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Increased ristocetin-cofactor in acute myocardial infarction: a component of the acute phase reaction
When compared to the values obtained in healthy normal-weight, normolipemic controls, the plasma level of ristocetin-cofactor (VIII:R-cof.) was found to be much higher in patients with acute myocardial infarction and in postoperative conditions (4--5 days after a major surgical intervention). A lesser increase of VIII:R-cof. was noted in atherosclerotic patients without acute occlusive accidents and no significant changes of this plasma factor could be observed in hyperlipemic subjects without obvious clinical atherosclerosis. Serial studies emphasized a tendency towards normalization of plasma VIII:R-cof. as the acute phenomena of a myocardial infarction subsided. The above mentioned data suggest that the high levels of VIII:R-cof. recorded in myocardial infarction are mainly caused by a systemic acute phase reaction and to a lesser extent by endothelial damage. Delayed clearance of VIII:R-cof. subsequent to a hepatic dysfunction or to a modified pattern of protein metabolism during the above mentioned acute phase reaction might also contribute to the high level of this plasma factor.
When compared to the values obtained in healthy normal-weight, normolipemic controls, the plasma level of ristocetin-cofactor (VIII:R-cof.) was found to be much higher in patients with acute myocardial infarction and in postoperative conditions (4--5 days after a major surgical intervention). A lesser increase of VIII:R-cof. was noted in atherosclerotic patients without acute occlusive accidents and no significant changes of this plasma factor could be observed in hyperlipemic subjects without obvious clinical atherosclerosis. Serial studies emphasized a tendency towards normalization of plasma VIII:R-cof. as the acute phenomena of a myocardial infarction subsided. The above mentioned data suggest that the high levels of VIII:R-cof. recorded in myocardial infarction are mainly caused by a systemic acute phase reaction and to a lesser extent by endothelial damage. Delayed clearance of VIII:R-cof. subsequent to a hepatic dysfunction or to a modified pattern of protein metabolism during the above mentioned acute phase reaction might also contribute to the high level of this plasma factor.