Effects of chronic hepatitis C infection on arterial stiffness

Chang Hua Chou, Chin Shan Ho, Wei-Chuan Tsai, Ming-Cheng Wang, Yau-Sheng Tsai, Zi-Yi Chen

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Nonalcoholic fatty liver disease (NAFLD) is associated with increased arterial stiffness. Although chronic hepatitis C virus (HCV) infection was shown to be associated with metabolic disorder and chronic inflammation, the effects of chronic HCV infection on arterial stiffness remain unclear. This study recruited 221 patients including 32 normal controls, 72 NAFLD patients, and 117 subjects with HCV infection. Arterial stiffness was assessed by peripheral arterial stiffness index, Compliance Index (CI), and central arterial stiffness index, Stiffness Index derived from digital volume pulse by photoplethysmography. Levels of oxidative stress marker and inflammatory markers were also measured. The HCV group had significantly lower CI (4.8 ± 3.1 units vs. 3.9 ± 2.1 units vs. 3.0 ± 1.7 units; P for trend <.001) and higher Stiffness Index (7.0 ± 1.6 m/s vs. 8.3 ± 2.3 m/s vs. 8.4 ± 2.3 m/s; P for trend =.001) compared with the normal controls and NAFLD groups. Multivariate linear regression analysis showed that CI was independently correlated with systolic blood pressure (beta = −0.202, P =.013) and HCV infection (beta = −0.216, P =.036). Chronic HCV infection was independently associated with peripheral arterial stiffness. Peripheral arterial stiffness in chronic HCV infection was not associated with a marker of general inflammation (high-sensitivity C-reactive protein); however, a role for more specific markers of inflammation cannot be ruled out.

Original languageEnglish
Pages (from-to)716-723
Number of pages8
JournalJournal of the American Society of Hypertension
Volume11
Issue number11
DOIs
Publication statusPublished - 2017 Nov 1

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Vascular Stiffness
Chronic Hepatitis C
Hepacivirus
Virus Diseases
Infection
Compliance
Inflammation
Photoplethysmography
Blood Pressure
C-Reactive Protein
Linear Models
Oxidative Stress
Regression Analysis
Non-alcoholic Fatty Liver Disease

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Effects of chronic hepatitis C infection on arterial stiffness",
abstract = "Nonalcoholic fatty liver disease (NAFLD) is associated with increased arterial stiffness. Although chronic hepatitis C virus (HCV) infection was shown to be associated with metabolic disorder and chronic inflammation, the effects of chronic HCV infection on arterial stiffness remain unclear. This study recruited 221 patients including 32 normal controls, 72 NAFLD patients, and 117 subjects with HCV infection. Arterial stiffness was assessed by peripheral arterial stiffness index, Compliance Index (CI), and central arterial stiffness index, Stiffness Index derived from digital volume pulse by photoplethysmography. Levels of oxidative stress marker and inflammatory markers were also measured. The HCV group had significantly lower CI (4.8 ± 3.1 units vs. 3.9 ± 2.1 units vs. 3.0 ± 1.7 units; P for trend <.001) and higher Stiffness Index (7.0 ± 1.6 m/s vs. 8.3 ± 2.3 m/s vs. 8.4 ± 2.3 m/s; P for trend =.001) compared with the normal controls and NAFLD groups. Multivariate linear regression analysis showed that CI was independently correlated with systolic blood pressure (beta = −0.202, P =.013) and HCV infection (beta = −0.216, P =.036). Chronic HCV infection was independently associated with peripheral arterial stiffness. Peripheral arterial stiffness in chronic HCV infection was not associated with a marker of general inflammation (high-sensitivity C-reactive protein); however, a role for more specific markers of inflammation cannot be ruled out.",
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Effects of chronic hepatitis C infection on arterial stiffness. / Chou, Chang Hua; Ho, Chin Shan; Tsai, Wei-Chuan; Wang, Ming-Cheng; Tsai, Yau-Sheng; Chen, Zi-Yi.

In: Journal of the American Society of Hypertension, Vol. 11, No. 11, 01.11.2017, p. 716-723.

Research output: Contribution to journalArticle

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