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A Simplified Stepwise Approach to Echo Guidance during Percutaneous Mitral Valve Repair
Published on: October 16, 2021
Effects of dapagliflozin on main pulmonary artery diameter in patients undergoing mitral valve replacement: a
Dong Wang1, Pengxin Liu1, Xiaodong Chen1
1Department of Cardiac Surgery, The Affiliated Hospital of Qingdao University, Qingdao, China.
Objective:
To investigate the effect of preoperative use of the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin on the perioperative main pulmonary artery (MPA) diameter in patients undergoing mitral valve replacement (MVR).
Methods:
This retrospective study analyzed 196 patients who underwent MVR at the Affiliated Hospital of Qingdao University between April 2020 and April 2025. Based on preoperative dapagliflozin use, patients were divided into a Dapagliflozin group (n = 39) and a Control group (n = 157). The baseline characteristics, perioperative echocardiographic parameters, and percentage changes in serological markers were compared between the two groups.
Results:
The baseline characteristics were balanced between the two groups. Postoperatively, the percentage change in MPA diameter was significantly lower in the Dapagliflozin group (-4.09% ± 16.77%) compared to the Control group (-2.21% ± 10.92%), with a statistically significant difference (p = 0.035). However, there were no significant differences in the percentage changes in pulmonary artery systolic pressure (PASP), left ventricular ejection fraction (LVEF), right ventricular function (TAPSE), right ventricular basal diameter (RVBD), or N-terminal pro-B-type natriuretic peptide (NT-proBNP).
Conclusion:
In patients undergoing mitral valve replacement, perioperative application of dapagliflozin was independently associated with a more stable and smaller main pulmonary artery diameter. This structural benefit was dissociated from changes in estimated pulmonary artery systolic pressure, suggesting that dapagliflozin may exert positive effects on the pulmonary artery via non-pressure-dependent direct vascular protective mechanisms.
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