Inflammatory Markers and Incident Heart Failure Risk in Older Adults
Open accessAbstract
Objectives The purpose of this study was to evaluate the association between inflammation and heart failure (HF) risk in older adults.Background Inflammation is associated with HF risk factors and also directly affects myocardial function.Methods The association of baseline serum concentrations of interleukin (IL)-6, tumor necrosis factor-alpha, and C-reactive protein (CRP) with incident HF was assessed with Cox models among 2,610 older persons without prevalent HF enrolled in the Health ABC (Health, Aging, and Body Composition) study (age 73.6 +/- 2.9 years; 48.3% men; 59.6% white).Results During follow-up (median 9.4 years), HF developed in 311 (11.9%) participants. In models controlling for clinical characteristics, ankle-arm index, and incident coronary heart disease, doubling of IL-6, tumor necrosis factor-alpha, and CRP concentrations was associated with 29% (95% confidence interval: 13% to 47%; p < 0.001), 46% (95% confidence interval: 17% to 84%; p = 0.001), and 9% (95% confidence interval: -1% to 24%; p = 0.087) increase in HF risk, respectively. In models including all 3 markers, IL-6, and tumor necrosis factor-alpha, but not CRP, remained significant. These associations were similar across sex and race and persisted in models accounting for death as a competing event. Post-HF ejection fraction was available in 239 (76.8%) cases; inflammatory markers had stronger association with HF with preserved ejection fraction. Repeat IL-6 and CRP determinations at 1-year follow-up did not provide incremental information. Addition of IL-6 to the clinical Health ABC HF model improved model discrimination (C index from 0.717 to 0.734; p = 0.001) and fit (decreased Bayes information criterion by 17.8; p < 0.001).Conclusions Inflammatory markers are associated with HF risk among older adults and may improve HF risk stratification.
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The inflammatory milieu further contributes to aging-associated functional decline via reactive oxidative species-mediated exacerbation of telomere dysfunction and accelerated muscle catabolism, promoting cell senescence and subsequent disease, frailty, and mortality.
“This inflammatory milieu further contributes to aging-associated functional decline via reactive oxidative species–mediated exacerbation of telomere dysfunction34 and accelerated muscle catabolism, promoting cell senescence and subsequent disease, frailty, and mortality.33,35,36”
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- Authors
- Kalogeropoulos, A., Georgiopoulou, V., Psaty, B. M., Rodondi, N., Smith, A. L., Harrison, D. G., Liu, Y., Hoffmann, U., Bauer, D. C., Newman, A. B., Kritchevsky, S. B., Harris, T. B., & Butler, J.
- Affiliations
- Emory University (US)
- University of Washington (US)
- University of Lausanne (CH)
- Wake Forest University (US)
- Harvard University (US)
- University of California, San Francisco (US)
- University of Pittsburgh (US)
- National Institutes of Health (US)
- Corresponding author
- Butler, Javed
- ORCID
- Venue
- Journal of the American College of Cardiology
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 55
- Issue
- 19
- Pages
- 2129-2137
- ISSN
- 0735-1097 (ISSN-L)
- PMC
- PMC3267799
- OpenAlex
- W1518273993
- Cited by
- 478
- References
- 55
- Citations by year
- 2026: 21 · 2025: 38 · 2024: 34 · 2023: 39 · 2022: 40 · 2021: 45 · 2020: 37 · 2019: 25 · 2018: 27 · 2017: 34 · 2016: 24 · 2015: 24 · 2014: 30 · 2013: 18 · 2012: 13
- FWCI
- 13.17
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of the American College of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion, other-oa)
- Funders
- Emory University
- National Institutes of Health (N01-AG-6-2103, n01ag062101-007, n01ag062103-006, N01‐AG‐6‐2106, n01ag062106-007, N01-AG-6-2101)
- National Institute on Aging (N01‐AG‐6–2101, R01AG028288, N01 AG062106, N01AG62106, N01-AG-62103, N01 AG062103, P30AG021332, N01 AG062101)
- National Heart, Lung, and Blood Institute (P01HL058000)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Oncology › Inflammatory Biomarkers in Disease Prognosis
- Keywords
- heart failure, inflammation, interleukin-6, TNF-α, C-reactive protein, older adults, incident heart failure risk, preserved ejection fraction, risk stratification, Health ABC Study, coronary artery disease
- MeSH terms
- Age Factors, Aged, Body Composition, C-Reactive Protein, Female, Health Status, Heart Failure, Humans, Male, Risk Factors, Tumor Necrosis Factor-alpha, Cohort Studies, Biomarkers, Interleukin-6, Incidence, Case-Control Studies
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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