Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function: The CARDIA Study

Lisa B. VanWagner; Jane E. Wilcox; Hongyan Ning; Cora E. Lewis; John Jeffrey Carr; Mary E. Rinella; Sanjiv J. Shah; Joao A.C. Lima; Donald M. Lloyd-Jones

doi:10.1161/JAHA.119.014279

Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function: The CARDIA Study

Lisa B. VanWagner, Jane E. Wilcox, Hongyan Ning, Cora E. Lewis, John Jeffrey Carr, Mary E. Rinella, Sanjiv J. Shah, Joao A.C. Lima, Donald M. Lloyd-Jones

School of Medicine

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is associated with high cardiovascular morbidity/mortality, including heart failure. Abnormalities in left ventricular (LV) structure/function are associated with heart failure risk. Methods and Results: Participants from the population-based CARDIA (Coronary Artery Risk Development in Young Adults) study year 25 exam (2010–2011, aged 43–55 years, 61% women, 48% black) with computed tomography measured liver fat and comprehensive echocardiography were included. Echocardiography was repeated at year 30 follow-up (aged 47–62 years, N=1827). NAFLD was defined as liver attenuation ≤40 HU after exclusions. LV geometry was classified into normal and abnormal by integrating relative wall thickness and LV mass index. Diastolic function was defined using Doppler and tissue Doppler imaging. Systolic function was assessed with myocardial strain measured by speckle tracking. NAFLD prevalence was 8.7% (n=159). NAFLD participants had higher LV mass, relative wall thickness, incident LV hypertrophy and abnormal LV geometry versus non-NAFLD (P<0.02). NAFLD participants had impaired LV relaxation (E/A ratio 1.1 versus 1.2), higher LV filling pressures (E/e′ ratio 7.9 versus 7.2), worse longitudinal strain (−13.9% versus −15.3%), and lower LV ejection fraction (58.9% versus 60.2%, P<0.01). In multivariable analyses adjusted for heart failure risk factors, NAFLD was independently associated with incident LV hypertrophy (odds ratio: 1.9, 95% CI: 1.1–3.4), abnormal LV geometry (odds ratio: 1.9, 1.1–3.3) and greater change in strain (odds ratio: 2.2, 1.1–4.7). Adjustment for body mass index attenuated associations to non-significance. Conclusions: NAFLD is associated with subclinical changes over time in LV structure/function and obesity explains much of the association. Presence of obesity in mid-life may identify an important at-risk population in whom to focus preventive heart failure strategies.

Original language	English (US)
Article number	e014279
Journal	Journal of the American Heart Association
Volume	9
Issue number	4
DOIs	https://doi.org/10.1161/JAHA.119.014279
State	Published - Feb 18 2020

Keywords

NAFLD
NASH
heart failure
metabolic syndrome
obesity

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine

Access to Document

10.1161/JAHA.119.014279

Cite this

VanWagner, L. B., Wilcox, J. E., Ning, H., Lewis, C. E., Carr, J. J., Rinella, M. E., Shah, S. J., Lima, J. A. C., & Lloyd-Jones, D. M. (2020). Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function: The CARDIA Study. Journal of the American Heart Association, 9(4), Article e014279. https://doi.org/10.1161/JAHA.119.014279

@article{5afaa0b4ea6e456997e8e9ae706e87b2,

title = "Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function: The CARDIA Study",

abstract = "Background: Non-alcoholic fatty liver disease (NAFLD) is associated with high cardiovascular morbidity/mortality, including heart failure. Abnormalities in left ventricular (LV) structure/function are associated with heart failure risk. Methods and Results: Participants from the population-based CARDIA (Coronary Artery Risk Development in Young Adults) study year 25 exam (2010–2011, aged 43–55 years, 61% women, 48% black) with computed tomography measured liver fat and comprehensive echocardiography were included. Echocardiography was repeated at year 30 follow-up (aged 47–62 years, N=1827). NAFLD was defined as liver attenuation ≤40 HU after exclusions. LV geometry was classified into normal and abnormal by integrating relative wall thickness and LV mass index. Diastolic function was defined using Doppler and tissue Doppler imaging. Systolic function was assessed with myocardial strain measured by speckle tracking. NAFLD prevalence was 8.7% (n=159). NAFLD participants had higher LV mass, relative wall thickness, incident LV hypertrophy and abnormal LV geometry versus non-NAFLD (P<0.02). NAFLD participants had impaired LV relaxation (E/A ratio 1.1 versus 1.2), higher LV filling pressures (E/e′ ratio 7.9 versus 7.2), worse longitudinal strain (−13.9% versus −15.3%), and lower LV ejection fraction (58.9% versus 60.2%, P<0.01). In multivariable analyses adjusted for heart failure risk factors, NAFLD was independently associated with incident LV hypertrophy (odds ratio: 1.9, 95% CI: 1.1–3.4), abnormal LV geometry (odds ratio: 1.9, 1.1–3.3) and greater change in strain (odds ratio: 2.2, 1.1–4.7). Adjustment for body mass index attenuated associations to non-significance. Conclusions: NAFLD is associated with subclinical changes over time in LV structure/function and obesity explains much of the association. Presence of obesity in mid-life may identify an important at-risk population in whom to focus preventive heart failure strategies.",

keywords = "NAFLD, NASH, heart failure, metabolic syndrome, obesity",

author = "VanWagner, {Lisa B.} and Wilcox, {Jane E.} and Hongyan Ning and Lewis, {Cora E.} and Carr, {John Jeffrey} and Rinella, {Mary E.} and Shah, {Sanjiv J.} and Lima, {Joao A.C.} and Lloyd-Jones, {Donald M.}",

note = "Funding Information: The CARDIA study is conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (HHSN268201800005I & HHSN268201800007I), Northwestern University (HHSN268201800003I), University of Minnesota (HHSN268201800006I), and Kaiser Foundation Research Institute (HHSN268201800004I). Dr VanWagner is supported by the National Institutes of Health's National Center for Advancing Translational Sciences (KL2 TR001424) and the National Heart, Lung, and Blood Institute (K23 HL136891). Dr Carr is supported by the National Institutes of Health (R01 HL098445). Dr Shah is supported by the National Institutes of Health (R01 HL107577 and R01 HL127028). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Publisher Copyright: {\textcopyright} 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.",

year = "2020",

month = feb,

day = "18",

doi = "10.1161/JAHA.119.014279",

language = "English (US)",

volume = "9",

journal = "Journal of the American Heart Association",

issn = "2047-9980",

publisher = "Wiley-Blackwell",

number = "4",

}

TY - JOUR

T1 - Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function

T2 - The CARDIA Study

AU - VanWagner, Lisa B.

AU - Wilcox, Jane E.

AU - Ning, Hongyan

AU - Lewis, Cora E.

AU - Carr, John Jeffrey

AU - Rinella, Mary E.

AU - Shah, Sanjiv J.

AU - Lima, Joao A.C.

AU - Lloyd-Jones, Donald M.

N1 - Funding Information: The CARDIA study is conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (HHSN268201800005I & HHSN268201800007I), Northwestern University (HHSN268201800003I), University of Minnesota (HHSN268201800006I), and Kaiser Foundation Research Institute (HHSN268201800004I). Dr VanWagner is supported by the National Institutes of Health's National Center for Advancing Translational Sciences (KL2 TR001424) and the National Heart, Lung, and Blood Institute (K23 HL136891). Dr Carr is supported by the National Institutes of Health (R01 HL098445). Dr Shah is supported by the National Institutes of Health (R01 HL107577 and R01 HL127028). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Publisher Copyright: © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

PY - 2020/2/18

Y1 - 2020/2/18

N2 - Background: Non-alcoholic fatty liver disease (NAFLD) is associated with high cardiovascular morbidity/mortality, including heart failure. Abnormalities in left ventricular (LV) structure/function are associated with heart failure risk. Methods and Results: Participants from the population-based CARDIA (Coronary Artery Risk Development in Young Adults) study year 25 exam (2010–2011, aged 43–55 years, 61% women, 48% black) with computed tomography measured liver fat and comprehensive echocardiography were included. Echocardiography was repeated at year 30 follow-up (aged 47–62 years, N=1827). NAFLD was defined as liver attenuation ≤40 HU after exclusions. LV geometry was classified into normal and abnormal by integrating relative wall thickness and LV mass index. Diastolic function was defined using Doppler and tissue Doppler imaging. Systolic function was assessed with myocardial strain measured by speckle tracking. NAFLD prevalence was 8.7% (n=159). NAFLD participants had higher LV mass, relative wall thickness, incident LV hypertrophy and abnormal LV geometry versus non-NAFLD (P<0.02). NAFLD participants had impaired LV relaxation (E/A ratio 1.1 versus 1.2), higher LV filling pressures (E/e′ ratio 7.9 versus 7.2), worse longitudinal strain (−13.9% versus −15.3%), and lower LV ejection fraction (58.9% versus 60.2%, P<0.01). In multivariable analyses adjusted for heart failure risk factors, NAFLD was independently associated with incident LV hypertrophy (odds ratio: 1.9, 95% CI: 1.1–3.4), abnormal LV geometry (odds ratio: 1.9, 1.1–3.3) and greater change in strain (odds ratio: 2.2, 1.1–4.7). Adjustment for body mass index attenuated associations to non-significance. Conclusions: NAFLD is associated with subclinical changes over time in LV structure/function and obesity explains much of the association. Presence of obesity in mid-life may identify an important at-risk population in whom to focus preventive heart failure strategies.

AB - Background: Non-alcoholic fatty liver disease (NAFLD) is associated with high cardiovascular morbidity/mortality, including heart failure. Abnormalities in left ventricular (LV) structure/function are associated with heart failure risk. Methods and Results: Participants from the population-based CARDIA (Coronary Artery Risk Development in Young Adults) study year 25 exam (2010–2011, aged 43–55 years, 61% women, 48% black) with computed tomography measured liver fat and comprehensive echocardiography were included. Echocardiography was repeated at year 30 follow-up (aged 47–62 years, N=1827). NAFLD was defined as liver attenuation ≤40 HU after exclusions. LV geometry was classified into normal and abnormal by integrating relative wall thickness and LV mass index. Diastolic function was defined using Doppler and tissue Doppler imaging. Systolic function was assessed with myocardial strain measured by speckle tracking. NAFLD prevalence was 8.7% (n=159). NAFLD participants had higher LV mass, relative wall thickness, incident LV hypertrophy and abnormal LV geometry versus non-NAFLD (P<0.02). NAFLD participants had impaired LV relaxation (E/A ratio 1.1 versus 1.2), higher LV filling pressures (E/e′ ratio 7.9 versus 7.2), worse longitudinal strain (−13.9% versus −15.3%), and lower LV ejection fraction (58.9% versus 60.2%, P<0.01). In multivariable analyses adjusted for heart failure risk factors, NAFLD was independently associated with incident LV hypertrophy (odds ratio: 1.9, 95% CI: 1.1–3.4), abnormal LV geometry (odds ratio: 1.9, 1.1–3.3) and greater change in strain (odds ratio: 2.2, 1.1–4.7). Adjustment for body mass index attenuated associations to non-significance. Conclusions: NAFLD is associated with subclinical changes over time in LV structure/function and obesity explains much of the association. Presence of obesity in mid-life may identify an important at-risk population in whom to focus preventive heart failure strategies.

KW - NAFLD

KW - NASH

KW - heart failure

KW - metabolic syndrome

KW - obesity

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U2 - 10.1161/JAHA.119.014279

DO - 10.1161/JAHA.119.014279

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AN - SCOPUS:85079645589

SN - 2047-9980

VL - 9

JO - Journal of the American Heart Association

JF - Journal of the American Heart Association

IS - 4

M1 - e014279

ER -

Longitudinal Association of Non-Alcoholic Fatty Liver Disease With Changes in Myocardial Structure and Function: The CARDIA Study

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