Thrombogenesis and inhibition of platelet aggregation. Experimental aspects and future approaches.
The pathophysiology of the acute coronary syndromes and of the progression of chronic coronary artery disease is complex, but in most cases it appears to be based on fixed atherosclerotic coronary disease with plaque rupture and superimposed thrombosis commonly followed by its organization by connective tissue. Furthermore, spontaneous or therapeutic reperfusion may be followed by re-thrombosis, as it may occur in reocclusion post-thrombolysis, which is another pathologic event of significant clinical importance. The mechanisms of thrombus formation in atherosclerosis are not fully understood, but clearly involve local blood flow conditions, in addition to vascular and blood-borne factors that regulate cell-substrate and cell-cell interactions. The evolving understanding of the mechanisms of local flow and of cell-wall and cell-cell interaction is helping in the development of future approaches for the prevention and management of thrombotic events.
Badimon
L
L
Division of Cardiology, Mount Sinai School of Medicine, New York.
Badimon
J J
JJ
Fuster
V
V
D000818:Animals; D003324:Coronary Artery Disease / Q000097:blood* / Q000188:drug therapy; D003328:Coronary Thrombosis / Q000097:blood* / Q000188:drug therapy; D006801:Humans; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*
D010975:Platelet Aggregation Inhibitors