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Fibrin clot properties in cardiovascular disease: from basic mechanisms to clinical practice

期刊

CARDIOVASCULAR RESEARCH
卷 119, 期 1, 页码 94-111

出版社

OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvad017

关键词

Fibrin clot; Fibrinolysis; Cardiovascular disease; Thrombosis

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Fibrinogen conversion and clot formation are crucial processes in coagulation cascade. Dense fibrin networks that are resistant to lysis have been associated with cardiovascular disease, while hypofibrinolysis is a persistent feature in patients with thrombotic events or stable coronary artery disease. Lifestyle modifications and certain medications can improve fibrin structure and function. Prospective studies have shown that prothrombotic fibrin clot phenotype can predict cardiovascular events. Furthermore, various factors, including mutations in fibrinogen molecules and clot-bound proteins, contribute to the prothrombotic fibrin clot phenotype. This review summarizes the mechanisms underlying unfavorable fibrin clot properties and their implications in cardiovascular disease and its thrombo-embolic manifestations.
Fibrinogen conversion into insoluble fibrin and the formation of a stable clot is the final step of the coagulation cascade. Fibrin clot porosity and its susceptibility to plasmin-mediated lysis are the key fibrin measures, describing the properties of clots prepared ex vivo from citrated plasma. Cardiovascular disease (CVD), referring to coronary heart disease, heart failure, stroke, and hypertension, has been shown to be associated with the formation of dense fibrin networks that are relatively resistant to lysis. Denser fibrin mesh characterized acute patients at the onset of myocardial infarction or ischaemic stroke, while hypofibrinolysis has been identified as a persistent fibrin feature in patients following thrombotic events or in those with stable coronary artery disease. Traditional cardiovascular risk factors, such as smoking, diabetes mellitus, hyperlipidaemia, obesity, and hypertension, have also been linked with unfavourably altered fibrin clot properties, while some lifestyle modifications and pharmacological treatment, in particular statins and anticoagulants, may improve fibrin structure and function. Prospective studies have suggested that prothrombotic fibrin clot phenotype can predict cardiovascular events in short- and long-term follow-ups. Mutations and splice variants of the fibrinogen molecule that have been proved to be associated with thrombophilia or increased cardiovascular risk, along with fibrinogen post-translational modifications, prothrombotic state, inflammation, platelet activation, and neutrophil extracellular traps formation, contribute also to prothrombotic fibrin clot phenotype. Moreover, about 500 clot-bound proteins have been identified within plasma fibrin clots, including fibronectin, alpha 2-antiplasmin, factor XIII, complement component C3, and histidine-rich glycoprotein. This review summarizes the current knowledge on the mechanisms underlying unfavourable fibrin clot properties and their implications in CVD and its thrombo-embolic manifestations.

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