Von-Willebrand-Factor And Coronary-Artery Disease

The value of studying factors of haemostasis and thrombosis in patients with coronary artery disease is established. The endothelial lesion and evolution of the thrombus play key roles in acute coronary syndromes and coronary angioplasty.The von Willebrand factor (VWF) is known for its participation in primary haemostasis. Deficits of this factor lead to a haemorrhagic syndrome, von Willebrand's disease. This glycoprotein is mainly synthesised by the endothelial cells. Its polymeric composition allows identification of two types of multimeres. The high molecular weight, active multimeres are liberated from the endothelium after stimulation by thrombin. Low molecular weight multimeres are less active and are secreted continuously. The VWF promotes platelet adhesion and facilitates platelet aggregation Experimental pig models with VWF deficiency show that this factor is essential for the constitution of an occlusive thrombus. Several physiopathological mechanisms interact to increase VWF concentrations during thrombosis : the endothelial lesion, adrenergic stimulation, acute phase reaction.Increased VWF concentrations have been reported in many clinical situations. The results are most demonstrative in coronary artery disease. The VWF is abnormally high from the time of hospital admission in patients with acute myocardial infarction and continues to increase up to the 5th day before falling, without returning to normal values, at the 15th day. It is a sensitive though not specific late diagnostic marker of myocardial infarc tion. Increased VWF concentrations are not proportional to the severity of coronary atherosclerosis. They are, however, related to the infarct size, to the inflammatory reaction and to the prothrombotic phase. The persistence of increased VWF three months after the primary infarct is a risk factor for death or reinfarction. The variations of VWF concentrations are not significant during successful myocardial revascularisation by thrombolysis. On the other hand, the VWF concentration continues to rise significantly after failed thrombolysis and direct or complementary angioplasty. During thrombolysis, the risk of haemorrhage is related to the increase in plasma concentrations of new fragments cleaved off the VWF.In uncomplicated successful coronary angioplasty, the risk in VWF concentration is no greater than that observed during diagnostic coronary angiography. Acute complications of angioplasty are related to the presence of very high VWF concentrations before the procedure.