[Ischemic disorders of cardiac rhythm: effects of the autonomic nervous system on electrophysiologic findings and pharmacotherapy].
The time course and frequency of ventricular arrhythmias in myocardial ischemia and myocardial necrosis are influenced by a great number of different factors. The most important are: size and localization of the ischemic area, mode of coronary artery occlusion (one stage occlusion, phasic, protracted or gradual occlusion), intermittent reperfusions, and influence of the autonomic nervous system. Autonomic factors influence both the mechanisms of arrhythmias and the results of pharmacological interventions. An increased sympathetic tone causes both in reversible myocardial ischemia and in partially irreversible myocardial necrosis a significant increase in incidence and severity of arrhythmias. The underlying mechanism of action is complex and includes enhanced automaticity, an increase in ischaemia-induced prolongation of conduction while the frequency of bidirectional conduction blockades is reduced, and an increase in dispersion of repolarization. Due to these various factors the preconditions for reentry are favourable. Vagal effects consist in an increase or decrease of frequency-related arrhythmias. Furthermore, indirect antifibrillatory effects are apparent due to an antagonism of sympathetic actions. The significance of autonomic factors for arrhythmogenesis following "early" reperfusion (i.e. arrhythmias occurring immediately after release of short-term coronary artery obstruction) has not yet been established. Reports in the literature suggesting antifibrillatory actions of sympathicolytics have not yet been confirmed. The results of antiarrhythmic pharmacotherapy are also influenced by autonomic factors, particularly increased sympathetic activity. At the very onset of acute myocardial ischemia, when sympathetic tone is markedly increased in most patients, class I antiarrhythmic agents, particularly those which cause a significant conduction delay display only weak antiarrhythmic effects or even no effectiveness at all. The frequency of ventricular fibrillation is not diminished. Various agents even produce significant arrhythmogenic effects. The electrophysiological mechanism of action is based on a further increase in ischemia-induced prolongation of conduction and in dispersion of conduction times. By contrast, beta-sympathicolytics, class III antiarrhythmic agents (d-Sotalol type) and calcium antagonists (Verapamil type) (the latter only at high doses) cause a decrease in ischemia-induced prolongation of conduction and in dispersion of conduction times thereby reducing the incidence of early ventricular fibrillation. In the stage of manifest necrosis the order of relative potency is reversed if the sympathetic tone is low.(ABSTRACT TRUNCATED AT 400 WORDS)
D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000503:physiopathology*; D001341:Autonomic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology*; D004562:Electrocardiography; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D011379:Prognosis; D014693:Ventricular Fibrillation / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents
Ischämische Herzrhythmusstörungen: Einflüsse des autonomen Nervensystems auf elektrophysiologische Befunde und Pharmakotherapie.