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Updated: Jul 6, 2026

The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
Published on: February 27, 2026
Thrombin activatable fibrinolysis inhibitor and other hemostatic parameters in patients with essential arterial
Jolanta Małyszko1, Justyna Tymcio
1Department of Nephrology and Transplantology, Medical University, Białystok, Poland. jomal@pczta.onet.pl
Introduction:
Hypertension is associated with hemostatic abnormalities and endothelial dysfunction. thrombin activatable fibrinolysis inhibitor (TAFI) is a glycoprotein linking coagulation and fibrinolysis. Objectives. We evaluated TAFI concentrations in patients with essential hypertension in relation to blood pressure. Additionally, we studied TAFI activator, thrombin activity (thrombin-antithrombin complexes--TAT, prothrombin fragments F1 + 2), thrombomodulin (TM)--a marker of endothelial cell injury, degree of plasmin generation (plasmin-antiplasmin complexes [PAP]), other markers of endothelial cell injury--von Willebrand factor (vWF).
Patients And Methods:
Seventy-two patients with essential hypertension (27 untreated, 13 treated with enalapril (angiotensin-converting enzyme inhibitor [ACEI]), 32 with beta-blocker, betaxolol). In every hypertensive patients ambulatory blood pressure measurements and echocardiography were performed.
Results:
All hypertensive patients did not differ with respect to age, creatinine, fibrinogen, D-dimers. In ACEI-treated patients a significantly higher TAFI concentration was observed when compared to beta-blocker-treated patients. In beta-blocker-treated patients both diastolic and systolic blood pressure were lower than in ACEI treated patients as well as ejection fraction, while serum triglycerides were higher. Diastolic blood pressure correlated significantly with TAFI concentrations in untreated patients (r = 0.27, p < 0.05), and in beta-blocker-treated patients (r = 0.25, p = 0.05), TAFI activity was inversely associated with interventricular septal diameter (r = -0.75, p < 0.01) in patients treated with ACEI.
Conclusions:
Elevated TAFI concentrations and enhanced thrombin generation in hypertensive patients may contribute to atherosclerosis progression in this population. Differences in the studied parameters may be due to a small sample size, monotherapy and potential effects of antihypertensive drugs on glicemia, ejection fraction and triglycerides.
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