Structural Pathways and Prevention of Heart Failure and Sudden Death
Structural Pathways and Prevention of Heart Failure and Sudden Death
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DOI：
10.1046/j.1540-8167.2003.02543.x
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发表时间：
2003-07
影响因子：
2.7
通讯作者：
A. Pacifico;P. D. Henry
中科院分区：
文献类型：
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作者：
A. Pacifico;P. D. Henry
我们回顾了与心力衰竭(HF)和心脏性猝死(SCD)相关的心肌疾病的宏观和微观解剖，并根据其结构途径重点介绍了SCD的预防。与没有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到6倍。流行病学上，心电图或超声心动图显示的左心室肥厚是一种有效的剂量依赖性SCD预测指标。血脂异常是冠心病的危险因素，可独立预测超声心动图肥大。在成人SCD尸检研究中，心脏重量增加和严重的冠状动脉疾病是恒定的发现，而急性冠状动脉血栓的发生率差异显著。SCD的心肌微观解剖结构尚不完全清楚，但可能包括常见的晚期心肌疾病的改变，包括心肌细胞肥大、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性细胞募集。肥大的心肌细胞表达“胎儿特异性”的遗传程序，这可以解释获得性长QT间期生理学与多形性室性心律失常的风险。与心力衰竭和高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-醛固酮途径上调有关。在结果试验中，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联合抑制这一途径可以显著降低总死亡率和SCD。相反，用离子通道激动剂进行的试验并不知道能减少结构性心脏病，但未能降低这些风险。装置疗法有效地预防了SCD，但双室起搏引起的重构是否减少了左心室质量仍不确定。(《心脏电生理杂志》，第14卷，第764-775页，2003年7月)
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. (J Cardiovasc Electrophysiol, Vol. 14, pp. 764‐775, July 2003)