[Myocardial infarct: an acute dysmetabolic disease].
It is hypothesised, on the basis of experimental observations on post-heparin plasma samples collected under post-prandial conditions, that variations in the activity of endothelial lipoproteinlipasic systems may be correlated to reductions in blood flow at coronary capillary level. More specifically, it is shown that a change in these enzymatic systems could determine "functional kidnapping" of heparin or other substances (glicosaminoglycans) engaged in the activation of Antithrombin III, with noteworthy haemorrheological consequences mediated by a variety of mechanisms. Relations between such haemorheological and metabolic changes further to activation of lipoprotein lipase are discussed and stress is laid on the importance both might have in the pathogenesis of myocardial infarction.
D000328:Adult; D000990:Antithrombin III / Q000037:antagonists & inhibitors; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D006025:Glycosaminoglycans / Q000378:metabolism; D006493:Heparin / Q000008:administration & dosage / Q000378:metabolism*; D006801:Humans; D007275:Injections, Intravenous; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000378:metabolism*
D006025:Glycosaminoglycans; C020341:glucosaminoglycans; D000990:Antithrombin III; D005340:Fibrinogen; D006493:Heparin; D008071:Lipoprotein Lipase
L'infarto del miocardio: malattia dismetabolica acuta.