Atheromatous plaque formation and thrombogenesis: formation, risk factors and therapeutic approaches

Angiographic and ultrasound analyses of the coronary arteries have confirme d the importance of acute thrombosis as the primary cause of myocardial inf arction and acute coronary syndromes. Intravenous treatments aimed at recan alizing the obstructed arteries can help achieve acute reperfusion of the o rgan, but often a thrombus-triggering plaque remains active for some time. It is not yet known how long a plaque remains active, but it has been shown that systemic markers of coagulation remain elevated as long as 6 months a fter the event. The presence of a residual mural thrombus overlying an acti ve plaque predisposes to recurrent thrombotic vessel occlusion. A fragmente d thrombus appears to be one of the most powerful thrombogenic substrates, and residual thrombus may predispose to recurrent thrombosis. Non-acute, ch ronic antithrombotic treatments and pharmacological interventions should ai m to block thrombosis and preserve vascular prostacyclin formation. Experim ental work has shogun that both aspirin and triflusal inhibit the growth of a thrombus on a fresh mural thrombus to the same extent, but triflusal was found to preserve cyclooxygenase-2 activity in the vessel wall. Research t o uncover the mechanism of action of triflusal at the vascular level is in progress. (C) 2001 The European Society of Cardiology.