Relation Between Severity of Coronary Artery Disease and Aorto-Ilio-Pudendal Artery Disease in Patients With Ischemic Heart Disease-Associated Vascular Erectile Dysfunction.

BACKGROUND: The angiographically documented association between severity of coronary artery disease (CAD) and aorto-ilio-pudendal (A-I-P) artery disease and vascular erectile dysfunction (ED) was not yet settled. AIM: To assess the relation between angiographically proved CAD and A-I-P artery disease in patients with ischemic heart disease (IHD)-associated vascular ED. METHODS: 60 men were assigned to 3 study groups: Group 1 (n = 25), patients who had IHD and ED; group 2 (n = 25), patients who had IHD and had no ED; group 3 (n = 10), patients who had ED and had no suspected IHD. All patients were subjected to detailed medical, cardiac, and sexual history. International Index of Erectile Function and penile color Doppler ultrasound were used to assess ED. Quantitative coronary angiography and invasive angiography were used to assess the vascular tree for the right and left (A-I-P) arteries. Endothelial markers, that is, endothelial microparticles and endothelial progenitor cells were also assessed. OUTCOMES: The main outcome measures are assessment of ED and angiographically proved CAD and A-I-P artery disease. RESULTS: The mean age ± SD of the 3 study groups were 50.4 ± 6.6, 51.4 ± 3.9, and 49.9 ± 6.1 years, respectively, with no statistically significant difference among groups (P = .380). There were significant higher rates of left main (LM) lesions (≥50%), CAD (≥70%), right and left internal pudendal artery lesions, and right and left internal iliac artery lesions in G1 in comparison with G2 and G3. Patients with ED alone had a higher rate of peripheral lesions compared with patients with CAD alone. 10 percent of patients with ED alone had CAD. Patients in G1 had notably higher rates of peripheral lesions than the other groups combined Patients with left internal pudendal artery lesions had a chance by 1.25 and 2.11 times to have LM lesions and significant CAD, respectively. There was a significant increase of endothelial microparticles in G1 in comparison with other groups (P < .05). CLINICAL IMPLICATIONS: The clinical implications are uses of peripheral angiograghy as a diagnostic tool in patients with CAD-associated vascular ED may have a clinical merit. STRENGTHS & LIMITATIONS: The strengths in the present study are the use of angiography, color Doppler ultrasound, and standardized instruments. The main limitations are the small sample size and lack of intervention and longitudinal data. CONCLUSION: ED correlates more with A-I-P vascular lesions compared with CAD alone. There was a statistically significant association between severity of CAD including LM significant lesions and A-I-P arteries disease in patients with CAD-associated vascular ED. Sanad AM, Younis SE, Oraby, MA, et al. Relation Between Severity of Coronary Artery Disease and Aorto-Ilio-Pudendal Artery Disease in Patients With Ischemic Heart Disease-Associated Vascular Erectile Dysfunction. J Sex Med 2020;17:1086-1093.

Impact of hepatitis C virus infection on neutrophil oxidative burst function in hemodialysis patients.

Polymorphonuclear leukocyte (PMN) functions have been studied extensively in hemodialysis (HD) patients; however, results are contradictory and the mechanisms that modulate phagocytosis and oxidative burst are not completely understood. Hepatitis C virus (HCV) is a frequent complication of HD that may be associated with disturbed PMN function; however, the impact of HCV infection on neutrophil oxidative burst function in HD patients is unknown. We investigated Neutrophil oxidative burst function in 24 HD patients (15 HCV-positive and, 9 HCV-negative patients) before and after dialysis. HCV-RNA was detected by RT-nested PCR while, quantitative measurement of oxidative burst function was assessed by flowcytometry. Neutrophil Oxidised burst function was significantly diminished in HD patients as comapred to controls (P = 0.001, oxidised PMN (%); P = 0.02 mean flueresnce intensity, MFI), and in pre-dialysis as compared to post-dialysis samples (oxidised PMNs (%): 60.5 +/- 3.2 vs. 72.1 +/- 3.9, P = 0.02); (MFI: 352 +/- 42 vs. 500 +/- 50, P = 0.03). Alteration in Neutrophil oxidative burst function in the pre-dialysis samples was significant in HCV-positive patients as compared to HCV-negative patients (oxidized PMNs (%): 50 +/- 2.9 vs. 63 +/- 5.1, P = 0.02); (MFI: 291 +/- 31 vs. 438 +/- 64, P = 0.006). Marked reduction in E. coli induced burst in pre-dialysis samples compared to post-dialysis was found in HCV-positive when compared to HCV-negative patients (oxidized PMNs (%): 50 +/- 2.9 vs. 74.8 +/- 4.7, P = 0.001), (MFI: 291 +/- 31 vs. 493 +/- 63, P = 0.002). In conclusion, a possible role of concomitant HCV infection in alteration of Neutrophil oxidative burst function is highly suggested.