Search for: [Abstract = "Both RVO and control groups did not differ with regard toage, gender, BMI, smoking status, medications, a previous myocardial infarction\/ stroke, lipid profile, creatinine,AlAT, PAI\-1, and a percentage of patients with CRP level≥3.36 mg\/l. RVO patients had higher percentage of arterial hypertension \(by 58%, p = 0.01\) and higher glucose \(by 4%,p = 0.01\), fibrinogen \(by 17%, p = 0.03\) and tPA \(by 59%, p= 0.001\) compared with controls. Platelet count \(by 10%, p= 0.001\) and total homocysteine \(by 14.5%, p = 0.001\) were lower in RVO group compared with controls. RVO patients were characterized by unfavorably altered plasma fibrin clot properties. Thirty per cent lower clot permeability was found in RVO patients compared with the control group \(6.9\[5.9–8.0\] vs 9.8 \[8.5–10.5\] 10\-9 cm2, p <0.0001\). Compared with controls, RVO patients had 11% shorter lag phase\(41.42 ± 4.59 vs 46.42 ± 4.12 s, p <0.0001\) indicating faster fibrin formation, and 19% greater ΔAbmax \(0.86 \[0.80–0.94\] vs 0.72 \[0.66–0.77\], p <0.0001\), indicating thicker fibrin fibers. D\-Dmax indicating thrombotic mass available for fibrinolytic agents was 22% higher in the RVO group \(4.04 \[3.48–4.55\] vs 3.32 \[3.26–3.43\] mg\/l, p <0.0001\) and29% longer t50% \(9.3 \[8.5–10.2\] vs 7.2 \[6.8–7.7\] min, p<0.0001\) compared with controls. Only D\-Drate was similarin both groups \(0.071 \[0.063–0.074\] vs 0.069 \[0.063–0.073\]mg\/l\/min, p = 0.223\). The differences remained statistically significant after adjustment for fibrinogen, glucose and platelet count. In the RVO group fibrinogen inversely correlated with Ks \(tau\-b = –0.414, p <0.0001\), lag phase\(tau\-b = –0.383, p <0.0001\), D\-Drate \(tau\-b = –0.490, p<0.0001\) and positively correlated with ΔAbmax \(tau\-b =0.276, p = 0.002\), t50% \(tau\-b = 0.350, p <0.0001\) and DDmax \(tau\-b = 0.324, p <0.0001\). RVO patients with CRP≥3.36 mg\/l had higher ΔAbmax \(0,95 \[0.87–1.01\] vs 0,85\[0.79–0.91\], p = 0.024\), longer t50% \(10.0 \[9.8–11.9\] vs 9.1\[8.5–10.1\] min, p = 0.007\), higher D\-Dmax \(4.75 \[4.04–5.45\] vs 3.95 \[3.44–4.42\] mg\/l, p = 0.004\) and lower D\-Drate \(0.063 \[0.059–0.79\] vs 0.071 \[0.065–0.079\]mg\/l\/min, p = 0.035\) compared with the RVO patients with CRP <3.36 mg\/l. In RVO patients age correlated positively with t50% \(tau\-b = 0.182, p = 0.047\). None of the parameters of fibrin clot showed associations with sex, smoking status, previous stroke or myocardial infarction,time from the RVO occurrence, PAI\-1, tPA, lipid variables, and glucose in RVO patients. Fibrin clot properties did not differ between patients with diagnosed BRVO or CRVO, with or without neovascurarization and macular edema,visual acuity <0.1 or ≥0.1, indicating the lack of correlation between severity of RVO and plasma fibrin clot properties.Two times higher prevalence of factor V Leiden was observed in RVO patients \(10.2%\) than in Polish general population \(approximately 5%\), but it was not associated with unfavorably altered plasma fibrin clot properties. In conclusion, the current results show that less porousplasma fibrin clots composed of thicker fibrils, displaying reduced susceptibility to lysis, are formed in RVO patients, like in those with coronary artery disease and deep vein thrombosis. Plasma fibrinogen and CRP levels have been recognized as the most important modulators of fibrin function in RVO. This original observation highlights a role of blood coagulation, particularly alterations in fibrin formation and degradation, in the pathogenesis of RVO."]

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