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PubMed1980

Amiodarone-induced ventricular fibrillation.

Amiodarone, 600 mg orally daily, was used in an attempt to control supraventricular tachyarrhythmias in a patient with the sick sinus syndrome. Twenty days from the onset of therapy the Q-T interval lengthened. Episodes of ventricular flutter, ventricular fibrillation and self-terminating ventricular tachyarrhythmia (torsade de pointes) developed on the 28th day of amiodarone therapy. Temporary cardiac pacing prevented further episodes of ventricular fibrillation. Despite the suggestion that this drug may be given in large doses for long periods of time since it has a wide safety margin, we feel that the risk of lethal arrhythmias is such that caution is required in its use.

Amiodarone↗
PubMed1982

[Clinical-electrophysiological findings in patients following ventricular fibrillation].

30 patients, successfully resuscitated from ventricular fibrillation outside acute myocardial infarction, were studied by programmed right-ventricular stimulation. The stimulation studies were carried out one week up to 1.5 years after the event (median two months). Mean age of the patients was 50.2 +/- 8.8 years, 27 were male. The majority of patients had coronary heart disease and/or localized or diffuse ventricular contraction abnormalities. In 26 patients the stimulation protocol included the application of premature single and double ventricular stimuli during sinus rhythm and a paced ventricular rhythm at cycle lengths of 500, 430, 370 and 330 msec until ventricular tachycardia, ventricular flutter or ventricular fibrillation were induced. 4 patients were studied only at a cycle length of 500 msec. Using this stimulation protocol, in 7 patients (26.9%) sustained ventricular tachycardia, in 5 patients (19.2%) ventricular flutter and in 7 patients (26.9%) ventricular fibrillation were induced. These arrhythmias were induced at a basic cycle length of 500 ms in 10 patients, at 430 ms in 3 patients, at 370 ms in 4 patients and at 330 ms in 2 patients. In the remaining patients, only ventricular echo beats (one to six) of the intra-ventricular reentry type were induced. Thus these results show a persistent increase in ventricular vulnerability in a high percentage of patients (73%), provided that appropriate stimulation techniques are used. These observations may have great importance for the management of these patients.

Arrhythmias, Cardiac↗
PubMed1982

Low energy countershock using an intravascular catheter in an acute cardiac care setting.

We examined the feasibility, effectiveness, and safety of using an intravascular catheter positioned in the right ventricular apex for countershock in a coronary care unit setting in 8 patients who had recurrent ventricular tachyarrhythmia. Countershock using 2.5 to 40 J stored energy (damped sinusoidal wave form) was attempted 115 times to terminate 100 episodes of ventricular tachyarrhythmia (ventricular tachycardia, 91; ventricular flutter, 3; ventricular fibrillation, 6). Eighty-six (87%) of 99 countershock attempts for ventricular tachycardia, 3 (60%) of 5 for ventricular flutter, and 4 (36%) of 11 for ventricular fibrillation were successful using this technique. The catheters remained in stable position for 1 to 16 days without dislodgment. A majority of the countershocks were delivered by the regular nursing staff in the coronary unit. We conclude that low energy countershock through an intravascular catheter system is feasible, safe, and effective in a coronary care unit setting. Such a system should be beneficial in the acute management of patients who have recurrent ventricular tachycardia or fibrillation. The catheter lead may also prove useful in managing ventricular tachyarrhythmias that occur during electrophysiologic studies.

Adult↗
PubMed1985

Clinical significance of ventricular fibrillation-flutter induced by ventricular programmed stimulation.

Two hundred twenty-four patients underwent ventricular programmed stimulation (VPS) without prior documentation of the clinical occurrence of sustained ventricular tachycardia (VT) or ventricular fibrillation-flutter (VF). Indications for VPS were: palpitations or nonsustained VT during ambulatory monitoring (85 patients), syncope or presyncope (137 patients), and a family history of sudden death (two patients). Sustained VF requiring transthoracic defibrillation was initiated by VPS in 18 patients (8.0%). Four patients were treated for inducible VF with antiarrhythmic agents directed by electropharmacologic testing; five patients were treated empirically; nine patients received no therapy. No patient has had a cardiac arrest or sudden death during a follow-up period 25.2 +/- 13.8 months (mean +/- standard deviation). VF was initiated by two ventricular extrastimuli in three patients and by three extrastimuli in 15 patients. The incidence of VF was similar in patients with and without previous symptoms (8.8% vs 6.9%) or heart disease (7.1% vs 9.6%). It was significantly higher when VPS at three ventricular sites with a current of 5 mA (pulse width 2 msec) was compared to programmed stimulation at two ventricular sites with a current twice diastolic threshold (pulse width 2 msec) (15.2% vs 3.0%, p less than 0.05). VF initiated by VPS in patients without prior VT or VF appears to be a nonspecific finding. Antiarrhythmic therapy for VF may not be necessary in these patients.

Adult↗
PubMedDate not supplied

Acute therapy of maternal and fetal arrhythmias during pregnancy.

Atrial premature beats are frequently diagnosed during pregnancy. Supraventricular tachycardia (atrial tachycardia, atrioventricular nodal reentrant tachycardia, circus movement tachycardia) is diagnosed less frequently. For acute therapy, electrical cardioversion with 50 to 100 J is indicated in all unstable patients. In stable supraventricular tachycardia, the initial therapy includes vagal maneuvers to terminate tachycardias. For short-term management, when vagal maneuvers fail, intravenous adenosine is the first choice drug and may safely terminate the arrhythmia. Ventricular premature beats are also frequently present during pregnancy and are benign in most patients; however, malignant ventricular tachyarrhythmias (sustained ventricular tachycardia, ventricular flutter, or ventricular fibrillation) may occur. Electrical cardioversion is necessary in all patients who are hemodynamically unstable with life-threatening ventricular tachyarrhythmias. In hemodynamically stable patients, initial therapy with ajmaline, procainamide, or lidocaine is indicated. In patients with syncopal ventricular tachycardia, ventricular fibrillation, ventricular flutter, or aborted sudden death, an implantable cardioverter-defibrillator is indicated. In patients with symptomatic bradycardia, a pacemaker can be implanted using echocardiography at any stage of pregnancy. The treatment of the pregnant patient with cardiac arrhythmias requires important modifications of the standard practice of arrhythmia management. The goal of therapy is to protect the patient and fetus through delivery, after which chronic or definitive therapy can be administered.

Anti-Arrhythmia Agents↗
PubMed1990

Different effects of epoprostenol on ischemia-induced ventricular arrhythmias in dogs.

In 60 randomized dogs the effects of epoprostenol infusion (100 ng/kg/min) on ischemia-induced premature ventricular contractions (PVCs), ventricular tachycardia (VT), ventricular flutters and ventricular fibrillation were studied. The circumflex coronary artery occlusion canine model of sudden death was used. The results demonstrate different effects of epoprostenol on ischemia-induced ventricular arrhythmias: 1) both postischemic (7 of 30 vs 15 of 30, p = 0.0298) and postreperfusion (5 of 23 vs 8 of 15, p = 0.0492) ventricular fibrillations were prevented in epoprostenol dogs with an improvement of the global survival rate (18 of 30 vs 7 of 30, p = 0.0019) as compared to controls; 2) in epoprostenol treated dogs a significantly increased incidence of non lethal arrhythmias-including ventricular flutters that occurred in 12 of 30 dogs vs 4 of 30 in controls (p = 0.0195)--was observed; 3) a positive correlation between the percent diastolic pressure fall 10 min after the start of epoprostenol infusion and the number of non lethal arrhythmias was noted. However, hemodynamic effects of the compound, suggesting an oxygen sparing action, did not preclude the antifibrillatory effectiveness. Thus, the antifibrillatory and antiarrhythmic effects of epoprostenol after circumflex coronary artery occlusion and reperfusion in dogs seem independent from one another.

Animals↗
PubMed1992

[Correlations between the different criteria of late potentials and results of programmed ventricular stimulation after myocardial infarction].

Five to ten per cent of survivors of acute myocardial infarction die within two years. The majority of these deaths are sudden and are attributed to a lethal ventricular arrhythmia. This is usually ventricular tachycardia degenerating to ventricular fibrillation. These post-infarction tachycardias are generally due to reentry. They require an anatomic arrhythmogenic substrate, a zone of delayed conduction. This can be detected as late potentials on signal averaged ECG. The triggering of a significant ventricular arrhythmia by ventricular stimulation is closely correlated to the occurrence of a severe ventricular arrhythmia in the months following infarction. Programmed ventricular stimulation could, therefore, help to identify patients requiring close follow-up and/or preventive antiarrhythmic therapy, but cannot be offered to all patients because of its invasive nature. Seventy nine post-infarction patients were studied prospectively. All underwent coronary angiography, signal averaging electrocardiography, and programmed ventricular stimulation at least 15 days after infarction. Fifty five patients had at least one criterion of late potentials (QRS duration > or = 110 ms and/or amplitude of the last 40 ms < 27 microV and/or duration of potentials of under 40 microV > 37 ms). Twenty four patients had no late potentials. The results of programmed stimulation were estimated to be positive when sustained or unsustained monomorphic ventricular tachycardia was triggered, and negative when ventricular fibrillation, ventricular flutter unsustained polymorphic ventricular tachycardia or no arrhythmia could be induced. Programmed ventricular pacing triggered 15 significant events, 17 unsustained polymorphic ventricular tachycardias, 13 ventricular flutters and 11 ventricular fibrillations. The exploration was negative in 23 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

[A portable device for checking equipment and programs of detecting flutter and fibrillation of heart ventricles in humans].

Facilities and programs of detecting ventricular flutter and ventricular fibrillation of the heart of man are important units of cardiomonitors. The life of cardiological patients staying at the departments for intensive care depend in many respects on the quality of the units in question. Using a portable simulator of three types of ventricular fibrillation and ventricular flutter it is possible to check up the service-ability and safety of the given units. The main parameters of the simulator are chosen on the basis of the statistical and spectral characteristics of real ventricular fibrillation and ventricular flutter, derived by the authors as a result of the experimental studies. Those characteristics can also be used for optimizing facilities and programs of detecting ventricular fibrillation and ventricular flutter.

Arrhythmias, Cardiac↗
PubMed1976

Arrhythmias in two patients with left ventricular bypass transplants.

Two patients who underwent left ventricular bypass transplants are described. Both patients sustained postoperative rhythm disturbances of their own hearts during sinus rhythm of the donor hearts. Illustrative examples of atrial flutter, ventricular flutter, ventricular fibrillation, blocked atrial extrasystoles, and double ventricular parasystole in the recipient hearts are presented. The patients tolerated all these arrhythmias well during uninterrupted sinus rhythm in the donor heart. The problems in interpretation of arrhythmias in the presence of two hearts are discussed.

Arrhythmias, Cardiac↗
PubMed2004

[Transthoracic defibrillation. Physiologic and pathophysiologic principles and their role in the outcome of resuscitation].

As one major link in the chain of survival, early transthoracic (external) cardiac defibrillation is aimed at the termination of ventricular flutter and ventricular fibrillation. Most important to the success of defibrillation is the passage of a defined amount of current through a critical mass of heart muscle. Different transthoracic resistances reduce the effective density of the current within the heart. As for other therapeutic intervention procedures, recommendations for the optimal strength of current to be applied to the fibrillating heart need to be evaluated and defined for therapeutical defibrillation too. Unnecessarily high current density causes damage to the heart and should be prevented. By using biphasic waveforms in contrast to monophasic impulses, the amount of current can be reduced but the same or even higher efficacy is attained. Therefore possible myocardial damage might be clearly reduced. Even with individually altered thoracic impedance effective conversion of cardiac rhythm can be achieved by device-controlled compensation and biphasic waveforms. According to their different mechanisms or origin (electrically induced or spontaneously caused by organic heart disease) the probability of successful conversion of the cardiac rhythm by one single electrical impulse varies. The optimum point in time for defibrillation during resuscitation needs to be redefined. In order to improve comparability, further studies should use standardized definitions for successful defibrillation relating to the resulting cardiac rhythm.

Cardiopulmonary Resuscitation↗
PubMed2006

[Ventricular tachycardia. Diagnostic spectrum and therapeutic measures].

The origin of ventricular tachycardia lies in the ventricular tissue and includes a variety of symptoms such as monomorphic and polymorphic ventricular tachyarrhythmia (VT), ventricular flutter and ventricular fibrillation. Due to transitions of one form of VT to another, any form of VT incurs in principal the risk of cardiac failure. Apart from different electrophysiologic mechanisms such as reentry or triggered activity, any occurrence of VT has to be considered in an individual context: VT can be caused by structural heart disease such as coronary artery disease or dilative cardiomyopathy, or primary electrical disease such as long or short QT syndromes or can even occur without any detectable cause (idiopathic VT). Correct identification of the underlying cause of the arrhythmia is essential for the prognosis, differential therapy and long-term treatment of patients.

Catheter Ablation↗
PubMed2006

Study of pathogenesis of ventricular arrhythmia in experimental rats by separation of sinus and ventricular substitutional rhythms.

Pathogenesis of cardiac arrhythmia was determined by EEC changes after ATP-induced complete atrioventricular block. The re-entry mechanism underlays extrasystoles with equal coupling intervals with complexes of ventricular substitution rhythms, which transformed into paroxysmal tachycardia with equal R-R intervals, ventricular flutter, and ventricular fibrillation. Ectopic automaticity was characterized by extrasystole unrelated to the complexes of substitutional rhythms, which was transformed into accelerated idioventricular rhythm and asystole. During trigger activity, the extrasystoles were associated with complexes of basic rhythm and transformed themselves into torsades de pointes and ventricular fibrillation.

Adenosine Triphosphate↗
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↗
PubMed1989

Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease.

The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed greater than or equal to 1 membrane-active antiarrhythmic drug (mean 2.2 +/- 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had greater than or equal to 1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 +/- 14 vs 86 +/- 11 beats/min, p less than 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 +/- 14 to 80 +/- 9 beats/min, p less than 0.001) than in nonresponders (from 86 +/- 11 to 74 +/- 9 beats/min, p less than 0.01) (p less than 0.05 between the groups), despite equal plasma propranolol concentrations (84 +/- 50 vs 88 +/- 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had greater than or equal to 1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after beta blockade (p less than 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 +/- 38 vs 302 +/- 66 ms, p less than 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.

Aged↗
PubMed1987

Do endogenous lipoproteins modulate the sensibility of animals against arrhythmogenic drugs?

The present study suggests that a diminished level of HDL is connected with an enhanced susceptibility to arrhythmogenic stimuli only in rats pretreated with a diet deficient in polyunsaturated fatty acids (PUFA), but not after a PUFA-rich or pellet diet. The endogenous level of total cholesterol did not influence the thresholds for ventricular flutter or ventricular fibrillation in aconitine-induced arrhythmia in rats or in ouabain-induced arrhythmia in guinea pigs.

Aconitine↗
PubMed2004

Severe frequent ventricular ectopy after exercise as a predictor of death in patients with heart failure.

OBJECTIVES: The study was done to determine the prognostic importance of frequent ventricular ectopy in recovery after exercise among patients with systolic heart failure (HF). BACKGROUND: Although ventricular ectopy during recovery after exercise predicts death in patients without HF, its prognostic importance in patients with significant ventricular dysfunction is unknown. METHODS: Systematic electrocardiographic data during rest, exercise, and recovery were gathered on 2,123 consecutive patients with left ventricular systolic ejection fraction <or=35% who were referred for symptom-limited metabolic treadmill exercise testing. Severe ventricular ectopy was defined as the presence of ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, polymorphic ventricular tachycardia, or ventricular fibrillation. The primary end point was all-cause mortality, with censoring for interval cardiac transplantation. RESULTS: Of 2,123 patients, 140 (7%) had severe ventricular ectopy during recovery. There were 530 deaths (median follow-up among survivors 2.9 years). Severe ventricular ectopy during recovery was associated with an increased risk of death (three-year death rates 37% vs. 22%, hazard ratio [HR] 1.76; 95% confidence interval [CI] 1.32 to 2.34, p < 0.0001). After adjustment for ventricular ectopy at rest and during exercise, peak oxygen uptake, and other potential confounders, severe ventricular ectopy during recovery remained predictive of death (adjusted HR 1.48; 95% CI 1.10 to 1.97; p = 0.0089), whereas ventricular ectopy during exercise was not predictive of death in this cohort. CONCLUSIONS: Severe ventricular ectopy during recovery after exercise is predictive of increased mortality in patients with severe HF and can be used as a prognostic indicator of adverse outcomes in HF cohorts.

Cohort Studies↗
PubMed1995

Implantable cardioverter-defibrillator. Evaluation of clinical neurologic outcome and electroencephalographic changes during implantation.

During placement of implantable cardioverter-defibrillators, ventricular arrhythmias are induced to test the function of the devices. Although cerebral hypoperfusion and ischemic electroencephalographic changes occur in patients while implantable cardioverter-defibrillators are being tested, no investigation has assessed neurologic outcome in these patients. Nine patients having either implantation or change of an implantable cardioverter-defibrillator underwent neurologic examination and neuropsychometric tests before and after the operation. After induction of general anesthesia and insertion of implantable cardioverter-defibrillator leads (when needed), ventricular fibrillation, ventricular flutter, or ventricular tachycardia, was induced by means of programmed electrical stimulation. Implantable cardioverter-defibrillator testing continued until satisfactory lead placement was confirmed. The intraoperative electroencephalographic recording was analyzed for evidence of ischemic change. In all, an electroencephalogram was recorded during 50 periods of circulatory arrest. Mean duration of the arrest periods was 13.6 seconds. By means of conventional visual inspection of the raw electroencephalogram, high-amplitude rhythmic delta or theta, voltage attenuation, or loss of fast frequency activity was observed in 30 of the arrests. By means of an automated technique of electroencephalographic interpretation based on power spectral analysis, electroencephalographic changes were correctly identified in 26 of the arrests. The incidence of these electroencephalographic changes was dependent on the arrest duration. The mean interval from arrest onset to electroencephalographic change was 7.5 seconds (standard deviation +/- 1.8 seconds). In patients with electroencephalographic changes during multiple arrests, no downward trend in this interval was detected in later arrests and no evidence of persistent ischemic change was observed in electroencephalograms recorded after the conclusion of implantable cardioverter-defibrillator testing. Postoperative neurologic and neuropsychometric testing was completed in eight patients, none of whom exhibited a new neurologic deficit, exacerbation of a preexisting neurologic condition, or significant deterioration in neuropsychometric performance. We conclude that the brief arrest of cerebral circulation induced during insertion of an implantable cardioverter-defibrillator is not associated with permanent neurologic injury.

Adult↗
PubMed1984

Implantation of automatic cardioverter-defibrillators via median sternotomy.

15 AICD (automatic implantable cardioverter-defibrillator) Model B units were implanted in 10 patients. The median sternotomy is our preferred surgical approach using a right atrial patch electrode, a left ventricular apex patch electrode, and two closely placed epicardial sensing electrodes. Follow-up is 109 patient months and all patients are alive. AICD units discharged for ventricular tachycardia, ventricular flutter, and ventricular fibrillation. Discharges also occurred for sinus tachycardia and atrial fibrillation above the rate limit in three units. Premature pulse generator depletion has occurred in four AICD-B units 3 to 18 months postimplant and appears due to a defect in original battery design. Discharge of the AICD for supraventricular tachycardia is a problem that will remain until a better means of differentiating supraventricular tachycardia from ventricular tachyarrhythmias is found. The AICD appears to prevent sudden death from ventricular tachyarrhythmias.

Adult↗