Hypofibrinolysis in atrial fibrillation

Citation
V. Roldan et al., Hypofibrinolysis in atrial fibrillation, AM HEART J, 136(6), 1998, pp. 956-960
Citations number
18
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
AMERICAN HEART JOURNAL
ISSN journal
00028703 → ACNP
Volume
136
Issue
6
Year of publication
1998
Pages
956 - 960
Database
ISI
SICI code
0002-8703(199812)136:6<956:HIAF>2.0.ZU;2-J
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 levers of modified antithrombin III (ATM), tissue plasminoge n activator (TPA), its inhibitor (PAI-1 ), TPA-PAI-1 complexes and plasmin- antiplasmin complexes (PAP), D-dimer, and fibrinogen were measured in plasm a from 36 patients with chronic atrial fibrillation. Fifteen patients had r heumatic mitral stenosis and 21 had nonrheumatic atrial fibrillation. Level s were compared with those found in the plasma of 20 healthy subjects. Tran sthoracic 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 rheum atic atrial fibrillation group also showed elevated levels of fibrinogen (P < .05). No significant differences were found in TPA and PAP. There were n o differences between rheumatic and nonrheumatic atrial fibrillation. Conclusions Atrial fibrillation shows a hypofibrinolytic state caused by el evated 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.