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Die chronische Herzinsuffizienz gleich welcher Ursache, stellt ein komplexes klinisches Syndrom dar, welches aufgrund der Einschrankung der Belastungstoleranz nicht nur die Lebensqualitat des Patienten mindert, sondern auch mit einem signifikant erhohten Risiko fur lebensbedrohliche ventrikulare Tachyarrhythmien verbunden ist. Ebenso wie die Ursachen der Herzinsuffizienz sind auch die Form und der Mechanismus ventrikularer Arrhythmien vielfaltig. So modulieren zellulare, myokardiale und extrakardiale Einflussfaktoren entscheidend die Auslosung und die Aggravation ventrikularer Tachyarrhythmien mit z. T. rascher Degeneration in Kammerflimmern.

During recent years, experimental data have collected convincing evidence for the fatal interaction of myocardial ischemia, ventricular tachyarrhythmias, and sudden cardiac death. In the clinical setting, data reporting on the daily relevance of such a fatal interaction lacked until recently. However, there is now increasing evidence from autoptic studies, from the evaluation of patients who survived one episode of sudden cardiac death, from the follow-up of these patients when treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and, most recently, from studies in patients with stable and especially unstable angina pectoris suffering from Holter-documented ischemic proarrhythmia, that acute and transient myocardial ischemia play an important role for the initiation as well as the aggravation of ventricular tachyarrhythmias and out-of-hospital sudden cardiac death. The present work is directed to summarize our clinical knowledge on this topic and to indicate that preventive strategies for myocardial ischemia are the “antiarrhythmic” of choice in patients with severe coronary artery disease and evidence for ischemic proarrhythmia.