Search for: [Abstract = "Plasma fibrin clot properties were expressed as permeation coefficient \(Ks\), turbidity measurements of fibrin polymerization \[lag phase, maximum absorbance \(Δ Abs\)\], plasma clot lysis assays in presence of recombinant tissue\-type plasminogen activator \(rtPA\) with \(t50%\) or without \(CLT\) exogenous thrombin and D\-dimer levels \[maximum concentration \(D\-D max\) and rate of increase \(D\-D rate\)\] in a fibrin clot perfusion model. The location of venous thrombosis in VTE patients was analyzed. Screening for thrombophilia and residual venous thrombosis \(RVT\) detection were also performed. Two groups did not differ with respect to demographic data and arterial hypertension, however overweight was more common in VTE patients. There were no differences in laboratory data between the groups at the baseline, except for higher CRP \(1.66 \[interquartile range 0.74\-2.22\] mg\/l vs 0.84 \[0.54\-1.12\] mg\/l, p= 0.03\), glucose \(5.66 ±0.36 mM vs. 5.44 ±0.36 mM, p= 0.03\) and t\-PA levels \(14.05 \[11.05\-17.35\] ng\/ml vs 10.80 \[10.10\-13.70\] ng\/ml, p= 0.015\) in VTE patients. Plasma fibrin clot variables prior to atorvastatin administration significantly differed between two groups. VTE patients displayed 9% faster protofibril formation and 14.2% thicker fibrin fiber formation, together with 27.4% lower clot permeability and 25% lysability compared to control group \(p for all <0.0001\). The presence of RVT in the lower extremity deep veins \(n=9\) led to faster protofibril \(lag phase 41.2 ±2.5 s vs 44.5 ±2.8 s, p= 0.005\) and thicker fibrin fiber \(Δ Abs 0.9 ±0.04 vs 0.8 ±0.06, p= 0.005\) formation together with lower clot permeability \(Ks 6.0 ±0.9 \*10\-9 cm2 vs 7.2 ±1.4 \*10\-9 cm2, p= 0.03\) and lysability \(t50% 10.6 \[9.5 – 11.3\] min vs 9.9 \[7.5 – 10.3\] min, p= 0.03\). In control group atorvastatin decreased total \(TC\), low\-density lipoprotein cholesterol \(LDL\-C\) and triglyceride levels \(p for all <0.05\), while CRP level remained unchanged. A reduction in CLT \(by 11%, p= 0.003\) was noted\; other fibrin parameters were unaltered. Atorvastatin in VTE patients resulted in TC, LDL\-C reduction \(p for all < 0.0001\), no change in CRP concentration and a decrease in tHcy \(by 31.6%, p= 0.006\), PAI\-1 \(by 19.4%, p= 0.009\), Lp\(a\) \(by 7.2%, p= 0.0006\) levels. VTE patients following atorvastatin administration had an increase in Ks \(by 23.2%, p< 0.0001\), lag phase \(by 4.5%, p= 0.04\), D\-D rate \(by 10.3%, p< 0.0001\) and decrease in Δ Abs \(by 4.5%, p= 0.002\), t50% \(by 19.9%, p< 0.0001\) and CLT \(by 13.7%, p= 0.0004\). Atorvastatin\-induced reduction of Δ Abs was more pronounced in patients with RVT as compared to patients without RVT \(0.10 ±0.07 vs 0.01 ±0.07, p= 0.005\), while CLT reduction was seen only in patients without RVT. D\-D rate increase following atorvastatin was higher in unprovoked \(n=10\) than provoked VTE \(0.012 mg\/l\/min ±0.01 vs 0.005 mg\/l\/min ±0.006, p= 0.044, respectively\). Patients with proximal venous thrombosis \(n=17\), contrary to distal thrombosis patients, displayed Δ Abs reduction following atorvastatin administration \(p= 0,01\). Thrombophilia \(n=14\) did not alter fibrin clot properties either before or after statin administration. The improvement of fibrin clot structure\/function in VTE patients after atorvastatin was unrelated to TC or tHcy, t\-PA, PAI\-1, F1.2, Lp\(a\) changes."]

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