| Summary: | 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 (APD 90) 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 APD 90 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 APD 90 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.
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