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 AF. 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.
Similar content being viewed by others
References
Cerebral Embolism Task Force. Cardiogenic brain embolism.Arch Neurol. 1986; 43:71–84.
Hinton RC, Kistler JP, Fallon JT, Freidlich AL, Fischer CM. Influence of etiology of atrial fibrillation on incidence of systemic embolism.Am J Cardiol. 1977;40:509–513.
Wolf PA, Dawber TT, Thomas HE Jr, Kannel WB. Epidemic assessment of chronic atrial fibrillation and risk of stroke: the Framingham Study.Neurology. 1978;28:973–977.
Roldan V, Marin F, Marco P, Martinez JG, Calatayud R, Sogorb F. Hypofibrinolysis in atrial fibrillation.Am Heart J. 1998;136: 956–960.
Lip GYH, Lowe GOD, Rumley A, Dunn FG. Increased markers of thrombogenesis in chronic atrial fibrillation: effects of warfarin treatment.Br Heart J. 1995;73:527–533.
Mitusch R, Siemens HJ, Garbe M, Wagner T, Sheikhzadeh A, Diederich KW. Detection of a hypercoagulable state in nonvalvular atrial fibrillation and the effect of anticoagulant therapy.Thromb Haemost. 1996;75:219–223.
Lip GYH, Lip PL, Zarifis J, Watson RDS, Lowe GDO. Fibrin D dimer and beta thromboglobulin as markers of thrombogenesis and platelet activation in atrial fibrillation.Circulation. 1996;94: 425–431.
Feng D, D’Agostino RB, Silbershatz H, et al. Hemostatic state and atrial fibrillation (the Framingham Offspring Study).Am J Cardiol. 2000;87:168–171.
Peverill RE, Harper RW, Gelman J, Gan TE, Herris G, Smolich JJ. Determinants of increased regional left atrial coagulation activity in patients with mitral stenosis.Circulation. 1996;94: 331–339.
Jafri SM, Caceres L, Rosman HS, et al. Activation of the coagulation system in women with mitral stenosis and sinus rhythm.Am J Cardiol. 1992;70;1217–1219.
Marin F, Roldan V, Monmeneu JV, et al. Prothrombotic state and elevated levels of plasminogen activator inhibitor-1 in mitral stenosis with and without atrial fibrillation.Am J Cardiol. 1999;84: 862–865.
Amiral J, Malmejec A, Gin H, et al. Evaluation of the fibrinolytic potential on plasma: physiological and pathological variations, and associations with cardiovascular disease risk factors.Fibrinolysis Proteolysis. 1999;13(suppl 1):1–10.
Peverill RE, Smolich JJ. Relation between atrial coagulation activity and levels of coagulation markers in peripheral samples.Am J Cardiol. 1999;84:760–761.
L-Saw-Hee FL, Blann AD, Goldsmith I, Lip GYH. Indexes of hypercoagulability measured in peripheral blood reflect levels in intracardiac blood in patients with atrial fibrillation secondary to mitral stenosis.Am J Cardiol. 1999;83:1206–1209.
Coulshed N, Epstein EJ, McKendrick CS, Galloway RN, Walker E. Systemic embolism in mitral valve disease.Br Heart J. 1970;32: 26–34.
İleri M, Büyükaşık Y, İleri ş, et al. Activation of blood coagulation in patients with mitral stenosis and sinus rhythm.Am J Cardiol. 1998:81;795–797.
Gustafsson C, Blombak M, Britton M, Hamsten A, Svensson J. Coagulation factors and the increased risk of stroke in non valvular atrial fibrillation.Stroke. 1990;21:47–51.
Mondillo S, Sabatini L, Agricola E, et al. Correlation between left atrial size, prothrombotic state and markers of endothelial dysfunction in patients with lone chronic nonrheumatic atrial fibrillation.Int J Cardiol. 2000;75:227–232.
Kumagai K, Fukunami M, Ohmori M, Kitabatake A, Kamada T, Haki N. Increased intravascular clotting in patients with chronic atrial fibrillation.J Am Coll Cardiol. 1990;16:377–400.
Author information
Authors and Affiliations
Corresponding author
About this article
Cite this article
Atalar, E., Özmen, F., Haznedaroğlu, İ. et al. Impaired Fibrinolytic Capacity in Rheumatic Mitral Stenosis with or without Atrial Fibrillation and Nonrheumatic Atrial Fibrillation. Int J Hematol 76, 192–195 (2002). https://doi.org/10.1007/BF02982584
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/BF02982584