Arrhythmogenic action of endothelin-1

Abstract

Dear Editor, ischemic ECG changes and yielded a prompt fall in It was highly interesting to read the 'Letter to the Editor' coronary blood flow. Due to 1 nmol ET-1 bolus, MAP by Duru et al. [1] regarding the arrhythmogenic action of shortening and the decrease of the upstroke velocity in endothelin-1 (ET-1). ET-1 is supposed to act as a paracrine LV MAP signals were observed (ischemic effect) folepi hormone released due to stretch or myocardial ischaemia lowed by an increase of MAPD in the reperfusion period 90 in vivo. ET-1 prolonged action potential duration with (direct effect) [7]. early afterdepolarization (EAD) formation in right bundle When applying three dimensional mapping during 60 branch cells [2]. In in vivo experimental studies mono-and pmol / min ET-1 infusion and LAD ligation electrophysiopolymorphic nonsustained and sustained ventricular tachlogical changes, local refractory period, left ventricular ycardias (VT) often accelerating into ventricular fibrillaconduction time and total activation pattern were also tion were observed during low dose (30-60 pmol / min) different in the two groups. Besides focal mechanisms, intracoronary (ic.) ET-1 administration [3]. At the time of macroreentry was also observed in the maintenance of the the appearance of nonsustained VT-s 30% reduction of arrhythmias induced by subtotal LAD ligation, while no coronary blood flow without ischemic ECG alterations signs of reentry could be found during ET-1 infusion [8]. were observed. Furthermore, no ischemic lactate elevation Certainly, we can not rule out the role of focal ischemia in the coronary sinus could be observed [4]. Following 60 of ET-1 infusion, and the first reports on severe ventricular pmol / min ic. ET-1 infusion, a continuous prolongation of arrhythmias due to high-dose bolus administration of ET-1 monophasic action potential (MAP) signs at 90% repolaripresumably referred to the secondary arrhythmogenic sation (MAPD ) was detected before arrhythmia formaeffect of ET-1 via strong coronary vasoconstriction, cor-90 tion in all investigated regions (right and left ventricular onary spasm or reperfusion. Presumably, ischemia can also apical / septal endocardial and right and left ventricular play an important role in the maintenance of ET-1 induced anterior epicardial sites). This was associated with EAD arrhythmias. However, direct arrhythmogenic effect of ETformation in approximately 50% of cases. However, the 1 infusion was proven by both in vivo and in vitro typical ischemic MAP changes, shortening of MAPD , experimental models.