The physiopathology of atherothrombosis is complex. The development and progression of this vascular disease involves the interactive processes of atherosclerotic lesions and the formation of thrombi. In and of itself, atherosclerosis is not deadly; the actual risk lies in the vulnerability of the arteriolosclerotic plaque to breakage. An ulceration, which is the rupture or breakage of the covered plaque, constitutes a complication that favors thrombosis. During these processes platelets are relevant factors, acting with the endothelial and inflammatory cells even at the premature stages of atherogenesis. The interaction of platelets with the endothelial cells (ECs) can occur in two ways: activated platelets joining intact ECs, or resting platelets joining activated ECs. Platelet molecules such as GPIIb-IIIa, CD40, CD40L and P-selectin, as well as microparticle platelets, are important in this process. In this review, the most important mechanisms by which platelets participate in the genesis of atherosclerotic lesions are described.

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