Heart failure is a common disease in aging western populations. Not only severe but even mild to moderate heart failure is associated with increasing risk for stroke. This can partly be attributed to concomitant atrial fibrillation, a well-known risk factor for stroke. Furthermore, the increased risk for thromboembolic events in congestive heart failure has been attributed to a hypercoagulable state including formation of intraventricular thrombi. However, more recently, enhanced platelet activation has been described in patients with heart failure in sinus rhythm. Vascular endothelial dysfunction and reduced formation of the platelet inhibitor nitric oxide appear to contribute to platelet activation in heart failure. This review article summarizes the historical knowledge of abnormal platelet function in heart failure, focuses on pathophysiological changes in heart failure which could influence platelet activation, and discusses drug regimens investigated in heart failure to reduce platelet activation either by direct anti-platelet effects or by modulating the release of platelet inhibiting substances.
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