Resting_Heart_Rate_CVD_Online-Only_Supplemental_Materials_12-15-20.pdf (132.43 kB)

Risk Factors for Longitudinal Resting Heart Rate and Its Associations With Cardiovascular Outcomes in the DCCT/EDIC Study

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posted on 25.02.2021, 23:29 by Sareh Keshavarzi, Barbara H. Braffett, Rodica Pop-Busui, Trevor J. Orchard, Elsayed Z. Soliman, Gayle M. Lorenzi, Annette Barnie, Amy B. Karger, Rose A. Gubitosi-Klug, Samuel Dagogo-Jack, Andrew D. Paterson, the DCCT/EDIC Research Group
Background: Individuals with diabetes have higher resting heart rate compared to those without, which may predict long-term cardiovascular (CVD) risk. Using data from the DCCT/EDIC study, we evaluated whether the beneficial effect of intensive vs. conventional diabetes therapy on heart rate persisted, the factors mediating the differences in heart rate between treatment groups, and the effects of heart rate on future CVD risk.

Research Design and Methods: Longitudinal changes in heart rate, from annual electrocardiograms over 22 years of EDIC follow-up, were evaluated in 1402 participants with type 1 diabetes. Linear mixed models were used to assess the effect of DCCT treatment group on mean heart rate over time and Cox proportional hazards models were used to estimate the effect of heart rate on CVD risk during DCCT/EDIC.

Results: At DCCT closeout, participants were 33±7 years old, 52% male, diabetes duration 12±5 years, and HbA1c 7.4±1.2% (intensive) and 9.1±1.6% (conventional). Through EDIC, participants in the intensive group had significantly lower heart rate compared to the conventional group. While significant group differences in heart rate were fully attenuated by DCCT/EDIC mean HbA1c, higher heart rate predicted CVD and major adverse cardiovascular events (MACE) independent of other risk factors.

Conclusion: After 22 years of follow-up, former intensive vs. conventional therapy remained significantly associated with lower heart rate, consistent with the long-term beneficial effects of intensive therapy on CVD. DCCT treatment group effects on heart rate were explained by differences in DCCT/EDIC mean HbA1c.

Funding

The DCCT/EDIC has been supported by cooperative agreement grants (1982-1993, 2012-2017, 2017-2022), and contracts (1982-2012) with the Division of Diabetes Endocrinology and Metabolic Diseases of the National Institute of Diabetes and Digestive and Kidney Disease (current grant numbers U01 DK094176 and U01 DK094157), and through support by the National Eye Institute, the National Institute of Neurologic Disorders and Stroke, the General Clinical Research Centers Program (1993-2007), and Clinical Translational Science Center Program (2006-present), Bethesda, Maryland, USA.

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