[From the physiopathology of thrombosis to therapeutic targets]

Structural changes in blood vessels associated with atherosclerosis are at the onset of arterial thrombosis. Thrombi form at the sites of plaque rupture. Plateletrich masses accumulate in the vessel lumen perturb blood flow, thereby aggravating ischemic syndromes. Other local modifications include the recruitment of cells with inflammatory and immunologic potential, showing how complicated this process is. The demonstration that aspirin lowered the number of thrombotic events was an important step in proving the value of anti-platelet therapy. Since then, newer strategies involving drugs acting on the fibrinogen receptor (the GPIIb-IIIa complex) or on ADP receptors have evolved largely as a result of the increased knowledge of the biological pathways of platelet aggregation. These drugs have given superior results in many international trials and their usefulness in interventional cardiology has been proven. Such encouraging progress also incites efforts to find new and improved targets for anti-platelet therapy as well as testing new associations of existing anti-platelet drugs which may also be used with anticoagulant therapies, and in the future, be combined with drugs directly preventing restenosis.