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

Kamaran Fatah; Angela Silveira; Per Tornvall; Fredrik Karpe; Margareta Blombäck; Anders Hamsten

doi:10.1055/s-0038-1650618

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1996; 76(04): 535-540
DOI: 10.1055/s-0038-1650618

Original Article

Schattauer GmbH Stuttgart

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

Kamaran Fatah

¹The Department of Laboratory Medicine/Coagulation Research, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

,

Angela Silveira

⁴The Atherosclerosis Research Unit, King Gustaf V Research Institute, Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

,

Per Tornvall

²The Division of Cardiology, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

⁴The Atherosclerosis Research Unit, King Gustaf V Research Institute, Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

,

Fredrik Karpe

³The Division of Internal Medicine, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

⁴The Atherosclerosis Research Unit, King Gustaf V Research Institute, Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

,

Margareta Blombäck

¹The Department of Laboratory Medicine/Coagulation Research, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

,

Anders Hamsten

³The Division of Internal Medicine, King Gustaf V Research Institute, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

⁴The Atherosclerosis Research Unit, King Gustaf V Research Institute, Department of Medicine, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden

› Institutsangaben

Abstract

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Summary

The 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.

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Referenzen

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