[Myocardial ischemia and ventricular arrhythmia].
A relation between myocardial ischemia and induction of ventricular arrhythmias can be demonstrated in patients with coronary heart disease--in contrast to patients with primary non ischemic cardiac diseases--using a combined metabolic-electrophysiological investigation protocol consisting of programmed atrial and ventricular stimulation with simultaneous measurement of the arterio/coronary venous difference for lactate, pyruvate, free fatty acids and amino acids. There are significant metabolic distinctions between both ischemic and non ischemic heart disease under pacing stress conditions as well as at rest. Areas of "hibernating myocardium" resp. "mismatch" zones in the myocardium showing reduced or abolished perfusion and preserved metabolism during scintographic SPECT/PET studies, may be found more often in patients with ventricular tachycardias (VT) or ventricular fibrillation (VF) in the chronic post myocardial infarction state than in patients without VT/VF. The proof of such zones may be considered a possible risk factor for arrhythmic events and sudden cardiac death after myocardial infarction. Hereby the concept of an interaction between acute and chronic ischemia triggering the onset of polymorphic VT or VF gaines increasing acceptance. In contrast, monomorphic reentrant VT are usually generated in the border zone of scarred areas where islands of vital fibers are surrounded by fibrotic tissue. These arrhythmogenic origin regions are characterized by a "match" pattern presenting a comparably severe reduction of perfusion and metabolism. Under those circumstances a control resp. suppression of the VT focus can only be provided by interventional techniques like catheter ablation, antitachycardiac surgery or implantation of a cardioverter/defibrillator beyond antiarrhythmic drug therapy. An antiischemic causal treatment (bypass surgery or angioplasty) represents for maximal 40% of patients with ischemically induced ventricular arrhythmias an adequate and sufficient therapeutic option. This pure antiischemic procedure seems to be justified especially in patients with preserved left ventricular function, proof of reversible ischemia and non inducibility of VT/VF following revascularization or non inducibility pre- and post intervention. In all other instances an additional treatment by antiarrhythmic drugs or preferably the implantable defibrillator is required.
Vester
E G
EG
Heinrich-Heine-Universität Düsseldorf Medizinische Klinik und Poliklinik B Klink für Kardiologie, Pneumologie und Angiologie.
D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000175:diagnosis / Q000503:physiopathology; D004562:Electrocardiography; D004734:Energy Metabolism / Q000502:physiology; D006801:Humans; D017202:Myocardial Ischemia / Q000175:diagnosis / Q000503:physiopathology*; D017682:Myocardial Stunning / Q000175:diagnosis / Q000503:physiopathology; D011379:Prognosis; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000503:physiopathology*
Myokardischämie und ventrikuläre Arrhythmien.