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PubMed1983

Prophylaxis of primary ventricular fibrillation with tocainide in acute myocardial infarction.

Within six hours of suspected acute myocardial infarction, 791 patients entered a randomised double blind study of combined intravenous and oral tocainide for the prophylaxis of primary ventricular fibrillation. Acute myocardial infarction was confirmed in 559 patients, of whom 278 had received tocainide. The study was terminated on the basis of a sequential statistical analysis which showed that in these patients tocainide was unlikely to reduce the incidence of primary ventricular fibrillation by as much as 50%, primary ventricular fibrillation having occurred in 4% of the tocainide and 2% of the placebo patients. Significantly fewer tocainide treated patients were withdrawn for other serious ventricular arrhythmias. Mortality (1% in the tocainide group and 2% in the placebo group) was low with no statistically significant differences between the active and placebo groups. Unwanted effects of treatment were infrequent and rarely troublesome both in patients with and without acute myocardial infarction. These results suggest that in the dosage used in this study tocainide does not exert an antifibrillatory action in the early phase of acute myocardial infarction.

Anti-Arrhythmia Agents↗

PubMed1982

[Physical training following myocardial infarct complicated by ventricular fibrillation].

Case histories of 4 patients with myocardial infarction are given, 3 had ventricular fibrillation during the acute period and one a month later after infarction. When discharged all of them completed a physical training program. They had no rhythm disorders and all returned to work. It is concluded that myocardial infarction cases who had had ventricular fibrillation can achieve complete rehabilitation, if there are no rhythm disorders during exercise. Physical training can be used for rehabilitation.

Adult↗

PubMed1995

Effect of myocardial infarction and ischemia on induction of cardiac reentries and ventricular fibrillation.

The present work is aimed at investigating the effects of myocardial infarction and ischemia on induction of ventricular fibrillation. Electrophysiologic effects of global and local ischemia (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms was studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local area of ischemia where effects of the dispersion of refractory periods are investigated is then simulated. This is made using a Gaussian distribution characterized by its mean and standard deviation. These simulations show that ischemia is capable of initiating reentry phenomena which propagate through the whole ventricle; they are responsible for ventricular fibrillation which causes sudden cardiac death, even when ischemia only involves limited parts of the myocardium. Statistical study of the probability of reentries as a function of both of the size of ischemic zones and the rate of dispersion of refractory periods shows that the latter parameter is of primary importance in triggering cardiac reentries.

Cell Hypoxia↗

PubMed1990

[Effects of ethmozine on ventricular fibrillation threshold in acute occlusion of the coronary artery in dogs].

In experiments on dogs with acute left descending coronary artery occlusion, ethmozine (3 mg/kg) was tested for effects on the threshold of ventricular fibrillation occurring as a result of high-frequency electric stimulation. Two hours after occlusion, the fibrillation threshold became significantly lower than the control values. Ethmozine used in this period enhanced the ventricular fibrillation threshold in some experiments and diminished it in the others. Four hours following the occlusion, the fibrillation threshold did not differ from the control ones. Ethmozine given in this period caused a significant increase in the ventricular fibrillation threshold. It was concluded that 4 hours after the onset of experimental myocardial infarction are the minimal time period following which administration of ethmozine failed to decrease electric stability of the heart.

Animals↗

PubMed2004

Mapping and ablation of ventricular fibrillation.

Sudden cardiac death frequently results from ventricular fibrillation (VF). While VF is frequently the eventual mode of death in patients with abnormal ventricular substrates, it has also been described in patients with structurally normally hearts. Until recently, the management of patients who have survived sudden cardiac death has focused on treating the consequences by implantation of a defibrillator. However, such therapy remains restricted in many countries, is associated with a prohibitive cost to the community, and may be a cause of significant morbidity in patients with frequent episodes or storms of arrhythmia. Evidence emerging from the study of fibrillation both in the atria and the ventricle suggests an important role for triggers arising from the Purkinje network or the right ventricular outflow tract in the initiation of VF. Initial experience in patients with idiopathic VF and even those with VF associated with abnormal repolarization syndromes (LQT or Brugada syndrome) or myocardial infarction suggests that long term suppression of recurrent VF may be feasible by the elimination of these triggers. With the development of new mapping and ablation technologies, and greater physician experience, catheter ablation of VF, with the ultimate aim of curing such patients at risks of sudden cardiac death, may not be an unrealistic goal in the future.

Electrocardiography↗

PubMed2006

Ventricular fibrillation due to severe hypokalemia induced by steroid treatment in a patient with thyrotoxic periodic paralysis.

We report a 25-year-old Japanese man with ventricular fibrillation associated with severe hypokalemia. He developed arm and leg paralysis. He had received 2 g of methylprednisolone because thoracic epidural hematoma had been suspected in another hospital. His serum potassium was 0.8 mEq/l on arrival at our hospital. Half an hour after arrival ventricular fibrillation occurred. Treatment with electric defibrillation 8 times was successful. Afterward Graves' disease was diagnosed, therefore, his clinical symptom was diagnosed as thyrotoxic periodic paralysis. We considered that the unusual condition of hyperthyroid-related hypokalemia worsened by steroid therapy induced the ventricular fibrillation.

Adult↗

PubMedDate not supplied

Administration of prostacyclin prevents ventricular fibrillation following coronary occlusion in conscious dogs.

The effects of prostacyclin (PGI2) on ventricular arrhythmias following 20 min of coronary occlusion and release were studied in 34 conscious dogs. We administered PGI2 at 100 ng/kg/min and did not observe significant changes in heart rate, blood pressure, or systemic vascular resistance. During the control period, heart rate was 97 +/- 30 (mean +/- SEM) vs. 99 +/- 28 in the PGI2-treated group. Mean arterial pressure was 115 +/- 26 mm Hg and 109 +/- 10 mm Hg in the control and PGI2 groups, respectively. Systemic vascular resistance declined minimally from 2,985 +/- 221 dyn . s . cm-5 to 2,484 +/- 135 dyn . s . cm-5 during the PGI2 infusion (p = NS). Following coronary occlusion, the frequency of ventricular fibrillation was reduced from 53% (9/17) in the control group to 6% (1/17) in the PGI2 group (p less than 0.01). Overall 80-min postinfarction survival was 64% in the group receiving PGI2 infusion compared to 24% in the control group (p less than 0.05). The effects of PGI2 in preventing ventricular fibrillation following acute coronary occlusion can be ascribed to a direct action of this prostaglandin on the myocardium, rather than to an indirect effect due to a reduction in systemic vascular resistance.

Animals↗

PubMed1981

The influence of contrast media additives upon ventricular fibrillation thresholds during coronary angiography in ischemic and normal canine hearts.

Contrast media additives that bind calcium lower the total dose necessary to induce fibrillation. The method of measuring ventricular fibrillation threshold during coronary arteriography is sensitive and allows dose comparison at volumes relevant to clinical use. We compared two commercial formulations of sodium/meglumine diatrizoate for their effects upon fibrillation threshold in normal and ischemic dog hearts. Even though the formulations differed only by their additives, Hypaque 76 was significantly less fibrillatory than Renografin 76. This was observed at two different doses and in both ischemic and non-ischemic hearts. We conclude that amounts of additives capable of binding calcium should be kept as low as possible in sodium/meglumine diatrizoate formulations that are used for coronary angiography.

Angiocardiography↗

PubMed1977

Linoleic acid and susceptibility to fatal ventricular fibrillation in rats.

The effect of linoleic acid on the induction of fatal ventricular fibrillation by intravenous CaCl2 (10%), was studied in rats fed for a month from weaning on a diet with either a high or low content of linoleic acid. Studies were performed in the basal state and after pretreatment with noradrenaline, which increased the sensitivity to CaCl2 equally in animals from both diet groups. Despite considerable differences in the linoleic acid levels in the plasma and myocardium, the two groups did not differ in the incidence of fatal ventricular fibrillation. Our conclusions concerning the effect of linoleic acid on cardiac arrhythmias, and sudden death in particular, are compared with those from other studies.

Animals↗

PubMed1997

Rhythm changes during resuscitation from ventricular fibrillation in relation to delay until defibrillation, number of shocks delivered and survival.

AIM: To describe rhythm changes during the initial phase of resuscitation from ventricular fibrillation in relation to the interval between collapse and defibrillation, to survival and to bystander-initiated cardiopulmonary resuscitation (CPR). PATIENTS: All patients who suffered out-of-hospital cardiac arrest between 1980 and 1992, who were reached by the emergency medical service system (EMS), in whom resuscitation attempts were initiated and who were found in ventricular fibrillation. RESULTS: In all, 1216 patients were included in the study. Among patients who converted to a pulse-generating rhythm after the first defibrillation (n = 119) were 56% discharged from hospital as compared with 6% among patients who converted to asystole. The corresponding figures after the third defibrillation were 49% and 2%, respectively, and after the fifth defibrillation 28% and 7%, respectively. Among patients in whom the first defibrillation took place less than 5 min after collapse, 28% directly converted to a pulse-generating rhythm as compared with 3% when the first defibrillation took place 12 min or more after collapse. CONCLUSION: Among patients who suffer out-of-hospital cardiac arrest and are found in ventricular fibrillation, there is a strong relationship between survival and initial rhythm changes after defibrillation. These rhythm changes are directly related to the interval between collapse and the first defibrillation.

Adolescent↗

PubMed1998

Comprehensive scheme for detection of ventricular fibrillation for implantable cardioverter defibrillators.

Implantable cardioverter defibrillators (ICDs) detect and defibrillate ventricular fibrillation (VF) and ventricular tachycardia (VT). Other therapies which use less energy are also available to terminate VT. Previous studies have shown that ICD rate schemes often misdiagnose VT as VF. In this study, an improved VF classification scheme was designed and tested, which employs the classic rate criteria plus paired signal concordance (PSC); PSC uniquely detects VF where VT and VF rates overlap (220-340 ms). Two signals from a bipolar pair (1 cm) recorded in a unipolar sense exhibit similar signal shape for concordant rhythms, such as sinus rhythm and VT, and disconcordance for VF. Once the rate criterion is met, PSC is measured by the peak normalized cross-correlation coefficient calculated over the depolarization. Variability, measured by a modified range, determined the contextual diagnosis over a passage. Sinus rhythm (20), VT (12), VF (22), atrial fibrillation (10), sinus rhythm with ventricular premature depolarizations (7), and polymorphic VT (4) passages were recorded from 38 patients. Rate-PSC was tested with unfiltered, digitized signals (1-500 Hz, 1,000 samples per second) and with filtered, downsampled signals (1-50 Hz, 100 samples per second). Sensitivity values, or percentage of correct VF detection, and specificity values, or detection of all other rhythms, were generated and compared with simulations of three commercial ICDs programmed to similar settings as rate-PSC and to nominal settings. The sensitivity values for rate-PSC with unfiltered and with filtered signals and for ICDs with 220 ms and with nominal settings were 100%, 100%, 48-80%, and 100%, respectively; the corresponding specificity values were 95%, 83%, 93%, and 7-13%, respectively. It was concluded that the rate-PSC scheme was able to reliably separate VF from other rhythms, even rhythms that have a variable morphology or variable rate. With the confidence of accurate VF detection, use of low-energy therapies for non-VF rhythms will increase device longevity and enhance patient comfort.

Computer Simulation↗

PubMed2004

Mode of initiation and ablation of ventricular fibrillation storms in patients with ischemic cardiomyopathy.

OBJECTIVES: We report on the initiation of ventricular fibrillation (VF) storm in patients with ischemic cardiomyopathy (ICM) and the results of targeted ablation to treat VF storm. BACKGROUND: Monomorphic premature ventricular contractions (PVCs) have been shown to initiate VF in patients without structural heart disease. METHODS: A total of 29 patients with ICM and documented VF initiation were identified. In 21 patients, VF storm was controlled with antiarrhythmic drugs and/or treatment of heart failure. Eight patients with VF (mean 52 +/- 25 episodes) refractory to medical management required ablation. All patients underwent three-dimensional electroanatomical mapping using CARTO (Biosense-Webster Inc., Diamond Bar, California), and PVCs were mapped when present. Scarred areas were identified using voltage mapping. RESULTS: Monomorphic PVCs initiated VF in all 29 identified patients. Five of eight patients requiring ablation had frequent PVCs that allowed PVC mapping. The earliest activation site was consistently located in the scar border zone. The PVCs were always preceded by a Purkinje-like potential (PLP). Ablation was successfully performed at these sites. In three patients, infrequent PVCs prevented mapping, but PLPs were recorded around the scar border. Ablation targeting these potentials along the scar border was successfully performed. During follow-up (10 +/- 6 months), one patient had a single VF episode and another developed sustained, monomorphic ventricular tachycardia. There was no recurrence of VF storm. CONCLUSIONS: Ventricular fibrillation in ICM is triggered by monomorphic PVCs originating from the scar border zone with preceding PLPs; targeting these PVCs may prevent VF recurrence. In the absence of PVCs, both substrate mapping and ablation appear to be equally effective.

Aged↗

PubMed1993

Antagonizing the hydroxyl ion free radical (HO.) does not abolish reperfusion ventricular fibrillation in anesthetized dogs.

1. The hypothesis that the hydroxyl ion free radical, HO; derived from O2 plays a pivotal role in the development of reperfusion ventricular fibrillation was tested in 63 anesthetized mongrel dogs of either sex weighing 14 +/- 7 kg submitted to 90-min coronary occlusion followed by 60-min reperfusion. 2. OH. was blocked by the iron chelator deferoxamine (DF, 500 mg) and by dimethylthiourea (DMTU, 500 mg/kg), a HO. scavenger both given iv over 30 min before reperfusion. 3. The frequency of reperfusion ventricular fibrillation was similar in all animals, i.e., 7/27 (26%) control dogs, 7/23 (30%) DF-treated dogs and 3/13 (23%) DMTU-treated dogs. Arterial pressure, heart rate and double product were not significantly different among the three groups during occlusion or reperfusion. The hemodynamic variables were also similar among dogs that fibrillated and those that did not. Likewise, extent of ischemic areas and necrosis was similar among the three experimental groups, with the control values being 34 +/- 4% and 14 +/- 5%, respectively. 4. We conclude that OH. does not play a major role in the induction of reperfusion ventricular fibrillation in the anesthetized dog with ischemia/necrosis.

Anesthesia↗

PubMed1991

Ventricular fibrillation in the Wolff-Parkinson-White syndrome.

Ventricular fibrillation (VF) is a well-known but rare complication of the Wolff-Parkinson-White syndrome (WPW). Clinical and electrophysiological data of 23 patients with spontaneous VF were compared with data from 100 consecutive patients with WPW without VF but with symptomatic supraventricular tachycardia. The 23 patients were collected in a multicentre retrospective study in seven European centres. VF occurred in only one patient who was receiving antiarrhythmic drugs, and was the first manifestation of the syndrome in six. No significant differences were found between those with VF and without VF in age, complaints of palpitations, syncope, and presence of structural heart disease. The retrograde effective refractory period of the accessory pathway, the atrial refractory period and the fastest atrial pacing rate with 1:1 anterograde conduction over the accessory pathway were similar in both groups. Significant differences were found for sex, permanent pre-excitation on the electrocardiogram, type of documented supraventricular tachyarrhythmias, shortest RR interval less than or equal to 220 ms during spontaneous atrial fibrillation (AF), inducibility of supraventricular tachycardias, ventricular effective refractory period less than or equal to 190 ms, mean shortest RR interval during induced AF less than or equal to 180 ms and presence of multiple accessory pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1975

Resuscitation from out-of-hospital ventricular fibrillation: 4 years follow-up.

In 51 months, 234 patients with out-of-hospital ventricular fibrillation (VF) were successfully resuscitated, hospitalized, and discharged home. Patients surviving an episode of primary ventricular fibrillation, that is, VF not associated with acute myocardial infarction, showed a 2-year mortality rate greater than three times that of survivors from VF associated with acute transmural infarction. Recurrent out-of-hospital VF was common, and a pattern of early recurrence was noted, with a median interval of 17 weeks in 34 documented cases. Ten patients were counted as long-term survivors from second episodes of out-of-hospital VF, one of whom survived a third episode. Coronary anatomy and ventricular function were studied in 29 survivors of primary VF. Of the 29 patients, 23 had coronary disease, considered "operable" in 17. Exercise testing and left ventricular function studies were normal or minimally abnormal in approximately half of these patients. There is an obvious need to develop effective measures to prevent primary VF, which commonly presents almost instantaneously, without prodromal symptoms.

Acute Disease↗

PubMed2002

Endocardial wave front organization during ventricular fibrillation in humans.

OBJECTIVES: This study was designed to characterize the organization of ventricular fibrillation (VF) on the endocardium of humans. BACKGROUND: Most proposed mechanisms for the maintenance of VF postulate the propagation of a number of activation wave fronts that reenter to maintain the arrhythmia. We tested the hypothesis that, in patients undergoing internal cardioverter-defibrillator implantation, VF consists primarily of a few large wave fronts on the endocardium. METHODS: Electrograms were recorded from a 36-electrode catheter in the left ventricle of 16 patients during VF. Activation times were chosen for a 2-s epoch for each fibrillation episode, and a two-dimensional Kolmogorov-Smirnov test was performed to determine if activation occurred randomly along the catheter over that time interval. The maximum cross-correlation was found for all possible pairs of electrodes on the catheter, and these values were plotted relative to the distance between the two electrodes. An exponential curve was then fit to the data, and a length constant was determined. Activation times were grouped into wave fronts along the catheter, and the lengths of the wave fronts were estimated. RESULTS: The Kolmogorov-Smirnov test showed that activation was not random along the catheter in any of the patients studied. The correlation length determined was 9 +/- 2 cm. The number of wave fronts recorded by the catheter was 9.2 +/- 2.9 wave fronts/s. The length of the pathway of each wave front along the catheter was 6.5 +/- 4.5 cm. CONCLUSIONS: Ventricular fibrillation is well organized on the endocardial surface of humans, consisting primarily of a few large wave fronts on the order of 6 to 9 cm.

Adult↗

PubMed1984

Autonomic mechanisms in ventricular fibrillation induced by myocardial ischemia during exercise in dogs with healed myocardial infarction. An experimental preparation for sudden cardiac death.

The relationship between activity of the autonomic nervous system, myocardial ischemia, and malignant arrhythmias has been investigated in a new experimental preparation for sudden death. Fifty-seven dogs were chronically instrumented and studied under control conditions (n = 15) and 1 month after production of an anterior myocardial infarction (n = 42). The protocol consisted in occluding the left circumflex coronary artery for 2 min, commencing at the last minute of an exercise stress test and extending through the first minute after cessation of exercise. With this protocol, ventricular fibrillation was observed in 40% of normal dogs and 66% of dogs with infarction. In 14 dogs with infarction, left stellectomy reduced the incidence of ventricular fibrillation to zero (p less than .001). The reflex changes in heart rate elicited within the first minute of ischemia during exercise in the animals that survived (from 204 +/- 14 to 198 +/- 31 beats/min, -6) were opposite those in animals that had ventricular fibrillation (from 208 +/- 24 to 229 +/- 30 beats/min, +21) (p less than .05). The ischemia-induced reduction in heart rate despite continuation of exercise suggests the presence in the dogs that survived of active vagal reflexes that may have played an important role in the maintenance of cardiac electrical stability. This preparation has the potential to induce ventricular fibrillation consistently in conscious animals by the interaction of a few clinically relevant factors (acute myocardial ischemia, submaximal exercise and its cessation, sympathetic and vagal reflexes, and heart rate) and offers the possibility of acquiring further insights into the mechanisms of malignant arrhythmias and evaluating novel strategies for targeted prevention.

Animals↗

PubMed1988

Late potentials in the acute phase of myocardial infarction indicate the risk of early ventricular fibrillation.

Late potentials occurring at the end of or after the QRS complex were recorded from the body surface by means of a high-gain ECG and the signal-averaging technique in 75 patients, within 24 h from the onset of symptoms of acute myocardial infarction. Late potentials were found in 20 patients (26.7%). Out of this group, eight (40%) developed ventricular fibrillation. There was only one incident of ventricular fibrillation among 55 patients without late potentials (1.8%, P less than 0.001). The three-month mortality after myocardial infarction was slightly higher in individuals with late potentials: 15% vs. 11.5%, but this difference was not statistically significant. We conclude that the presence of late potentials recorded in the acute phase of myocardial infarction indicates a risk of ventricular fibrillation, but this was not associated with an increased mortality rate during the three-month follow-up.

Action Potentials↗