Association between non-alcoholic fatty liver disease and subclinical coronary atherosclerosis: An observational cohort study

Lee, Seung Bum; Park, Gyung‐Min; Lee, Jong‐Young; Lee, Byung Uk; Park, Jae Ho; Kim, Byung Gyu; Jung, Seok Won; Jeong, In Du; Bang, Sung-Jo; Shin, Jüng Woo; Park, Neung Hwa; Yang, Dong Hyun; Kang, Joon‐Won; Lim, Tae‐Hwan; Kim, Hong‐Kyu; Choe, Jaewon; Lee, Han Chu

doi:10.1016/j.jhep.2017.12.012

Cited by 123 publications

(80 citation statements)

References 33 publications

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“…These estimate the 10‐year risk of atherosclerotic cardiovascular events (including acute coronary syndrome and stroke) and have been validated in large cohorts of the general population. However, patients with NAFLD may be considered of higher risk as NAFLD is associated with various markers of subclinical atherosclerosis and high‐risk coronary disease . Furthermore, the Framingham risk score does not include key features of the metabolic syndrome (including obesity and insulin resistance), which are evidently important risk factors for atherosclerotic events in those with NAFLD .…”

Section: Introductionmentioning

confidence: 99%

Derivation and validation of a cardiovascular risk score for prediction of major acute cardiovascular events in non‐alcoholic fatty liver disease; the importance of an elevated mean platelet volume

Abeles

Mullish

Forlano

et al. 2019

Aliment Pharmacol Ther

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Summary Background Atherosclerotic cardiovascular disease is a key cause of morbidity in non‐alcoholic fatty liver disease (NAFLD) but appropriate means to predict major acute cardiovascular events (MACE) are lacking. Aim To design a bespoke cardiovascular risk score in NAFLD. Methods A retrospective derivation (2008‐2016, 356 patients) and a prospective validation (2016‐ 2017, 111 patients) NAFLD cohort study was performed. Clinical and biochemical data were recorded at enrolment and mean platelet volume (MPV), Qrisk2 and Framingham scores were recorded one year prior to MACE (Cardiovascular death, acute coronary syndrome, stroke and transient ischaemic attack). Results The derivation and validation cohorts were well‐matched, with MACE prevalence 12.6% and 12%, respectively. On univariate analysis, age, diabetes, advanced fibrosis, collagen proportionate area >5%, MPV and liver stiffness were associated with MACE. After multivariate analysis, age, diabetes and MPV remained independently predictive of MACE. The “NAFLD CV‐risk score” was generated using binary logistic regression: 0.06*(Age) + 0.963*(MPV) + 0.26*(DM1) – 16.44; 1Diabetes mellitus: 1: present; 2: absent. (AUROC 0.84). A cut‐off of −3.98 gave a sensitivity 97%, specificity 27%, PPV 16%, and NPV 99%. An MPV alone of >10.05 gave a sensitivity 97%, specificity 59%, PPV 24% and NPV 97% (AUROC 0.83). Validation cohort AUROCs were comparable at 0.77 (NAFLD CV‐risk) and 0.72 (MPV). In the full cohort, the NAFLD CV‐risk score and MPV outperformed both Qrisk2 and Framingham scores. Conclusions The NAFLD CV risk score and MPV accurately predict 1‐year risk of MACE, thereby allowing better identification of patients that require optimisation of their cardiovascular risk profile.

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Section: Introductionmentioning

confidence: 99%

Derivation and validation of a cardiovascular risk score for prediction of major acute cardiovascular events in non‐alcoholic fatty liver disease; the importance of an elevated mean platelet volume

Abeles

Mullish

Forlano

et al. 2019

Aliment Pharmacol Ther

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“…A recent meta-analysis of 26 studies (total of 85 395 participants) determined a significant independent association between NAFLD and subclinical atherosclerosis, identified by carotid artery intima-media thickness, arterial stiffness, coronary artery calcification and endothelial dysfunction [1 ▪▪ ]. Further independent association between NAFLD and noncalcified coronary artery plaques was provided through a cross-sectional study of 5121 individuals with no prior history of coronary artery disease [2 ▪▪ ]. The biological mechanisms responsible for this association are complex, involving hepatic insulin resistance, altered hepatocyte lipoprotein metabolism and dyslipidemia, and chronic hepatocyte inflammation – all in response to hepatic exposure to high concentrations of fatty acids.…”

Section: Introductionmentioning

confidence: 99%

Non-parenchymal hepatic cell lipotoxicity and the coordinated progression of non-alcoholic fatty liver disease and atherosclerosis

Peters¹,

Wilson²,

Borradaile³

2018

Current Opinion in Lipidology

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Purpose of reviewNon-alcoholic fatty liver disease (NAFLD) appears to be independently associated with the development of atherosclerosis. The biological mechanisms underlying this association are complex, and likely involve liver-resident cell types other than hepatocytes. Thus, we review recent evidence that non-parenchymal hepatic cell responses to lipid excess contribute to the pathogenesis of both NAFLD and atherosclerosis.Recent findingsSignificant independent associations between NAFLD and atherosclerosis have been identified through cross-sectional studies and meta-analyses. Mechanistic studies in cell cultures and in rodent models suggest that liver-resident macrophages, activated hepatic stellate cells (HSC) and liver sinusoidal endothelial cells (LSEC) mount lipotoxic responses under NAFLD conditions which can contribute to the progression of both NAFLD and atherosclerosis.SummaryNon-parenchymal hepatic cell types exhibit some similarity in their responses to lipid excess, and in their pathogenic mechanisms, which likely contribute to the coordinated progression of NAFLD and atherosclerosis. In response to lipotoxic conditions, macrophages, Kupffer cells and HSC initiate robust inflammatory responses, whereas LSEC generate excess reactive oxygen species (ROS). The extent to which inflammatory cytokines and ROS produced by non-parenchymal cells contribute to the progression of both NAFLD and atherosclerosis warrants further investigation.

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“…The basic demographic information was collected from a database maintained by the Health Screening and Promotion Center at the Asan Medical Center. Past medical history including angina, myocardial infarction, stroke, structural heart disease, open heart surgery, percutaneous coronary intervention, previous cardiac procedures, diabetes mellitus, hypertension, or hyperlipidemia; a family history of CAD; and smoking status was taken from the responses in the systemized self-report questionnaire issued prior to the general health examination [17].…”

Section: Clinical and Laboratory Measurementsmentioning

confidence: 99%

Homocysteine is not a risk factor for subclinical coronary atherosclerosis in asymptomatic individuals

Park

et al. 2020

PLoS ONE

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BackgroundHomocysteine has been known as a risk factor for cardiovascular disease. This study sought to evaluate the influence of homocysteine on the risk of subclinical coronary atherosclerosis in asymptomatic individuals. MethodsWe reviewed 3,186 asymptomatic individuals (mean age 53.8 ± 8.0 years, 2,202 men [69.1%]) with no prior history of coronary artery disease who voluntarily underwent coronary computed tomographic angiography (CCTA) and laboratory tests as part of a general health examination. The subjects were stratified into tertiles according to their homocysteine levels. The degree and extent of subclinical coronary atherosclerosis were assessed by CCTA. Logistic regression analysis was used to determine the association between homocysteine levels and subclinical coronary atherosclerosis. ResultsThe prevalence of significant coronary artery stenosis, any atherosclerotic, calcified, mixed, and non-calcified plaques increased with homocysteine tertiles (all p < 0.05). However, after adjustment for cardiovascular risk factors, there were no statistically significant differences in the adjusted odds ratios (ORs) for any atherosclerotic plaque (OR 1.06; 95% CI [confidence interval] 0.85-1.32; p = 0.610), calcified plaques (OR 1.17; 95% CI 0.92-1.48; p = PLOS ONE PLOS ONE | https://doi. Data Availability Statement:Data cannot be shared publicly because data contain potentially identifying or sensitive patient information. Interested readers can request the data from the 0.199), non-calcified plaques (OR 0.80; 95% CI 0.61-1.04; p = 0.089), and mixed plaques (OR 1.42; 95% CI 0.96-2.11; p = 0.077) between the third and first homocysteine tertiles. In addition, the adjusted OR for significant coronary artery stenosis (OR 0.92; 95% CI 0.63-1.36; p = 0.687) did not differ between the first and third tertiles.

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Association between non-alcoholic fatty liver disease and subclinical coronary atherosclerosis: An observational cohort study

Cited by 123 publications

References 33 publications

Derivation and validation of a cardiovascular risk score for prediction of major acute cardiovascular events in non‐alcoholic fatty liver disease; the importance of an elevated mean platelet volume

Derivation and validation of a cardiovascular risk score for prediction of major acute cardiovascular events in non‐alcoholic fatty liver disease; the importance of an elevated mean platelet volume

Non-parenchymal hepatic cell lipotoxicity and the coordinated progression of non-alcoholic fatty liver disease and atherosclerosis

Homocysteine is not a risk factor for subclinical coronary atherosclerosis in asymptomatic individuals

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