Computer simulations demonstrate that acute regional ischemia dramatically reduces action potential duration and alters the ionic basis of depolarization, with premature stimuli leading to slow Ca2+-dependent responses.
May promote reentry via slow Ca2+-dependent conduction in ischemia; leaves open clinical translation from animal models.
In this paper, computer simulations have been carried out to investigate the main features of propagated cardiac action potentials in myocardial tissue in the presence of regional acute ischemia. For this purpose, we have used a modified version of Luo-Rudy phase II model of the ventricular action potential, in which the formulation of the ATP-sensitive K/sup +/ current proposed by Ferrero et al. has been included, to simulate electrical activity in a 1-dimensional model of myocardial tissue. Both extracellular [K/sup +/] and K/sub ATP/ current are conveniently modified along the strand to simulate the normal zone, electrophysiological border-zone and central ischemic zone, each of them 1 cm long. Control electrical stimuli with a basic cycle length of 500 milliseconds were applied to the first cell of the normal zone, and a premature stimulus was applied to the normal side of the ischemic border-zone. The results show that action potentials in the ischemic central zone arising from control stimulation, (a) result from Na/sup +/-mediated depressed fast responses, with Ca/sup 2+/ current playing also an important role in depolarization, and (b) their duration is dramatically reduced when compared to those in the normal zone. Premature action potentials in the central zone show very low upstroke velocities and result from slow Ca/sup 2+/-dependent responses.
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Ferrero et al. (1997) studied this question.
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