Thrombosis/platelets and other blood factors in acute coronary syndromes.
We support the concept of a common anatomic and physiologic link between the acute coronary syndromes, which consists of plaque fissuring or rupture, leading to exposure of the circulating blood to collagen, lipids, and smooth muscle cells. This, in turn, results in marked platelet activation and the initiation of the coagulation sequence, both of which lead to thrombus formation. What determines the clinical outcome in these patients is the suddenness of coronary occlusion, the completeness of blood flow deprivation, and most importantly, its duration. In unstable angina, either plaque disruption resulting in an abrupt change in its morphologic configuration with reduction of coronary blood flow or increased myocardial oxygen demand are associated with increased exertional symptoms. In rest angina, two events may take place: formation of a transient and labile thrombus due to platelet and clotting activation, or vasospasm associated with the release of platelet-derived vasoconstrictive substances or loss of endothelial relaxing properties. As a result, transient myocardial ischemia occurs, which may be intermittent and recurrent and may progress to myocardial infarction or sudden death. In myocardial infarction, plaque rupture is usually more severe, leading to the formation of an occlusive or near-occlusive thrombus which may be more persistent and fixed to the arterial wall. The duration of coronary blood flow deprivation needs to be sufficiently long in order to produce myocardial cell death. Moreover, the difference between Q-wave and non-Q-wave infarction is probably determined by the duration of blood flow obstruction, being longer in the former. The presence of a functionally adequate collateral circulation will, in part, determine the survival of the area of myocardium at jeopardy. The coronary events that take place in ischemic sudden death are probably similar to those in unstable angina, namely plaque rupture with thrombus formation. In sudden death, the resulting myocardial ischemia may precipitate fatal ventricular arrhythmias. Alternatively, platelet microemboli from ulcerated arterial plaques may produce multiple areas of myocardial necrosis which can result in electrical instability and ventricular fibrillation.
Stein
B
B
Badimon
L
L
Israel
D H
DH
Badimon
J J
JJ
Fuster
V
V
D000787:Angina Pectoris / Q000209:etiology; D003327:Coronary Disease / Q000503:physiopathology*; D003328:Coronary Thrombosis / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D003645:Death, Sudden / Q000209:etiology; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology