Pacifico Antonio, Henry Philip D
Texas Arrhythmia Institute and Baylor College of Medicine, Scorlock Tower, Suite 620, 6560 Fannin Street, Houston, TX 77030, USA.
J Cardiovasc Electrophysiol. 2003 Jul;14(7):764-75. doi: 10.1046/j.1540-8167.2003.02543.x.
We review the macroscopic and microscopic anatomy of myocardial disease associated with heart failure (HF) and sudden cardiac death (SCD) and focus on the prevention of SCD in light of its structural pathways. Compared to patients without SCD, patients with SCD exhibit 5- to 6-fold increases in the risks of ventricular arrhythmias and SCD. Epidemiologically, left ventricular hypertrophy by ECG or echocardiography acts as a potent dose-dependent SCD predictor. Dyslipidemia, a coronary disease risk factor, independently predicts echocardiographic hypertrophy. In adult SCD autopsy studies, increases in heart weight and severe coronary disease are constant findings, whereas rates of acute coronary thrombi vary remarkably. The microscopic myocardial anatomy of SCD is incompletely defined but may include prevalent changes of advanced myocardial disease, including cardiomyocyte hypertrophy, cardiomyocyte apoptosis, fibroblast hyperplasia, diffuse and focal matrix protein accumulation, and recruitment of inflammatory cells. Hypertrophied cardiomyocytes express "fetospecific" genetic programs that can account for acquired long QT physiology with risk for polymorphic ventricular arrhythmias. Structural heart disease associated with HF and high SCD risk is causally related to an up-regulation of the adrenergic renin-angiotensin-aldosterone pathway. In outcome trials, suppression of this pathway with combinations of beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin-II receptor blockers, and mineralocorticoid receptor blockers have achieved substantial total mortality and SCD reductions. Contrarily, trials with ion channel-active agents that are not known to reduce structural heart disease have failed to reduce these risks. Device therapy effectively prevents SCD, but whether biventricular pacing-induced remodeling decreases left ventricular mass remains uncertain.
我们回顾了与心力衰竭（HF）和心源性猝死（SCD）相关的心肌病的宏观和微观解剖结构，并根据其结构途径重点关注SCD的预防。与无SCD的患者相比，SCD患者发生室性心律失常和SCD的风险增加了5至6倍。从流行病学角度来看，心电图或超声心动图显示的左心室肥厚是一种强有力的剂量依赖性SCD预测指标。血脂异常作为冠心病的危险因素，可独立预测超声心动图显示的心肌肥厚。在成人SCD尸检研究中，心脏重量增加和严重冠心病是常见发现，而急性冠状动脉血栓形成的发生率差异很大。SCD的微观心肌解剖结构尚未完全明确，但可能包括晚期心肌病的普遍变化，如心肌细胞肥大、心肌细胞凋亡、成纤维细胞增生、弥漫性和局灶性基质蛋白积聚以及炎症细胞募集。肥厚的心肌细胞表达“胎儿特异性”基因程序，这可能导致获得性长QT生理状态并伴有多形性室性心律失常的风险。与HF和高SCD风险相关的结构性心脏病与肾上腺素能肾素-血管紧张素-醛固酮途径的上调存在因果关系。在结局试验中，联合使用β受体阻滞剂、血管紧张素转换酶抑制剂、血管紧张素II受体阻滞剂和盐皮质激素受体阻滞剂抑制该途径已使总死亡率和SCD大幅降低。相反，使用已知不会减轻结构性心脏病的离子通道活性药物的试验未能降低这些风险。器械治疗可有效预防SCD，但双心室起搏诱导的重塑是否能减轻左心室重量仍不确定。
