Pathophysiology of coronary occlusion in acute infarction.
Coronary angiography has proved beyond doubt that complete coronary occlusion is the rule in the very early hours of infarction. The 60% to 80% rate of coronary recanalization after thrombolytic therapy has proved that thrombosis is a major component of the occlusion at the time when the procedure is performed a few hours after the onset of symptoms. However, the trigger for coronary thrombosis and the causes of failure of thrombolytic therapy are still a matter of speculation. The relatively rare occurrence of acute coronary occlusion in the life of an individual with even severe coronary disease can be explained on the basis of the necessity of either extremely powerful isolated stimuli, which only occurs rarely, or the casual simultaneous presence in one coronary arterial segment of multiple unfavorable events, such as plaque fissuring, enhanced reactivity of coronary smooth muscle to constrictor stimuli and displacement of the thrombotic-thrombolytic equilibrium toward thrombosis. Coronary artery constriction possibly caused by vasoconstrictor substances released by thrombus, represents the potential element of a vicious cycle causing persistent coronary occlusion and reocclusion when reflow occurs with thrombolysis.
D000925:Anticoagulants / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D001792:Blood Platelets / Q000502:physiology; D003329:Coronary Vasospasm / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D003645:Death, Sudden / Q000209:etiology; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000517:prevention & control
D000925:Anticoagulants; D001241:Aspirin