Kjekshus J
Department of Medicine, Baerum Hospital, Sandvika, Norway.
Am J Cardiol. 1990 May 22;65(19):42I-48I. doi: 10.1016/0002-9149(90)90125-k.
The extent and severity of myocardial dysfunction and risk of dying are associated with the occurrence of ventricular arrhythmias. However, there is a dissociation between the frequency of ventricular arrhythmias and the prevalence of sudden death among patients with congestive heart failure. Sudden death occurs in 8 to 10% of New York Heart Association functional class I patients and in 20% of class II, III and IV patients, despite increased frequency of malignant arrhythmias and functional deterioration. Yearly mortality rates increase from 12 to 15% in class I and II and is 60% in class IV. Sudden death in class I and II is 50 to 60% of all deaths, whereas in class IV it amounts to only 20 to 30%. The most important cause of death in class IV is progressive congestive heart failure. Ventricular arrhythmia is a trigger event in the development of fatal arrhythmia which depends on a substrate of myocardial scar tissue, hypertrophy and aberrant conducting pathways. However, regional myocardial ischemia, transmembrane electrolyte differences and myocardial stores of catecholamines are important modulators. Depletion of myocardial catecholamines and down-regulation of myocardial beta-adrenergic receptors in the myocardium may explain tolerance to ventricular tachyarrhythmias observed in patients with severe congestive heart failure and intolerance to conventional antiarrhythmic drugs. Although angiotensin-converting enzyme (ACE) inhibitors may reduce ventricular arrhythmias, the important role of ACE inhibitors in severe congestive heart failure is to prevent progression of myocardial dysfunction and congestive heart failure. To date, however, ACE inhibitors have not been demonstrated to have a significant effect on the incidence of sudden death. This does not preclude an effect on fatal arrhythmias among patients with milder heart failure and intact stores of myocardial catecholamines.
心肌功能障碍的程度和严重性以及死亡风险与室性心律失常的发生有关。然而，在充血性心力衰竭患者中，室性心律失常的频率与猝死的发生率之间存在脱节。纽约心脏协会心功能I级患者中，猝死发生率为8%至10%，而II级、III级和IV级患者中为20%，尽管恶性心律失常的频率增加且功能恶化。I级和II级患者的年死亡率从12%升至15%，IV级患者为60%。I级和II级患者的猝死占所有死亡的50%至60%，而IV级患者仅占20%至30%。IV级患者最重要的死亡原因是进行性充血性心力衰竭。室性心律失常是致命性心律失常发生过程中的触发事件，其取决于心肌瘢痕组织、肥厚和异常传导通路的基质。然而，局部心肌缺血、跨膜电解质差异和心肌儿茶酚胺储备是重要的调节因素。心肌儿茶酚胺的耗竭以及心肌中β-肾上腺素能受体的下调，可能解释了重度充血性心力衰竭患者对室性快速心律失常的耐受性以及对传统抗心律失常药物的不耐受性。尽管血管紧张素转换酶（ACE）抑制剂可能减少室性心律失常，但ACE抑制剂在重度充血性心力衰竭中的重要作用是防止心肌功能障碍和充血性心力衰竭的进展。然而，迄今为止，尚未证明ACE抑制剂对猝死发生率有显著影响。这并不排除其对心力衰竭较轻且心肌儿茶酚胺储备完整的患者的致命性心律失常有影响。
