Author + information
- Received May 4, 2017
- Revision received July 14, 2017
- Accepted August 7, 2017
- Published online December 25, 2017.
- Claire A. Lawson, RN, BA, MA, PhDa,b,∗ (, )
- Peter W. Jones, BSc, MSc, PhDc,
- Lucy Teece, MSc, BScc,
- Sandra B. Dunbar, RN, PhDd,
- Petar M. Seferovic, MD, PhDe,
- Kamlesh Khunti, MD, PhDa,
- Mamas Mamas, BM, BCh, MA, DPhilb and
- Umesh T. Kadam, MPhil, MSc, PhDa,b
- aUniversity of Leicester, Diabetes Research Centre, Leicester Diabetes Centre, Leicester General Hospital, Leicester LE5 4PW, United Kingdom
- bKeele Cardiovascular Research Group, Centre for Prognosis Research, Institute of Primary Care and Health Sciences, University of Keele, Stoke-on-Trent, United Kingdom
- cFaculty of Medicine and Health Sciences, University of Keele, Stoke-on-Trent, United Kingdom
- dDepartment of Medicine, Emory University, Atlanta, Georgia
- eSchool of Medicine, University of Belgrade, Belgrade, Serbia
- ↵∗Address for correspondence:
Dr. Claire A. Lawson, Leicester Diabetes Centre, Leicester LE5 4PW, United Kingdom.
Objectives This study sought to investigate in the general heart failure (HF) population, whether the associations between type 2 diabetes (T2D) and risk of hospitalization and death, are modified by changing glycemic or drug treatment intensity.
Background In the general HF population, T2D confers a higher risk of poor outcomes, but whether this risk is modified by the diabetes status is unknown.
Methods A nested case-control study in an incident HF database cohort (2002 to 2014) compared patients with T2D with those without for risk of all-cause first hospitalization and death. T2D was stratified by categories of glycosylated hemoglobin (HbA1c) or drug treatments measured 6 months before hospitalization and 1 year before death and compared with the HF group without T2D.
Results In HF, T2D was associated with risk of first hospitalization (adjusted odds ratio [aOR]: 1.29; 95% confidence interval [CI]: 1.24 to 1.34) and mortality (aOR: 1.24; 95% CI: 1.29 to 1.40). Stratification of T2D by HbA1c levels, compared with the reference HF group without T2D, showed U-shaped associations with both outcomes. Highest risk categories were HbA1c >9.5% (hospitalization, aOR: 1.75; 95% CI: 1.52 to 2.02; mortality, aOR: 1.30; 95% CI: 1.24 to 1.47) and <5.5% (hospitalization, aOR: 1.42; 95% CI: 1.12 to 1.80; mortality, aOR: 1.29; 95% CI: 1.10 to 1.51, respectively). T2D group with change in HbA1c of >1% decrease was associated with hospitalization (aOR: 1.33; 95% CI: 1.18 to 1.49) and mortality (aOR: 1.36; 95% CI: 1.24 to 1.48). T2D drug group associations with hospitalization were no medication (aOR: 1.12; 95% CI: 1.04 to 1.19), oral antihyperglycemic only (aOR: 1.34; 95% CI: 1.27 to 1.41), oral antihyperglycemic+insulin (aOR: 1.36; 95% CI: 1.21 to 1.52), and insulin only (aOR: 1.61; 95% CI: 1.43 to 1.81); and with mortality for the same drug groups were 1.31 (95% CI: 1.23 to 1.39), 1.16 (95% CI: 1.11 to 1.22), 1.19 (95% CI: 1.06 to 1.34), and 1.43 (95% CI: 1.31 to 1.57), respectively. The T2D group with reduced drug treatments were associated with hospitalization (aOR: 2.13; 95% CI: 1.68 to 2.69) and mortality (aOR: 2.09; 95% CI: 1.81 to 2.41).
Conclusions In the general HF population, T2D stratified by glycemic control and drug treatments showed differential risk associations. Routine measures of dynamic diabetes status provide important prognostic indication of poor outcomes in HF.
This work was supported by a National Institute for Health Research (United Kingdom) Doctoral Fellowship (grant no. NIHR-DRF-2012-05-288). The study sponsors had no role in study design; in the collection, analysis, and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication. The views and opinions expressed therein are those of the authors and do not necessarily reflect those of the National Institute for Health Research (UK). Dr. Khunti has received research grant support and speaker honoraria from as well as served on the advisory board for Amgen, AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Novartis, Roche, Servier, Sanofi, Merck Sharp & Dohme Ltd., and Novo Nordisk. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received May 4, 2017.
- Revision received July 14, 2017.
- Accepted August 7, 2017.
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