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Over a six-month period, SGLT2 inhibition with empagliflozin did not change left ventricular structure or function compared with placebo in people without diabetes or significant heart failure.
Sodium-glucose co-transporter 2 (SGLT2) inhibition with empagliflozin did not lead to significant changes in left ventricular (LV) structure or function among individuals without diabetes or significant heart failure, compared with placebo.
The findings from the Empagliflozin and Cardiac Remodeling in People Without Diabetes (EMPA-HEART 2 CardioLink-7) trial were presented in a session at the American Heart Association (AHA) Scientific Sessions 2022 in Chicago.
“This suggests that in a broader and potentially lower risk cohort of individuals without diabetes, significant LV hypertrophy and a median baseline NT-proBNP of ~ 50pg/mL, short-term SGLT2 inhibition (e.g., the 6 months study duration in EMPA-HEART 2) is unlikely to be associated with changes in LV structure or function,” wrote study author Subodh Verma, MD, PhD, Division of Cardiac Surgery, St. Michael’s Hospital, University of Toronto.
As SGLT2 inhibitors have proven benefit across the spectrum of heart failure, it has been considered that the medication class may lead to greater benefit if introduced earlier in the natural history of heart failure.
The randomized trial compared empagliflozin to placebo in a cohort without diabetes and not enriched for significant heart failure and evaluated the change in left ventricular mass over 6-months by cardiac magnetic resonance imaging (cMRI). Study enrollment occurred between April 2021 and January 2022 at two sites in Canada and one site in Taiwan.
The primary outcome was the change in left ventricular mass indexed (LVMI) to baseline body surface area between the baseline and month 6 visits in the empagliflozin and placebo groups. Further measures included in the 6-month between-group changes in LV end-diastolic and end-systolic volume and LVEF.
Of the 227 individuals who provided informed consent, 169 were randomized to either empagliflozin 10 mg/day (n = 85) or placebo (n = 84) for six months. The study population consisted of 141 men (83%) and had a mean age of 59.3 ± 10.5 years. Baseline LVMI was reported as 63.2 ± 17.9 g/m2 and 63.8 ± 14.0 g/m2 for the empagliflozin- and placebo-assigned groups, respectively.
The difference in LV mass at 6 months in the empagliflozin group compared to the placebo group adjusted for baseline LV mass was -0.83 (95% confidence interval [CI], -4.5 to 2.8; P = .65). Regarding the primary outcome, the difference in LVMi at 6 months in the empagliflozin group compared with the placebo group, adjusted for baseline LVMi, was -0.30 mg (95% CI, -2.1 to 1.5; P = .74).
Investigators had enrolled a population without significant heart failure, as explained by the baseline NT-proBNP levels. The median baseline NT-proBNP was 51 pg/mL and 55 pg/mL for the empagliflozin- and placebo-assigned groups, respectively.
Data show the 6-month treatment effect of empagliflozin versus placebo on blood pressure and NT-proBNP were -1.3 mmHg (95% CI, -5.2 to 2.6 mmHg; P = .52), 0.69 mmHg (95% CI, -1.9 to 3.3 mmHg; P = .60), and -6.1 pg/mL (95% CI, -37.0 to 24.8 pg/mL; P = .70) for systolic blood pressure, diastolic blood pressure, and NT-proBNP, respectively.
There were no clinically meaningful between-group differences in LV volumes or ejection fraction reported by investigators. Investigators noted that empagliflozin was well-tolerated and there were comparable adverse outcome rates between study arms.
The study, “Empagliflozin and Left Ventricular Remodeling in People Without Diabetes: Primary Results of the EMPA-HEART2 CardioLink-7 Randomized Clinical Trial,” was published in Circulation.