Effects of atorvastatin on reactive hyperaemia and the thrombosis–fibrinolysis system in patients with heart failure. Issue 1 (16th December 2004)

• Record Type: Journal Article
• Authors: Tousoulis, D; Antoniades, C; Bosinakou, E; Kotsopoulou, M; Tsioufis, C; Tentolouris, C; Trikas, A; Pitsavos, C; Stefanadis, C
• Is Part Of: Heart. Volume 91:Issue 1(2005)
• Page Start: 27
• Page End: 31
• Publication Date: 2004-12-16
• Subjects: eNOS, endothelial nitric oxide synthase -- FBF, forearm blood flow -- ELISA, enzyme linked immunosorbent assay -- NTG%, forearm vasodilatory response to nitrate -- PAI-1, plasminogen activator inhibitor 1 -- RH%, forearm vasodilatory response to reactive hyperaemia -- TNFα, tumour necrosis factor α -- tPA, tissue plasminogen activator; heart failure -- statins -- endothelium -- thrombosis -- fibrinolysis; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/hrt.2003.027110
• Languages: English
• ISSNs: 1355-6037

Abstract

Abstract : Objective: To investigate the effects of short term atorvastatin treatment on forearm vasodilatory response to reactive hyperaemia (RH%) and on components of the thrombosis–fibrinolysis system (antithrombin III, proteins and S, factors V and VII, von Willebrand factor, tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI-1)) in patients with heart failure. Patients and methods: 35 patients with heart failure were enrolled in this study; 17 patients received atorvastatin 10 mg/day and 18 patients received no statin for four weeks. Forearm blood flow (FBF) was measured by venous occlusion strain gauge plethysmography. RH% and forearm vasodilatory response to nitrate were defined as the percentage change of FBF from rest to the maximum flow during reactive hyperaemia and after nitrate administration, respectively. Plasma concentrations of antithrombin III, protein C, protein S, factor V, factor VII, von Willebrand factor, tPA, and PAI-1 were determined before and after treatment. Results: Maximum hyperaemic FBF remained unchanged in both groups. Baseline FBF was slightly but not significantly decreased in the atorvastatin treated group. RH% was significantly increased only in the atorvastatin treated group, from mean (SD) 42.44 (18.9)% to 83.7 (36.1)% (p < 0.01). Plasma concentrations of antithrombin III (from mean (SD) 81.7 (11.37)% to 73.5 (13.8)%), protein C (from mean (SD) 88.3 (26.9)% to 63.9 (25.0)%), factor V (from mean (SD) 126.2 (33.4)% to 94.9 (29.8)%), tPA (from median (25th–75th percentile) 11.68 (8.60–20.95) ng/ml to 10.30 (8.65–15.12) ng/ml), and PAI-1 (from median (25th–75th percentile) 3.10 (2.15–4.40) IU/l to 1.90 (0.75–3.0) IU/l) were significantly decreased in the atorvastatin treated group (p < 0.05) but not in the control group. Plasma concentrations of von Willebrand factor, factor VII, and protein S remained unaffected in both groups. Conclusion: Atorvastatin did not change the maximum hyperaemic flow, although it decreased plasma concentrations of antithrombin III, protein C, factor V, tPA, and PAI-1 in patients with heart failure. Therefore, short term treatment with atorvastatin may affect the expression of both endothelium and liver derived components of the thrombosis–fibrinolysis system in patients with heart failure.