There are no studies to date on the early changes in the hemostasis profile of patients with paroxysmal atrial fibrillation (PAF).Given the key role of the fibrinolytic system in maintaining blood fluidity, our aim was to examine its activity in patients with clinical manifestation of the disease <24 hours.We studied 51 nonanticoagulated patients with a first episode of the disease (26 men, 25 women; mean age 59.84 ± 1.60 years) and 52 controls (26 men, 26 women; mean age 59.50 ± 1.46 years) who matched the patients in terms of gender, age, comorbidities, and conducted treatment. Using enzyme-linked immunoassays and colorimetric assays we assessed the plasminogen activity, tissue plasminogen activator level (t-PA), plasminogen activator inhibitor 1 activity (PAI-1), α2-antiplasmin activity (α2-AP), D-dimer level, and vitronectin level. Blood samples were collected immediately after hospitalization.Patients were hospitalized between the second and twenty fourth hours (mean 8.14 ± 0.76 hours) after the onset of PAF. Compared to controls, plasminogen (159.40 ± 4.81 vs 100.2 ± 2.88%, P < 0.001) and t-PA levels (11.25 ± 0.35 vs 6.05 ± 0.31 ng/mL, P < 0.001) were significantly higher in the patient group. PAI-1 activity (7.33 ± 0.37 vs 15.15 ± 0.52 AU/mL, P < 0.001) and α2-AP (112.9 ± 2.80 vs 125.60 ± 3.74%, P < 0.05) as well as vitronectin plasma levels (134.7 ± 5.83 vs 287.3 ± 10.44 mcg/mL, P < 0.001) were lower in the PAF group. Conversely, the levels of D-dimer in patients were significantly higher (0.53 ± 0.07 vs 0.33 ± 0.02 ng/mL, P < 0.05).Early changes in the fibrinolytic system occur in PAF, suggesting their close relationship with the manifestation of the disease. There is high plasma fibrinolytic activity, during the very first 24 hours of the disease, which is most likely a pathophysiological response to the intensified procoagulation process.
Introduction Paroxysmal atrial fibrillation (PAF) is a well-documented prothrombotic state that carries significant embolic risk. However, precise hemostatic changes in the very early stage of the disease are not completely studied. The aim of the study was to study von Willebrand factor (vWF) and coagulation factor VIII (FVIII) plasma levels and activity in the first hours (up to 24 h) of PAF clinical manifestation. Material and methods We selected consecutively 51 non-anticoagulated patients (26 men, 25 women, mean age: 59.84 ±1.60) with PAF and 52 controls (26 men, 26 women, mean age: 59.50 ±1.46 years) corresponding in gender, accompanying diseases and conducted treatment. The indicators were examined using enzyme-linked immunoassays and photometric tests. Results All patients were hospitalized between the 2 nd and 24 th h after the onset of arrhythmia (mean: 8.14 ±0.74 h). Higher FVIII levels (107.52 ±3.48% vs. 93.85 ±2.93%, p < 0.05) and activity (200.03 ±11.11% vs. 109.73 ±4.90%, p < 0.001) were found in the PAF group. vWF levels (178.40 ±12.95% vs. 119.53 ±6.12%, p < 0.001) and activity (200.92 ±12.45% vs. 110.80 ±5.14%, p < 0.001) were also higher. These changes did not depend on age, sex, body mass index or CHA 2 DS 2 -VASc score in the PAF group ( p > 0.05). PAF duration was a significant predictor of increased FVIII levels and activity. Increased PAF duration was followed by increased values of the factors ( r = 0.85, p < 0.001; r = 0.83, p < 0.001). Conclusions The results presented an activated coagulation cascade and endothelial injury, suggesting hypercoagulability still in the early hours of PAF. These changes in PAF did not correlate with CHA 2 DS 2 -VASc score risk factors, outlining PAF as a possible independent embolic risk factor.
Background: Atrial fibrillation (AF) is a hypercoagulable state. However, the intimate mechanisms leading to impaired coagulation and the timing of their activation are unclear. The aim of the study was to investigate the factors that initiate the coagulation cascade in the early hours (up to 48 h) of clinical manifestation of paroxysmal atrial fibrillation (PAF).Methods: Tissue factor (TF) level, coagulation activity of factor VII (FVIIa), factor XII (FXIIa) and factor XI (FXIa) were measured in plasma of 51 non-anticoagulated patients (26 men and 25 women, aged 59.84 ± 11.42 years) and 52 controls (26 men and 26 women, aged 59.50 ± 10.53 years) by enzyme-linked immunoassays and kinetic assays.Results: TF was higher in the PAF group (268.63 ± 90.62 pg/mL vs. 170.21 ± 66.19 pg/mL, P < 0.001) as well as FVIIa (170.82±59.39% vs. 95.17±37.90%, P < 0.001), FXIIa (218.31±84.04% vs. 148.41±53.94%, P < 0.001) and FXIa (178.41±55.94% vs. 111.75±37.33%, P < 0.001). Regression analysis showed that in the first 6 h of the disease, increase in time led to increase in FXIIa (r = 0.25, P < 0.05), FXIa (r = 0.75, P < 0.05), TF level (r = 0.25, P < 0.05) and FVIIa (r = 0.25, P < 0.05). Conclusion:Hemocoagulation changes were observed even < 6 h after the onset of the disease. They suggest that PAF has an early tendency for hypercoagulability, with the involvement of the intrinsic and extrinsic pathways of coagulation.
Background: Increased coagulation activity has been established in paroxysmal atrial fibrillation (PAF), but data on the anticoagulant system are scarce. Purpose: To examine the protein C anticoagulant pathway in the early hours of the disease. Materials and Methods: Fifty-one patients (26 men and 25 women; mean age 59.84 + 1.60 years) and 52 controls (26 men and 26 women; mean age 59.50 + 1.46 years) were selected for the study. Protein C antigen and its activity, total protein S, free protein S and its activity, soluble forms of endothelial protein C receptor (sEPCR), and thrombomodulin (sTM) were examined in the plasma. Results: The indicators were studied in patients between the 2nd and the 24th hour after the onset of arrhythmia. Levels of protein C were significantly elevated in patients compared to controls (111.40% + 6.66% vs 94.83% + 4.47%; P ¼ .039). Protein C activity showed significant reduction in PAF (73.13% + 5.80% vs 103.3% + 3.80%; P < .001). Total protein S levels did not differ significantly (108.20% + 4.07% vs 102.40% + 3.65%; P ¼ .30). Free protein S (76.81% + 6.01% vs 122.10% + 3.97%; P < .001) and its activity (71.39% + 6.27% vs 119.50% + 6.54%; P < .001) were reduced in patients. Higher levels of sEPCR (203.10 + 10.33 vs 133.10 + 7.37 ng/mL; P < .001) and sTM (6.50+0.40 vs 4.48+0.28 ng/mL; P < .001) were measured in PAF. Conclusion: Protein C activity is reduced still in the first hours (until the 24th hour) of PAF clinical manifestation, determining reduced activity of the anticoagulant pathway as a whole. The established low levels of free protein S and its activity as well as low sEPCR and sTM levels are a possible explanation of the changes in protein C activity.
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