Abstract 13520: Empagliflozin Reduces Markers of Arterial Stiffness, Vascular Resistance and Cardiac Workload in EMPA-REG OUTCOME
Introduction: In EMPA-REG OUTCOME®, empagliflozin added to standard of care in patients with type 2 diabetes and established vascular disease, significantly reduced the primary composite outcome of CV death, non-fatal myocardial infarction or non-fatal stroke, a result driven mainly by a 38% reduction in CV death. We aimed to assess the vascular effects of empagliflozin in the trial, beyond its recognized effects in reducing systolic blood pressure (SBP) and diastolic BP (DBP).
Hypothesis: We hypothesized that empagliflozin reduced 1) pulse pressure (PP), a vascular marker of arterial stiffness determined by the cardiac output, the stiffness of elastic central arteries and wave reflection (PP = SBP - DBP), 2) mean arterial pressure (MAP), a measure reflecting the cardiac cycle determined by the cardiac output, systemic vascular resistance, and central venous pressure (MAP = ([2 x diastolic BP]+ systolic BP)/3), and 3) the double product (DP), a marker of cardiac workload and an indirect measure of myocardial oxygen demand (DP = heart rate x SBP).
Methods: Patients with type 2 diabetes and high CV risk were randomised to receive placebo, empagliflozin 10 mg, or empagliflozin 25 mg in addition to standard of care. We analysed changes from baseline to week 164 for SBP, DBP, HR, PP, MAP and DP, between treatment and placebo groups using a mixed model repeated measures analysis.
Results: In total, 2333, 2345 and 2342 patients received placebo, empagliflozin 10 mg and empagliflozin 25 mg, respectively and followed for a median period of 3.1 years. There were nominal significantly greater reductions in PP, MAP and DP with empagliflozin treatment as compared with placebo (Table), without increases in mean HR (Table).
Conclusions: Empagliflozin had favorable effects on BP, arterial stiffness, vascular resistance and on the indirect measure of cardiac workload. Further analyses are needed to determine the potential contribution of these changes to the reduction in CV mortality.
Author Disclosures: R.J. Chilton: Consultant/Advisory Board; Modest; Boehringer Ingelheim, Merck Sharp and Dohme, Pfizer and Takeda. L. Gullestad: Consultant/Advisory Board; Modest; Boehringer Ingelheim. D. Fitchett: Consultant/Advisory Board; Modest; Boehringer Ingelheim, Novo Nordisk, AstraZeneca, Sanofi, and Merck & Co. S.E. Inzucchi: Consultant/Advisory Board; Modest; Boehringer Ingelheim, Merck & Co, Janssen, Novo Nordisk, Sanofi, Regeron, Intarcia, Lexicon, Poxel, and Eli Lilly and Company. M. Mattheus: Employment; Significant; Boehringer Ingelheim. H. Woerle: Employment; Significant; Boehringer Ingelheim. O. Johansen: Employment; Significant; Boehringer Ingelheim.
- © 2016 by American Heart Association, Inc.