Hepatitis C Virus Clearance by Direct-Acting Antivirals Agents Improves Endothelial Dysfunction and Subclinical
Rocío Muñoz-Hernández1,2, Javier Ampuero1,2,3, Raquel Millán1
1SeLiver Group, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla, España.
Insights
Hepatitis C virus (HCV) clearance significantly improves cardiovascular health by reducing endothelial dysfunction and subclinical atherosclerosis. Treatment with direct-acting antivirals enhances vascular function and lowers key inflammatory markers.
Area of Science:
- Cardiovascular disease
- Hepatology
- Vascular biology
Background:
- Hepatitis C virus (HCV) infection is linked to increased cardiovascular (CV) risk.
- Direct-acting antiviral agents (DAAs) offer a curative treatment for HCV.
- The impact of HCV clearance on CV risk factors requires further investigation.
Purpose of the Study:
- To evaluate the effect of sustained virological response (SVR) after DAA treatment on endothelial dysfunction and subclinical atherosclerosis in HCV patients.
- To analyze changes in CV risk markers following HCV eradication.
Main Methods:
- Prospective study of 114 HCV patients treated with DAAs.
- Assessment of endothelial dysfunction (laser Doppler flowmetry) and subclinical atherosclerosis (ABI) at baseline, 12 weeks (SVR), and 1 year post-treatment.
- Measurement of lipid profile, oxidative stress markers (OLAbs), adhesion molecules (VCAM, e-selectin), angiogenesis markers, apoptotic microparticles (EMPs, PMPs), and cell-free DNA (cfDNA).
Main Results:
- HCV clearance improved endothelial function, indicated by increased hyperemia (P=0.013), and reduced levels of VCAM, e-selectin (P<0.001), and cfDNA (P=0.017).
- Subclinical atherosclerosis improved, with a significant increase in ABI (P<0.001) in patients with baseline atherosclerosis.
- Levels of endothelial and platelet microparticles (EMPs, PMPs) decreased post-SVR and at follow-up (P=0.006, P=0.002).
Conclusions:
- Sustained virological response achieved with DAAs improves endothelial dysfunction and subclinical atherosclerosis in HCV patients.
- HCV clearance positively impacts vascular health by reducing inflammatory and pro-apoptotic markers.
- This study highlights the cardiovascular benefits of HCV eradication therapy.
Introduction:
Hepatitis C virus (HCV) infection has been related to increased cardiovascular (CV) risk. The aim of this study was to analyze the impact of sustained virological response (SVR) on endothelial dysfunction and subclinical atherosclerosis in patients with hepatitis C virus treated with direct-acting antiviral agents.
Methods:
A total of 114 patients were prospectively recruited and underwent CV risk assessment including (i) endothelial dysfunction determined through laser Doppler flowmetry and (ii) subclinical atherosclerosis, elucidated by the ankle-brachial index (ABI). Atherogenic lipid profile (total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and triglycerides); markers of oxidative stress (oxidized low-density lipoprotein antibodies [OLAbs]), soluble markers of adhesion (vascular cell adhesion molecule [VCAM], e-selectin, and soluble markers of angiogenesis; and vascular endothelial growth factor, endothelial [EMPs] and platelet [PMPs] apoptotic microparticles, and cell-free DNA [cfDNA]) were measured. All determinations were performed at baseline, 12 weeks (SVR time), and 1 year after treatment.
Results:
In patients with endothelial dysfunction, area of hyperemia improved after virus clearance (P = 0.013) and was related to significant decrease in VCAM, e-selectin (P < 0.001), and cfDNA (P = 0.017) and to increased OLAb levels (P = 0.001). In patients with subclinical atherosclerosis at baseline, a significantly improved ABI was seen after HCV clearance (P < 0.001). Levels of both EMPs and PMPs also decreased after SVR and at follow-up (P = 0.006 and P = 0.002, respectively).
Discussion:
HCV clearance improved not only liver function but also endothelial dysfunction and subclinical atherosclerosis promoted by decrease in levels of VCAM, e-selectin, cfDNA, and PMPs and EMPs.
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