P299 - EMPAGLIFLOZIN AND LEFT ATRIOVENTRICULAR COUPLING INDEX IN PATIENTS WITH TYPE 2 DIABETES MELLITUS AND CORONARY ARTERY DISEASE: INSIGHTS FROM THE EMPA-HEART CARDIOLINK‐6 RANDOMIZED CONTROLLED TRIAL

Background: Although randomized controlled trials have established the efficacy of SGLT2 inhibitors in preventing cardiovascular death and heart failure in patients with diabetes, the mechanisms underlying these benefits remain incompletely understood. Left atrioventricular coupling index (LACI), defined as the ratio between the left atrial (LA) volume at left ventricular end-diastole (LAEDV) and left ventricular (LV) end-diastolic volume (LVEDV), reflects the complex interplay between LA and LV function. A higher LACI indicates more severe LV diastolic dysfunction and is a novel adverse prognosticator in diverse patient populations. The randomized controlled EMPA-HEART CardioLink-6 trial demonstrated that LV mass indexed to body surface area (LVMi) was significantly reduced after 6 months of empagliflozin treatment. This post-hoc sub-analysis of the EMPA-Heart CardioLink-6 trial evaluated the effect of empagliflozin on LACI in patients with diabetes and coronary artery disease.

METHODS AND RESULTS: EMPA-HEART CardioLink-6 assigned 97 patients with type 2 diabetes and coronary artery disease to either empagliflozin 10 mg daily or placebo for 6 months. LA and LV volumes at baseline and 6 months were independently measured on cardiac MRI by blinded readers. The change in LACI was compared between the empagliflozin and placebo groups using ANCOVA adjusted for baseline values. Spearman’s rho correlation coefficient was used to assess the relationship between baseline LACI, blood pressure, NT-pro-BNP, and LVMi.

In total, 90 patients (mean age 63 years; 7.8% women; 44 and 46 patients in the empagliflozin and placebo arms, respectively) with complete LACI data were included. At baseline, LAEDV index (27.6±8.3 ml/m2), LVEDV index(67.3±16.0ml/m2), LV ejection fraction(56.8±8.0%), LVMi (60.7±11.9g/m2) and LACI (0.18±0.8) were similar between the 2 groups. At baseline, LACI was significantly correlated with LVMi (rho=-0.27, p=0.009), but not (both p>0.10) with systolic blood pressure (rho=-0.14) or NT-pro-BNP (rho=0.019).

Over 6 months, there was no difference in the change in LACI with an adjusted difference of 0.0020 (95% CI: -0.024 to 0.027, p=0.91). Furthermore, the narrow 95% CI ruled out a meaningful difference in LACI changes between the 2 arms. There was no significant correlation between changes in LACI and LVMi (rho=-0.072, p=0.50).

Conclusion: In this study, treatment with empagliflozin for 6 months did not affect LACI in patients with diabetes and coronary artery disease. This suggests that the cardiovascular benefits of SGLT2 inhibitors may not be mediated by changes in LACI. Given the short duration of follow-up and small sample size, further studies are needed to confirm these findings.