Early SGLT2 inhibitor use is associated with improved left atrial strain following acute coronary syndrome

Abstract

Aim

Left atrial (LA) strain, a novel marker of LA function, reliably predicts diastolic dysfunction. SGLT2 inhibitors improve heart failure outcomes, but limited data exists regarding their use in the immediate aftermath of acute coronary syndrome (ACS). We studied the effect of empagliflozin on LA strain in patients with type 2 diabetes (T2D) and ACS.

Methods

Patients with ACS and T2D were identified and empagliflozin was initiated in eligible patients prior to discharge. Patients not initiated on empagliflozin were analysed as a comparator group. A blinded investigator assessed LA strain using baseline and 3–6 month follow-up echocardiograms.

Results

Forty-four participants (n = 22 each group) were included. Baseline characteristics and LA strain were similar in the two groups. LA reservoir, conduit and contractile strain increased in empagliflozin group (28.0 ± 8.4% to 34.6 ± 12.2% p < 0.001, 14.5 ± 5.4% to 16.7 ± 7.0% p = 0.034, 13.5 ± 5.2% to 17.9 ± 7.2% p = 0.005, respectively) but remained unchanged in comparison group (29.2 ± 6.7% to 28.8 ± 7.0%, 12.8 ± 4.2% to 13.3 ± 4.7%, 16.7 ± 5.3% to 15.5 ± 4.5%, respectively, p = NS). The difference in change between groups was significant for LA reservoir (p = 0.003) and contractile strain (p = 0.005).

Conclusion

In patients with ACS and T2D, addition of empagliflozin to standard ACS therapy prior to discharge is associated with improved LA function.

Keywords:

• Left atrial strain
• empagliflozin
• diastolic function
• acute coronary syndrome

Authors’ contributions

All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by Amro Sehly and Nick Lan. The first draft of the manuscript was written by Amro Sehly and all authors commented on previous versions of the manuscript. All authors read and approved the final manuscript.

Ethics approval and consent

Ethical approval was obtained from the South Metropolitan Health Service Human Research Ethics Committee (RGS-3023) and the study was conducted according to the principles of the Declaration of Helsinki. All participants provided written informed consent.

Disclosure statement

PGF has received speaker honoraria and conference support from Sanofi, MSD, Boehringer Ingelheim, Lilly, AstraZeneca and Novo Nordisk. BBY has received speaker honoraria and conference support from Sanofi, MSD, Boehringer Ingelheim, Lilly, AstraZeneca, Novo Nordisk, and Takeda, and has participated in advisory committees for Sanofi, Lilly, and Novartis. GD reports paid lectures from AstraZeneca, Pfizer and Amgen not related to the topic in the manuscript and provides consultancy services and has equity interest in Artrya Ltd. NSRL has received research funding from Sanofi as part of a Clinical Fellowship in Endocrinology and Diabetes, education support from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Eli Lilly and Novartis, speaker honoraria from AstraZeneca, Boehringer Ingelheim, Eli Lilly, Novartis and Sanofi, and has participated in advisory boards for Eli Lilly.

Additional information

Funding

We would like to thank Diabetes Research Western Australia for their ongoing funding support of this work.