2 FORMS OF SPIRAL-WAVE REENTRY IN AN IONIC MODEL OF ISCHEMIC VENTRICULAR MYOCARDIUM

It is well known that there is considerable spatial inhomogeneity in t he electrical properties of heart muscle, and that the many interventi ons that increase this initial degree of inhomogeneity all make it eas ier to induce certain cardiac arrhythmias. We consider here the specif ic example of myocardial ischemia, which greatly increases the electri cal heterogeneity of ventricular tissue, and often triggers life-threa tening cardiac arrhythmias such as ventricular tachycardia and ventric ular fibrillation. There is growing evidence that spiral-wave activity underlies these reentrant arrhythmias. We thus investigate whether sp iral waves might be induced in a realistic model of inhomogeneous vent ricular myocardium. We first modify the Luo and Rudy [Circ. Res. 68, 1 501-1526 (1991)] ionic model of cardiac ventricular muscle so as to ob tain maintained spiral-wave activity in a two-dimensional homogeneous sheet of ventricular muscle. Regional ischemia is simulated by raising the external potassium concentration ([K+](o)) from its nominal value of 5.4 mM in a subsection of the sheet, thus creating a localized inh omogeneity. Spiral-wave activity is induced using a pacing protocol in which the pacing frequency is gradually increased. When [K+](o) is su fficiently high in the abnormal area (e.g., 20 mM), there is complete block of propagation of the action potential into that area, resulting in a free end or wave break as the activation wave front encounters t he abnormal area. As pacing continues, the free end of the activation wave front traveling in the normal area increasingly separates or deta ches from the border between normal and abnormal tissue, eventually re sulting in the formation of a maintained spiral wave, whose core lies entirely within an area of normal tissue lying outside of the abnormal area (''type I'' spiral wave). At lower [K+](o) (e.g., 10.5 mM) in th e abnormal area, there is no longer complete block of propagation into the abnormal area; instead, there is partial entrance block into the abnormal area, as well as exit block out of that area. In this case, a different kind of spiral wave (transient ''type II'' spiral wave) can be evoked, whose induction involves retrograde propagation of the act ion potential through the abnormal area. The number of turns made by t he type II spiral wave depends on several factors, including the level of [K+](o) within the abnormal area and its physical size. If the pac ing protocol is changed by adding two additional stimuli, a type I spi ral wave is instead produced at [K+](o)=10.5 mM. When pacing is contin ued beyond this point, apparently aperiodic multiple spiral-wave activ ity is seen during pacing. We discuss the relevance of our results for arrythmogenesis in both the ischemic and nonischemic heart. (C) 1998 American Institute of Physics.