Kendler Kenneth S, Gardner Charles O, Fiske Amy, Gatz Margaret
Virginia Institute for Psychiatric and Behavioral Genetics, Department of Psychiatry, Virginia Commonwealth University School of Medicine, Richmond, Virginia 23298-0126, USA.
Arch Gen Psychiatry. 2009 Aug;66(8):857-63. doi: 10.1001/archgenpsychiatry.2009.94.
Major depresssion (MD) and coronary artery disease (CAD) frequently co-occur. The mechanisms of comorbidity are uncertain.
To clarify sources of MD-CAD comorbidity.
Major depression was assessed at the time of the personal interview, and CAD from hospital discharge records and death certificates.
Swedish population-based twin registry.
The study included 30 374 twins with a mean age of 57 years. Main Outcome Measure Modified DSM-IV diagnosis of MD or diagnosis of CAD.
Lifetime association between MD and CAD was modest (odds ratio, approximately 1.3). In time-dependent Cox analyses, onset of CAD produced concurrent and ongoing hazard ratios for MD of 2.83 and 1.75. These risks increased if the diagnosis of CAD was restricted to myocardial infarction. Onset of MD increased the concurrent and ongoing hazard ratios for CAD to 2.53 and 1.17. The ongoing CAD risk was strongly associated with depressive severity and recurrence. Twin models showed that the modest comorbidity between MD and CAD in women arose primarily from shared genetic effects, although the genetic correlation was small (+0.16). In men, the source of comorbidity was moderated by age, being environmental in older members and largely genetic in younger members of the sample.
Although the MD-CAD relationship across the lifespan is modest, time-dependent models reveal stronger associations. The sustained effect of CAD onset on MD risk is much stronger than vice versa. The effect of MD on CAD is largely acute, and the longer-term effects are apparently mediated via depressive recurrence. When examined separately, in men, environmental effects, which are often acute, play a large role in MD-CAD comorbidity, whereas in women, chronic effects, which are in part genetic, are more important. In men, genetic sources of MD-CAD comorbidity are more important in younger members of the sample.
重度抑郁症（MD）与冠状动脉疾病（CAD）经常同时出现。共病机制尚不确定。
阐明MD - CAD共病的根源。
在个人访谈时评估重度抑郁症，并根据医院出院记录和死亡证明确定CAD情况。
瑞典基于人群的双胞胎登记处。
该研究纳入了30374对双胞胎，平均年龄为57岁。主要观察指标为改良的DSM - IV对MD的诊断或CAD的诊断。
MD与CAD的终生关联较弱（优势比约为1.3）。在时间依赖性Cox分析中，CAD的发病导致MD的并发和持续风险比分别为2.83和1.75。如果将CAD的诊断仅限于心肌梗死，这些风险会增加。MD的发病使CAD的并发和持续风险比分别增至2.53和1.17。持续的CAD风险与抑郁严重程度和复发密切相关。双胞胎模型显示，女性中MD与CAD之间的弱共病主要源于共同的遗传效应，尽管遗传相关性较小（+0.16）。在男性中，共病的根源受年龄影响，样本中年龄较大者为环境因素，年龄较小者主要为遗传因素。
尽管MD - CAD在整个生命周期中的关系较弱，但时间依赖性模型显示出更强的关联。CAD发病对MD风险的持续影响远强于反之情况。MD对CAD的影响主要是急性的，长期影响显然是通过抑郁复发介导的。分别来看，在男性中，通常为急性的环境因素在MD - CAD共病中起很大作用，而在女性中，部分为遗传的慢性因素更为重要。在男性中，MD - CAD共病的遗传因素在样本中年龄较小者更为重要。
