Platelet/vessel wall interactions, rheologic factors and thrombogenic substrate in acute coronary syndromes: preventive strategies.
Thrombosis is an important pathogenetic factor in acute coronary syndromes, including unstable angina, myocardial infarction and sudden death. In all of these conditions, atherosclerotic plaque fissuring is a key inciting event. Minor injury to the vessel wall brings into play interactions between platelets and the wall. Platelet adhesion and aggregation ensue, modulated by a number of factors and substances. More severe injury to the vessel wall exposes the blood to other thrombogenic substances. Platelet deposition is also affected by rheologic (blood flow) factors at the site of injury, depending on the degree of stenosis and the resulting shear rates. The mechanism of unstable angina appears to be related to these factors in the following sequence: mild stenosis and minor injury with plaque fissuring, platelet responses, labile thrombosis, intermittent ischemia and pain at rest. Vasoconstriction may contribute to the symptoms. Although developing from the same origin, infarction may stem from a greater degree of vessel wall damage resulting in more permanent thrombus. Such considerations provide a focus for preventive strategies, including the optimal use of current inhibitors of platelet adhesion and aggregation and the application of peptide receptor blockers and monoclonal antibodies. Also important is control of rheologic factors by preventing stenosis or correcting it with angioplasty and thrombolytic therapy. Further elucidation of the critical role of thrombosis in coronary syndromes will facilitate progress toward the ultimate goal of primary prevention.
Adams
P C
PC
Mount Sinai School of Medicine, City University of New York, New York 10029.
Fuster
V
V
Badimon
L
L
Badimon
J J
JJ
Chesebro
J H
JH
D001783:Blood Flow Velocity; D001792:Blood Platelets / Q000502:physiology*; D003327:Coronary Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D006801:Humans; D012212:Rheology; D013927:Thrombosis / Q000503:physiopathology*