Abstract
Cardiac memory (CM) can alter the configuration of action potentials and the transmural repolarization gradient in ventricular tissue. This study evaluated the effects of CM on ventricular arrhythmogenicity. A total of 20 patients (12 females, 8 males; mean age, 46 +/- 13 years) were enrolled. The following indicators were measured to evaluate ventricular arrhythmogenicity: (1) the action potential duration at 90% repolarization (APD90) recorded from the right ventricular apex (RVA); (2) the maximal slope of the action potential duration restitution curve (APDR) constructed by programmed extra stimuli from RVA; and (3) the maximal corrected QT interval (QTc) and QT interval dispersion (QTd). The short-term CM was induced by constant pacing from the RVA at a pacing cycle length (PCL) of 400 ms for 20 minutes. After induction of CM, the mean APD90 were significantly shortened at both PCLs of 600 ms and 400 ms (252.9 +/- 6.4 ms vs. 235.6 +/- 6.4 ms and 231.2 +/- 6.4 ms vs. 214.4 +/- 7.3 ms, respectively; p = 0.001). No significant change regarding the maximal slopes of APDR were found at both PCLs of 600 ms and 400 ms (1.05 +/- 0.09 vs. 0.96 +/- 0.11 and 0.85 +/- 0.08 vs. 0.84 +/- 0.09, respectively). QTc (417.3 +/- 9.1 ms vs. 454.7 +/- 8.3 ms; p = 0.001), but not QTd (63.4 +/- 5.4 ms vs. 65.7 +/- 6.1 ms), was significantly shortened. Short-term CM significantly decreased ventricular APD90 and QTc, but did not significantly change the maximal slope of APDR or QTd. These results suggest that CM might not have a significant effect on ventricular arrhythmogenicity.