Depression acts as a pathophysiological risk factor for cardiovascular disease development, highlighting the need to address it proactively rather than viewing it solely as a consequence of vascular events.
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May warrant depression screening in CVD prevention; leaves open whether treatment reduces events in trials.
The coexistence of depression and cardiovascular disease (CVD) is regularly discussed, and much debated. There is strong evidence that there are pathophysiological mechanisms, particularly endothelial dysfunction, altered platelet aggregation, and hyperactivation of the thrombosis cascade, which coexist with hypothalamic-pituitary-adrenocortical axis dysfunction, and link depression to CVD. Therefore, depression should not be automatically considered to be a consequence of life impairment due to myocardial infarction or major stroke. Probably, it should be considered as one of the many other stressful events, or "genetic reactions to life", which are risk factors for CVD development. This review will examine the significance of depression in clinical daily practice, its pathophysiology as a determinant in vascular events, and its real importance in, before, and after many CVD events.
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Moretti et al. (2011) studied this question.
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