Fibrin Gel Network Characteristics and Coronary Heart Disease: Relations to Plasma Fibrinogen Concentration, Acute Phase Protein, Serum Lipoproteins and Coronary Atherosclerosis

Fatah, K.; Hamsten, Anders; Blombäck, Birger; Blombäck, Margareta

doi:10.1055/s-0038-1656337

Cited by 169 publications

(123 citation statements)

References 38 publications

(47 reference statements)

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“…In the present study, the most powerful determinants of fibrin gel permeability (Ks) were changes in levels of P-fibrinogen and cholesterol. These findings are in line with studies by Fatah et al [11,25], showing associations between fibrin gel porosity and fibrinogen and lipoproteins, respectively, in patients with myocardial infarction at a young age. However, in one of those studies the strongest determinant of fibrin gel structure was found to be the acute-phase reactant orosomucoid [11], and an association was demonstrated between proneness to form a tight and rigid fibrin network and premature coronary artery disease [11].…”

Section: Discussionsupporting

confidence: 93%

“…These findings are in line with studies by Fatah et al [11,25], showing associations between fibrin gel porosity and fibrinogen and lipoproteins, respectively, in patients with myocardial infarction at a young age. However, in one of those studies the strongest determinant of fibrin gel structure was found to be the acute-phase reactant orosomucoid [11], and an association was demonstrated between proneness to form a tight and rigid fibrin network and premature coronary artery disease [11]. In a later study [25], also consisting of non-diabetic patients with coronary artery disease, the abnormalities of fibrin gel structure were related to an impaired fibrinolytic function secondary to a raised level of plasma plasminogen activator inhibitor 1 (PAI-1).…”

Section: Discussionsupporting

confidence: 93%

“…myocardial infarction, further indicated by a tight and rigid fibrin gel structure prior to CSII. Despite a markedly improved metabolic control during CSII, the levels of hs-CRP, S-AA and E-selectin, which also is an endothelial marker, were not significantly reduced, and in contrast to the study by Fatah et al [11], no relationships were found between the inflammatory markers and the fibrin gel characteristics. Neither were there any significant correlations between the levels of plasma fibrinogen and S-AA or hs-CRP, suggesting that plasma fibrinogen is influenced by other factors in addition to inflammation [27,28].…”

Section: Discussioncontrasting

confidence: 88%

“…Abnormal architectures of the fibrin network have been described in different diseases, e.g. in diabetes mellitus [10], myocardial infarction [11], nephrotic syndrome [12]. In those studies, the permeability coefficient (Ks) and fiber mass-length ratio (m) were decreased.…”

Section: Introductionmentioning

confidence: 99%

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Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion

Jörneskog

et al. 2003

Journal of Thrombosis and Haemostasis

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Summary. Background: Patients with Type 1 diabetes have a tighter plasma fibrin gel structure, to which impaired glycemic control might contribute. Improved glycemic control can be achieved with continuous subcutaneous insulin infusion (CSII). Objectives: The aim of the present study was to investigate the effect of CSII on plasma fibrin gel properties and circulating markers of inflammatory activity in patients with Type 1 diabetes. Patients and methods: Twenty-eight patients were investigated before and after 4-6 months' treatment with CSII. Fibrin gel structure formed in vitro from plasma samples was investigated by liquid permeation of hydrated fibrin gel networks. Pfibrinogen was analyzed by a syneresis method. Comparisons were made between patients with improved (> 0.5%) and unchanged (< 0.5%) glucosylated hemoglobin (HbA1c) during CSII. Results: Eighteen patients showed improved and 10 patients unchanged HbA 1c during CSII. P-fibrinogen, high sensitive C-reactive protein and serum amyloid A-antigen were not significantly changed, while fibrin gel permeability (Ks) and fiber mass-length ratio (m) increased in both groups (P < 0.02). P-insulin and triglycerides decreased (P < 0.05) in both groups, while reductions of total cholesterol and intercellular adhesion molecule-1 were seen only in patients with improved HbA 1c (P < 0.05). Absolute changes in Ks were inversely correlated to changes in plasma fibrinogen (r ¼ 0.50; P < 0.01) and in LDLcholesterol (r ¼ 0.46; P < 0.05). Conclusions: Treatment with CSII in patients with Type 1 diabetes is associated with increased plasma fibrin gel porosity. Slight attenuation of the inflammatory activity was also observed. The changes in fibrin gel porosity seem to be mainly mediated by changes in plasma fibrinogen and blood lipids, and are probably secondary to improved insulin sensitivity.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Discussioncontrasting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion

Jörneskog

et al. 2003

Journal of Thrombosis and Haemostasis

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“…19,20 After MI, fibrin clots have reduced permeability and a lower fiber mass-to-length ratio. 13,21 There are independent associations between permeability and the extent and severity of coronary artery stenosis and also of fibrinolytic activity. Patients with severe coronary artery disease have more rigid clot structures and an elevated fiber mass-to-length ratio.…”

Section: Abnormal Clot Architecture and Atherothrombotic Vascular Dismentioning

confidence: 99%

Genetic and Environmental Determinants of Fibrin Structure and Function

Scott

Ariëns

Grant

2004

ATVB

138

129

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Abstract-The formation of a fibrin clot is one of the key events in atherothrombotic vascular disease. The structure of the fibrin clot and the genetic and environmental factors that modify it have effects on its biological function. Alterations in fibrin structure and function have implications for the clinical presentation of vascular disease. This review briefly describes the key features involved in the formation of a fibrin clot, its typical structure, and function. This is followed by a review of the current literature on genetic and environmental influences on fibrin structure/function and the relationship to clinical disease. Key Words: fibrin Ⅲ hemostatis Ⅲ genetic Ⅲ environment Ⅲ atherothrombosis D iseases associated with the development of thrombosis are a major cause of morbidity and mortality in the developed world. Atherothrombotic vascular disorders develop over many decades and involve the interaction of classic atherogenic risk factors such as diabetes, hyperlipidemia, and hypertension with abnormalities of the inflammatory and hemostatic systems. Arterial disease develops in a high-pressure, high-flow system, with lipid deposition and smooth muscle hyperplasia occurring to form an atherosclerotic plaque. 1 Subsequently, the plaque becomes unstable and ruptures exposing a prothrombotic lipid core activating the clotting cascade and leading to the development of a platelet-rich fibrin blood clot and arterial thrombotic occlusion. The extent of this process determines clinical outcome, ranging from no clinically noticeable event to acute coronary artery syndromes including myocardial infarction (MI), cerebrovascular and peripheral vascular disease, or sudden death. The Formation of a Fibrin ClotFibrin is the major protein constituent of the blood clot and is formed from fibrinogen, a glycoprotein that circulates largely inactively, in the blood stream. Fibrinogen consists of 6 polypeptide chains (A␣, B␤, ␥) 2 held together by disulphide bonds in a molecule with bilateral symmetry (Figure 1). The molecule consists of 3 main structural regions, 2,3 including a central region (E), which contains fibrinopeptides A and B and the amino acid termini of all 6 polypeptide chains, 2 distal regions (D) connected to the E region by 2 ␣-helical coiled segments and the D regions containing the carboxyl termini of the B␤ and ␥ chains, and those of the A␣ chain, which extend to form relatively flexible ␣C-domains, each ending in a globular domain. 2,3 In situations of tissue injury and inflammation, thrombin is generated after cleavage of prothrombin by the Xase complex. Thrombin subsequently binds to fibrinogen and cleaves the amino termini of the fibrinogen A␣ and B␤ chains at region E. This results in the release of fibrinopeptides A and B from fibrinogen, producing fibrin and initiating fibrin clot formation. Release of fibrinopeptide A by thrombin is fast and exposes a polymerization site on the E region of fibrin. 4,5 This combines with a complementary binding site on the ␥ chain in the D region of an adjac...

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Racial and genetic determinants of plasma factor XIII activity

et al. 2000

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Factor XIII (F XIII), a plasma transglutaminase, is essential for normal hemostasis and fibrinolysis. Plasma F XIII consists of two catalytic A (F XIIIA) and two non‐catalytic B (F XIIIB) subunits. Activated F XIII is involved in the formation of fibrin gel by covalently crosslinking fibrin monomers. As the characteristics of the fibrin gel structure have been shown to be associated with the risk of coronary heart disease (CHD), F XIII activity may play a seminal role in its etiology. In this investigation, we determined plasma F XIII activity in two racial groups, including Asian Indians (n = 258) and Chinese (n = 385). Adjusted plasma F XIII activity was significantly higher in Indian men (142 vs. 110%; P < 0.0001) and women (158 vs. 111%; P < 0.0001) than their Chinese counterparts. As compared to Indians where the distribution of F XIII activity was almost normal, in Chinese it was skewed towards low activity. In both racial groups, bivariate and multivariate analyses showed strong correlation of F XIII activity with plasma fibrinogen and plasminogen levels. Race explained about 25% of the variation in F XIII activity even after the adjustment of significant correlates. We also determined the contribution of common genetic polymorphisms in the F XIIIA and F XIIIB genes in affecting plasma F XIII activity. Both loci showed significant and independent effects on plasma F XIII activity in Indians (F XIIIA, P < 0.01; F XIIIB, P < 0.05) and Chinese (F XIIIA, P < 0.0001; F XIIIB, P < 0.13) in a gene dosage fashion. This study shows that both racial and genetic components play a significant role in determining plasma F XIII activity, and consequently it may affect the quantitative risk of CHD. Genet. Epidemiol. 19:440–455, 2000. © 2000 Wiley‐Liss, Inc.

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Fibrin Gel Network Characteristics and Coronary Heart Disease: Relations to Plasma Fibrinogen Concentration, Acute Phase Protein, Serum Lipoproteins and Coronary Atherosclerosis

Cited by 169 publications

References 38 publications

Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion

Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion

Genetic and Environmental Determinants of Fibrin Structure and Function

Racial and genetic determinants of plasma factor XIII activity

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