Key result
HCV coinfection in HIV is not associated with impaired endothelial function or increased CIMT.
Why the study?
Does HCV coinfection worsen endothelial function and subclinical atherosclerosis in HIV-infected patients?
Cross-Sectional (n=201)
Single-blind
No
Does HCV coinfection worsen endothelial function and subclinical atherosclerosis in HIV-infected patients?
Absolute Event Rate: 6.21% vs 5.54%
p-value: p=0.37
HCV coinfection in HIV patients increases circulating cell adhesion molecules but does not significantly worsen endothelial function or subclinical atherosclerosis.
HCV coinfection may not worsen endothelial function or atherosclerosis in HIV; leaves open whether adhesion molecule changes affect clinical events.
BACKGROUND: Relationship of hepatitis C virus (HCV) infection with an increased risk of cardiovascular disease (CVD) in HIV-infected patients remains controversial. We evaluated endothelial function and subclinical atherosclerosis in HIV-infected patients with and without HCV. METHODS: Flow-mediated dilatation (FMD) of the brachial artery and circulating levels of cell adhesion molecules (CAM) were measured in HCV/HIV-coinfected and HIV-monoinfected patients. Subclinical atherosclerosis was assessed by carotid intima-media thickness (cIMT). RESULTS: 63 (31%) HCV/HIV-coinfected and 138 (69%) HIV-monoinfected patients were included. Median soluble vascular CAM-1 (sVCAM-1) and intercellular CAM-1 (sICAM-1) levels were significantly higher in HIV/HCV-coinfected patients (P < 0.001 for both cases). Median (interquartile range) FMD was 6.21% (2.86-9.62) in HCV/HIV-coinfected and 5.54% (2.13-9.13) in HIV-monoinfected patients (P = 0.37). Adjustment for variables associated with HCV and FMD disclosed similar results. FMD correlated inversely with cIMT and age. Carotid IMT did not differ between HCV/HIV-coinfected and HIV-monoinfected patients in unadjusted (0.61 [0.55-0.65] mm vs 0.60 [0.53-0.72] mm; P = 0.39) or adjusted analyses. CONCLUSION: HCV infection was associated with higher levels of sICAM-1 and sVCAM-1, but no evidence of increased subclinical atherosclerosis was found when endothelial function was evaluated through FMD, or when assessing the cIMT.
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Masiá et al. (2011) conducted a cross-sectional in HIV infection (n=201). Hepatitis C virus (HCV) coinfection vs. HIV monoinfection (without HCV) was evaluated on Flow-mediated dilatation (FMD) of the brachial artery (p=0.37). Hepatitis C virus coinfection in HIV-infected patients was not associated with impaired endothelial function measured by brachial flow-mediated dilatation (6.21% vs 5.54%, P=0.37) or increased carotid intima-media thickness.
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