Abstract
Acute myocardial infarction (AMI) can no longer be considered as a single event, but as a series of episodes. In most of the cases, the initial event may be the induction of a severe spasm of the coronary artery by vasoconstrictive substance released from aggregated platelets. These spasms are followed by dilatation, which is caused by substances set free from the ischemic tissue. Dilatation then results in a washing-out of vasoactive mediators (as well as myoglobin) and platelets, which is reflected as a peak in the blood myoglobin concentration-time curve. The local depletion of vasodilative metabolites allows a further contraction of the coronary vessel. A new accumulation of platelets then stimulates another spasm. This vicious circle (thrombo-ischemic re-entry-mechanism) is repeated several times and can be interrupted by the systemic administration of thrombolytic drugs (streptokinase).