posted on 2021-02-25, 23:29authored bySareh 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
<b>Background:</b>
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.
<p><b>Research
Design and Methods:</b> 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. </p>
<p><b>Results:</b>
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.<i> </i></p>
<p><b>Conclusion:</b>
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.</p>
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.