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SUPPLEMENTAL_INFORMATION_CLEAN_5-22-2022.pdf (276.19 kB)

THE ASSOCIATION OF MEASURES OF CARDIOVASCULAR AUTONOMIC FUNCTION, HEART RATE, AND ORTHOSTATIC HYPOTENSION WITH INCIDENT GLUCOSE DISORDERS

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posted on 2022-08-02, 12:41 authored by Joshua I. Barzilay, William Tressel, Mary L. Biggs, Phyllis K. Stein, Jorge R. Kizer, Sanyog G. Shitole, Yakubu Bene-Alhasan, Kenneth J. Mukamal

  

Background: The autonomic nervous system (ANS) innervates pancreatic endocrine cells, muscle, and liver, all of which participate in glucose metabolism. We tested whether measures of cardiovascular ANS function are independently associated with incident diabetes and annual change in fasting glucose (FG) levels, as well as with insulin secretion and insulin sensitivity, in older non-diabetic adults.

Methods: Heart rate (HR) and measures of HR variability (HRV) were derived from 24-hour electrocardiographic monitoring. Blood pressure, seated and standing, was measured. Cox proportional hazards models and linear mixed models were used to analyze the associations between HRV, HR, and orthostatic hypotension (SBP >20 mmHg decline) and incident diabetes or longitudinal FG change.

Results: The mean annual unadjusted FG change was 1 mg/dL. Higher detrended fluctuation analyses (DFA) values, averaged over 4-11 (DFA1) or 12-20 beats (DFA2) - reflecting greater vs less organization of beat-to-beat intervals - were associated with less FG increase over time (per 1-SD increment: DFA1: -0.49 mg/dL/year [-0.96, -0.03]; DFA2: -0.55 mg/dL/year [-1.02, -0.09]). In mutually adjusted analyses, higher standard deviation of the N-N interval (SDNN) was associated with less FG increase over time (per 1-SD increment: SDNN: -0.62 mg/dL/year [-1.22, -0.03]). Higher values of DFA1, DFA2, and SDNN were each associated with greater insulin secretion and insulin sensitivity but not with incident diabetes. We observed no association of HR or orthostatic hypotension with diabetes or FG change.  

Conclusion: Specific measures of cardiac autonomic function are prospectively related to FG level changes and insulin secretion and action. 

Funding

This research was supported by contracts HHSN268201200036C, HHSN268200800007C, HHSN268201800001C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, N01HC85086, 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 (NINDS). Additional support was provided by R01AG023629 from the National Institute on Aging (NIA). A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

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