Journal
AMERICAN JOURNAL OF HYPERTENSION
Volume 26, Issue 5, Pages 608-616Publisher
OXFORD UNIV PRESS
DOI: 10.1093/ajh/hps098
Keywords
arterial stiffness; atorvastatin; blood pressure; hypertension; pulse-wave velocity; wave reflections
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Funding
- Pfizer Hellas S.A.
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BACKGROUND Experimental and clinical data suggest that statins exert anti-inflammatory and antiproliferative actions on vasculature beyond their lipid-lowering properties. Whether these pleiotropic effects of statins translate into a beneficial effect on arterial stiffness is not clear. This study aimed to evaluate the potential effects of low-dose atorvastatin treatment on arterial stiffness and central arterial pressure waveforms in patients with mild hypertension and hypercholesterolemia. METHODS In a double-blind, randomized, placebo-controlled fashion, 50 hypertensive and hypercholesterolemic patients were allocated to receive 10 mg of atorvastatin or placebo for 26 weeks. Arterial stiffness was assessed by aortic pulse-wave velocity (PWV) using a Sphygmocor device. Central arterial pressure waveform parameters were estimated by radial artery applanation tonometry. Heart rate-adjusted augmentation index (Alx(75)) was used as measure of wave reflections. RESULTS At study end, aortic PWV (9.0 +/- 1.5 vs. 10.9 +/- 2.6 m/sec; P<0.001) and Alx(75) (24.9% +/- 9.7% vs 28.8% +/- 11.8%; P < 0.001) were significantly lower in the atorvastatin group than that placebo group. Furthermore, decreases in central aortic systolic blood pressure and pulse pressure were evident at study-end with atorvastatin but not with placebo (130 +/- 8 vs. 138 +/- 6 mm Hg, P < 0.001; 48 +/- 7 vs. 53 +/- 6 mm Hg, P < 0.05, respectively). Atorvastatin-induced reductions in aortic PWV during follow-up showed significant associations with changes in Alx(75) and central aortic systolic blood pressure and pulse pressure. CONCLUSIONS This study shows that low-dose atorvastatin treatment improves arterial stiffness and exerts a reduction on central aortic pressures. These effects may represent a potential mechanism of cardiovascular risk reduction observed with statin use.
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