Association of Total Atherosclerotic Burden with Progression of Penile Vascular Disease

Abstract

Background: Erectile dysfunction (ED) is an early manifestation of a generalized arterial disease. The association between penile vascular disease progression and total atherosclerotic burden was investigated using a classification that incorporates ultrasonographic assessments of intima media thickness (IMT) and plaques from both the carotid and femoral arteries. Methods: Sixty-five ED patients (mean age, 56 -10 yrs) were evaluated for cavernous vascular disease severity using penile Doppler ultrasound. Ultrasonographic assessments of IMT, lumen diameter, and plaques in the carotid and femoral arteries were evaluated, and patients were classified according to an ultrasound-based morphological system. Results: Based on the results of ultrasonic assessments, patients were divided into two groups-a high-score group and a low-score group. Patients in the high-score group had increased intima-media ( > 1.0 mm) and/or plaque in any of the four arteries. Patients in the low-score group had normal carotid and femoral IMT and an absence of plaques in all four arteries. While the two groups did not differ in blood pressure parameters, metabolic profile, and smoking status, high-score patients (n = 31) had significantly decreased age-adjusted peak systolic velocity (25.2 cm versus 32.3 cm/s, P < 0.01) and a longer duration of ED (3.8 years versus 2 years, P < 0.05), compared with low-score patients (n = 34). In the high-score group, score level was inversely correlated with peak systolic velocity after adjusting for age and systolic blood pressure (b = -0.322, P = 0.025). There also was a positive linear relation of ED duration with prevalence of high score (P < 0.05). Conclusions: In patients with vasculogenic ED, ultrasound findings of penile vasculature damage and longstanding ED correlate significantly with increasing carotid and femoral atherosclerotic burden. These data suggest a close interrelationship between progression of vasculogenic ED and peripheral atherosclerosis.