TY - JOUR
T1 - The association of non-alcoholic fatty liver disease and cardiac structure and function—Framingham Heart Study
AU - Chiu, Laura S.
AU - Pedley, Alison
AU - Massaro, Joseph M.
AU - Benjamin, Emelia J.
AU - Mitchell, Gary F.
AU - McManus, David D.
AU - Aragam, Jayashri
AU - Vasan, Ramachandran S.
AU - Cheng, Susan
AU - Long, Michelle T.
N1 - Funding Information:
This work was supported by: National Heart, Lung, and Blood Institute contracts N01‐HC‐25195 and HHSN268201500001l (Dr. Vasan) and grants R01HL126136 (Mitchell/Vasan), R01HL080124, R01HL077477, and 5R01AG047645 (Dr. Vasan), 1R01HL128914 and 2R01HL092577 (Dr. Benjamin), and the National Institute of Diabetes and Digestive and Kidney Diseases K23 DK113252 and the Boston University School of Medicine Department of Medicine (Long). Dr. Cheng was supported by R01HL131532, R01HL134168, R01HL143227 and R01HL142983 from the NIH. Dr. McManus was supported by KL2RR031981, 5R01HL126977‐02, 1R15HL121761‐01‐A1 and IUH2TR000921‐02 from the NIH. Career Investment Award to Dr. Long. Dr. Vasan is supported in part by the Evans Medical Foundation and the Jay and Louis Coffman Endowment from the Boston University School of Medicine.
Funding Information:
The authors disclose the following potential conflicts of interest: Dr. Gary F. Mitchell is the owner of Cardiovascular Engineering, Inc., serves as a consultant to and receives honoraria from Novartis, Merck, Servier, and Philips Healthcare, and is funded by research grants from Novartis and the National Institutes of Health (NIH). Dr. Susan Cheng serves as a consultant to Zogenix. Dr. David D. McManus serves as a consultant to and receives honoraria from Bristol‐Meyers Squibb, Pfizer, FlexCon, and Samsung Semiconductor and is an equity stakeholder in Mobile Sense Technologies, LLC. The remaining authors disclose no conflicts.
Publisher Copyright:
© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2020/10/1
Y1 - 2020/10/1
N2 - Background & Aims: Non-alcoholic fatty liver disease confers increased risk for cardiovascular disease, including heart failure (HF), for reasons that remain unclear. Possible pathways could involve an association of liver fat with cardiac structural or functional abnormalities even after accounting for body size. Methods: We analysed N = 2356 Framingham Heart Study participants (age 52 ± 12 years, 52% women) who underwent echocardiography and standardized computed tomography measures of liver fat. Results: In cross-sectional multivariable regression models adjusted for age, gender, cohort and cardiovascular risk factors, liver fat was positively associated with left ventricular (LV) mass (β = 1.45; 95% confidence interval (CI): 0.01, 2.88), LV wall thickness (β = 0.01; 95% CI: 0.00, 0.02), mass volume ratio (β = 0.02; 95% CI 0.01, 0.03), mitral peak velocity (E) (β = 0.83; 95% CI 0.31, 1.36) and LV filling pressure (E/e′ ratio) (β = 0.16; 95% CI 0.09, 0.23); and inversely associated with global systolic longitudinal strain (β = 0.20, 95% CI 0.07, 0.33), diastolic annular velocity (e′) (β = −0.12; 95% CI − 0.22, −0.03), and E/A ratio (β = −0.01; 95% CI − 0.02, −0.00). After additional adjustment for body mass index (BMI), statistical significance was attenuated for all associations except for that of greater liver fat with increased LV filling pressure, a possible precursor to HF (β = 0.11; 95% CI 0.03, 0.18). Conclusion: Increased liver fat was associated with multiple subclinical cardiac dysfunction measures, with most of associations mediated by obesity. Interestingly, the association of liver fat and LV filling pressure was only partially mediated by BMI, suggesting a possible direct effect of liver fat on LV filling pressure. Further confirmatory studies are needed.
AB - Background & Aims: Non-alcoholic fatty liver disease confers increased risk for cardiovascular disease, including heart failure (HF), for reasons that remain unclear. Possible pathways could involve an association of liver fat with cardiac structural or functional abnormalities even after accounting for body size. Methods: We analysed N = 2356 Framingham Heart Study participants (age 52 ± 12 years, 52% women) who underwent echocardiography and standardized computed tomography measures of liver fat. Results: In cross-sectional multivariable regression models adjusted for age, gender, cohort and cardiovascular risk factors, liver fat was positively associated with left ventricular (LV) mass (β = 1.45; 95% confidence interval (CI): 0.01, 2.88), LV wall thickness (β = 0.01; 95% CI: 0.00, 0.02), mass volume ratio (β = 0.02; 95% CI 0.01, 0.03), mitral peak velocity (E) (β = 0.83; 95% CI 0.31, 1.36) and LV filling pressure (E/e′ ratio) (β = 0.16; 95% CI 0.09, 0.23); and inversely associated with global systolic longitudinal strain (β = 0.20, 95% CI 0.07, 0.33), diastolic annular velocity (e′) (β = −0.12; 95% CI − 0.22, −0.03), and E/A ratio (β = −0.01; 95% CI − 0.02, −0.00). After additional adjustment for body mass index (BMI), statistical significance was attenuated for all associations except for that of greater liver fat with increased LV filling pressure, a possible precursor to HF (β = 0.11; 95% CI 0.03, 0.18). Conclusion: Increased liver fat was associated with multiple subclinical cardiac dysfunction measures, with most of associations mediated by obesity. Interestingly, the association of liver fat and LV filling pressure was only partially mediated by BMI, suggesting a possible direct effect of liver fat on LV filling pressure. Further confirmatory studies are needed.
KW - heart failure
KW - non-alcoholic fatty liver disease
KW - subclinical cardiovascular disease
UR - http://www.scopus.com/inward/record.url?scp=85088384472&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85088384472&partnerID=8YFLogxK
U2 - 10.1111/liv.14600
DO - 10.1111/liv.14600
M3 - Article
C2 - 32654390
AN - SCOPUS:85088384472
VL - 40
SP - 2445
EP - 2454
JO - Liver International
JF - Liver International
SN - 1478-3223
IS - 10
ER -