Otto A Sanchez1, Mariana Lazo-Elizondo2, Irfan Zeb3, Russell P Tracy4, Ryan Bradley5, Daniel A Duprez6, Hossein Bahrami7, Carmen A Peralta8, Lori B Daniels9, João A Lima10, Alan Maisel11, David R Jacobs12, Mathew J Budoff13. 1. Department of Internal Medicine, Division of Renal Diseases and Hypertension, University of Minnesota, 717 Delaware, Mail Code 1932, Minneapolis, MN 55414. Electronic address: sanc0050@umn.edu. 2. Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD; Department of Epidemiology and the Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD. Electronic address: mlazo@jhu.edu. 3. Department of Cardiology, Mount Sinai St. Luke's Roosevelt Hospital (Bronx-Lebanon Hospital Center). Electronic address: izeb82@gmail.com. 4. University of Vermont College of Medicine, Burlington, VT 05405. Electronic address: russell.tracy@uvm.edu. 5. National College of Natural Medicine, SW Porter Street, Portland, OR 97201. Electronic address: rbradley@ncnm.edu. 6. Division of Cardiology, University of Minnesota, 420 Delaware St. SE. Mayo Mail Code 508, Minneapolis, MN 55455. Electronic address: dupre007@umn.edu. 7. Stanford Cardiovascular Institute, Stanford University. Electronic address: hbahrami@stanford.edu. 8. School of Medicine, University of California San Francisco, 33 Parnassus Ave, UC Hall, San Francisco, CA 94143. Electronic address: CarmenAlicia.Peralta@ucsf.edu. 9. Division of Cardiology, University of California, San Diego, Sulpizio Cardiovascular Center, 9434 Medical Center Drive, La Jolla, CA 92037. Electronic address: lbdaniels@ucsd.edu. 10. Division of Cardiology, Johns Hopkins Bayview Medical Center, 4940 Eastern Avenue, Baltimore, MD 21224. Electronic address: jlima@jhmi.edu. 11. School of Medicine, University of California, 3350 La Jolla Village Drive, Cardiology Section, mc 9111A, San Diego, CA 92161. Electronic address: amaisel@ucsd.edu. 12. School of Public Health, Division of Epidemiology & Community Health, University of Minnesota, Minneapolis, MN. Electronic address: jacob004@umn.edu. 13. Los Angeles Biomedical Research Institute, Division of Cardiology, Harbor-UCLA Medical Center, Los Angeles, CA. Electronic address: mbudoff@labiomed.org.
Abstract
BACKGROUND AND AIMS: N-terminal pro B-type natriuretic peptide (NT-proBNP) is inversely associated with diabetes mellitus, obesity and metabolic syndrome. We aim to characterize the association between NT-proBNP and nonalcoholic fatty liver disease (NAFLD), a condition strongly associated with metabolic syndrome. METHODS: 4529 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) free of cardiovascular disease, without self-reported liver disease and not diabetic at their baseline visit in 2000-2002 were included in this analysis. NAFLD was defined by a liver attenuation <40 HU. Relative prevalence (RP) for NAFLD was assessed adjusted for age, race, and sex, percentage of dietary calories derived from fat, total intentional exercise, alcoholic drinks per week, and interleukin-6 by quintiles of NT-proBNP. Adjusted linear spline model was used to characterize a non-linear association between NT-proBNP and liver fat. The inflection point (IP) was the NT-proBNP concentration where there was a change in slope in the association between liver attenuation and NT-proBNP. RESULTS: RP for NAFLD decreased by 30% from the lowest to the highest quintile of NT-proBNP, p=0.01. We observed an inverse linear association between NT-proBNP and liver fat, which plateaued (IP) at an NT-proBNP concentration of 45pg/mL. Linear regression coefficient (SE) per unit of NT-proBNP less than and greater than or equal to IP was of 0.05 (0.02), p=0.001 and 0.0006 (0.0008), p=0.5, respectively; differences between slopes, p<0.0001. CONCLUSIONS: In this cross-sectional study of a community based multiethnic sample of non-diabetic adults, low levels of NT-proBNP are associated with greater prevalence of NAFLD.
BACKGROUND AND AIMS: N-terminal pro B-type natriuretic peptide (NT-proBNP) is inversely associated with diabetes mellitus, obesity and metabolic syndrome. We aim to characterize the association between NT-proBNP and nonalcoholic fatty liver disease (NAFLD), a condition strongly associated with metabolic syndrome. METHODS: 4529 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) free of cardiovascular disease, without self-reported liver disease and not diabetic at their baseline visit in 2000-2002 were included in this analysis. NAFLD was defined by a liver attenuation <40 HU. Relative prevalence (RP) for NAFLD was assessed adjusted for age, race, and sex, percentage of dietary calories derived from fat, total intentional exercise, alcoholic drinks per week, and interleukin-6 by quintiles of NT-proBNP. Adjusted linear spline model was used to characterize a non-linear association between NT-proBNP and liver fat. The inflection point (IP) was the NT-proBNP concentration where there was a change in slope in the association between liver attenuation and NT-proBNP. RESULTS: RP for NAFLD decreased by 30% from the lowest to the highest quintile of NT-proBNP, p=0.01. We observed an inverse linear association between NT-proBNP and liver fat, which plateaued (IP) at an NT-proBNP concentration of 45pg/mL. Linear regression coefficient (SE) per unit of NT-proBNP less than and greater than or equal to IP was of 0.05 (0.02), p=0.001 and 0.0006 (0.0008), p=0.5, respectively; differences between slopes, p<0.0001. CONCLUSIONS: In this cross-sectional study of a community based multiethnic sample of non-diabetic adults, low levels of NT-proBNP are associated with greater prevalence of NAFLD.
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