TY - JOUR
T1 - Apolipoprotein E Polymorphism, Cardiac Remodeling, and Heart Failure in the ARIC Study
AU - Selvaraj, SENTHIL
AU - CLAGGETT, BRIAN
AU - JOHANSEN, MICHELLE C.
AU - CUNNINGHAM, JONATHAN W.
AU - GOTTESMAN, REBECCA F.
AU - YU, B. I.N.G.
AU - Boerwinkle, Eric
AU - MOSLEY, THOMAS H.
AU - SHAH, AMIL M.
AU - SOLOMON, SCOTT D.
N1 - Funding Information:
Funding: The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services (contract numbers HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I and HHSN268201700005I). The authors thank the staff and participants of the ARIC study for their important contributions. The work for this manuscript was also supported by NHLBI grants R01HL135008, R01HL143224, and R01HL150342 (Amil M. Shah).
Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2022/7
Y1 - 2022/7
N2 - Background: β-Amyloid has recently been discovered in the myocardium of patients with Alzheimer's disease (AD). Whether genetic variation in apolipoprotein E (APOE) ɛ4, a common variant associated with Alzheimer's disease, is associated with incident heart failure (HF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and cardiac structure and function is unknown. Methods and Results: We studied 15,064 White and Black participants in the Atherosclerosis Risk in Communities, relating genotype status at visit 1 (1987–1989) to incident HF hospitalization using Cox regression. At visits 2, 4, and 5, we assessed NT-proBNP levels by genotype. At visits 3 and 5, we related Aβ peptides to incident HF. At visit 5 (2011–2013, n = 6251), we assessed the relationship of genotype with prevalent HF and echocardiographic parameters. The mean participant age was 54.7 ± 5.8 years, 45% were men, and 73% were White. At visit 5, there was no difference in prevalent HF by genotype. The APOE ε4 carriers did not have increased risk for HF hospitalization. The APOE ε4 genotype was not associated with cardiac structure and function or NT-proBNP levels. The Aβ peptides were not associated with incident HF after multivariable adjustment. Conclusions: A genetic predisposition to Alzheimer's disease through APOE ε4 is not associated with an increased prevalence of HF, HF hospitalization, myocardial remodeling, or biochemical evidence of HF.
AB - Background: β-Amyloid has recently been discovered in the myocardium of patients with Alzheimer's disease (AD). Whether genetic variation in apolipoprotein E (APOE) ɛ4, a common variant associated with Alzheimer's disease, is associated with incident heart failure (HF), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and cardiac structure and function is unknown. Methods and Results: We studied 15,064 White and Black participants in the Atherosclerosis Risk in Communities, relating genotype status at visit 1 (1987–1989) to incident HF hospitalization using Cox regression. At visits 2, 4, and 5, we assessed NT-proBNP levels by genotype. At visits 3 and 5, we related Aβ peptides to incident HF. At visit 5 (2011–2013, n = 6251), we assessed the relationship of genotype with prevalent HF and echocardiographic parameters. The mean participant age was 54.7 ± 5.8 years, 45% were men, and 73% were White. At visit 5, there was no difference in prevalent HF by genotype. The APOE ε4 carriers did not have increased risk for HF hospitalization. The APOE ε4 genotype was not associated with cardiac structure and function or NT-proBNP levels. The Aβ peptides were not associated with incident HF after multivariable adjustment. Conclusions: A genetic predisposition to Alzheimer's disease through APOE ε4 is not associated with an increased prevalence of HF, HF hospitalization, myocardial remodeling, or biochemical evidence of HF.
KW - APOE ɛ4
KW - Alzheimer's disease
KW - cardiac remodeling
KW - heart failure
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U2 - 10.1016/j.cardfail.2021.12.011
DO - 10.1016/j.cardfail.2021.12.011
M3 - Article
C2 - 34965472
AN - SCOPUS:85123374183
SN - 1071-9164
VL - 28
SP - 1128
EP - 1136
JO - Journal of cardiac failure
JF - Journal of cardiac failure
IS - 7
ER -