We previously showed that eradication of HCV in HIV/HCV-coinfected patients was associated a near-significant increase in the risk of cardiovascular events (Hepatology 2017; 66:344). We compared changes in 10-year Framingham cardiovascular risk (10y-CVR) and changes in noninvasive tests for preclinical atherosclerosis in coinfected patients with and without SVR receiving anti-HCV therapy (anti-HCV Rx).
We performed a multicenter prospective study between February 2012 and March 2014. Serum lipids, 10y-CVR, arterial stiffness by carotid-femoral pulse wave velocity (PWV), and carotid intima-medial thickness (cIMT) by B-mode ultrasound were assessed at baseline and 96 wk after initiation of anti-HCV Rx. Age at baseline was computed for estimation of 10y-CVR at both time-points.
We recruited 262 patients. Median age, 48 yr; males, 77%; prior IDU, 78%; HCV genotype-1, 65%; median liver stiffness, 13 kPa; anti-HCV Rx, pegylated interferon and ribavirin (PR) plus 1 direct-acting antiviral (DAA) 54%, PR 33%; all-oral DAA, 13%; concomitant ART, 98%. A total of 163 (62%) patients achieved SVR. After the exclusion of patients who died or were lost to follow-up and of those initiating statin therapy during the study period, paired measurements (baseline and wk 96) were available from 227 patients for 10y-CVR, from 128 patients for PWV, and from 49 patients for cIMT. No significant differences were found at baseline in these variables between responders and nonresponders (Table). Significantly higher changes (∆) in LDL-C and 10y-CVR were observed in responders than in non-responders (Table). No significant differences were found in ∆-PWV or ∆-cIMT between responders and nonresponders (Table).
We found that eradication of HCV in coinfected patients was associated with an increase in 10y-CVR. This change was driven by an increase in serum LDL-C. Eradication of HCV was not associated with improvements in noninvasive tests for preclinical atherosclerosis.