Abstract 13363: Renoprotective Effects of Empagliflozin in Patients With Acute Myocardial Infarction and Type 2 Diabetes Mellitus; Subgroup Analysis of the Embody Trial

• Published in: Circulation (New York, N.Y.) N.Y.), 2020-11, Vol.142 (Suppl_3 Suppl 3), p.A13363-A13363
• Main Authors: Mozawa, Kosuke, Kubota, Yoshiaki, Hoshika, Yu, Tara, Shuhei, Tokita, Yukichi, Yodogawa, Kenji, Iwasaki, Yu-ki, Yamamoto, Takeshi, Takano, Hitoshi, Tsukada, Yayoi, Asai, Kuniya, Miyamoto, Masaaki, Miyauchi, Yasushi, Kodani, Eitaro, Maruyama, Mitsunori, Tanabe, Jun, Shimizu, Wataru
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.142.suppl_3.13363

IntroductionAlthough renoprotective effect of sodium glucose co-transporter-2 (SGLT2) inhibitors has been recognized in the patients with heart failure or type 2 diabetes mellitus (T2DM), this protection has not been fully examined in patients with acute myocardial infarction (AMI). We therefore examined renoprotection of the SGLT2 inhibitor empagliflozin in patients with AMI and T2DM. MethodsThe EMBODY trial was a prospective, multicenter, randomized, double-blind, placebo-controlled trial to identify the effect of the SGLT inhibitor on cardiac sympathetic hyperactivity in patients with AMI and T2DM in Japan. One hundred and five patients were randomized (1:1) to receive once-daily 10-mg empagliflozin, or placebo 2 weeks after the onset of AMI. In this sub-analysis, we specifically focused on the time-course of renal function on baseline, weeks 4, 12 and 24. ResultsOverall, 96 patients (64±11 y, 78 male) were included in the full analysis set (n = 46 and 50 in empagliflozin and placebo groups, respectively). In the placebo group, estimated glomerular filtration rate (eGFR) decreased from 66.1 at baseline to 62.8 mL/min/1.73m2 on week 24, (P = 0.02). On the other hand, the empagliflozin group did not worsen it (from 64.6 to 64.4 mL/min/1.73m2, P = 0.84). The empagliflozin group exhibited the significant reduction in systolic blood pressure and uric acid level from baseline to week 24 (129.7 mmHg to 123.1 mmHg, P = 0.004, and 5.8 mg/dL to 4.9 mg/dL, P < 0.0001, respectively), whereas the reduction was not significant in the placebo group (123.1 mmHg to 126.2 mmHg, P = 0.19, and 5.7 mg/dL to 5.8 mg/dL, P = 0.82, respectively). The change in eGFR from baseline to 24 weeks was negatively correlated with the changes in uric acid in the placebo group (r=0.685, P