Key result
M-TEER is linked to a ~2 mm TAPSE improvement at 1 year in baseline RV dysfunction.
Why the study?
This study aimed to assess changes in LV and RV size and function at 1 year after successful M-TEER, stratified by baseline RV function.
Does baseline right ventricular dysfunction affect biventricular remodeling after successful mitral transcatheter edge-to-edge repair in patients with severe mitral regurgitation?
Observational (n=96)
No
Does baseline right ventricular dysfunction affect biventricular remodeling after successful mitral transcatheter edge-to-edge repair in patients with severe mitral regurgitation?
Absolute Event Rate: 16% vs 14%
p-value: p=0.010
Successful mitral transcatheter edge-to-edge repair leads to positive biventricular remodeling and improved right ventricular systolic function at 1 year, regardless of the presence of baseline right ventricular dysfunction.
Similar post-M-TEER biventricular remodeling regardless of baseline RV function should not yet guide selection; leaves open validation in prospective trials.
Purpose: This study aims to retrospectively utilize the echocardiographic analysis to assess the changes in the left ventricle (LV) and right ventricle (RV) size and function after 1 year of repair, in patients who underwent successful mitral transcatheter edge-to-edge repair (M-TEER), stratified by their baseline RV function. Methods: A total of 112 patients were enrolled. Sixteen patients (14.2%) died during the 1 st year postprocedure, so that they were excluded from the study due to the nonavailability of follow-up echocardiography. Ninety-six patients were included in a single-center, observational study with 67 (69.7%) males and a mean age of 61 ± 14 years. All patients who were selected ( n = 96) had completed a 1-year follow-up after M-TEER therapy. Patients were stratified into two groups: right ventricular dysfunction ( RVdysf) group (Tricsupid annular plane systolic excursion [TAPSE] <17 mm, [ n = 59]) and No-RVdysf group (TAPSE < 17 mm, [ n = 37]). Results: Procedural success was reported in 94.8% and at baseline RV-dysf group showed greater LV end-systolic dimension (left ventricular end-systolic diameter 53 mm vs. 48 mm, P = 0.022), LV end-systolic volume (LVESV 142 ml vs. 89 ml, P = 0.028), and significantly lower LV ejection fraction (LVEF 29.7% vs. 35.8%, P = 0.038). In the RVDysf group, RV dimensions did not change significantly at follow-up but TAPSE showed improvement in RV function after mitral TEER therapy (TAPSE at baseline 14 vs. follow-up 16 mm, P = 0.010). The right ventricular systolic pressure (RVSP) also decreased significantly in the RVdysf group (RVSP 55 vs. 42.5 mmHg, P = 0.000). The left atrial volume decreased significantly (54 ml/m 2 vs. 47 ml/m 2 , P = 0.002), but no significant change was seen in the right atrial volume in this group of patients. When comparing the median differences of both groups at baseline and follow-up, some parameters show slight numerical differences between the groups, the P values generally indicate a lack of statistically significant differences. Conclusions: Patients with preexistent RV dysfunction showed greater biventricular enlargement and impaired systolic function compared to those with normal RV function. At 1-year follow-up, the M-TEER therapy resulted in positive left ventricular remodeling and improvement in right ventricular systolic function in patients with baseline RV dysfunction, but the magnitude of these improvements was not statistically different from those observed in patients with normal RV function.
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Shah et al. (2025) conducted an observational in Severe mitral regurgitation (n=96). Baseline right ventricular dysfunction vs. Normal right ventricular function was evaluated on Change in tricuspid annular plane systolic excursion (TAPSE) from baseline to 1-year follow-up in the RV dysfunction group (p=0.010). M-TEER improved TAPSE at 1 year in patients with baseline RV dysfunction (14 to 16 mm, P=0.010), though improvements did not differ significantly from patients with normal RV function.
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