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

L. Badimon*, G. Vilahur, S. Sanchez and X. Duran

Cardiovascular Research Center, Instituto de Investigaciones Biomédicas de Barcelona and Consejo Superior de Investigaciones Científicas, Hospital Santa Creu i San Pau-Universidad Autómoma de Barcelona, 08034 Barcelona, Spain

* Correspondence: Professor Lina Badimon, Centro de Investigación y Desarrollo-CSIC, Jordi Girona, 18-26, 08034 Barcelona, Spain.

Abstract

Angiographic and ultrasound analyses of the coronary arteries have confirmed the importance of acute thrombosis as the primary cause of myocardial infarction and acute coronary syndromes. Intravenous treatments aimed at recanalizing the obstructed arteries can help achieve acute reperfusion of the organ, 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 after the event. The presence of a residual mural thrombus overlying an active plaque predisposes to recurrent thrombosic vessel occlusion. A fragmented thrombus appears to be one of the most powerful thrombogenic substrates, and residual thrombus may predispose to recurrent thrombosis. Non-acute, chronic antithrombotic treatments and pharmacological interventions should aim to block thrombosis and preserve vascular prostacyclin formation. Experimental work has shown 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 to uncover the mechanism of action of triflusal at the vascular level is in progress.

Key Words: Atherogenesis • lipids • platelets • thrombosis • triflusal


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