Increased Ristocetin-Cofactor in Acute Myocardial Infarction: a Component of the Acute Phase Reaction

Abstract

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.

Fibrin D-Dimer, Haemostatic Factors and Peripheral Arterial Disease

“…We found that, in men, von Willebrand factor was related to the ABPI. Likewise, several case-control studies of peripheral arterial disease have reported higher levels in the cases (8,16,17). The ARIC study (18) reported associations between increased baseline von Wille brand factor and prevalent cases of stroke, coronary heart disease and peripheral arterial disease.…”

Von Willebrand Factor, Plasminogen Activator Inhibitor-1 and C-Reactive Protein Are Markers of Thrombolytic Efficacy in Acute Myocardial Infarction

“…The circulating levels of von Willebrand factor, plasminogen activator inhibitor-1 and C-reactive protein increase during the acute-phase that follows myocardial infarction (20)(21)(22)(23)(24). The induction of these factors is probably triggered by soluble inflammatory mediators, such as interleukin-1 and tumour ne crosis factor (25)(26)(27)(28).…”

Thirty years in hemostasis research in Cluj Napoca

“…According to clinical observation and laboratory data it was considered that the increase of plasmatic level of von Willebrand factor in patients with myocardial infarction is more likely a consequence of the reaction of endothelial cells to adrenergic and proinflammatory stimuli, rather than a simple leakage of vWF from injured endothelia (8). This interpretation is accepted and cited by many authors such as Schorer et al (9), Pottinger et al (10) It is worth mentioning that some genetic hemostasis defects were detected by the research group in Cluj Napoca.…”