American heart journal · 1998
Hypofibrinolysis in atrial fibrillation.
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Roldán V, Marín F, Marco P, Martínez J G, Calatayud R, Sogorb F
Аннотация
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.
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.