Henagliflozin added to standard therapy significantly reduced left ventricular mass index compared to standard therapy alone at 6 months (-2.62 vs +4.35 g/m2; P=0.007).
Cohort (n=132)
No
Does henagliflozin attenuate adverse ventricular remodeling and improve cardiometabolic parameters in patients with type 2 diabetes and hypertension?
In patients with T2DM and hypertension, the addition of henagliflozin to standard therapy for 6 months significantly attenuates adverse left ventricular remodeling and improves cardiometabolic parameters.
Absolute Event Rate: -2.62% vs 4.35%
p-value: p=0.007
Abstract Background Henagliflozin has demonstrated favorable glycemic and metabolic effects in phase III trials. However, real-world evidence regarding its impact on cardiac structure—particularly left ventricular mass index (LVMI)—in patients with type 2 diabetes mellitus (T2DM) and concomitant hypertension remains lacking. Methods In this single-center, retrospective cohort study, 183 patients with T2DM and hypertension were enrolled. After 1:1 propensity score matching, 132 patients (henagliflozin group, n = 66; control group, n = 66) were included in the primary analysis. The henagliflozin group received henagliflozin 10 mg once daily added to standard-of-care therapy, whereas the control group received standard therapy alone. The primary outcome was the change in LVMI from baseline to 6 months. Secondary outcomes included changes in other echocardiographic parameters (LVEF, E/e′, left atrial diameter, LVEDd, IVSd, LVPWT), glycemic indices (FPG, HbA1c), blood pressure, body mass index (BMI), inflammatory markers, and renal function. Results At 6 months, LVMI decreased in the henagliflozin group (from 87.90 ± 18.32 to 85.28 ± 18.20 g/m 2 ; mean change − 2.62 ± 13.00 g/m 2 ) but increased in the control group (from 83.46 ± 18.22 to 87.81 ± 16.53 g/m 2 ; mean change + 4.35 ± 15.88 g/m 2 ; between-group P = 0.007). Additionally, henagliflozin treatment was associated with significant reductions in left atrial diameter (between-group P = 0.035), E/e′ ratio ( P = 0.044), interventricular septal thickness ( P = 0.030), and left ventricular posterior wall thickness ( P = 0.018), as well as a modest increase in LVEF ( P = 0.045). Compared with the control group, the henagliflozin group also exhibited greater reductions in fasting plasma glucose (− 0.97 vs. + 0.16 mmol/L; P = 0.037), HbA1c (− 0.42% vs. + 0.04%; P = 0.021), systolic blood pressure (− 9.45 vs. − 1.95 mmHg; P = 0.023), diastolic blood pressure (− 3.38 vs. 0.68 mmHg; P = 0.029), and BMI (− 0.45 vs. 0.00 kg/m 2 ; P = 0.023). Conclusions In patients with T2DM and hypertension, the addition of henagliflozin to standard therapy over 6 months was associated with significant attenuation of adverse ventricular remodeling—as evidenced by reductions in LVMI, left atrial diameter, and diastolic filling indices—alongside clinically meaningful improvements in glycemic control, blood pressure, and body weight.
Luo et al. (Sat,) conducted a cohort in Type 2 diabetes mellitus and hypertension (n=132). Henagliflozin vs. Standard therapy alone was evaluated on Change in left ventricular mass index (LVMI) from baseline to 6 months (p=0.007). Henagliflozin added to standard therapy significantly reduced left ventricular mass index compared to standard therapy alone at 6 months (-2.62 vs +4.35 g/m2; P=0.007).
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