Cardiovascular Division, Washington University School of Medicine, St. Louis, MO, USA.
Circ Arrhythm Electrophysiol. 2012 Aug 1;5(4):773-81. doi: 10.1161/CIRCEP.112.970491. Epub 2012 Jul 6.
Cardiac memory refers to the observation that altered cardiac electrical activation results in repolarization changes that persist after the restoration of a normal activation pattern. Animal studies, however, have yielded disparate conclusions, both regarding the spatial pattern of repolarization changes in cardiac memory and the underlying mechanisms. The present study was undertaken to produce 3-dimensional images of the repolarization changes underlying long-term cardiac memory in humans.
Nine adult subjects with structurally normal hearts and dual-chamber pacemakers were enrolled in the study. Noninvasive electrocardiographic imaging was used before and after 1 month of ventricular pacing to reconstruct epicardial activation and repolarization patterns. Eight subjects exhibited cardiac memory in response to ventricular pacing. In all subjects, ventricular pacing resulted in a prolongation of the activation recovery interval (a surrogate for action potential duration) in the region close to the site of pacemaker-induced activation from 228.4±7.6 ms during sinus rhythm to 328.3±6.2 ms during cardiac memory. As a consequence, increases are observed in both apical-basal and right-left ventricular gradients of repolarization, resulting in a significant increase in the dispersion of repolarization.
These results demonstrate that electrical remodeling in response to ventricular pacing in human subjects results in action potential prolongation near the site of abnormal activation and a marked dispersion of repolarization. This dispersion of repolarization is potentially arrhythmogenic and, intriguingly, was less evident during continuous right ventricular pacing, suggesting the novel possibility that continuous right ventricular pacing at least partially suppresses pacemaker-induced cardiac memory.
心脏记忆是指观察到改变心脏电激活会导致复极变化,这些变化在恢复正常激活模式后仍然存在。然而,动物研究对于心脏记忆中复极变化的空间模式和潜在机制得出了不同的结论。本研究旨在生成人类长期心脏记忆下复极变化的 3 维图像。
9 名结构正常的成年患者和双腔起搏器被纳入研究。在 1 个月的心室起搏前后,使用非侵入性心电图成像来重建心外膜激活和复极模式。8 名患者对心室起搏表现出心脏记忆。在所有患者中,心室起搏导致起搏器诱导的激活部位附近的激活恢复间隔(动作电位持续时间的替代指标)延长,从窦性节律时的 228.4±7.6ms 延长至心脏记忆时的 328.3±6.2ms。因此,在顶端-基底和右-左心室复极梯度中观察到复极的增加,导致复极离散度显著增加。
这些结果表明,人类对心室起搏的电重构导致异常激活部位附近的动作电位延长和复极离散度显著增加。这种复极离散度可能是心律失常的潜在原因,有趣的是,在连续右心室起搏期间,这种离散度不那么明显,这表明连续右心室起搏至少部分抑制了起搏器诱导的心脏记忆的新可能性。