Swann Michael H, Nakagawa Hiroshi, Vanoli Emilio, Lazzara Ralph, Schwartz Peter J, Adamson Philip B
Physiology and Medicine Cardiology Cardiac Arrhythmia Research Institute WK Warren Medical Research Institute, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma 73190, USA.
J Cardiovasc Electrophysiol. 2003 Aug;14(8):873-9. doi: 10.1046/j.1540-8167.2003.03100.x.
Repolarization Heterogeneity and Sudden Death Risk.
The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear.
Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 +/- 10 msec vs 222 +/- 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 +/- 1.5 msec/mmHg vs 28 +/- 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 +/- 42 msec, basal anterior wall vs 197 +/- 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization.
Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias.
复极异质性与猝死风险
本研究旨在探讨心内膜心室复极特征是否与猝死的不同风险相关。体表QT间期延长与心肌梗死（MI）后心律失常风险增加相关，但QT延长的潜在机制及其与致死性心律失常的关系尚不清楚。
在12只犬前壁心肌梗死后1个月进行运动试验并短暂结扎回旋支冠状动脉时评估心室颤动（VF）风险。易感犬（n = 5）在短暂缺血发作期间发生VF，而抗性犬未发生（n = 7）。静息时测量体表QT间期。通过超声心动图确定的四个独特区域获得左心室复极的心内膜电解剖导管图，并在组间进行比较。与抗性犬相比，易感犬的特征是体表QT间期延长（240±10毫秒对222±7毫秒，P = 0.04）。此外，它们的压力反射敏感性较低（9.7±1.5毫秒/毫米汞柱对28±9.8毫秒/毫米汞柱，P <0.01），对急性缺血有心动过速反应，提示更强的交感神经反射倾向更高。易感犬体表QT间期延长是由于心内膜左心室复极的显著异质性（基底前壁为239±42毫秒，侧壁为197±35毫秒；P <0.001）。抗性动物的心内膜复极无区域差异。
心肌梗死后交感神经激活不仅会导致不良的结构重塑，还会导致不良的电生理重塑，从而导致心室复极异质性，并形成有利于致死性折返性心律失常的心肌基质。
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