Author + information
- Received April 14, 2019
- Revision received June 17, 2019
- Accepted July 19, 2019
- Published online September 2, 2019.
- aNational Heart and Lung Institute, Imperial College, London, United Kingdom
- bPostgraduate Medical School, University of Hertfordshire, Hertfordshire, United Kingdom
- cLiverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart and Chest Hospital, Liverpool, United Kingdom
- dAalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Aalborg, Denmark
- ↵∗Address for correspondence:
Dr. Diana A. Gorog, National Heart and Lung Institute, Dovehouse Street, London SW3 6LR, United Kingdom.
• Endogenous fibrinolysis is a natural defense against lasting arterial thrombotic occlusion.
• Impaired fibrinolysis is detectable with global assays in a number of patients with ACS and CVD.
• Impaired fibrinolysis is a strong, independent and novel marker of cardiovascular risk.
• Future trials of pharmacotherapy to enhance chronic fibrinolytic status are required to reduce cardiovascular risk.
Endogenous fibrinolysis is a powerful natural defense mechanism against lasting arterial thrombotic occlusion. Recent prospective studies have shown that impaired endogenous fibrinolysis (or hypofibrinolysis) can be detected in a significant number of patients with acute coronary syndrome (ACS) using global assays and is a strong marker of future cardiovascular risk. This novel risk biomarker is independent of traditional cardiovascular risk factors and unaffected by antiplatelet therapy. Most prospective prognostic data have been obtained using a global assay using native whole blood at high shear or plasma turbidimetric assays, which are described herein. Tests of endogenous fibrinolysis could be used to identify patients with ACS who, despite antiplatelet therapy, remain at high cardiovascular risk. This review discusses the impact of currently available medications and those in development that favorably modulate fibrinolytic status and may offer a potential new avenue to improve outcomes in ACS.
Dr. Gorog is related through family to a company director in Thromboquest Ltd, but neither she, nor her spouse, nor children have financial involvement or equity interest in and have received no financial assistance, support, or grants from the aforementioned. Dr. Lip has reported that he has no relationships relevant to the contents of this paper to disclose.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received April 14, 2019.
- Revision received June 17, 2019.
- Accepted July 19, 2019.
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