Impaired fibrinolytic capacity in rheumatic mitral stenosis with or without atrial fibrillation and nonrheumatic atrial fibrillation.
ABSTRACT Chronic atrial fibrillation (AF) has often been associated with systemic embolization, and patients with mitral stenosis (MS) have the highest thromboembolic risk. Increased risk of thromboembolism could be in part due to impaired fibrinolytic function. Global fibrinolytic capacity (GFC) is an innovative technique for evaluating the entire fibrinolytic system. The aim of our study was to evaluate fibrinolytic activity in patients with rheumatic and nonrheumatic chronic AE To investigate fibrinolytic activity, we assessed GFC in peripheral blood samples of 32 patients with nonrheumatic AF (14 women; mean age, 56 +/- 1 years), 30 patients with rheumatic MS and AF (23 women; mean age, 35 +/- 9 years), and 32 patients with rheumatic MS and sinus rhythm (24 women; mean age, 36 +/- 8 years). The control group comprised 30 healthy adult subjects in normal sinus rhythm. Patients with chronic AF (rheumatic and nonrheumatic) had lower GFC than did the controls (P = .0001). The rheumatic AF group also showed decreased levels of GFC compared with the nonrheumatic AF group, with the rheumatic MS and sinus rhythm group, and with controls (P = .03, P = .02, P = .0001, respectively). GFC was lower in patients with rheumatic MS and sinus rhythm than in controls (P = .003). Although there were correlations between GFC and mitral valve area, transmitral mean gradient, left atrial diameter, and mitral calcification in patients with rheumatic MS, multivariate analysis showed only transmitral gradient as an independent factor affecting GFC. Patients with AF have decreased GFC, a finding that suggests the presence of a hypofibrinolytic state. Fibrinolytic dysfunction was more pronounced in rheumatic MS patients with AF than in those with nonrheumatic AF. Moreover, patients with rheumatic MS and sinus rhythm had decreased global fibrinolytic activity. Hypofibrinolysis documented by decreased GFC can be one of the important causes of increased risk of embolism in patients with AF and rheumatic MS.
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ABSTRACT: Background There is a high incidence of systemic embolism in patients with chronic atrial fibrillation. A hypercoagulable state has been demonstrated, but the fibrinolytic system is rarely studied. Methods Plasma levels of modified antithrombin III (ATM), tissue plasminogen activator (TPA), its inhibitor (PAI-1), TPA–PAI-1 complexes and plasmin-antiplasmin complexes (PAP), d -dimer, and fibrinogen were measured in plasma from 36 patients with chronic atrial fibrillation. Fifteen patients had rheumatic mitral stenosis and 21 had nonrheumatic atrial fibrillation. Levels were compared with those found in the plasma of 20 healthy subjects. Transthoracic echocardiographic studies were done. Results Patients with atrial fibrillation had higher plasma levels of ATM, d -dimer, PAI-1, and TPA–PAI-1 complexes than controls (P < .001). The rheumatic atrial fibrillation group also showed elevated levels of fibrinogen (P < .05). No significant differences were found in TPA and PAP. There were no differences between rheumatic and nonrheumatic atrial fibrillation. Conclusions Atrial fibrillation shows a hypofibrinolytic state caused by elevated PAI-1 levels with no increase in PAP complex concentration. Elevated plasma d -dimer levels suggest increased intravascular thrombogenesis. This may contribute to increased risk of thrombosis. (Am Heart J 1998;136:956-60.)American Heart Journal 12/1998; · 4.50 Impact Factor
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ABSTRACT: Systemic embolism is a frequent complication in mitral stenosis (MS).1 Its incidence increases with age and the presence of atrial fibrillation.2,3 Although patients with MS and sinus rhythm can also develop systemic emboli, the frequency of this event is lower in these patients than in those with atrial fibrillation.1 Patients with MS and atrial fibrillation are considered at high risk of systemic embolism and require anticoagulant therapy.4 Because patients with MS and sinus rhythm are considered at low risk for systemic embolism, anticoagulant therapy is not routinely recommended.4 It is desirable to identify patients with MS in sinus rhythm who are at high risk for systemic embolism. There are no reliable clinical or laboratory parameters available to stratify this risk. Recently developed assays are capable of detecting peptides released during activation of the coagulation cascade and thrombogenesis.5,6 Measurement of these markers may be used to identify patients at risk for thromboembolism. This study was performed to test the hypothesis that there is activation of coagulation in patients with MS and sinus rhythm. Fibrinolytic activity was assayed by measuring D-dimers that are generated from plasmic degradation of cross-linked fibrin.5 Thrombin activation was assayed by measuring thrombinantithrombin III complexes.6The American Journal of Cardiology 12/1992; 70(13):1217-9. · 3.21 Impact Factor
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ABSTRACT: Atrial fibrillation is associated with a prothrombotic state and endothelial dysfunction. To understand whether the prothrombotic state was correlated with endothelial dysfunction and whether the latter was related to atrial dimension (endocardial damage), we studied systemic hemocoagulative activity and markers of endothelial dysfunction in 45 patients with chronic nonrheumatic atrial fibrillation and in 35 controls. We assessed fibrinogen, antithrombin III, protein C, markers of platelet activation (platelet factor 4 and beta-thromboglobulin) as markers of fibrinolysis, and D-dimer, tissue plasminogen activator, plasminogen activator inhibitor, von Willebrand's factor and soluble thrombomodulin as endothelial dysfunction. Plasma fibrinogen (P<0. 005), platelet factor 4 (P<0.001), thromboglobulin (P<0.001), D-dimer (P<0.03), tissue plasminogen activator (P<0.006), plasminogen activator inhibitor (P<0.04) and both von Willebrand's factor (P<0.0001) and soluble thrombomodulin (P<0.03) were significantly higher in the patients than in the controls. Positive significant linear correlations were found between fibrinogen and markers of endothelial dysfunction and left atrial volume and fibrinogen or markers of endothelial dysfunction. These findings confirm that chronic nonrheumatic atrial fibrillation is associated with a prothrombotic state but also suggest that there is a correlation between endothelial dysfunction, coagulation factors and left atrial dimension.International Journal of Cardiology 09/2000; 75(2-3):227-32. · 5.51 Impact Factor