Elkhattib I, Raafat KW, Elsayed B, Elnaggar M. Chronic hepatitis C and the risk for atherosclerotic and cardiomyopathic heart disease. World J Hepatol 2025; 17(8): 108678 [DOI: 10.4254/wjh.v17.i8.108678]
Corresponding Author of This Article
Ismail Elkhattib, MD, Division of Gastroenterology and Hepatology, University of Nebraska Medical Center, 80 Seymour Street, Omaha, NE 68105, United States. ismailkhattib89@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Basant Elsayed, Faculty of Medicine, Ain Shams University, Cairo 10533, Egypt
Mohamed Elnaggar, Department of Hospital Medicine, Hartford Hospital, Hartford, CT 06102, United States
Co-first authors: Ismail Elkhattib and Kareem Wael Raafat.
Author contributions: Elkhattib I participated in the design and structure of the manuscript; Rafaat KW and Elnaggar M contributed to the review of literature, writing and elaboration of the tables; Elsayed B reviewed the paper. Elkhattib I and Rafaat KW contributed equally to this work as co-first authors.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ismail Elkhattib, MD, Division of Gastroenterology and Hepatology, University of Nebraska Medical Center, 80 Seymour Street, Omaha, NE 68105, United States. ismailkhattib89@gmail.com
Received: April 20, 2025 Revised: June 5, 2025 Accepted: July 9, 2025 Published online: August 27, 2025 Processing time: 129 Days and 9.1 Hours
Abstract
Hepatitis C virus (HCV) infection has been increasingly associated with cardiovascular complications, particularly atherosclerosis and cardiomyopathy, in addition to its primary hepatic effects. Studies indicate a higher prevalence of carotid atherosclerosis in patients with chronic hepatitis C infection, with viral load and steatosis emerging as independent risk factors. HCV-related atherosclerosis appears to develop through complex processes involving endothelial dysfunction, inflammation, oxidative stress, and immune dysregulation. Key cytokines, including tumor necrosis factor-alpha and interleukin-6, increase inflammatory responses, while oxidative stress markers, such as malondialdehyde, are associated with an increased risk of atherogenesis. In addition, HCV infection has been linked to cardiomyopathy. Direct viral effects, including HCV replication within cardiomyocytes and cytotoxicity induced by viral proteins, lead to myocardial injury and functional decline. Indirectly, HCV triggers immune-mediated damage, with heightened pro-inflammatory cytokines exacerbating cardiomyocyte apoptosis and fibrosis. Furthermore, HCV infection promotes a procoagulant imbalance, as evidenced by elevated factor VIII levels and thrombin potential, contributing to the increased cardiovascular risk. While substantial evidence indicates a relationship between HCV and cardiovascular disease, further research is needed to establish causality and guide therapeutic interventions.
Core Tip: Hepatitis C virus (HCV) infection has been shown to contribute to cardiovascular complications, extending beyond its liver-related effects. This review highlights the link between HCV and various examples of these complications, such as atherosclerosis and cardiomyopathy, emphasizing the roles of chronic inflammation, oxidative stress, immune dysregulation, and coagulation imbalance. Understanding these mechanisms may help guide future research and improve cardiovascular risk assessment and management in patients with chronic HCV infection.
