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Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review
Hepatitis C (HCV) infection has an estimated global prevalence of 2.5%, causing chronic liver disease in 170 million people worldwide. Recent data has identified HCV infection as a risk factor for subclinical and clinical cardiovascular disease (CVD), but these data have been mixed and whether HCV i...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
XIA & HE Publishing Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5719192/ https://www.ncbi.nlm.nih.gov/pubmed/29226101 http://dx.doi.org/10.14218/JCTH.2017.00021 |
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author | Babiker, Ahmed Jeudy, Jean Kligerman, Seth Khambaty, Miriam Shah, Anoop Bagchi, Shashwatee |
author_facet | Babiker, Ahmed Jeudy, Jean Kligerman, Seth Khambaty, Miriam Shah, Anoop Bagchi, Shashwatee |
author_sort | Babiker, Ahmed |
collection | PubMed |
description | Hepatitis C (HCV) infection has an estimated global prevalence of 2.5%, causing chronic liver disease in 170 million people worldwide. Recent data has identified HCV infection as a risk factor for subclinical and clinical cardiovascular disease (CVD), but these data have been mixed and whether HCV is an independent risk factor for development of CVD remains controversial. In this review, we present the literature regarding the association of HCV with subclinical and clinical CVD and the possible underlying mechanisms leading to increased CVD among those infected with HCV. HCV infection leads to increased CVD via direct and indirect mechanisms with chronic inflammation, endothelial dysfunction and direct invasion of the arterial wall cited as possible mechanisms. Our review showed that HCV infection, particularly chronic HCV infection, appears to lead to increased subclinical CVD most consistently and potentially also to increased clinical CVD outcomes, leading to increased morbidity and mortality. Furthermore, the majority of studies evaluating the impact of HCV therapy on CVD morbidity and mortality showed an improvement in subclinical and clinical CVD endpoints in patients who were successfully treated and achieved sustained viral suppression. These results are of particular interest following the development of new direct antiviral agents which have made HCV eradication simple and feasible for many more patients globally, and in doing so may possibly reduce CVD morbidity and mortality in those with chronic HCV infection. |
format | Online Article Text |
id | pubmed-5719192 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | XIA & HE Publishing Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57191922017-12-08 Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review Babiker, Ahmed Jeudy, Jean Kligerman, Seth Khambaty, Miriam Shah, Anoop Bagchi, Shashwatee J Clin Transl Hepatol Review Article Hepatitis C (HCV) infection has an estimated global prevalence of 2.5%, causing chronic liver disease in 170 million people worldwide. Recent data has identified HCV infection as a risk factor for subclinical and clinical cardiovascular disease (CVD), but these data have been mixed and whether HCV is an independent risk factor for development of CVD remains controversial. In this review, we present the literature regarding the association of HCV with subclinical and clinical CVD and the possible underlying mechanisms leading to increased CVD among those infected with HCV. HCV infection leads to increased CVD via direct and indirect mechanisms with chronic inflammation, endothelial dysfunction and direct invasion of the arterial wall cited as possible mechanisms. Our review showed that HCV infection, particularly chronic HCV infection, appears to lead to increased subclinical CVD most consistently and potentially also to increased clinical CVD outcomes, leading to increased morbidity and mortality. Furthermore, the majority of studies evaluating the impact of HCV therapy on CVD morbidity and mortality showed an improvement in subclinical and clinical CVD endpoints in patients who were successfully treated and achieved sustained viral suppression. These results are of particular interest following the development of new direct antiviral agents which have made HCV eradication simple and feasible for many more patients globally, and in doing so may possibly reduce CVD morbidity and mortality in those with chronic HCV infection. XIA & HE Publishing Inc. 2017-08-31 2017-12-28 /pmc/articles/PMC5719192/ /pubmed/29226101 http://dx.doi.org/10.14218/JCTH.2017.00021 Text en © 2017 Authors. http://creativecommons.org/licenses/by-nc/4.0/ This article has been published under the terms of Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0), which permits noncommercial unrestricted use, distribution, and reproduction in any medium, provided that the following statement is provided. “This article has been published in Journal of Clinical and Translational Hepatology at DOI: 10.14218/JCTH.2017.00021 and can also be viewed on the Journal’s website at http://www.jcthnet.com”. |
spellingShingle | Review Article Babiker, Ahmed Jeudy, Jean Kligerman, Seth Khambaty, Miriam Shah, Anoop Bagchi, Shashwatee Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title | Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title_full | Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title_fullStr | Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title_full_unstemmed | Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title_short | Risk of Cardiovascular Disease Due to Chronic Hepatitis C Infection: A Review |
title_sort | risk of cardiovascular disease due to chronic hepatitis c infection: a review |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5719192/ https://www.ncbi.nlm.nih.gov/pubmed/29226101 http://dx.doi.org/10.14218/JCTH.2017.00021 |
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