Proneness to Formation of Tight and Rigid Fibrin Gel Structures in Men with Myocardial Infarction at a Young Age

Abstract

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.