Effect of sildenafil in cavernous arteries of patients with erectile dysfunction.

INTRODUCTION Sildenafil citrate is a type 5 phosphodiesterase inhibitor, which has demonstrated excellent results in the treatment of erectile dysfunction. The effect of sildenafil citrate in the cavernous arteries of patients with erectile dysfunction has not been established yet. The objective of this study was to assess the effect of sildenafil citrate in the cavernous arteries of patients with erectile dysfunction, following an intracavernous injection of alprostadil. MATERIALS AND METHODS 29 male patients, with mean age of 53.8 years (32 to 75 years), were prospectively evaluated. The mean time with complaint of erectile dysfunction was 50.5 months (6 to 168 months). Each patient was his own control. Patients underwent a measurement of peak systolic velocity before and after use of sildenafil citrate associated with 5 micrograms of alprostadil, through ultrasonic velocitometry Knoll/MIDUS system. In the interval between measurements, approximately 15 days, patients used 3 tablets of sildenafil at home with their partners. RESULTS Using only 5 mcg of alprostadil, average peak systolic velocity was 23.9 cm/s, and when associated to 50 mg of sildenafil it was 24.8 cm/s. Despite the increase in the flow rate caused by sildenafil, the difference was not statistically significant, Z calculated = - 0.695 NS (Wilcoxon test). Twenty one of the 29 patients (72.4%) showed global improvement in sexual performance with the use of sildenafil citrate at home. There was not a statistically significant correlation between the global response to sildenafil citrate and the increase in the peak systolic velocity. CONCLUSION We concluded that, even though the use of 50 mg of sildenafil citrate associated with 5 mcg of alprostadil provides an increase in the peak systolic velocity of the cavernous arteries, there was no statistic difference in relation to alprostadil alone. There was no correlation between the global response to sildenafil and the increase in the peak systolic velocity.