Depression, ischaemic heart disease and cerebrovascular disease are important causes of morbidity and are among the leading contributors to global health burden. These conditions often occur in the same patient, resulting in considerably greater effect on health than combinations of chronic diseases without depression. The frequent occurrence of these conditions in the same patient raises the possibility of a common genetic predisposition, similar risk factors or a pathophysiological link. Serotoninergic and adrenergic signalling play important roles in causing major depression and also in platelet activation and aggregation, which underlies vascular disease. This review discusses the potential pathophysiological link between major depression and conditions in which platelet activation plays an important role and also provides evidence linking the use of the most commonly used antidepressant drugs (i.e. the selective serotonin re-uptake inhibitors) to increased risk of bleeding.
Depression accelerates the development and progression of cardiovascular disease and confers an increased risk of mortality. Platelets share biochemical similarity with the central nervous system, particularly in the uptake, storage, and metabolism of serotonin. Given this similarity, and considering the central role of platelets in the biology of cardiovascular disease, it is highly plausible that platelets play an important role in the increased cardiovascular risk of patients with depression. This article provides a comprehensive review of the evidence in this area and shows that the relationship between depression and platelet function is hardly straightforward. Whereas many studies have found that patients with depression have exaggerated platelet activation, quite a number of others show no such relationship or even lower levels of platelet activation in patients with depression. Larger, carefully designed, adequately powered studies with standardized methods of assessing platelet function are needed to address this issue.
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