Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis · 2016
Impaired plasma clot lysis and its determinants in patients with obstructive sleep apnea syndrome.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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Borratynska Anna, Stopyra-Pach Katarzyna, Fil Korneliusz, Undas Anetta
Аннотация
Evidence indicates that hypercoagulability and impaired fibrinolysis have been observed in patients with obstructive sleep apnea syndrome (OSAS). It is unclear which factors determine prolonged fibrin clot lysis in OSAS. One hundred and sixty-five consecutive patients suspected of OSAS underwent overnight polysomnography. Prior to polysomnography, we determined plasma clot lysis time (CLT), plasminogen activator inhibitor (PAI)-1 antigen, activated thrombin-activatable fibrinolysis inhibitor (TAFIa), plasmin, and antiplasmin. OSAS was diagnosed in 110 (66.7%) patients, including 35 (31.8%) with severe OSAS, 26 (23.6%) with moderate OSAS, and 49 (44.6%) mild OSAS. Compared with 55 (33.3%) individuals in whom OSAS was not confirmed, OSAS patients had prolonged CLT (+12.8%), associated with higher PAI-1 antigen (+18.1%) (after adjustment for age, diabetes, and body mass index; both P < 0.01) and similar levels of TAFIa, plasmin, or antiplasmin. PAI-1, TAFIa, and CLT correlated positively with apnea/hypopnea index, which reflects the severity of OSAS (R = 0.66, P < 0.001; R = 0.29, P = 0.002; R = 0.55, P = 0.001, respectively), and with other polysomnography parameters, with the most potent correlations observed for desaturation index. Regression analysis adjusted for potential confounders showed that in OSAS, CLT was independently predicted by apnea/hypopnea index (B = 0.29, P = 0.002), PAI-1 (B = 0.42, P < 0.001), and TAFIa (B = 0.81, P = 0.044), whereas both PAI-1 and TAFIa were predicted only by desaturation index (B = 0.24, P = 0.002; and B = 0.14, P = 0.001, respectively). The severity of OSAS is closely associated with hypofibrinolysis measured in a global plasma-based assay, driven largely by PAI-1. Attenuated fibrinolysis might contribute to high risk of thromboembolic events in this disease.