Depression

Patients with myocardial infarction who suffer from a depression are at increased risk of dying of a subsequent heart attack or some other complication of coronary artery disease (CAD). A considerable body of research has provided evidence that a major depression, which is found in 16 to 23 percent of patients with CAD, but also subliminal depressive symptoms are independent risk factors for an unfavourable outcome of CAD. However, it is not yet clear whether depression is a causal risk factor having impact on the course of the heart disease or merely a prognostic marker that allows predicting the outcomes of interest, without any causal influence on them. Several pathways between depression and CAD have been discussed. These include behavioral mechanisms such as low compliance with both medical treatment and life style recommendations as well as neurobiological links. Much attention has been paid to the hypothalamic-pituitary-adrenocortical and sympathomedullary hyperactivity found in depression. Other possible links include diminished heart rate variability, stress-induced ischemia, platelet activation, and immunological dysregulation. To resolve the issue whether depression is a causal risk factor or only a prognostic marker, experimental studies are needed to evaluate interventions aimed at improving depression and test whether mortality is subsequently reduced. Such studies brought in the past mixed results. Whereas comprehensive intervention programs including risk factor management have produced a reduction in both coronary morbidity and mortality, a recent multicenter study providing either cognitive-behavioral therapy or usual care to depressed patients with CAD could not demonstrate a survival benefit among the participants of the intervention. Finally, results of evaluation studies regarding integrated disease management programs for patients with comorbid depression are presented.