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Biomedical subjects

G E Gendlin

Publications and source records attributed to G E Gendlin.

17 recordsLinked to original sources
PubMed1992

[Myocardial perfusion in mitral valve prolapse with arrhythmic syndrome].

Myocardial perfusion was studied in 12 patients with mitral valve prolapse concurrent with cardiac arrhythmias by using two-dimensional 201Tl myocardial scintigraphy at rest and during exercise test. Signs of myocardial ischemia were revealed only in one case. Five patients were found to have steady-state perfusion defects whose extent correlated with the depth of mitral valve prolapse. There was an irregular distribution of myocardial blood flow, which ceased on exercise in 10 out of 12 patients. Patients with ventricular premature contraction displayed a decreased reserve of myocardial blood flow as compared to those with supraventricular premature contraction, presumably by enhancing myocardial perfusion at rest.

Adult↗
PubMed1991

[Physical exertion tolerance and its determining factors in hypertrophic cardiomyopathy].

A contribution of specific features of myocardial hypertrophy and hypercontractility left ventricular diastolic dysfunction to decreased exercise tolerance and developed coronary failure is discussed on the basis of results obtained from a bicycle ergometric test performed in 40 patients with hypertrophic cardiomyopathy. Thallium-201 myocardial scintigraphy conducted at the maximum exercise in 17 patients revealed a reduction in coronary reserve with increased myocardial mass index that was higher than the critical value. An implication of severe myocardial hypertrophy in the presence with coexisting left ventricular posterior wall hypertrophy and impaired perfusion/mass ratios is considered as a risk factor for death of patients with hypertrophic cardiomyopathy.

Adult↗
PubMed1978

[Prevention of ventricular fibrillation in animal experiments].

The precursors of ventricular fibrillation and asystole developing after ligation of a branch of the coronary artery and adrenalin injection were studied in 30 albino rats. The comparative efficacy of antiarrhythmic agents (ajmalin, lidocaine, isoptin, visken) in the prevention of ventricular fibrillation induced by electric current was determined in 40 rats. Ventricular extrasystole and tachysystole as well as the block of the bundle of His branch were the most common precursors of ventricular fibrillation. In some experiments fibrillation was preceded by complete atrioventricular block, cardiac fibrillation, sinus bradycardia, nonparoxysmal ventricular tachycardia, and excaped ventricular contractions. Ventricular asystole was most frequently preceded by complete atrioventricular block and the bundle of His branch block. Among the antiarrhythmic agents studied, ajmalin proved most effective in prevention of ventricular fibrillation; it raised the fibrillation threshold in all animals. Lidocaine, which produced a prophylactic effect in 50% of experiments, was second in effectiveness. Changes in the ventricular fibrillation threshold due to the effect of these agents were statistically significant on the average. Isoptin and visken proved to be less effective.

Ajmaline↗
PubMed1977

[Parasystolic arrhythmias].

The observation was conducted in 24 patients with parasystolic arrhythmias, 13 of them having parasystolic extrasystoles, and 11--paroxysmal and non-paroxysmal parasystolic tachycardia. Ventricular parasystole was found in 21 patients, atrial--in 3, atrioventricular--in 2; three patients had double parasystole with two ectopic centers. In the majority of patients their parasystole took a persistent, but relatively benign course, however one patient with ventricular parasystolic tachycardia persisting for many years had repeated ventricular fibrillations. For the treatment of supraventricular parasystolic arrhythmias beta-adrenergic receptors blocking agents, Isoptine, cardiac glycosides were used; in ventricular parasystole the more effective drugs are Lidocain, Novocainamid, Ajmalin.

Cardiac Complexes, Premature↗
PubMed1976

[Syndrome of sino-atrial node asthenia].

Under observation were kept 80 patients with signs pointing to the sick sinus syndrome. Most of them suffered from ischemic heart disease, from atherosclerotic cardiosclerosis and acute myocardial infarction. Persistent sinus bradycardia with active and passive heterotopic arrhythmias were recorded in 42 patients. Sino-auricular block of the II and III degrees or asystolia of the atria with ectopic arrhythmias were observed in 37 cases. A number of patients displayed fibrillary bradyarrhythmia, extrasystole with post-extrasystolic depression of the rhythm and other disturbances. The so-called tachycardia-bradycardia syndrome characterized by the presence of tachycardiac arrhythmias occurring against the background of a marked bradycardia was registered in 25 persons. Fifteen patients demonstrated attackes of the Morgagni-Adams-Stokes syndrome, usually associated with lengthy periods of cardiac asystole. The treatment of ectopic arrhythmias in patients with the sick sinus syndrome presents considerable difficulties, but in many of them these disorders could be successfully eliminated by a careful and rigidly controlled application of antiarrhythmic agents (isoptin, ajmalin, pulsnorma, rhythmodan, beta-adrenergical blocking agents). For some patients exhibiting a tendency toward asystole electric stimulation of the heart is indicated.

Aged↗
PubMed1975

[Atrio-ventricular dissociation].

Cardiac rhythm disorders called atrioventricular dissociation, especially the so-called dissociation with interference have been causing controversy among the cardiologists for a long time. The latter term implies an independent activity of the atria and ventricles, that is in no way connected with an orthograde atrioventricular block, and that develops in the presence of intermittent normal conductivity of sinus impulses. This disorder is always of a secondary nature and it may be due to the disorders in the formation of the primary rhythm, or conductivity of the impulse (passive form), or acceleration of the secondary rhythm (active form). The causes of such atrioventricular dissociation may lie in sinus bradycardia, sinoauricular or incomplete atrioventricular block, compensatory pauses after extra-systoles, atrioventricular and ventricular tachycardia (paroxysmal or nonparoxysmal) with a retrograde atrioventricular block, etc. Examples of ECG patterns illustrating most of the above mechanisms are presented. Due to the existence of several mechanisms that cause atrioventricular dissociation, and due to the fact that individual authors imply different meanings by the term "interference", it seems reasonable to abandon the term "dissociation with interference". In such case it would seem more appropriate to call the state a primary rhythm or conductivity disorder indicating an incomplete atrioventricular dissociation for a proper choice of therapy.

Adult↗