HR during the whole 24-hour period (r = 0.08). The acrophase of the circadian rhythm of HR (on -47 degrees, i.e. at 03.08 h) was shifted to the acrophase of VFT. The circadian rhythms of RT before the application of the anaesthetic agent and under general anaesthesia before the operative interventions had a very similar course with the nearly corresponding acrophases as the circadian rhythm of VFT. It is concluded that the electrical stability of the rat heart measured by VFT shows the significant circadian rhythm in a parallel with the circadian rhythm of RT and probably without dependence on the changes of HR.

Animals↗
PubMed1990

Role of calcium and the calcium channel in the initiation and maintenance of ventricular fibrillation.

The cellular events during the initiation and maintenance of ventricular fibrillation (VF) are poorly understood. We developed a nonischemic, isolated, perfused rabbit Langendorff preparation in which sustained VF could be induced by alternating current (AC) and which allowed changes in perfusate composition. We also used Na(+)-K+ pump inhibition (10 microM ouabain or K(+)-free perfusate) to induce VF. AC stimulation or Na(+)-K+ pump inhibition always initiated VF. Calcium channel blockade by verapamil or nitrendipine uniformly inhibited the initiation of VF in both models. During Na(+)-K+ pump inhibition, 1) VF was prevented by calcium channel blockade, despite evidence of Ca2+ overload, and 2) abolition of spontaneous sarcoplasmic reticulum-generated cytosolic Ca2+ oscillations by ryanodine or Na+ channel blockade with tetrodotoxin did not prevent VF initiation. Lowering extracellular [Ca2+] to 80 microM uniformly prevented the initiation of VF due to Na(+)-K+ pump inhibition but not that due to AC stimulation. VF maintenance also was studied using 1) reduction in perfusate [Ca2+], 2) blockade of Ca2+ channels, or 3) electrical defibrillation. Decreasing the perfusate [Ca2+] to 80 microM resulted in defibrillation during VF whether induced by AC or Na(+)-K+ pump inhibition. Verapamil or nitrendipine also resulted in defibrillation regardless of the initiation method. Electrical defibrillation was successful only in AC-induced VF. The results demonstrate that VF can be initiated and maintained in a nonischemic rabbit Langendorff preparation. The data suggest that increases in slow channel Ca2+ flux, as opposed to increases in cytosolic Ca2+ per se, were necessary for the initiation and maintenance of VF. The data, however, do not exclude an important role for cytosolic Ca2+ in the modulation of VF.

Animals↗
PubMed2001

Scaling exponent predicts defibrillation success for out-of-hospital ventricular fibrillation cardiac arrest.

BACKGROUND: -Defibrillator shocks often fail to terminate ventricular fibrillation (VF) in out-of-hospital cardiac arrest (OOHCA), and repeated failed shocks can worsen the subsequent response to therapy. Because the VF waveform changes with increasing duration of VF, it is possible that ECG analyses could estimate the preshock likelihood of defibrillation success. This study examined whether an amplitude-independent measure of preshock VF waveform morphology predicts outcome after defibrillation. Methods and Results-Clinical data and ECG recordings from an automated external defibrillator were obtained for 75 subjects with OOHCA in a suburban community with police first responders and a paramedic-based emergency medical system. An estimate of the fractal self-similarity dimension, the scaling exponent, was calculated off-line for the VF waveform preceding shocks. Success of the first shock was determined from the recordings. Return of pulses and survival were determined by chart review. The first shock resulted in an organized rhythm in 43% of cases, and 17% of cases survived to hospital discharge. A lower mean value of the scaling exponent was observed for cases in which the first defibrillation resulted in an organized rhythm (P:=0.004), for cases with return of pulses (P:=0.049), and for cases surviving to hospital discharge (P:<0.001). Receiver operator curves revealed the utility of the scaling exponent for predicting the probability of restoring an organized rhythm (area under the curve=0.70) and of survival (area under the curve=0.84). CONCLUSIONS: -The VF waveform in OOHCA can be quantified with the scaling exponent, which predicts the probability of first-shock defibrillation and survival to hospital discharge.

Aged↗
PubMed1985

Reperfusion-induced ventricular fibrillation. Modification by pharmacological agents.

We have assessed the ability of several of the main groups of antiarrhythmic agents to modify the incidence of reperfusion-induced ventricular fibrillation in the isolated working rat heart preparation with transient coronary artery occlusion. Hearts were perfused with Krebs-Henseleit medium containing 5 microM epinephrine to provide some level of exogenous catecholamine support. Compounds selected were: the fast sodium channel inhibitors lignocaine (1 and 10 microM) and prenylamine (4 microM) (the latter also possessing slow calcium channel antagonistic actions); the beta-adrenergic blocking agents oxprenolol (1.2 microM), timolol (0.13 microM), metoprolol (1.0 microM), and acebutolol (5.6 microM); and the slow calcium channel antagonist nifedipine (0.05 and 0.5 microM). After 15 min of coronary artery occlusion, over 90% of control hearts fibrillated 30-60 sec after the onset of reperfusion. Drugs reduced this to the following: prenylamine, 0% (p less than 0.001); 1 microM lignocaine, 83%; 10 microM lignocaine, 33% (p less than 0.01); oxprenolol, 92% (NS); timolol, 92% (NS); metoprolol, 42% (p less than 0.01); acebutolol, 67% (p less than 0.05); 0.05 microM nifedipine, 83% (NS); and 0.5 microM nifedipine, 67% (NS). Thus, inhibition of the fast inward sodium channel with agents such as prenylamine and lignocaine, (when begun before coronary-artery occlusion) offers maximal protection against reperfusion-induced ventricular fibrillation, while beta-blockade with timolol and oxprenolol and slow calcium channel inhibition with nifedipine do not offer any significant protection. The beta-blocking agents metoprolol and acebutolol produce a partial reduction that may be due to a membrane-stabilizing action, rather than to beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1987

Effects of metoprolol, alone and in combination with lidocaine, on ventricular fibrillation threshold: comparison with atenolol, propranolol, and pindolol.

Metoprolol and other beta-adrenergic blocking drugs are known to exert cardioprotective effects that include significant reduction in occurrence of ventricular fibrillation (VF) following myocardial ischemia and infarction. To help determine the mechanism of these cardioprotective effects, this study evaluated the effect of equipotent beta-blocking doses of metoprolol and three other beta-blockers with differing ancillary properties on ventricular fibrillation threshold (VFT) in the normal canine heart. Metoprolol tartrate (1.0 mg/kg i.v.), atenolol (0.3 mg/kg i.v.), propranolol hydrochloride (0.3 mg/kg i.v.), pindolol (0.03 mg/kg i.v.), or saline control (0.9% NaCl solution; vehicle) was given, alone and in combination with lidocaine (L), to groups of six pentobarbital (32.5 mg/kg i.v.) anesthetized mongrel dogs after control VFT and control isoproterenol-induced (ISO) positive chronotropic effects had been determined. The D- (membrane stabilizing, non-beta blocking) and L- (beta blocking) isomers of propranolol also were administered to separate groups of six anesthetized dogs in a dose of 0.3 mg/kg i.v. Blood samples (venous) were taken before drug or vehicle administration, 10 min after drug/vehicle administration and at half-hour intervals thereafter during experimentation. ISO responses and VFT were determined 5 and 15 min, respectively, after drug/vehicle administration and at half-hour intervals for a total experimental period of 165 min. VF was induced with a train of pulses (5 s, 100 Hz, 3-ms duration, 250-omega resistance) applied by bipolar platinum electrodes to a paced heart (200 beats/min). Voltage (V) was increased every 60 sec (0.25-V increments between 0-3.5 V and 0.5-V increments greater than 3.5 V) until VF occurred. Metoprolol increased VFT significantly (p less than 0.05) and maximally (max delta V = 2.3 +/- 0.7 V) at 135 min postdrug when the ISO-induced increase in heart rate was inhibited (%I ISO) by less than 53%. Max delta V was not significantly increased following i.v. administration of atenolol (0.8 +/- 0.6 V), pindolol (0.1 +/- 0.1 V), or saline (0.1 +/- 0.1 V). Max delta V was 0.5 +/- 0.2 in the D-propranolol-treated group and 0.5 +/- 0.3 in the L-propranolol-treated group. These values did not differ from max delta V obtained in the propranolol-treated group (0.6 +/- 0.4 V). Changes in VFT for all groups were, over time, negatively correlated with %I ISO and were not dependent on membrane stabilizing effect (metoprolol, propranolol (D,DL), pindolol), intrinsic sympathomimetic activity (pindolol), or cardioselectivity (metoprolol, atenolol).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Dietary lipid modulation of ventricular fibrillation threshold in the marmoset monkey.

Programmed electrical stimulation was used to examine the ability of long-term dietary lipid modulation to influence myocardial vulnerability to the induction of ventricular fibrillation in adult marmoset monkeys (Callithrix jacchus). Marmosets fed diets supplemented (to a total of 28.5% of the energy as fat) with polyunsaturated fatty acid (PUFA)-rich tuna fish oil or sunflower seed oil had significantly elevated mean ventricular fibrillation threshold compared with those fed a saturated animal fat supplemented diet or a reference diet not supplemented with fat (11.2% of the energy as fat). Fibrillation threshold was reduced during acute myocardial ischemia induced by coronary artery occlusion but still remained higher in the PUFA-fed animals than either the control or the ischemic threshold in reference or saturated fat supplemented animals. Dietary tuna fish oil was associated with a low incidence of sustained fibrillation episodes and no fatalities. These results indicate that myocardial substrate vulnerability to arrhythmic stimuli is increased during ischemia in a nonhuman primate model but dietary PUFA can reduce vulnerability under both normal and ischemic conditions. Reduced dietary fat intake alone was without effect.

Animals↗
PubMed2004

Total failure to sense ventricular fibrillation with inappropriate defibrillator sensitivity adjustment.

Automatic Sensitivity Control, unique to St. Jude defibrillators, allows for programmable sensitivity threshold and refractory periods. However, inappropriate programming can lead to marked undersensing and potentially lethal complications. We report a case of complete failure to sense ventricular fibrillation with inappropriate sensitivity adjustments. Detailed review of the parameters with induction of ventricular fibrillation must be performed to assure adequate safety.

Aged↗