RESULTS For the comparison of statins ( + /- sildenafil ) with placebo ( + /- sildenafil ) , the mean International Index of Erectile Function ( IIEF-5 ) ( the st and ardized mean difference [ SMD ] = 3.23 , 95 % confidence interval [ CI ] = -1.65 to 4.80 , P < 0.0001 ) indicated that statins ( + /- sildenafil ) showed statistically significantly greater improvements in the mean IIEF-5 compared with placebo ( + /- sildenafil ) .
For the comparison of statins plus sildenafil with placebo plus sildenafil , the mean IIEF-5 ( SMD = 3.60 , 95 % CI = 2.64 to 4.56 , P < 0.00001 ) , the IIEF domain ( SMD = 4.88 , 95%CI = 3.01 to 6.74 , P < 0.00001 ) , and the global efficacy question ( odds ratio = 6.44 , 95 % CI = 2.92 to 14.23 , P < 0.00001 ) showed that compared with placebo plus sildenafil , statins plus sildenafil clearly improved erectile function .
CONCLUSIONS This meta- analysis indicates that statins ( + /- sildenafil ) may improve ED compared with placebo ( + /- sildenafil )
INTRODUCTION It is not known if statins will improve symptoms in patients with established erectile dysfunction ( ED ) .
AIM We carried out a systematic review and meta- analysis to assess the effect of statins on ED .
Atorvastatin Restores Endothelial Function in Normocholesterolemic Smokers Independent of Changes in Low-Density Lipoprotein
Cigarette smoking impairs endothelial function . Hydroxymethylglutaryl ( HMG ) CoA reductase inhibitors ( statins ) may favorably affect endothelial function via nonlipid mechanisms . We tested the hypothesis that statins would improve endothelial function independent of changes in lipids in cigarette smokers . Twenty normocholesterolemic cigarette smokers and 20 matched healthy control subjects were r and omized to atorvastatin 40 mg daily or placebo for 4 weeks , washed out for 4 weeks , and then crossed-over to the other treatment . Baseline low-density lipoprotein ( LDL ) levels were similar in smokers and healthy subjects , 103±22 versus 95±27 mg/dL , respectively ( P = NS ) and were reduced similarly in smokers and control subjects by atorvastatin , to 55±30 and 58±20 mg/dL , respectively ( P = NS ) . Vascular ultrasonography was used to determine brachial artery , flow-mediated , endothelium-dependent , and nitroglycerin-mediated , endothelium-independent vasodilation . To eluci date potential molecular mechanisms that may account for changes in endothelial function , skin biopsy specimens were assayed for eNOS mRNA , eNOS activity , and nitrotyrosine . Endothelium-dependent vasodilation was less in smokers than nonsmoking control subjects during placebo treatment , 8.0±0.6 % versus 12.1±1.1 % , ( P=0.003 ) . Atorvastatin  increased endothelium-dependent vasodilation in smokers to 10.5±1.3 % ( P=0.017 versus placebo ) but did not change endothelium-dependent vasodilation in control subjects ( to 11.0±0.8 % , P = NS ) . Endothelium-independent vasodilation did not differ between groups during placebo treatment and was not significantly affected by atorvastatin . Multivariate analysis did not demonstrate any association between baseline lipid levels or the change in lipid levels and endothelium-dependent vasodilation . Cutaneous nitrotyrosine levels and skin microvessel eNOS mRNA , but not ENOS activity , were increased in smokers compared with controls but unaffected by atorvastatin treatment . Atorvastatin  restores endothelium-dependent vasodilation in normocholesterolemic cigarette smokers independent of changes in lipids . These results are consistent with a lipid-independent vascular benefit of statins but could not be explained by changes in eNOS message and tissue oxidative stress . These findings implicate a potential role for statin therapy to restore endothelial function and thereby investigate vascular disease in cigarette smokers
RESULTS For the comparison of statins ( + /- sildenafil ) with placebo ( + /- sildenafil ) , the mean International Index of Erectile Function ( IIEF-5 ) ( the st and ardized mean difference [ SMD ] = 3.23 , 95 % confidence interval [ CI ] = -1.65 to 4.80 , P < 0.0001 ) indicated that statins ( + /- sildenafil ) showed statistically significantly greater improvements in the mean IIEF-5 compared with placebo ( + /- sildenafil ) .
For the comparison of statins plus sildenafil with placebo plus sildenafil , the mean IIEF-5 ( SMD = 3.60 , 95 % CI = 2.64 to 4.56 , P < 0.00001 ) , the IIEF domain ( SMD = 4.88 , 95%CI = 3.01 to 6.74 , P < 0.00001 ) , and the global efficacy question ( odds ratio = 6.44 , 95 % CI = 2.92 to 14.23 , P < 0.00001 ) showed that compared with placebo plus sildenafil , statins plus sildenafil clearly improved erectile function .
CONCLUSIONS This meta- analysis indicates that statins ( + /- sildenafil ) may improve ED compared with placebo ( + /- sildenafil )
INTRODUCTION It is not known if statins will improve symptoms in patients with established erectile dysfunction ( ED ) .
AIM We carried out a systematic review and meta- analysis to assess the effect of statins on ED .