Decreased prostaglandin-I2 stability in acute myocardial infarction.
It has been demonstrated that under certain conditions the in-vitro half-life of biologically active PGI2 in plasma is extremely shortened, which may result in-vivo in a local haemostatic imbalance. In 36 patients suffering from acute myocardial infarction a sequential change in in-vitro half-life of synthetic PGI2 was therefore studied during 3 weeks. 21 patients admitted turning out not to develop myocardial infarction served as follow-up controls. During and shortly after the acute episode the plasmatic half-life of PGI2 in-vitro was shortened by about 40%, improving continuously thereafter. No certain influence of either risk factors, sex or age could be discovered. A possible influence of various drugs administered in the hospital period has been excluded in 43 patients with proven coronary artery disease. No such changes occurred during acute angina pectoris attack in 12 patients. It remains to be established, whether the short-lasting destabilisation of PGI2 may be an acute disease-associated finding, or an important pathogenetic factor.
Sinzinger
H
H
Atherosclerosis Research Group (ATK) Austrian Academy of Sciences, Vienna.
Fitscha
P
P
Tiso
B
B
D000368:Aged; D000787:Angina Pectoris / Q000097:blood; D003327:Coronary Disease / Q000097:blood; D011464:Epoprostenol / Q000097:blood*; D005260:Female; D006207:Half-Life; D006801:Humans; D006951:Hyperlipoproteinemias / Q000097:blood; D006973:Hypertension / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood*; D012307:Risk Factors; D012907:Smoking / Q000097:blood
D011464:Epoprostenol