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Biomedical subjects

H Garan

Publications and source records attributed to H Garan.

121 records · Page 7Linked to original sources
PubMed1981

Centrally mediated effect of phenytoin on digoxin-induced ventricular arrhythmias.

Studies on the efficacy of phenytoin administered directly into the cerebrospinal fluid in protecting against digoxin-induced arrhythmias were carried out in 20 anesthetized dogs. Phenytoin was administered in an average dose of 10 mg directly into the cisterna magna of 10 dogs. The other control dogs received only the vehicle for phenytoin intrathecally. Both groups of dogs subsequently received a toxic dose of digoxin (0.2 mg/kg) intravenously. The time after intravenous digoxin to the onset of ventricular premature beats, ventricular tachycardia and ventricular fibrillation (VF) was significantly shorter in control animals compared to the phenytoin-treated dogs. In the control group, one dog survived the 3-h observation period without developing ventricular fibrillation, whereas 5 of the 10 phenytoin-treated dogs survived this period without VF (P less than 0.05). Phenytoin had a similar protective effect against digoxin-induced arrhythmias in 10 other dogs that received phenytoin intravenously. In the animals that received phenytoin intrathecally, plasma concentrations of phenytoin were undetectable. Thus, in this experimental model, phenytoin exerts a protective effect against digoxin-induced ventricular arrhythmias which is mediated via the central nervous system.

Animals↗
PubMed1981

Repetitive responses to single ventricular extrastimuli in patients with serious ventricular arrhythmias: incidence and clinical significance.

Electrophysiologic studies were carried out in 85 patients with serious ventricular arrhythmias: 44 with recurrent sustained ventricular tachycardia (group A), 16 with recurrent nonsustained ventricular tachycardia (group B), and 25 with recent prehospital ventricular fibrillation not associated with acute myocardial infarction (group C). Programmed ventricular stimulation from the right ventricular apex included premature stimulation during normal sinus rhythm, atrial pacing, and ventricular pacing, as well as brief bursts of rapid ventricular pacing (RVP). A repetitive ventricular response (RVR) was defined as one or more non-stimulated premature ventricular depolarizations in response to a single paced premature ventricular depolarization during normal sinus rhythm or atrial pacing. RVRs were observed in seven of 44 (16%) group A patients, one of 16 (6%) group B patients, and three of 25 (12%) group C patients. In contrast, single and double premature ventricular stimuli during ventricular pacing and/or bursts of RVP resulted in the reproducible initiation of ventricular tachycardia in 40 of 44 (91%) group A patients, 10 of 16 (63%) group B patients, and 19 of 25 (76%) group C patients. We conclude that RVRs to single ventricular extrastimuli during normal sinus rhythm or atrial pacing are rare, and therefore are an insensitive index of susceptibility to serious ventricular arrhythmias in these patients.

Adult↗
PubMed1981

Intracardiac electrophysiologic techniques in recurrent syncope of unknown case.

Twenty-five patients with recurrent episodes of syncope, unexplained despite thorough medical and neurologic evaluation, underwent intracardiac electrophysiologic study with programmed stimulation. Electrophysiologic study yielded a presumptive diagnosis in 17 patients: nine with rapid ventricular tachycardia by programmed stimulation, three with intra-His conduction delays, one with symptomatic atrial flutter, one with sick sinus syndrome, and three with persistent hypervagotonia manifested as atropine-reversible prolongation of atrioventricular nodal refractoriness. Therapy based on these findings provided complete symptomatic relief in 14 and improvement in one of these 17 patients during a mean follow-up of 18 +/- 10 months. Therapy based on electrophysiologic testing was ineffective in two of the 17 patients. Syncope persisted in four of the eight patients in whom electrophysiologic study did not define a probable arrhythmic mechanism. These observations indicate that full electrophysiologic evaluation with programmed stimulation is useful in the diagnosis and therapy of recurrent unexplained syncope.

Adolescent↗
PubMed1980

Out-of-hospital cardiac arrest: electrophysiologic observations and selection of long-term antiarrhythmic therapy.

We performed electrophysiologic studies in 31 survivors of out-of-hospital cardiac arrest not associated with acute myocardial infarction. At the time of resuscitation, eight patients had sustained ventricular tachycardia and 23 patients had ventricular fibrillation. Programmed right ventricular stimulation later revealed electrically inducible ventricular arrhythmias in 25 of the 31 patients (81 per cent). Complete suppression of electrically inducible ventricular arrhythmias was achieved with antiarrhythmic therapy in 19 of these 25 patients. None of the 19 patients in whom the inducible arrhythmias was suppressed before discharge has died suddenly or had a symptomatic arrhythmia after a mean follow-up of 15 months (range, five to 26 months). Of the six patients in whom inducible arrhythmias could not be suppressed, three died suddenly (one in the hospital) within six months. We conclude that ventricular arrhythmias can be initiated and reproduced by programmed ventricular stimulation in a majority of patients who have been resuscitated after out-of-hospital cardiac arrest and that complete suppression of these arrhythmias with anti-arrhythmic therapy is highly predictive of survival for at least one year.

Adult↗
PubMed1980

Permanent radiofrequency ventricular pacing for management of drug-resistant ventricular tachycardia.

Three patients with frequent episodes of symptomatic, sustained ventricular tachycardia that often required physician intervention were treated with a permanent patient-activated radiofrequency ventricular pacemaker for self-termination of ventricular tachycarida. Before pacemaker implantation, electrophysiologic testing revealed the tachycardia to be resistant to all approved and several investigational antiarrhythmic drugs. In all three patients, ventricular tachycardia was reliably and reproducibly terminated with brief bursts of rapid right ventricular apical pacing over several hundred trials. No patient had rapid ventricular pacing-induced acceleration of ventricular tachycardia or pacing-induced ventricular fibrillation. Since the implantation of a radiofrequency ventricular pacemaker an average of 13.7 months ago, all episodes of ventricular tachycardia (average 43/patient) have been terminated successfully by radiofrequency pacing, and no patient has required hospitalization for an arrhythmia-related problem.

Aged↗
PubMed1980

Neural effect of digitalis glycosides on gracilis vascular resistance in hypotension.

This study was undertaken to investigate the effect of intravenous acetylstrophanthidine and digoxin on the gracilis vascular resistance of hypotensive dogs. The gracilis muscle was isolated and separately perfused, but the nerve to the muscle was left intact. Acetylstrophanthidin, 0.5 mg iv, and digoxin, 1.0 mg iv, both produced a sustained vasodilator response in the gracilis vascular bed of all the hypotensive animals (mean arterial pressure 50 mmHg). A short-lasting vasoconstriction preceded the vasodilation in response to acetylstrophanthidin in 6 of the 8 animals. Prior local alpha-adrenergic blockade with phenoxybenzamine did not have any significant effect on vasodilation. Prior local cholinergic receptor blockade with atropine, however, abolished the sustained vasodilator response, thus indicating that the mechanism responsible for this neurogenic effect is cholinergic. In contrast, in the normotensive dogs, the response to intravenously administered digoxin was sustained vasoconstriction, which was abolished by prior local alpha-adrenergic receptor blockade. Thus, the effect of digitalis glycosides on peripheral vascular resistance is importantly affected by the background level of sympathetic activity.

Animals↗
PubMed1980

Sustained ventricular tachycardia in recent canine myocardial infarction.

To study recurrent ventricular tachycardia in the late phase or myocardial infarction (MI), transmural anteroapical infarcts were created by ligation of the left anterior descending (LAD) coronary artery in 25 dogs. Twenty dogs survived LAD ligation and underwent an open-chest electrophysiologic study an average of 20 days after MI. Programmed electrical stimulation was carried out using the extrastimulus technique and short bursts of rapid ventricular pacing via bipolar electrodes positioned at multiple left ventricular endocardial sites. Sixteen dogs had electrically induced ventricular tachycardia, and in 11, sustained ventricular tachycardia was reproducibly initiated and terminated by programmed ventricular stimulation. Short bursts of rapid left ventricular pacing from areas in periinfarct zone was the most effective technique for initiating ventricular tachycardia. The electrophysiologic phenomena in this model of sustained ventricular tachycardia in 3-week-old MI included electrically induced changes in rate and morphology and biventricular capture without termination during tachycardia.

Animals↗
PubMed1974

The neurogenic vasoconstrictor effect of digitalis on coronary vascular resistance.

The coronary vasoconstrictor properties of digitals were evaluated in 61 anesthetized, openchest dogs after coronary sinus cannulation and under conditions of a constant heart rate (atrioventricular pacing) and near-constant blood pressure. The contribution of alpha adrenergic receptor stimulation to the digitalis-induced increase in coronary vascular resistance (CVR) was examined. With Na pentobarbital anesthesia (16 dogs), intravenous acetylstrophanthidin (0.5 mg) caused a significant (P<0.05) rise in CVR from 1 through 9 min after injection. The peak increase was +11+/-2% SE of the control of 1.8+/-0.2 mm Hg/cm(3)/min. The mean time to peak effect was 3 min, and to recovery was 21 min. Prior alpha adrenergic receptor blockade with phenoxybenzamine in 11 animals reduced (P<0.05) the acetylstrophanthidin-induced peak of CVR and substantially decreased (P<0.05) the time to recovery (5 min). Intravenous digoxin (1.0 mg) with Na pentobarbital anesthesia (five dogs) had no significant effect on CVR. However, with chloralose and urethane anesthesia (nine dogs) the same dose of digoxin produced a significant rise in CVR from 3 through 30 min. The peak increase was +20+/-3% of control (1.4+/-0.1 mm Hg/cm(3)/min). One-third the dose of intravenous digoxin (0.35 mg) produced a 9.5+/-1.0% increase in CVR (five additional dogs). Myocardial oxygen consumption did not change significantly in nine dogs after intravenous digoxin. In 10 additional dogs pretreated with phenoxy-benzamine and in 7 dogs pretreated with mecamylamine, the increase in CVR did not occur after 1.0 mg of intravenous digoxin. Thus there is a coronary vasoconstrictor effect of intravenous acetylstrophanthidin and digoxin, of rapid onset, which is mediated through alpha adrenergic receptor stimulation.

Blood Pressure↗
PubMed1974

The central nervous system as a site of action for the coronary vasoconstrictor effect of digoxin.

Digitalis is known to have a vasoconstrictor effect in the coronary circulation. Recent studies have demonstrated that the coronary vasoconstrictor effects of acetylstrophanthidin and digoxin are neurally mediated via alpha adrenergic fibers. In the present study, experiments were done in 20 dogs anesthetized with chloralose and urethane to study the central nervous system as a possible site of action for this vasoconstrictor effect of digoxin. After the intravenous administration of 1.0 mg digoxin, cerebrospinal fluid concentrations of digoxin rose to a peak of 2.3+/-0.4 (SEM) ng/ml at 15 min, temporally corresponding to the peak in coronary vascular resistance change of +20.0+/-2.5% of control in the paced canine heart. Submicrogram digoxin injections into the lateral cerebral ventricle produced a significant increase in coronary vascular resistance, the latter injection producing a peak increase in coronary vascular resistance of 12.4+/-1.2% of control. Cross-perfusion experiments, where the isolated head of the operative dog was perfused from a donor dog receiving digoxin, thus keeping digoxin levels in the remainder of the operative dog very low, showed a similar degree of coronary vasoconstriction. Thus, the central nervous system appears to be an important site of action for the early coronary vasoconstrictor effect of digoxin.

Animals↗
PubMedDate not supplied

A perspective on the ESVEM trial current knowledge: sotalol should not be the first-line agent in the management of ventricular arrhythmias.

The Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial has recently shown the superiority of sotalol over class-1 agents in lowering the rate of recurrence of ventricular tachyarrhythmias. However, this study was not placebo-controlled, and amiodarone was not included as one of the antiarrhythmic drugs in the trial. Randomized comparative trials between sotalol and amiodarone are available, but the results are inconclusive mainly because of small sample sizes. Because of the specific pharmacokinetics of amiodarone, sotalol has become the first-line agent in the management of ventricular arrhythmias. Because this policy is based on expediency rather than follow-up data, the long-term efficacy, morbidity, and safety of sotalol should be compared with those of amiodarone as well as of nonpharmacological treatment modes for ventricular tachyarrhythmias, such as implantable cardioverter defibrillator therapy in prospective trials. Until these issues are resolved, it is incorrect to say that sotalol should be the first-line agent in the management of ventricular arrhythmias.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

A perspective on the ESVEM trial and current knowledge: catheter ablation for ventricular tachyarrhythmias.

Although an effective and potentially curative technique for treating idiopathic ventricular tachycardia, map-guided transcatheter radiofrequency ablation is far from optimal for ventricular tachyarrhythmias in patients with advanced ischemic or other types of organic heart disease. First, this technique can be applied only to a minority of patients with structural heart disease, who can tolerate relatively long episodes of induced ventricular tachycardia necessary for mapping and successful ablation. Second, the success rate is lower and recurrence higher in patients with organic heart disease. Finally, for patients who lose consciousness during tachycardia or who present with prehospital cardiac arrest, transcatheter radiofrequency ablation is inappropriate as definitive treatment. At best, it is palliative and may be used to suppress relatively slow, frequent, or incessant ventricular tachycardias but does not obviate the need for other therapies such as cardioverter-defibrillator implantation or antiarrhythmic drug therapy.

Catheter Ablation↗