Abstract
Background: Periodontal disease (PD), resulting from inflammatory host response to dysbiotic subgingival microbiota, has been linked to cardiovascular disease; however, its relationship to heart failure (HF) and its subtypes (heart failure with reduced ejection fraction [HFrEF] and heart failure with preserved ejection fraction [HFpEF]) is unexplored. Objectives: The authors hypothesize that the presence of PD is associated with increased risk of incident HF, HFpEF, and HFrEF. Methods: A total of 6,707 participants (mean age 63 ± 6 years) of the ARIC (Atherosclerosis Risk In Communities) study with full-mouth periodontal examination at visit 4 (1996-1998) and longitudinal follow-up for any incident HF (visit 4 to 2018), or incident HFpEF and HFrEF (2005-2018) were included. Periodontal status was classified as follows: healthy, PD (as per Periodontal Profile Classification [PPC]), or edentulous. Multivariable-adjusted Cox proportional hazards models were used to calculate HRs and 95% CIs for the association between PPC levels and incident HF, HFpEF, or HFrEF. Additionally, biomarkers of inflammation (C-reactive protein [CRP]) and congestion (N-terminal brain natriuretic peptide [NT-proBNP]) were assessed. Results: In total, 1,178 incident HF cases occurred (350 HFpEF, 319 HFrEF, and 509 HF of unknown type) over a median of 13 years. Of these cases, 59% had PD, whereas 18% were edentulous. PD was associated with an increased risk for HFpEF (HR: 1.35 [95% CI: 0.98-1.86]) and significantly increased risk for HFrEF (HR: 1.69 [95% CI: 1.18-2.43]), as was edentulism: HFpEF (HR: 2.00 [95% CI: 1.37-2.93]), HFrEF (HR: 2.19 [95% CI: 1.43-3.36]). Edentulism was associated with unfavorable change in CRP and NT-proBNP, whereas PD was associated only with CRP. Conclusions: Periodontal status was associated with incident HF, HFpEF, and HFrEF, as well as unfavorable changes in CRP and NT-proBNP.
Original language | English |
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Pages (from-to) | 731-741 |
Number of pages | 11 |
Journal | JACC: Heart Failure |
Volume | 10 |
Issue number | 10 |
DOIs | |
Publication status | Published - Oct 2022 |
Bibliographical note
Publisher Copyright:© 2022 American College of Cardiology Foundation
Funding
The ARIC 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, under Contract numbers (75N92022D00001, 75N92022D00002, 75N92022D00003, 75N92022D00004, 75N92022D00005). Ms Molinsky was supported by institutional training grant T32HL007779 from the National Institutes of Health, and Dr Lutsey was supported by K24 HL 159246. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Funders | Funder number |
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National Institutes of Health | |
U.S. Department of Health and Human Services | 75N92022D00003, 75N92022D00004, 75N92022D00001, K24 HL 159246, 75N92022D00002, 75N92022D00005 |
National Heart, Lung, and Blood Institute | T32HL007779 |
ASJC Scopus Subject Areas
- Cardiology and Cardiovascular Medicine