A role for the renin-angiotensin system in the evolution of cardiac memory

Angiotensin II and Cardiac Memory. Introduction: We studied the role of the cardiac renin-angiotensin II system in the genesis of cardiac memory, in w hich T wave changes induced by ventricular pacing (VP) accumulate and persi st during subsequent sinus rhythm. Methods and Results: Anesthetized dogs were instrumented via a thoracotomy and three 20-minute runs of VP were interspersed with periods of normal sin us rhythm sufficient to permit T wave recovery to 90% of control. Memory wa s quantified as the change (Delta) in T wave vector angle showing accumulat ion over the three monitoring periods. In five control dogs T wave vector = -27 +/- 49 degrees, and this shifted by 104 degrees (P < 0.05) over the th ree postpacing recovery periods. In seven dogs infused with the I receptor blocker saralasin, five infused with the angiotensin-converting enzyme inhi bitor captopril, and four infused with the tissue protease inhibitor chymos tatin, there were significant reductions in the incidence and the accumulat ion of memory. In four other experiments, we used isolated, blood-perfused canine hearts to demonstrate that VP used to induce memory alters the contr actile pattern of the left ventricle, Conclusions: We propose that the alteration in myocardial stretch induced b y pacing activates angiotensin II synthesis by cardiac cells. We propose, f urther that the endogenous cardiac renin-angiotensin II system (blocked by saralasin, captopril and by chymostatin) is an important contributor to the induction of memory.