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Rheumatoid arthritis (RA) is associated with an excessive risk of cardiovascular morbidity and mortality, and inflammation appears to be the missing link explaining this markedly elevated risk.1 Inflammation is a potent inducer of coagulation and fibrinolysis and may contribute to atherosclerotic and thrombotic components of cardiovascular events.2 Thrombin-activatable fibrinolysis inhibitor (TAFI), a procarboxypeptidase in plasma, is a regulatory protein of the coagulation/fibrinolysis balance as well as inflammation. TAFIa, the activated form of TAFI, acts by removing C-terminal arginine and lysine residues from substrates such as fibrin degradation products, bradykinin and the anaphylatoxins C3a and C5a. Elevated TAFI levels may reflect an enhanced risk of developing cardiovascular …
Competing interests: None declared.
Ethics approval: The local ethics committees approved the study protocol and all participants provided written informed consent.
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