Apolipoprotein E Polymorphism, Cardiac Remodeling, and Heart Failure in the ARIC Study.

TitleApolipoprotein E Polymorphism, Cardiac Remodeling, and Heart Failure in the ARIC Study.
Publication TypeJournal Article
Year of Publication2022
AuthorsSelvaraj, S, Claggett, B, Johansen, MC, Cunningham, JW, Gottesman, RF, Yu, B, Boerwinkle, E, Mosley, TH, Shah, AM, Solomon, SD
JournalJ Card Fail
Volume28
Issue7
Pagination1128-1136
Date Published2022 Jul
ISSN1532-8414
KeywordsAlzheimer Disease, Apolipoprotein E4, Apolipoproteins E, Biomarkers, Female, Heart Failure, Humans, Male, Middle Aged, Natriuretic Peptide, Brain, Peptide Fragments, Ventricular Remodeling
Abstract

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.

DOI10.1016/j.cardfail.2021.12.011
Alternate JournalJ Card Fail
PubMed ID34965472
Grant ListHHSN268201700001I / HL / NHLBI NIH HHS / United States
R01 HL150342 / HL / NHLBI NIH HHS / United States
HHSN268201700004I / HL / NHLBI NIH HHS / United States
HHSN268201700002I / HL / NHLBI NIH HHS / United States
HHSN268201700003I / HL / NHLBI NIH HHS / United States
R01 HL070825 / HL / NHLBI NIH HHS / United States
R01 HL143224 / HL / NHLBI NIH HHS / United States
R01 HL135008 / HL / NHLBI NIH HHS / United States
HHSN268201700005I / HL / NHLBI NIH HHS / United States

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