Pravastatin improves lipid profiles but not endothelial function
31 January 2005. Related: Conference reports, Side effects, Lipodystrophy and metabolic complications, Lipodystrophy Workshop (IWADRW) 6th Washington 2004.
Graham McKerrow, HIV i-Base
Pravastatin improves the dyslipidaemia of HIV-positive people on ART but this does not translate to improved endothelial function (EF). Persistently elevated C-reactive protein (CRP) values suggest that there may be an ongoing stimulus towards cardiovascular (CV) risk that has yet to be elucidated, Sklar and colleagues in the United States conclude from a randomised, placebo-controlled, crossover study.
Twenty-three HIV-positive patients on stable ART completed the study to evaluate the effect of pravastatin (40mg) on endothelial function, which was assessed by flow-mediated vasodilation of the brachial artery.
At baseline, HIV-positive individuals demonstrated abnormal EF compared with an otherwise healthy, HIV-negative population (mean +/- SEM, 7.0+/-0.5% HIV vs. 10.1+/-0.9 controls, p=0.002). Active treatment with pravastatin significantly reduced total cholesterol (mean -36+/-5 mg/dL, p<.001), LDL-cholesterol (-30+/-4, p<.001), and triglycerides (-69+/-25, p=.01). There was no effect on HDL-cholesterol or measures of insulin resistance.
Despite the overall improvement in metabolic risk profiles, pravastatin showed no consistent or significant improvement in EF (mean 7.0% on drug, 7.3% on placebo, P=0.68). CRP values were similarly unaffected (mean 6.3 on drug, 6.7 on placebo, p=0.85); there was no significant correlation between FMD and CRP at baseline (correlation coefficient = -0.16, p=0.45)
Reference:
Sklar PA, Grubb JR, Voell JD et al. Endothelial dysfunction in HIV-infected patients on CART does not improve even when lipid profiles improve on pravastatin. 6th Lipodystrophy Workshop (6th IWADRLH), Washington, 2004. Abstract 24. Antiviral Therapy 2004; 9:L15.