Hepatitis C virus clearance by direct-acting antivirals agents improves endothelial dysfunction and subclinical atherosclerosis: HEPCAR study

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 d...

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Detalles Bibliográficos
Autores: Muñoz Hernández, Rocío, Ampuero Herrojo, Javier, Millán, Raquel, Gil Gómez, Antonio, Rojas, Ángela, Macher, Hada C., Stiefel García-Junco, Pablo Enrique, Romero Gómez, Manuel, Gallego Durán, Rocío, Maya Miles, Douglas
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2020
País:España
Institución:Universidad de Sevilla (US)
Repositorio:idUS. Depósito de Investigación de la Universidad de Sevilla
OAI Identifier:oai:idus.us.es:11441/151971
Acceso en línea:https://hdl.handle.net/11441/151971
https://doi.org/10.14309/ctg.0000000000000203
Access Level:acceso abierto
Palabra clave:Hepatitis C virus (HCV)
Sustained virological response (SVR)
Endothelial dysfunction
Subclinical atherosclerosis
Cardiovascular (CV) risk
Descripción
Sumario: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 5 0.013) and was related to significant decrease in VCAM, e-selectin (P < 0.001), and cfDNA (P 5 0.017) and to increased OLAb levels (P 5 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 5 0.006 and P 5 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.