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Published on: February 28, 2012
[Improvement in fibrinolytic function following anticoagulant treatment in chronic rheumatic atrial fibrillation]
F Marín Ortuño1, V Roldán Schilling, P Marco Vera
1Sección de Cardiología, Hospital General Universitario de Elche, Alicante.
Insights
Patients with rheumatic atrial fibrillation have impaired fibrinolysis, indicated by higher PAI-1 levels. Oral anticoagulation therapy improved these fibrinolytic markers over six months, reducing thromboembolic risk.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Rheumatic atrial fibrillation (AF) patients face high systemic embolism risk, necessitating oral anticoagulation.
- Fibrinolytic function in these patients is not well understood.
- This study investigates fibrinolytic activation markers in rheumatic AF patients before and during anticoagulation therapy.
Purpose of the Study:
- To evaluate fibrinolytic activation markers (tPA, PAI-1, PAP, D-dimer) in rheumatic AF patients.
- To assess changes in these markers after initiating oral anticoagulation.
- To explore the relationship between fibrinolytic markers and left atrial diameter/mitral area.
Main Methods:
- Measured tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), plasmin-antiplasmin complexes (PAP), and D-dimer in 13 rheumatic AF patients and 20 healthy controls.
- Assessed fibrinolytic markers at baseline, 1 month, and 6 months post-anticoagulation initiation.
- Utilized transthoracic echocardiography to measure left atrial diameter and mitral area.
Main Results:
- Rheumatic AF patients exhibited elevated PAI-1 and D-dimer levels compared to controls.
- A correlation was observed between left atrial diameter and baseline t-PA levels.
- Anticoagulation therapy led to significant reductions in t-PA, PAI-1, and D-dimer, with a concurrent increase in PAP levels.
Conclusions:
- Rheumatic AF patients present with a hypofibrinolytic state, primarily due to elevated PAI-1.
- Oral anticoagulation therapy demonstrates a positive impact on fibrinolytic function markers within six months.
- These findings support the prophylactic role of oral anticoagulants in mitigating thromboembolic risk in rheumatic AF.
Introduction And Objectives:
Patients with rheumatic atrial fibrillation are considered at high risk of systemic embolism and require oral anticoagulation. Fibrinolytic function has been little studied. We evaluated fibrinolytic activation markers before starting anticoagulation, at 1 and 6 months following the introduction of oral anticoagulation therapy. We analyzed the relationship with left atrial diameter and mitral area.
Methods:
Tissue plasminogen activator (tPA), its inhibitor (PAI-1), plasmin-antiplasmin complexes (PAP) and D-dimer were measured in 13 patients with rheumatic atrial fibrillation. Basal levels were compared with those found in plasma of 20 healthy subjects matched by sex and age. Transthoracic echocardiography was made.
Results:
A significant increase for PAI-1 and D-dimer levels were detected in patients with atrial fibrillation group (p < 0.05), with no differences in tPA and PAP concentrations. Significant correlation between left atrial diameter and basal t-PA levels was found. Levels of t-PA, PAI-1 and D-dimer decreased significantly under anticoagulation therapy, whereas PAP levels were significantly increased.
Conclusions:
Patients with rheumatic atrial fibrillation show a relative hypofibrinolytic state due to elevated PAI-1 levels with no increase in PAP concentration. At six months of anticoagulation therapy, an improvement of fibrinolytic function markers was observed. This is consistent with the prophylactic effect of oral anticoagulants therapy against thromboembolic risk.
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