Incident prolonged QT interval in midlife and late-life cognitive performance.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2020
Historique:
received: 23 08 2019
accepted: 08 02 2020
entrez: 26 2 2020
pubmed: 26 2 2020
medline: 21 5 2020
Statut: epublish

Résumé

Measures of cardiac ventricular electrophysiology have been associated with cognitive performance in cross-sectional studies. We sought to evaluate the association of worsening ventricular repolarization in midlife, as measured by incident prolonged QT interval, with cognitive decline in late life. Midlife QT interval was assessed by electrocardiography during three study visits from 1965/68 to 1971/74 in a cohort of Japanese American men aged 46-68 at Exam 1 from the Honolulu Heart Study. We defined incident prolonged QT as the QT interval in the upper quartile at Exam 2 or 3 after QT interval in lower three quartiles at Exam 1. Cognitive performance was assessed at least once using the Cognitive Abilities Screening Instrument (CASI), scored using item response theory (CASI-IRT), during four subsequent visits from 1991/93 to 1999/2000 among 2,511 of the 4,737 men in the Honolulu-Asia Aging Study otherwise eligible for inclusion in analyses. We used marginal structural modeling to determine the association of incident prolonged QT with cognitive decline, using weighting to account for confounding and attrition. Incident prolonged QT interval in midlife was not associated with late-life CASI-IRT at cognitive baseline (estimated difference in CASI-IRT: 0.04; 95% CI: -0.28, 0.35; p = 0.81), or change in CASI-IRT over time (estimated difference in annual change in CASI-IRT: -0.002; 95%CI: -0.013, 0.010; p = 0.79). Findings were consistent across sensitivity analyses. Although many midlife cardiovascular risk factors and cardiac structure and function measures are associated with late-life cognitive decline, incident prolonged QT interval in midlife was not associated with late-life cognitive performance or cognitive decline.

Sections du résumé

BACKGROUND
Measures of cardiac ventricular electrophysiology have been associated with cognitive performance in cross-sectional studies. We sought to evaluate the association of worsening ventricular repolarization in midlife, as measured by incident prolonged QT interval, with cognitive decline in late life.
METHODS
Midlife QT interval was assessed by electrocardiography during three study visits from 1965/68 to 1971/74 in a cohort of Japanese American men aged 46-68 at Exam 1 from the Honolulu Heart Study. We defined incident prolonged QT as the QT interval in the upper quartile at Exam 2 or 3 after QT interval in lower three quartiles at Exam 1. Cognitive performance was assessed at least once using the Cognitive Abilities Screening Instrument (CASI), scored using item response theory (CASI-IRT), during four subsequent visits from 1991/93 to 1999/2000 among 2,511 of the 4,737 men in the Honolulu-Asia Aging Study otherwise eligible for inclusion in analyses. We used marginal structural modeling to determine the association of incident prolonged QT with cognitive decline, using weighting to account for confounding and attrition.
RESULTS
Incident prolonged QT interval in midlife was not associated with late-life CASI-IRT at cognitive baseline (estimated difference in CASI-IRT: 0.04; 95% CI: -0.28, 0.35; p = 0.81), or change in CASI-IRT over time (estimated difference in annual change in CASI-IRT: -0.002; 95%CI: -0.013, 0.010; p = 0.79). Findings were consistent across sensitivity analyses.
CONCLUSIONS
Although many midlife cardiovascular risk factors and cardiac structure and function measures are associated with late-life cognitive decline, incident prolonged QT interval in midlife was not associated with late-life cognitive performance or cognitive decline.

Identifiants

pubmed: 32097438
doi: 10.1371/journal.pone.0229519
pii: PONE-D-19-23773
pmc: PMC7041789
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0229519

Subventions

Organisme : NIA NIH HHS
ID : R01 AG058772
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005136
Pays : United States
Organisme : NIA NIH HHS
ID : P01 AG036694
Pays : United States
Organisme : NIA NIH HHS
ID : K23 AG042492
Pays : United States
Organisme : NIA NIH HHS
ID : R13 AG030995
Pays : United States

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Claudia K Suemoto (CK)

Division of Geriatrics, University of São Paulo Medical School, São Paulo, Brazil.

Laura E Gibbons (LE)

Harborview Medical Center, University of Washington, Seattle, Washington, United States of America.

Evan L Thacker (EL)

Department of Public Health, Brigham Young University, Provo, Utah, United States of America.

Jonathan D Jackson (JD)

Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.

Claudia L Satizabal (CL)

Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, United States of America.
UT Health San Antonio, San Antonio, Texas, United States of America.

Brianne M Bettcher (BM)

Departments of Neurosurgery and Neurology, Rocky Mountain Alzheimer's Disease Center, University of Colorado Anschutz School of Medicine, Aurora, Colorado, United States of America.

Lenore Launer (L)

National Institute on Aging, Bethesda, Maryland, United States of America.

Caroline Phillips (C)

National Institute on Aging, Bethesda, Maryland, United States of America.

Lon R White (LR)

Departments of Medicine and Geriatrics, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii, United States of America.

Melinda C Power (MC)

Department of Epidemiology and Biostatistics, George Washington University Milken Institute of Public Health, Washington, DC, United States of America.

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