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Effect of atorvastatin on plasma levels of asymmetric dimethylarginine in patients with non‐ischaemic heart failure
Author(s) -
Young Joanna M.,
Strey Christopher H.,
George Peter M.,
Florkowski Christopher M.,
Sies Christiaan W.,
Frampton Christopher M.,
Scott Russell S.
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.03.010
Subject(s) - asymmetric dimethylarginine , medicine , endothelial dysfunction , atorvastatin , heart failure , cardiology , enos , statin , ejection fraction , arginine , endocrinology , nitric oxide , nitric oxide synthase , biochemistry , chemistry , amino acid
Background: Elevated plasma levels of asymmetric dimethylarginine (ADMA), an endothelial nitric oxide synthase (eNOS) inhibitor, may contribute to endothelial dysfunction in chronic heart failure (CHF). Since statins upregulate eNOS and ameliorate endothelial dysfunction in non‐ischaemic CHF, we hypothesized that this may be in part through modification of ADMA. Aim: To evaluate the effect of atorvastatin on the relationship between ADMA and endothelial function in non‐ischaemic CHF. Methods: Twenty‐four patients with CHF (ejection fraction <40%, New York Heart Association Functional Classes II and III) were randomised to atorvastatin treatment (40 mg) or placebo once daily for 6 weeks in a double‐blinded, placebo‐controlled crossover study. Plasma ADMA and L ‐arginine levels were measured by HPLC. Endothelial function was assessed by flow‐mediated dilatation and invasive forearm plethysmography. Results: Post‐statin therapy, endothelial function was improved ( p <0.05) independent of LDL‐cholesterol reductions, but no changes were observed in ADMA levels or the L ‐arginine to ADMA ratio. There was a trend for ADMA to inversely correlate with endothelial function at baseline. Conclusions: Short‐term atorvastatin treatment in non‐ischaemic CHF improves endothelial function but has no effect on ADMA or the L ‐arginine to ADMA ratio. Our finding suggests that the observed statin‐induced improvements in endothelial function are likely mediated via alternative pathways.