Fibrinolysis in Acute and Chronic Cardiovascular Disease

Noppadol Kietsiriroje; Robert A.S. Ariëns; Ramzi A. Ajjan

doi:10.1055/s-0040-1718923

Seminars in Thrombosis and Hemostasis, Table of Contents

Semin Thromb Hemost 2021; 47(05): 490-505
DOI: 10.1055/s-0040-1718923

Review Article

Fibrinolysis in Acute and Chronic Cardiovascular Disease

Noppadol Kietsiriroje

¹Department of Metabolic Medicine, Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom

²Endocrinology and Metabolism Unit, Department of Internal Medicine, Faculty of Medicine, Prince of Songkla University, Hatyai, Songkhla, Thailand

,

Robert A.S. Ariëns

¹Department of Metabolic Medicine, Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom

,

Ramzi A. Ajjan

¹Department of Metabolic Medicine, Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom

› Author Affiliations

Abstract

The formation of an obstructive thrombus within an artery remains a major cause of mortality and morbidity worldwide. Despite effective inhibition of platelet function by modern antiplatelet therapies, these agents fail to fully eliminate atherothrombotic risk. This may well be related to extensive vascular disease, beyond the protective abilities of the treatment agents used. However, recent evidence suggests that residual vascular risk in those treated with modern antiplatelet therapies is related, at least in part, to impaired fibrin clot lysis. In this review, we attempt to shed more light on the role of hypofibrinolysis in predisposition to arterial vascular events. We provide a brief overview of the coagulation system followed by addressing the role of impaired fibrin clot lysis in acute and chronic vascular conditions, including coronary artery, cerebrovascular, and peripheral vascular disease. We also discuss the role of combined anticoagulant and antiplatelet therapies to reduce the risk of arterial thrombotic events, addressing both efficacy and safety of such an approach. We conclude that impaired fibrin clot lysis appears to contribute to residual thrombosis risk in individuals with arterial disease on antiplatelet therapy, and targeting proteins in the fibrinolytic system represents a viable strategy to improve outcome in this population. Future work is required to refine the antithrombotic approach by modulating pathological abnormalities in the fibrinolytic system and tailoring therapy according to the need of each individual.

Keywords

fibrinolysis - fibrin - lysis time - cardiovascular disease

Full Text

References

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