Long-Term Effect of Inhibition of the Angiotensin-Converting Enzyme (ACE) on Cavernosal Perfusion in Men with Atherosclerotic Erectile Dysfunction: A Pilot Study

Abstract

Introduction Impaired perfusion of the corpora cavernosa is considered an important causal factor of erectile dysfunction (ED) in the aging male with atherosclerosis. Aim On the basis of this notion, we hypothesized that inhibition of angiotensin-converting enzyme (ACE) may have a structural beneficial effect on cavernosal perfusion and subsequently on erectile function in men with impaired cavernosal perfusion. Methods A total of 59 men with atherosclerotic ED (mean age, 60.0 ± 6.8 years) and impaired cavernosal perfusion, as demonstrated with penile-pharmaco duplex ultrasonography, were randomized between an ACE inhibitor and placebo treatment arm. The minimum period of intervention was 26 weeks (26–46 weeks). The goal of the study was to demonstrate an improvement of (i) cavernosal arterial perfusion demonstrated by a decrease of blood flow velocity waveform; and (ii) erectile function in the erection domain of the International Index of Erectile Function. Results Cavernosal perfusion improved significantly (paired samples t-test, P < 0.05) in both study arms, but the improvement did not differ significantly (anova, P > 0.05) between both arms. The number of sexually active men increased, and the severity of ED decreased in both groups. Conclusion Although a persisting improvement of cavernosal perfusion by at least a 6 month-administration of an ACE inhibitor in men with advanced atherosclerotic ED could not be demonstrated in this pilot study, the beneficial effect on cavernosal perfusion, sexual activity, and erectile function in all participants of this study is remarkable. This pilot study warrants a follow-up study in sexually more active men with ED and less advanced atherosclerosis to show that ACE inhibition may result in persisting improvement of cavernosal perfusion.

Effect of prescription medications on erectile dysfunction

“…In a separate studying comparing quinapril against placebo for the treatment of hypertensive men with atherosclerotic ED, researchers found that cavernosal perfusion significantly improved in both groups. This suggests a possible psychological component to the perceived improvement in erectile function in men who use ACE inhibitors 34. Overall, ACE inhibitors likely do not adversely affect erectile function and may improve function in men with metabolic syndrome and atherosclerotic ED.…”

Telmisartan, ramipril and their combination improve endothelial function in different tissues in a murine model of cholesterol‐induced atherosclerosis

“…Previously, we observed reduction of vascular oxidative stress and endothelial dysfunction with subsequent improvement of endothelial function of penile tissue in apolipoprotein‐E‐deficient (ApoE −/− ) treated with the AT 1 receptor antagonist irbesartan, which is in line with clinical findings of advantageous effects of AT 1 receptor blockade in hypertensive patients (Fogari et al ., 2001; Dusing, 2003; Baumhakel et al ., 2008). For reduction of Ang II formation via angiotensin converting enzyme (ACE) inhibitors, comparable effects have been described (Dorrance et al ., 2002; Speel et al ., 2005).…”

Erectile dysfunction in heart failure patients: a critical reappraisal

“…Investigators attributed these results to the reduction in the vasospastic effect and free radical generation by angiotensin II and to enhancement of endothelial NO production. Moreover, in a pilot study enalapril showed a positive effect on cavernosal perfusion and erectile function in middle aged patients with atherosclerotic ED (mean age 60 AE 6.8 years) (Speel et al, 2005). In a cross-over study, Fogari et al (2001) treated 160 hypertensive men without prior sexual dysfunction with carvedilol or valsartan; patients were divided in two groups and assumed placebo for 4 weeks, then carvedilol 50 mg/die or valsartan 80 mg/die for 16 weeks and then, after additional 4 weeks placebo step, switched to the other drug for 16 weeks.…”