Acquired dysfibrinogenemia in atherosclerotic vascular disease

Abstract

Acquired qualitative abnormalities of fibrinogen molecules, termed acquired dysfibrinogenemia, have been demonstrated in several disease states mostly related to prothrombotic tendency, including multiple myeloma and liver disease. Fibrin is abundant in atherosclerotic plaques. Altered plasma fibrin properties, reflected usually by reduced clot permeability and impaired fibrinolysis, have been reported in patients with acute or prior myocardial infarction, ischemic stroke, and peripheral artery disease. Moreover, prothrombotic clot phenotype has been observed in patients with previous no-reflow phenomenon and stent thrombosis. Growing evidence indicates that acquired dysfibrinogenemia contributes to the progression of atherosclerotic vascular disease and the occurrence of its thrombotic manifestations. The review summarizes current knowledge on the links between fibrin clot phenotype and atherosclerotic vascular disease and describes a wide spectrum of cardiovascular risk factors as modifiers of fibrin network characteristics.

Abnormalities in blood coagulation, fibrinolysis, and platelet activation in adult patients after the Fontan procedure

“…To assess fibrinolysis efficiency, we used the plasma-based clot lysis assay, in which coagulation is initiated by a tissue factor without addition of human thrombin, and tissue-type plasminogen activator is used. 18 In our study, CLT was prolonged in adult Fontan patients and correlated positively with PAI-1 antigen, TAFI activity, and F1.2. It remains to be established whether CLT might help identify subjects at increased risk of thromboembolic events among those patients.…”

Association of serum resistin with peripheral arterial disease

“…Furthermore, animal studies have proved the existence of a causal relationship between resistin and atherosclerosis progression. 17 However, there was little data on the relationship between resistin and PAD, which has many features characteristic of a pathobiological process akin to CAD, including chronic inflammation, endothelial dysfunction, lipoprotein deposition, smooth cell dysfunction, and altered fibrin clot formation/degradation, 18 which is why we designed this study to investigate the relationship between resistin and the extent of PAD. However, our study was a clinical observation and did not explore the mechanisms by which resistin levels were increased in PAD patients.…”

Altered plasma fibrin clot properties and fibrinolysis in patients with multiple myeloma

“…Finally, elucidation of the exact molecular mechanisms underlying the observed links between fibrin structure and multiple myeloma was beyond the scope of the current study. A potential contributor might be oxidative modification of the fibrinogen molecules [15,16]. Our preliminary findings suggest that compared with the effect of ferric chloride on clot properties in controls, plasma from MM patients is more sensitive to negative changes induced by iron on plasma fibrin clot permeability and lysability (A. Undas, unpublished data).…”

“…Few small studies or case reports, performed using plasmabased assays and purified immunoglobulins, investigated fibrin clot properties in MM. They reported heterogeneous effects of IgG paraproteins on fibrin that encompassed disturbed fibrin polymerization and slow clot lysis in association with IgG concentrations supported by markedly abnormal clot morphology on scanning electron microscopy images [16][17][18]. To our knowledge, the current study presents the first comprehensive evaluation of plasma fibrin clot structure and function in MM patients.…”