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SummaryWhen 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.

SummaryWhen compared to normal weight normolipidemic control subjects, dilute blood clot lysis time was found to be obviously (p <0.001) prolonged in hypertriglyceridemic patients without proteinuria and slightly (p <0.05) accelerated in hyperlipidemic nephrotic patients in spite of their very high levels of plasma fibrinogen. As a result the ratio plasma fibrinogen (mg/dl) per clot lysis time (minutes) was 1.241 ± 0.08 (X ± SEM) in control subjects, 0.574 ± 0.07 in hypertriglyceridemic patients and 2.69 ± 0.172 in nephrotic patients. This finding suggesting that a larger amount of fibrin is rather readily dispersed from dilute blood clots of nephrotic patients was associated with higher levels of plasma t-PA: Ag (9.45 ng/ml ± 1.18 in nephrotic patients versus 5.8 ng/ml ± 1.23 in controls before venous occlusion and respectively 33.1 ng/ml ± 3.83 versus 20.3 ± 3.40 in controls after venous occlusion). Plasminogen activator activity of the euglobulins as assessed by the bovine fibrin-agarose plate was significantly higher in nephrotic patients only after venous occlusion. Plasma samples of nephrotic patients exerted a more potent inhibition of fibrinolysis in a urokinase activated system. This effect was, however, mainly due to the high levels of α2 macroglobulin in nephrotic plasma which apparently have little influence on dilute blood clot lysis time.