Decrease of delayed rectifier currents in the subacute phase of infarction.

Abstract

See article by Jiang et al. [1] (pages 34–43) in this issue. The paper of Jiang et al. [1] in this issue of Cardiovascular Research – ‘Delayed rectifier K currents have reduced amplitudes and altered kinetics in myocytes from infarcted canine ventricle’ – forms the coping-stone in a long series of investigations into the mechanisms underlying arrhythmias post myocardial infarction (in terms of altered ionic currents). In this paper, delayed rectifier currents were characterized in ventricular myocytes isolated from the surviving layer of epicardium overlying a 5 day-old infarct, the epicardial borderzone (EBZ). This canine model of myocardial infarction, caused by complete occlusion of the left anterior descending coronary artery, has been thoroughly studied over the past decades. It has been demonstrated that during the healing phase post infarction (days to weeks after coronary occlusion), inducible ventricular tachycardias are a consequence of reentrant excitation localized to this EBZ (see for review [2]). Previous experimental studies on whole hearts and multicellular preparations already indicated important changes in cellular electrophysiology in the EBZ besides changes in anatomy relevant for reentry. Electrophysiological properties of the surviving epicardial fibers 5 days after coronary occlusion are characterized by a reduction in resting membrane potential, action potential amplitude and Vmax of phase 0 (upstroke velocity), partly contributing to slowed conduction. Additionally, action potentials had a brief plateau phase and thereby action potential duration was decreased [2,3]. Despite the latter, prolonged effective and relative refractory periods were observed … * Tel.: +31-20-566-3269; fax: +31-20-697-5458 m.w.veldkamp{at}amc.uva.nl