期刊
JOURNAL OF CARDIAC FAILURE
卷 28, 期 7, 页码 1128-1136出版社
CHURCHILL LIVINGSTONE INC MEDICAL PUBLISHERS
DOI: 10.1016/j.cardfail.2021.12.011
关键词
APOE epsilon 4; cardiac remodeling; Alzheimer's disease; heart failure
资金
- National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services [HHSN268201700001I, HHSN268201700002I, HHSN268201700003I, HHSN268201700004I, HHSN268201700005I]
- NHLBI [R01HL135008, R01HL143224, R01HL150342]
The genetic predisposition to Alzheimer's disease through APOEε4 is not associated with an increased prevalence of HF, HF hospitalization, myocardial remodeling, or biochemical evidence of HF.
Background: beta-Amyloid has recently been discovered in the myocardium of patients with Alzheimer's disease (AD). Whether genetic variation in apolipoprotein E (APOE) epsilon 4, 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 A beta 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 epsilon 4 carriers did not have increased risk for HF hospitalization. The APOE epsilon 4 genotype was not associated with cardiac structure and function or NT-proBNP levels. The A beta peptides were not associated with incident HF after multivariable adjustment. Conclusions: A genetic predisposition to Alzheimer's disease through APOE epsilon 4 is not associated with an increased prevalence of HF, HF hospitalization, myocardial remodeling, or biochemical evidence of HF.
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