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
