The association between chronic hepatitis C infection and cardiovascular risk

P. Pateria; Gary Jeffrey; Gerry Macquillan; D. Speers; Helena Ching; M.A. Chinnaratha; Gerald Watts; Leon Adams

doi:10.1111/imj.12936

The association between chronic hepatitis C infection and cardiovascular risk

P. Pateria, Gary Jeffrey, Gerry Macquillan, D. Speers, Helena Ching, M.A. Chinnaratha, Gerald Watts, Leon Adams

Graduate Research School

Research output: Contribution to journal › Article

13 Citations (Scopus)

Abstract

© 2016 Royal Australasian College of Physicians.Background: Vascular disease is a common cause of death in patients with chronic hepatitis C (CHC) infection; however, the association between CHC and atherosclerosis is unclear. Aims: To determine whether patients with CHC have increased subclinical vascular disease and whether genotype or antiviral treatment modifies this risk. Methods: Fifty CHC patients and 22 age-matched and sex-matched healthy controls underwent clinical and biochemical assessment for vascular risk factors. In addition, vascular risk was assessed by measuring arterial stiffness (aortic augmentation index and carotid-femoral pulse wave velocity (PWV)), endothelial dysfunction (brachial artery flow-mediated dilatation (FMD) and dilatation post-glycerol trinitrate administration) and carotid intima-media thickness (CIMT). Assessment was repeated in subset of CHC patients (n=12) undergoing antiviral treatment 18months after initiation of treatment. Results: Baseline vascular risk factors and measures of arterial stiffness, endothelial dysfunction and CIMT were not different between cases and controls (P > 0.2 for all). Genotype 1 CHC patients had greater endothelial dysfunction with lower FMD (8.2 ± 3.5% vs 10.9 ± 5.2%, P = 0.03) and higher right CIMT (0.6 ± 0.1mm vs 0.5 ± 0.07mm, P = 0.04) compared with non-genotype 1. Patients who achieved sustained virological response (7/12) showed significant improvement in insulin resistance (homeostasis model of assessment of insulin resistance 2.3 ± 1.2 vs 1.8 ± 0.8, P = 0.02) and arterial stiffness (PWV 7.4 ± 1.1m/s vs 6.5 ± 0.6m/s, P = 0.04). Conclusions: Subclinical vascular disease is not greater in CHC subjects compared with controls. However, among CHC subjects, genotype 1 infection is associated with greater endothelial dysfunction and increased carotid-intima medial thickness compared with non-genotype 1 infection. Successful viral eradication may improve insulin resistance and arterial stiffness.

Original language	English
Pages (from-to)	63-70
Journal	Internal Medicine Journal
Volume	46
Issue number	1
DOIs	https://doi.org/10.1111/imj.12936
Publication status	Published - 2016

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@article{da050220c173428099fe4050f7f9bf52,

title = "The association between chronic hepatitis C infection and cardiovascular risk",

abstract = "{\textcopyright} 2016 Royal Australasian College of Physicians.Background: Vascular disease is a common cause of death in patients with chronic hepatitis C (CHC) infection; however, the association between CHC and atherosclerosis is unclear. Aims: To determine whether patients with CHC have increased subclinical vascular disease and whether genotype or antiviral treatment modifies this risk. Methods: Fifty CHC patients and 22 age-matched and sex-matched healthy controls underwent clinical and biochemical assessment for vascular risk factors. In addition, vascular risk was assessed by measuring arterial stiffness (aortic augmentation index and carotid-femoral pulse wave velocity (PWV)), endothelial dysfunction (brachial artery flow-mediated dilatation (FMD) and dilatation post-glycerol trinitrate administration) and carotid intima-media thickness (CIMT). Assessment was repeated in subset of CHC patients (n=12) undergoing antiviral treatment 18months after initiation of treatment. Results: Baseline vascular risk factors and measures of arterial stiffness, endothelial dysfunction and CIMT were not different between cases and controls (P > 0.2 for all). Genotype 1 CHC patients had greater endothelial dysfunction with lower FMD (8.2 ± 3.5% vs 10.9 ± 5.2%, P = 0.03) and higher right CIMT (0.6 ± 0.1mm vs 0.5 ± 0.07mm, P = 0.04) compared with non-genotype 1. Patients who achieved sustained virological response (7/12) showed significant improvement in insulin resistance (homeostasis model of assessment of insulin resistance 2.3 ± 1.2 vs 1.8 ± 0.8, P = 0.02) and arterial stiffness (PWV 7.4 ± 1.1m/s vs 6.5 ± 0.6m/s, P = 0.04). Conclusions: Subclinical vascular disease is not greater in CHC subjects compared with controls. However, among CHC subjects, genotype 1 infection is associated with greater endothelial dysfunction and increased carotid-intima medial thickness compared with non-genotype 1 infection. Successful viral eradication may improve insulin resistance and arterial stiffness.",

author = "P. Pateria and Gary Jeffrey and Gerry Macquillan and D. Speers and Helena Ching and M.A. Chinnaratha and Gerald Watts and Leon Adams",

year = "2016",

doi = "10.1111/imj.12936",

language = "English",

volume = "46",

pages = "63--70",

journal = "Internal Medicine Journal (Print)",

issn = "1444-0903",

publisher = "John Wiley & Sons",

number = "1",

}

TY - JOUR

T1 - The association between chronic hepatitis C infection and cardiovascular risk

AU - Pateria, P.

AU - Jeffrey, Gary

AU - Macquillan, Gerry

AU - Speers, D.

AU - Ching, Helena

AU - Chinnaratha, M.A.

AU - Watts, Gerald

AU - Adams, Leon

PY - 2016

Y1 - 2016

N2 - © 2016 Royal Australasian College of Physicians.Background: Vascular disease is a common cause of death in patients with chronic hepatitis C (CHC) infection; however, the association between CHC and atherosclerosis is unclear. Aims: To determine whether patients with CHC have increased subclinical vascular disease and whether genotype or antiviral treatment modifies this risk. Methods: Fifty CHC patients and 22 age-matched and sex-matched healthy controls underwent clinical and biochemical assessment for vascular risk factors. In addition, vascular risk was assessed by measuring arterial stiffness (aortic augmentation index and carotid-femoral pulse wave velocity (PWV)), endothelial dysfunction (brachial artery flow-mediated dilatation (FMD) and dilatation post-glycerol trinitrate administration) and carotid intima-media thickness (CIMT). Assessment was repeated in subset of CHC patients (n=12) undergoing antiviral treatment 18months after initiation of treatment. Results: Baseline vascular risk factors and measures of arterial stiffness, endothelial dysfunction and CIMT were not different between cases and controls (P > 0.2 for all). Genotype 1 CHC patients had greater endothelial dysfunction with lower FMD (8.2 ± 3.5% vs 10.9 ± 5.2%, P = 0.03) and higher right CIMT (0.6 ± 0.1mm vs 0.5 ± 0.07mm, P = 0.04) compared with non-genotype 1. Patients who achieved sustained virological response (7/12) showed significant improvement in insulin resistance (homeostasis model of assessment of insulin resistance 2.3 ± 1.2 vs 1.8 ± 0.8, P = 0.02) and arterial stiffness (PWV 7.4 ± 1.1m/s vs 6.5 ± 0.6m/s, P = 0.04). Conclusions: Subclinical vascular disease is not greater in CHC subjects compared with controls. However, among CHC subjects, genotype 1 infection is associated with greater endothelial dysfunction and increased carotid-intima medial thickness compared with non-genotype 1 infection. Successful viral eradication may improve insulin resistance and arterial stiffness.

AB - © 2016 Royal Australasian College of Physicians.Background: Vascular disease is a common cause of death in patients with chronic hepatitis C (CHC) infection; however, the association between CHC and atherosclerosis is unclear. Aims: To determine whether patients with CHC have increased subclinical vascular disease and whether genotype or antiviral treatment modifies this risk. Methods: Fifty CHC patients and 22 age-matched and sex-matched healthy controls underwent clinical and biochemical assessment for vascular risk factors. In addition, vascular risk was assessed by measuring arterial stiffness (aortic augmentation index and carotid-femoral pulse wave velocity (PWV)), endothelial dysfunction (brachial artery flow-mediated dilatation (FMD) and dilatation post-glycerol trinitrate administration) and carotid intima-media thickness (CIMT). Assessment was repeated in subset of CHC patients (n=12) undergoing antiviral treatment 18months after initiation of treatment. Results: Baseline vascular risk factors and measures of arterial stiffness, endothelial dysfunction and CIMT were not different between cases and controls (P > 0.2 for all). Genotype 1 CHC patients had greater endothelial dysfunction with lower FMD (8.2 ± 3.5% vs 10.9 ± 5.2%, P = 0.03) and higher right CIMT (0.6 ± 0.1mm vs 0.5 ± 0.07mm, P = 0.04) compared with non-genotype 1. Patients who achieved sustained virological response (7/12) showed significant improvement in insulin resistance (homeostasis model of assessment of insulin resistance 2.3 ± 1.2 vs 1.8 ± 0.8, P = 0.02) and arterial stiffness (PWV 7.4 ± 1.1m/s vs 6.5 ± 0.6m/s, P = 0.04). Conclusions: Subclinical vascular disease is not greater in CHC subjects compared with controls. However, among CHC subjects, genotype 1 infection is associated with greater endothelial dysfunction and increased carotid-intima medial thickness compared with non-genotype 1 infection. Successful viral eradication may improve insulin resistance and arterial stiffness.

U2 - 10.1111/imj.12936

DO - 10.1111/imj.12936

M3 - Article

C2 - 26477784

VL - 46

SP - 63

EP - 70

JO - Internal Medicine Journal (Print)

JF - Internal Medicine Journal (Print)

SN - 1444-0903

IS - 1

ER -