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  • Title: [Divergent time courses of ventricular vulnerability of the heart to ventricular tachycardias and ventricular fibrillation in the early necrosis stage of acute experimental myocardial infarct].
    Author: Gülker H, Thale J, Heuer H, Zurstegge KM, Bender F.
    Journal: Z Kardiol; 1983 Dec; 72(12):711-7. PubMed ID: 6198813.
    Abstract:
    UNLABELLED: Early necrosis in acute experimental myocardial infarction is characterized by severe ventricular dysrhythmias beginning approx. 6 hours after coronary artery occlusion and persisting for 2-5 days. It was the aim of this study to investigate the comparative changes in ventricular vulnerability to spontaneous and stimulus-induced tachycardia and fibrillation during early necrosis 6-18 hours following acute coronary artery occlusion. RESULTS: 1) The thresholds for repetitive extrasystoles and for ventricular fibrillation determined via electrodes placed on to the endocardium of the right and left ventricle outside of the ischemic area are within the normal range of the non-ischemic heart. 2) Both stimulation thresholds increase significantly within the area of infarction and in many cases are not inducible any more after 18 hours of ischemia, whatever amount of current is applied. 3) Sustained ventricular tachycardia can be induced in about 30% of cases after an occlusion lasting approx. 6 hours and in about 80% after an occlusion period of 18 hours. 4) Electrically induced ventricular tachycardias differ from spontaneously occurring VT in so far as the former appear to be due to a reentry mechanism, whereas the latter seem to be "accelerated ventricular rhythms" and thus of focal origin. Our results demonstrate that enhanced ventricular vulnerability during early necrosis in acute myocardial infarction is predominantly due to ventricular tachycardia rather than to ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
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