Propagation of arterial thrombi: local and remote contributory factors.

It is a common understanding that the rupture of an atheroma in the coronary arteries is the initial event in the onset of arterial thrombosis resulting in myocardial infarction.1 Ex vivo perfusion experiments using human blood have clearly demonstrated that platelet accumulation occurs immediately when the subendothelial matrix, such as collagen, is exposed to the blood stream.2 However, initiation of platelet thrombus formation after endothelial disruption resulting in exposure of the subendothelial matrix does not directly represent the onset of symptomatic atherothrombotic diseases, such as myocardial infarction, which were caused by thrombotic arterial occlusion. For example, coronary intervention, while causing damage to the endothelium, does not, in most cases, result in any symptomatic myocardial ischemia. Moreover, recent advances in clinical imaging techniques, such as intracoronary ultrasonography, have revealed a much higher incidence of atheroma rupture than of symptomatic atherothrombotic coronary artery diseases, including myocardial infarction and unstable angina pectoris.3,4 These observations suggest the contribution of propagating factors for thrombus growth, besides exposure of the subendothelial matrix due to endothelial disruption, in the onset of symptomatic arterial thrombotic diseases.