CARDIOVASCULAR MEDICINE

Short-term statin treatment improves endothelial function and neurohormonal imbalance in normocholesterolaemic patients with non-ischaemic heart failure

C H Strey¹, J M Young², J H Lainchbury², C M Frampton², M G Nicholls³, A M Richards², R S Scott²

¹ Department of Endocrinology, Addenbrooke’s Hospital, Cambridge University Hospitals, Cambridge, UK
² Lipid and Diabetes Research and Department of Medicine, Christchurch Hospital and Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand
³ Department of Internal Medicine, Faculty of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates

Correspondence to:
Professor Russell S Scott
Lipid and Diabetes Research, Christchurch Hospital and Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand; russell.scott{at}chmeds.ac.nz

Objectives: To investigate the effect of short-term statin treatment on impaired endothelium-dependent vasodilatation and haemodynamic abnormalities typically occurring in chronic heart failure (CHF).

Methods: In a double-blind, crossover study endothelium-dependent vasodilatation was measured in conduit and resistance vessels of 23 patients with non-ischaemic CHF after 6 weeks of placebo and 40 mg atorvastatin. The haemodynamic impact was assessed by cardioendocrine hormones, echocardiography and clinical indicators of CHF.

Results: Cholesterol concentrations were population average (low density lipoprotein 3.56 (SEM 0.16) mmol/l, triglycerides 1.70 (0.20) mmol/l and high density lipoprotein 1.17 (0.07) mmol/l). In resistance vessels, the area under the curve ratio during acetylcholine infusion increased from 9.2 (1.9) with placebo to 12.2 (2.1) with statin (p < 0.01). This improvement was reversed during co-infusion with the nitric oxide antagonist N^G-monomethyl-L-arginine. In conduit arteries, flow-mediated dilatation increased from 5.64 (SEM 0.88)% with placebo to 6.83 (0.97)% with statin (p < 0.05). Endothelium-independent vasodilatation did not change (p = 0.68 for conduit and p = 0.45 for resistance vessels). Endothelin 1 and atrial natriuretic peptide (ANP) decreased from 1.57 (0.08) and 51.3 (1.0) with placebo to 1.42 (0.09) pg/ml (p < 0.05) and 42.1 (7.5) pmol/l (p < 0.05), respectively, with statin.

Conclusions: In patients with non-ischaemic CHF and population-average cholesterol concentrations, short-term statin treatment improves endothelial function in conduit and resistance vessels and lowers plasma endothelin 1 and ANP concentrations.

Abbreviations: ANP, atrial natriuretic peptide; BNP, B-type natriuretic peptide; CHF, chronic heart failure; CNP, C-type natriuretic peptide; CV, coefficient of variation; EID, endothelium-independent dilatation; FMD, flow-mediated dilatation; LDL, low density lipoprotein; L-NMMA, N^G-monomethyl-L-arginine; NO, nitric oxide

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