Hypertension is complicated by thrombosis-related events (such as myocardial infarction and stroke), and despite the high vascular pressures, these thrombotic occlusive events paradoxically occur more often than hemorrhagic episodes. The predisposition for thrombogenesis is increased in hypertension, which leads to changes in the platelets, endothelium, and matrix metalloproteinases and their inhibitors, as well as the coagulation and fibrinolytic pathways, which help promote the induction and the maintenance of this prothrombotic or hypercoagulable state. Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. These changes can, to a certain degree, be reversed by the treatment of hypertension, although the effects may be inconsistent. The evidence for antithrombotic therapy is less consistent, but in "high risk" hypertensive patients, antiplatelet therapy is useful.