Search for: [Abstract = "Venous thromboembolism \(VTE\), comprising deep vein thrombosis and pulmonary embolism, affects 1\-3 per 1000 persons per year. The pathogenesis of VTE is multifactorial and not fully understood. Recently VTE patients have been shown to display unfavorably altered fibrin clots as compared to healthy individuals. Inhibitors of 3\-hydroxy\-3\-methylglutaryl\-coenzyme A reductase \(statins\) not only reduce cholesterol biosynthesis, but also attenuate blood coagulation including favorable alteration of fibrin clots properties, as seen in coronary artery disease patients and in low cardiovascular risk subjects. Rosuvastatin has been reported to reduce the risk of VTE within a 2\-year period. It is unknown whether statin\-related alteration of fibrin properties occurs in VTE patients. The aim of the study was to evaluate atorvastatin induced alterations of fibrin clots in VTE patients and in disease control group matched for cardiovascular risk factors. 25 volunteers without VTE \(control group\) and 28 VTE patients were enrolled to the open\-label intervention study. Inclusion criteria for control group were low cardiovascular risk \(SCORE <5%\) and \- for VTE patients \- documented venous thrombosis within previous 30 months with over 1 month anticoagulation withdrawal prior to the enrollment. Exclusion criteria from control group was a history of any thrombosis, and for VTE patients a history of arterial thrombosis. Angina, acute thrombosis, diabetes, haemorrhagic diathesis, autoimmune diseases, hypo\- or hyperthyroidism, acute inflammation, medication usage \(beside antihypertensive drugs\) and severe comorbidities were the exclusion criteria for both groups. Study participants received atorvastatin \(Sortis, Pfizer\) 40 mg\/day for 3 days. Fasting blood was collected before intake of the first dose and after 3 days of atorvastatin administration. Lipid profiles, high\-sensitivity C\-reactive protein \(CRP\), other serum routine parameters, fibrinogen concentrations, D\-dimers, prothrombin fragment 1.2 \(F1.2\), tissue plasminogen activator \(t\-PA\), plasminogen activator inhibitor\-1 \(PAI\-1\), lipoprotein\(a\) \[Lp\(a\)\] and total homocysteine \(tHcy\) were determined."]

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