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L Mary-Rabine

Publications and source records attributed to L Mary-Rabine.

At least 19 recordsLinked to original sources
PubMed1997

Atrial flutter: historical background.

For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.

Animals↗
PubMed1990

Clinical efficacy of flecainide acetate in atrial fibrillation.

Seventy-seven patients with symptomatic atrial fibrillation (AF) received oral flecainide acetate (247 +/- 8 mg/day). In 66 patients, previous antiarrhythmic trials consisted of 1-9 drugs. In 55 cases, AF was paroxysmal. It was persistent in 22 patients. Conversion and/or no recurrence of AF was achieved in 40 patients (52%) by flecainide alone and in 11 (14%) by the combination of flecainide and amiodarone. The mean flecainide serum level was 535 +/- 46 ng/ml. Age, presence of coronary artery disease or electrocardiographic parameters were not useful for predicting clinical response. In persistent AF, flecainide efficacy decreased with the duration of arrhythmia. Side effects concerned conduction (26%) and congestive heart failure (5%).

Adult↗
PubMed1988

Long term evaluation of flecainide acetate in supraventricular tachyarrhythmias.

Fifty-five patients (34 males, 21 females) have been treated for resistant paroxysmal atrial fibrillation (39 cases) or supraventricular tachycardia (16 cases) for 3 to 32 months. Most of these patients were free of heart disease but were severely limited in their daily activities by the arrhythmia. Most were resistant to membrane-stabilizing agents or to amiodarone. Complete suppression of the arrhythmia was achieved in 44 patients (by flecainide alone in 38 patients and by a combination of flecainide and amiodarone in 6 patients). In 6 other cases, a significant reduction in the number of attacks and a concomitant improvement in the quality of life was obtained (by flecainide alone in 2, and by the combination of flecainide and amiodarone in 4). Five patients remained uncontrolled. This experience demonstrates that flecainide is highly effective in refractory atrial tachyarrhythmias. It allows a reduction in the dosage of amiodarone when both drugs are combined.

Administration, Oral↗
PubMed1986

Long-term sotalol therapy in patients with ventricular arrhythmias.

Sotalol, a beta adrenergic antagonist that prolongs action potential duration and refractoriness, was administered to ten patients with chronic, symptomatic ventricular ectopic activity. Eight patients had ischaemic heart disease, one patient congestive cardiomyopathy, and one patient atypical chest pain and no structural abnormality. Twenty-four hour Holter ECG tapes were analyzed during a drug-free period, and after three and six months of continuous Sotalol therapy. Satisfactory control of ventricular premature contractions was initially achieved in nine patients. Longer follow-up confirmed maintenance of antiarrhythmic efficacy in five (50%) patients. Sotalol was especially effective in reducing high grade arrhythmias (couplets, "R on T" VPCs). That efficacy and the low frequency of side-effects make Sotalol an agent of notable value in suppressing ventricular arrhythmias, especially in patients who require antianginal therapy.

Aged↗
PubMed1983

The relationship of human atrial cellular electrophysiology to clinical function and ultrastructure.

Although previous studies have described the electrophysiological and ultrastructural characteristics of human cardiac fibers, no attempt has been made as yet to describe quantitatively the relationship between the ultrastructural and cellular electrophysiological derangements occurring with cardiac disease, and their clinical manifestations. In this study, we used standard microelectrode techniques to record the action potential characteristics of human atrial fibers obtained during cardiac surgery and correlated the electrophysiological parameters with clinical and ultrastructural data. Ultrastructure was studied by optical and electron microscopy. We found a multiple linear regression among maximum diastolic potential, atrial size and pressure, P wave duration and ultrastructure changes. Proliferations of Z band material, widening of intercalated discs, and degenerative changes were quantified and correlated with electrophysiological and clinical data. These studies emphasize the relationship between hemodynamic anomalies and resultant changes in both human atrial fiber structure and electrical function. Finally, the likelihood of occurrence of arrhythmias can be predicted using the analytic method described.

Adolescent↗
PubMed1982

Electrophysiologic characteristics of human ventricular and Purkinje fibers.

We studied the electrophysiologic characteristics of ventricular muscle and Purkinje fibers from the hearts of five patients undergoing cardiac transplantation. All five patients had congestive failure and coronary artery disease before surgery and were receiving digitalis therapy. Ventricular muscle had a maximal diastolic potential (MDP) of -78 +/- 1 mV (mean +/- SEM), an action potential (AP) amplitude of 104 +/- 2 mV, a phase 0 upstroke velocity (Vmax) of 297 +/- 19 V/sec and an AP duration at 50% repolarization (APD50) of 190 +/- 4 msec. Purkinje fibers had an MDP of -80 +/- 2 mV, an AP amplitude of 107 +/- 2 mV, a Vmax of 388 +/- 25 V/sec and an APD50 of 195 +/- 9 msec. Fibers from infarcted sections of the heart had significantly longer APD than those from noninfarcted, which resulted in marked dispersion of APD in infarcted and adjacent zones. Both epinephrine and ouabain induced delayed after depolarizations in Purkinje fiber. This suggest that delayed after depolarizations and resultant triggered activity can occur in the human ventricle.

Action Potentials↗
PubMed1980

Combined mexiletine and amiodarone treatment of refractory recurrent ventricular tachycardia.

A combined mexiletine and amiodarone treatment was applied in nine cases with recurrent refractory ventricular tachycardia. During the first two days of treatment, mexiletine and amiodarone were perfused intravenously at a dose of 1,000 mg. and 1,500 mg. per 24 hours, respectively. Simultaneously amiodarone was also given orally at a dose of 600 mg. per 24 hours. From the third day onwards, the intravenous administration was interrupted and both drugs were continued orally at a dose of 600 mg. daily. The first three patients were very critically ill and had had at least five episodes of ventricular tachycardia per 24 hours during the last 10 days in the intensive care unit. The treatment resulted in total suppression of the tachycardic episodes within three days after initiation of therapy. In the remaining six cases, ventricular tachycardia was easily initiated by programmed electrical stimulation of the heart. No arrhythmia could be elicited by repeated testing on the seventh day of treatment. The mean follow-up period was 6 months. Two patients with poor left ventricular function died in intractable heart failure. Another one died suddenly 4-1/2 months after his release from the hospital. He had a large aneurysm and whether he continued his treatment is unknown. A fourth patient had an aneurysmectomy; he suffered a recurrence, and died at his second operation. All the others presently remain asymptomatic. The association of a class I (mexiletine) with a class III (amiodarone) agent is theoretically attractive for the treatment of refractory ventricular arrhythmias. The present findings corroborate this hypothesis, but show that this association is not able to protect individuals with severe underlying myocardial damage.

Adult↗
PubMed1980

Severe conduction disturbances and ventricular arrhythmias complicating mediastinal irradiation for Hodgkin's disease: a case report.

A 27-year-old male had undergone mediastinal and retroperitoneal irradiation for stage IIIA Hodgkin's disease at age 19. When he was admitted to the hospital, because of lightheadedness and syncope, trifascicular bundle branch block was noted and the patient underwent a clinical electrophysiological investigation. AH and HV intervals were prolonged and ventricular fibrillation was induced during programmed right ventricular stimulation. Serial electrophysiological studies allowed us to prescribe effective antiarrhythmic drug therapy with no recurrence of symptoms during a follow-up period of 12 months.

Adult↗