Two hundred and fourteen patients were initially included. Of 76 patients with a positive HCV antibody assay, 5 patients were excluded because of negative HCV RNA, 5 patients because of previous therapy for HCV and a negative HCV viral load, and 3 patients due to HCV infection with positive HBV antigenemia, leaving 63 (31%) patients with HCV/HIV coinfection and 138 (69%) HIV-monoinfected patients. Characteristics of the patients are listed in Table . Patients with HCV/HIV coinfection were more frequently intravenous drug users, were less likely to belong to the C CDC category, and tended to receive more frequently protease inhibitors and to be men. Among traditional cardiovascular risk factors, patients with HCV/HIV coinfection were more frequently smokers, and had a lower prevalence of dyslipidemia, lipid-lowering therapy, lower systolic blood pressure, lower total cholesterol, and LDL-cholesterol.
Median sVCAM-1 and sICAM-1 levels were significantly higher in HIV/HCV-coinfected than in HIV-monoinfected patients (P < 0.001 for both cases, Table ). When adjustment was performed for the variables associated with HCV (see Table ), sICAM-1 levels were still 62.4% higher in HIV/HCV coinfected patients (P < 0.001), and sVCAM-1 tended to be higher (33.1%, P = 0.08) (Table ). sICAM-1 continued to be higher in HCV-coinfected individuals when only those with an HIV viral load < 50 copies/ml were selected (Table ). There was a high correlation of sICAM-1 and sVCAM-1 with APRI (Spearman's rho = 0.42 and 0.45 respectively) and FIB-4 Spearman's rho = 0.34 and 0.39 respectively) fibrosis indexes (P < 0.001 in all cases). HCV viral load correlated with sVCAM-1 (Spearman's rho 0.36, P = 0.008), and to a lesser extent with sICAM-1 (Spearman's rho 0.25, P = 0.07). No differences between genotypes were found for sVCAM-1 or sICAM-1 in unadjusted analyses, nor after adjustment for variables associated with HCV (P = 0.66 and P = 0.46 respectively).
Association of HIV and HIV/HCV infection with flow-mediated dilatation, carotid intima-media thickness, and circulating levels of cell adhesion molecules
Median (IQR) FMD was 6.21% (2.86-9.62)% in patients HCV/HIV-coinfected and 5.54% (2.13-9.13)% in HIV-monoinfected patients (P = 0.37). No correlation was found between FMD and APRI or FIB-4 indexes. Factors associated with a lower FMD in univariate analysis were male sex (P = 0.001), dyslipidemia (P = 0.003), hypertension (P = 0.02), diabetes (P = 0.02), and lipodystrophy (P = 0.009). FMD correlated inversely with the cIMT (Spearman's rho = -0.32; P < 0.001) and with age (Spearman's rho = -0.23; P = 0.001).
Table shows the effect of HCV coinfection on FMD values. After adjustment for the variables associated with HCV and with FMD (Table ) and for baseline artery diameter, FMD remained not statistically different when patients HCV/HIV-coinfected and HIV-monoinfected were compared (17.23% higher FMD values in HCV/HIV-coinfected patients, P = 0.53). To avoid the effect of HIV viremia on the endothelial function, the same analyses were performed only in patients with undetectable viral load (< 50 copies/ml) (Table ). FMD was again not different according to HCV status.
The influence of HCV genotype on FMD was also explored. FMD values did not differ between patients with genotypes 1/4 and 2/3 (P = 0.32). Adjusted analysis generated similar results (P = 0.49).
Carotid IMT did not differ between HCV/HIV-coinfected and HIV-monoinfected patients (0.61 [0.55-0.65] mm vs 0.60 [0.53-0.72] mm; P = 0.39). After adjustment for the variables associated with HCV, the difference between the two groups remained non-significant (Table ). Analysis by genotypes yielded similar results, with no significant changes after adjustment (data not shown).