It has been shown by a number of authors that early myocardial infarct
ion constitutes a dynamic process of cyclic oscillation between corona
ry occlusion and spontaneous coronary reopening. Infarct-markers, such
as ST-segment elevation, serum-creatine kinase isoenzyme MB, the atri
onatriuretic peptide (ANP) and serum-myoglobin (Mb) exhibit cyclic beh
aviour pattern during early AMI and thus reflect episodes of intermitt
ent, spontaneous reperfusion. The latter have recently been verified b
y angiography. The mechanism underlying the phenomena seen in early my
ocardial infarction is likely to be based on a constant vasoconstricti
ve stimulus, deriving from aggregating platelets. The vasoconstriction
subsequent to platelet aggregation produces an initial episode of myo
cardial ischemia. This episode is followed by a hypoxia of the artery
wall. Reactive coronary dilation secondary to ischemia is than promote
d by the release of vasoactive by-products of anaerobic glycolysis as
well as changes in the open propability of certain transmembrane ion c
hannels. Thereafter, the initial coronary occlusion is interrupted by
transient vasodilation. A wave of reperfusion follows and leads to reo
xygenation and wash-out of ischemia-induced vasodilative components as
well as biochemical markers. The vasoconstrictive forces then take ov
er again. This results in repeated waves of reperfusion. A number of a
rguments in favour of this concepts are discussed in this paper.