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WASHINGTON, DC—Recently, the Food and Drug Administration (FDA) approved new labeling for empagliflozin-containing medications adding data which showed that the sodium-glucose co-transporter 2 (SGLT2) inhibitor reduced the risk of cardiovascular (CV) death vs. placebo when added to standard of care type 2 diabetes (T2D) and CV medicine in adults with T2D and established CV disease.
To understand the degree to which this risk reduction with empagliflozin may be explained by changes seen in conventional CV factors, lead study author David H. Fitchett, from St. Michael’s Hospital, University of Toronto, Canada, used the UKPDS Outcomes Model v2 to simulate 3 years of CV event rates using data from 7,020 patients in the EMPA-REG OUTCOME study. The findings were presented at the ACC.17 Scientific Session.
The CV risk factors included atrial fibrillation, smoking, albuminuria, HDL and LDL cholesterol, systolic BP, HbA1c, heart rate, white blood cell count, hemoglobin and estimated glomerular filtration rate; history of ischemic heart disease, heart failure, amputation, blindness, renal failure, stroke, myocardial infarction (MI) or ulcer were also included. To calculate modeled CV relative risk reductions (RRRs), estimated absolute event rates for both empagliflozin and placebo treated patients were used.
“Multiple simulations were performed for each participant to minimize first and second order uncertainty and to optimize the precision of the confidence intervals surrounding the cardiovascular risk point estimates,” the authors noted.
Compared to observed RRRs, the simulated results imply that empagliflozin would reduce absolute placebo rates for CV death by 3%, MI (fatal and nonfatal) by 2%, all-cause mortality by 4%, heart failure by 5%, and stroke (fatal and nonfatal) by 6%.
“Empagliflozin-associated changes in conventional cardiovascular risk factor values recorded in the EMPA-REG OUTCOME trial appear to explain only a small proportion of the actual cardiovascular risk reductions observed for key endpoints,” concluded Fitchett. Other risk-reducing mechanisms need to be studied to see if the “observed changes in risk can be explained by other factors or possibly a drug specific effect, the authors added.
