Introduction

Arterial thrombus formation seems to be an important factor in the conversion of chronic to acute atherosclerotic coronary events after plaque rupture, in the progression of coronary disease and in the acute phase of revascularization interventions. The presence of intraluminal thrombi, both in unstable angina and in acute myocardial infarction, has been documented in pathological, angiographic, angioscopic and intravascular ultrasound studies. In contrast with the very high incidence of thrombi in acute myocardial infarction, its incidence in unstable angina varies significantly among different studies, related, in part, to the interval between the onset of symptoms and the angiographic study. Presumably, the thrombus is occlusive at the time of anginal pain and later may become subocclusive and slowly lysed or digested. Local and systemic thrombogenic risk factors at the time of coronary plaque disruption may influence the type of thrombus and, hence, the different pathological and clinical syndromes [1].

Thrombosis: platelets and coagulation

In severe injury, with exposure of components of the plaque, as in spontaneous plaque rupture or in angioplasty, marked platelet aggregation with mural thrombus formation follows. Vascular injury of this magnitude stimulates thrombin formation through both the intrinsic (surface-activated) and extrinsic (tissue factor-dependent) coagulation pathways, in which the platelet membrane facilitates interactions between clotting factors. This concept of vascular injury as a trigger of the platelet coagulation response is important in understanding the pathogenesis of the various vascular diseases associated with atherosclerosis and coronary artery disease.