SummaryThe native fibrin gel structure formed in vitro from plasma samples was examined by liquid permeation of hydrated fibrin gel networks in 38 unselected men who had suffered a myocardial infarction before the age of 45 years and in 88 age-matched population-based control men. Both the fibrin gel porosity (permeability coefficient, Ks) and the calculated fiber mass-length ratio varied considerably within the two groups, but were generally lower in the patients. Ks was 8.3 ± 5.2 cm2 × 109 (mean ± SD) in the patient group and 12.5 ± 5.7cm2 × 109 among controls (p <0.001). The corresponding figures for fiber mass-length ratio were 13.1 ± 7.7 and 16.5 ± 7.5 Dalton/ cm × 10−13, respectively (p <0.01). Around 50% of the patients had Ks values below the 10th percentile of the control group. A strong inverse correlation was seen between plasma plasminogen activator inhibitor-1 (PAI-1) activity and Ks (r = -0.603, p <0.001) or fiber mass-length ratio (r = -0.565, p <0.001) in the patient group. Corresponding weaker associations of PAI-1 with fibrin gel properties were also present in the control group. In addition, inverse relationships of very low density lipoprotein (VLDL) triglyceride concentrations to Ks (r = -0.362, p <0.001) and fiber mass-length ratio (r = -0.283, p <0.01) were found among the controls. Proneness to formation of tight and rigid fibrin gel networks with abnormal architecture in vitro is in vivo associated with myocardial infarction at a young age. Impaired fibrinolytic function secondary to a raised plasma PAI-1 activity level is associated with abnormal fibrin gel structure.
SummaryThe native fibrin gel structure formed in vitro from plasma samples was examined by liquid permeation of the hydrated fibrin gel networks in 18 men who had suffered a myocardial infarction before the age of 45 years and in 20 control subjects. Patients with an elevated plasma fibrinogen concentration had a considerably lower fibrin gel porosity (permeability coefficient, K
s) compared with patients with a normal plasma fibrinogen level and with controls. The calculated fiber mass-length ratio of the fibrin gel networks was decreased in both patient groups. Gel porosity differed markedly between individuals at a given plasma fibrinogen concentration. Fairly strong inverse correlations were found between plasma orosomucoid level on the one hand and K
s (r = –0.617, p <0.01) or fiber mass-length ratio (r = –0.499, p <0.05) on the other. The low density lipoprotein (LDL) cholesterol concentration also correlated inversely with K
s (r = –0.471, p <0.05) and fiber mass-length ratio (r = –.522, p <0.05). Significant inverse relations, which were independent of plasma fibrinogen and lipoprotein concentrations, were detected between K
s (r = –.519, p <0.05) and calculated fiber mass-length ratio (r = –.723, p <0.001) and number and severity of coronary artery stenoses determined by angiography. A proneness to formation of tight, rigid and space-filling fibrin network structures with small pores thus appears to be associated with premature coronary artery disease.
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