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Dysregulated carbohydrate and lipid metabolism and risk of atrial fibrillation in advanced old age
  1. Cara N Pellegrini1,2,
  2. Petra Buzkova3,
  3. Adam Oesterle1,2,
  4. Susan R Heckbert4,
  5. Russell P Tracy5,
  6. David S Siscovick6,
  7. Kenneth J Mukamal7,
  8. Luc Djoussé8,
  9. Jorge R Kizer1,2
  1. 1Medical Service, San Francisco VA Health Care System, San Francisco, CA, USA
  2. 2Medicine, University of California, San Francisco, San Francisco, CA, USA
  3. 3Biostatics, University of Washington, Seattle, Washington, USA
  4. 4Epidemiology, University of Washington, Seattle, WA, USA
  5. 5Pathology and Biochemistry, University of Vermont, Burlington, Vermont, USA
  6. 6Medicine and Epidemiology, New York Academy of Medicine, New York, New York, USA
  7. 7Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  8. 8Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Cara N Pellegrini, University of California San Francisco, San Francisco, USA; cara.pellegrini{at}ucsf.edu

Abstract

Objective Obesity and dysmetabolism are major risk factors for atrial fibrillation (AF). Fasting and postload levels of glucose and non-esterified fatty acids (NEFAs) reflect different facets of metabolic regulation. We sought to study their respective contributions to AF risk concurrently.

Methods We assessed levels of fasting and postload glucose and NEFA in the Cardiovascular Health Study to identify associations with AF incidence and, secondarily, with ECG parameters of AF risk available at baseline. Linear and Cox regressions were performed.

Results The study included 1876 participants (age 77.7±4.4). During the median follow-up of 11.4 years, 717 cases of incident AF occurred. After adjustment for potential confounders, postload glucose showed an association with incident AF (HR per SD increment of postload glucose=1.11, 95% CI 1.02 to 1.21, p=0.017). Both glucose measures, but not NEFA, were positively associated with higher P wave terminal force in V1 (PTFV1); the association remained significant only for postload glucose when the two measures were entered together (β per SD increment=138 μV·ms, 95% CI 15 to 260, p=0.028). Exploratory analyses showed significant interaction by sex for fasting NEFA (pinteraction=0.044) and postload glucose (pinteraction=0.015) relative to AF, with relationships stronger in women. For postload glucose, the association with incident AF was observed among women but not among men.

Conclusions Among older adults, postload glucose was positively associated with incident AF, with consistent findings for PTFV1. In exploratory analyses, the relationship with AF appeared specific to women. These findings require further study but suggest that interventions to address postprandial dysglycaemia late in life might reduce AF.

  • atrial fibrillation
  • epidemiology

Data availability statement

Data are available upon reasonable request.

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Data availability statement

Data are available upon reasonable request.

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Footnotes

  • Twitter @CaraPellegrini

  • Contributors Planning for this research was conducted by CNP, AO, SRH, RPT, DSS, KJM, LD and JRK.The project was conducted by CNP, PB, KJM, LD and JRK. All authors were involved in reporting the work. CNP serves as guarantor.

  • Funding This research was supported by contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086 and 75N92021D00006, and grants U01HL080295 and U01HL130114 from the National Heart, Lung, and Blood Institute (NHLBI), with additional contribution from the National Institute of Neurological Disorders and Stroke. Additional support was provided by R01AG023629 and R01AG053325 from the National Institute on Aging, and K24 HL135413 from NHBLI.

  • Competing interests JRK reports stock ownership in Abbott, Bristol-Myers Squibb, Johnson & Johnson, Medtronic, Merck and Pfizer.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.