 Another platelet-related factor believed to contribute to cardiovascular thrombosis is the presence of larger, more reactive platelets in patients with acute ischemic events 19-21. The increase in platelet size, which is in compensation for a persistent decrease in platelet count, results from the ongoing consumption of platelets in unstable angina; this is not seen in an acute myocardial infarction. In addition, platelets from patients with unstable angina, as determined by studying platelet aggregability ex vivo, are hyperaggregable. These effects promote thrombus growth, limitation of blood flow, and acute ischemia. 