Cyclic phenomena in early myocardial infarction.
It has been shown by a number of authors that early myocardial infarction constitutes a dynamic process of cyclic oscillation between coronary occlusion and spontaneous coronary reopening. Infarct-markers, such as ST-segment elevation, serum-creatine kinase isoenzyme MB, the atrionatriuretic peptide (ANP) and serum-myoglobin (Mb) exhibit cyclic behaviour pattern during early AMI and thus reflect episodes of intermittent, spontaneous reperfusion. The latter have recently been verified by angiography. The mechanism underlying the phenomena seen in early myocardial infarction is likely to be based on a constant vasoconstrictive stimulus, deriving from aggregating platelets. The vasoconstriction subsequent to platelet aggregation produces an initial episode of myocardial ischemia. This episode is followed by a hypoxia of the artery wall. Reactive coronary dilation secondary to ischemia is than promoted by the release of vasoactive by-products of anaerobic glycolysis as well as changes in the open propability of certain transmembrane ion channels. Thereafter, the initial coronary occlusion is interrupted by transient vasodilation. A wave of reperfusion follows and leads to reoxygenation and wash-out of ischemia-induced vasodilative components as well as biochemical markers. The vasoconstrictive forces then take over again. This results in repeated waves of reperfusion. A number of arguments in favour of this concepts are discussed in this paper.
Gasser
R
R
Department of Medicine, University of Graz, Austria.
Schafhalter-Zoppoth
I
I
Schwarz
T
T
Eber
B
B
Köppel
H
H
Lechleitner
P
P
Puschendorf
B
B
Dienstl
F
F
Klein
W
W
D009320:Atrial Natriuretic Factor / Q000502:physiology; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D006801:Humans; D009203:Myocardial Infarction / Q000503:physiopathology*; D015539:Platelet Activation / Q000502:physiology*; D014661:Vasoconstriction / Q000502:physiology*
D009320:Atrial Natriuretic Factor