DEPRESSION AND MORTALITY FOLLOWING MYOCARDIAL INFARCTION

描述：临床抑郁症是死亡率的一个强有力的危险因素 急性心肌梗死（MI）后，人们对心肌梗死的了解甚少。 解释这种效应的潜在机制。 的主要目的 这项研究是为了检查最合理的候选机制之一， 自主神经张力改变 480例符合DSM-IV的MI后患者 严重或轻微抑郁症的人参加了 NHLBI赞助的ENRICHD（增强冠心病康复） 临床试验，480名非抑郁的心肌梗死后患者被排除在 ENRICHD，将在两年期间从四个月开始招募 ENRICHD临床中心。 之后将记录24小时动态ECG 出院时获得心率变异性、心肌 缺血和室性心律失常。 患者将在18岁时接受随访 个月，心理和医疗终点，包括死亡率，将是 确定。 主要分析将确定心率是否 变异性解释了预期的 与非抑郁组相比，抑郁的影响，以及这种影响是否 主要集中在室性心律失常患者， 心室功能障碍 研究的第二个目的是确定临床特征或亚型 抑郁症可能与特别高的死亡风险有关， 并伴有自主神经张力改变，如症状严重程度，共病焦虑， 或敌意 这项机制研究将补充临床数据， 从ENRICHD试验中获得，而且成本要高得多 很难独立进行比较研究。 澄清 这一基本机制将大大提高 流行病学证据表明，抑郁症会增加MI后的死亡率 患者，并允许进一步细化风险分层， 最高风险的患者可以被识别和治疗， 咄咄逼人

DESCRIPTION: Clinical depression is a powerful risk factor for mortality after an acute myocardial infarction (MI), yet little is known about the underlying mechanisms that account for this effect. The primary purpose of this study is to examine one of the most plausible candidate mechanisms, altered autonomic tone. Four hundred eighty post-MI patients with DSM-IV major or minor depression who are enrolled in the Usual Care arm of the NHLBI-sponsored ENRICHD (Enhancing Recovery in Coronary Heart Disease) clinical trial, and 480 non-depressed post-MI patients excluded from ENRICHD, will be recruited for this study during a two year period from four ENRICHD clinical centers. A 24 hour ambulatory ECG will be recorded after hospital discharge to obtain data on heart rate variability, myocardial ischemia, and ventricular arrhythmias. Patients will be followed up at 18 months, and psychosocial and medical endpoints, including mortality, will be ascertained. The primary analysis will determine whether heart rate variability accounts for the significantly higher mortality expected in the depressed compared to the non-depressed group, and whether this effect is largely concentrated in patients with ventricular arrhythmias and left ventricular dysfunction. The second purpose of the study is to identify clinical features or subtypes of depression that may be associated with a particularly high mortality risk and with altered autonomic tone, such as symptom severity, comorbid anxiety, or hostility. This mechanistic study will complement the clinical data to be obtained from the ENRICHD trial, and it would be considerably more costly and difficult to conduct a comparable study independently. Clarification of the underlying mechanism will greatly enhance the credibility of the epidemiological evidence that depression increases mortality in post-MI patients, and permit further refinements in risk stratification so that the patients at highest risk can be identified and treated the most aggressively.