Pathophysiology of arterial thrombosis.

Abstract

It is today an established fact that myocardial infarction in most cases is due to the obstruction by thrombi of the coronary vessels (5, 15, 2 as well as 3 for further references). Thus Bulkley and Hutchins (5) find, in 88% of all post-mortem examinations, in patients with aterosclerotic coronary artery disease, evidence for the existence of thrombi. Thus, arterial thrombosis is a major contributing factor to myocardial infarction and its pathophysiology therefore deserves every attention. Arterial thrombi as a rule start from a vascular lesion, most often from ruptured atheromas and have been shown to progress from a primary deposite of blood platelets. Thus, arterial thrombosis in many respects appears as the pathological deviation from a physiological process, i.e. the formation of a hemostatic plug. It appears appropriate to deal first with the mechanisms which are involved in the production of a platelet aggregate, which by its self, or by virtue of its procoagulant properties and subsequent fibrin formation, is capable of occluding a blood vessel.