Abstract
Background
A small baseline mitral valve area (MVA) raises concern for iatrogenic mitral stenosis due to increased transmitral pressure gradients (TMPG) after mitral transcatheter edge-to-edge repair (M-TEER). Outcomes in patients with MVA <4.0 cm² remain limited, as this population has been largely excluded from clinical trials.
Methods
We retrospectively analyzed 305 consecutive patients who underwent M-TEER (2014-2022). Patients were stratified by baseline MVA (<4.0 cm2 vs. ≥4.0 cm2). The primary endpoint was 2-year all-cause mortality. Secondary endpoints included heart failure hospitalization (HFH), mitral regurgitation (MR) reduction, New York Heart Association functional class improvement, and postprocedural TMPG.
Results
Of 305 patients, 66 (21.6%) had MVA <4.0 cm². Women were more prevalent in the small MVA group (57.6% vs. 42.7%; p = 0.03). Patients with smaller MVA received fewer clips (1.3 ± 0.07 vs. 1.5 ± 0.04; p = 0.03). Procedural success and in-hospital outcomes were comparable. At discharge, residual MR (<moderate) and New York Heart Association class were similar, although TMPG was higher in the small group (3.9 ± 0.2 vs. 3.3 ± 0.1 mmHg; p = 0.006). At 30 days and 1 year, mortality, HFH, and residual MR rates remained similar. Two-year Kaplan–Meier analyses showed no differences in survival, HFH, or composite outcomes. In multivariable analysis, age, creatinine, and hemoglobin predicted mortality, while age, LVEF, and hemoglobin predicted the composite outcome. Indexed MVA did not predict mortality or elevated TMPG.
Conclusions
M-TEER can be safely and effectively performed in patients with baseline MVA <4.0 cm2 without adverse clinical outcomes through 2 years.
Keywords: MitraClip, Mitral regurgitation, Mitral transcatheter edge-to-edge repair, Mitral valve area, Percutaneous mitral valve repair
Highlights
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M-TEER is safe and effective in patients with baseline MVA <4.0 cm2, achieving similar MR reduction and NYHA improvement as those with MVA ≥4.0 cm2.
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Smaller MVA is associated with higher postprocedural TMPG and fewer clips, but these differences do not impact clinical outcomes.
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Two-year survival and HFH are comparable between patients with MVA <3.5 cm2 and 3.5 to 4.0 cm2.
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Clinical factors (age, preprocedural hemoglobin, creatinine, and LVEF) remain the strongest predictors of adverse outcomes.
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MVA <3.0 cm2 remains challenging and unsuitable for M-TEER; larger studies are needed to define limits in extremely small valve areas.
Introduction
Mitral transcatheter edge-to-edge repair (M-TEER) offers a percutaneous alternative to surgical mitral valve (MV) repair for patients with symptomatic severe primary mitral regurgitation (MR) who are deemed high or prohibitive surgical risk and for patients with symptomatic severe secondary MR who have been treated with maximally tolerated guideline-directed medical therapy.1 Similar to the surgical Alfieri stitch, M-TEER effectively reduces MR by approximating the anterior and posterior MV leaflets, thus creating a double-orifice configuration that reduces the mitral valve area (MVA).2,3
Multiple studies have shown that M-TEER can result in a 30% to 65% reduction in MVA, especially in cases requiring multiple clips.4, 5, 6 Baseline MVA <4.0 cm2 and a baseline transmitral pressure gradient (TMPG) >4 mmHg have been associated with an increased risk of elevated postprocedural TMPG, which is considered an independent predictor of adverse outcomes after M-TEER.7,8,9 To mitigate the risk of iatrogenic mitral stenosis, M-TEER is generally reserved for patients with a baseline MVA >4.0 cm2. In fact, major clinical trials and registries have excluded patients with MVA<4.0 cm2.10,11,12,13
However, in real-world practice, patients with small MVA and severe symptomatic MR may not have alternative treatment options due to high or prohibitive surgical risk, advanced comorbidities, and 80% to 90% or higher screen failure rates for transcatheter MV replacement.14 In these challenging cases, M-TEER is still performed despite the baseline MVA <4.0 cm2, particularly when symptom burden and heart failure risk outweigh the potential risk of iatrogenic mitral stenosis. The exclusion of patients with small MVAs from pivotal trials has led to uncertainty in clinical decision-making for this population, and data on the feasibility, durability, and outcomes of M-TEER in patients with MVA <4.0 cm2 remain limited. In this study, we aimed to evaluate the procedural and clinical outcomes of M-TEER in patients with severe MR with baseline MVA <4.0 cm2.
Methods
Study Population
We retrospectively analyzed data from 367 consecutive patients with moderate-to-severe or severe MR who underwent M-TEER using the MitraClip system (Abbott Vascular, Illinois, USA) at Houston Methodist Hospital between 2014 and 2022. Eligibility for M-TEER was determined by a multidisciplinary heart team, including interventional cardiologists, interventional echocardiographers, and cardiothoracic surgeons.
Eligible candidates included patients with symptomatic primary MR, deemed high-risk or prohibitive risk for surgery, and those with secondary MR who remained symptomatic despite maximally tolerated guideline-directed medical therapy and had favorable mitral anatomy for M-TEER.1 Patients without baseline MVA measurements were excluded from this study. Patients were stratified into 2 groups according to baseline MVA<4.0 cm2 (n = 66) and MVA ≥4.0 cm2 (n = 239) (Figure 1).
Figure 1.
Patient inclusion chart.
Abbreviations: M-TEER, mitral transcatheter edge-to-edge repair; MVA, mitral valve area.
This study was approved by the Houston Methodist Institutional Review Board and conducted in accordance with the Declaration of Helsinki. Given its retrospective design, informed consent was waived.
Echocardiographic Analysis
MR was categorized as primary, secondary, or mixed according to American Society of Echocardiography guidelines.15 All patients underwent three-dimensional (3D) transesophageal echocardiography (TEE), performed by experienced interventional echocardiographers using the Philips i33 system (Philips Healthcare, Amsterdam, Netherlands). MVA was measured via 3D planimetry in diastole.
Intraprocedural 3D TEE was used to guide device placement and leaflet grasping. Postprocedural transthoracic echocardiography was performed prior to discharge to assess residual MR severity (using color Doppler) and TMPG via continuous-wave Doppler and at follow-up. MR severity was graded as mild, moderate, moderate-to-severe, or severe in accordance with the American Society of Echocardiography guidelines.16 Tricuspid regurgitation was graded using similar criteria, and right heart parameters including estimated right atrial pressure and pulmonary artery systolic pressure were recorded.17 Mitral annular calcification (MAC) was assessed based on the distribution of calcium within the annulus: mild MAC was defined as focal, noncontiguous calcification involving less than 180° of the annular circumference; moderate as continuous calcification spanning 180° to 270°; and severe as continuous calcification extending over 270° or more of the annular circumference.18
MVA was indexed to body surface area (BSA) by dividing the measured MVA by the BSA, generating the indexed MVA expressed in cm2/m2. This index accounts for patient body size to allow standardized comparisons.
M-TEER Procedure
M-TEER was performed using standard transcatheter techniques via transfemoral venous access. Under general anesthesia, transseptal puncture was guided by fluoroscopy and TEE. A 24-F transseptal sheath was used to measure baseline left atrial pressure (LAP) and V wave prior to insertion of the clip delivery system. LAP and V wave were continuously monitored throughout the procedure. The clip delivery system was advanced across the MV to grasp and approximate the mitral leaflets at the site of the regurgitation. Adequacy of clip positioning and MR reduction was assessed in real time using TEE. Additional clips were implanted as needed to achieve optimal MR reduction. Following the final clip deployment, direct LAP and V wave measurements were repeated before withdrawing the sheath from the left atrium to the right atrium.
Data Collection and Study Endpoints
Clinical, procedural, and echocardiographic data were manually extracted from electronic health records. Postprocedural outcomes and follow-up were assessed through electronic health record review, including emergency department visits, hospitalizations, and outpatient clinic documentation.
The primary endpoint was all-cause mortality at 2 years, heart failure hospitalizations (HFH) within 2 years, and a composite outcome of mortality and HFH at 2 years. Secondary endpoints included change in MR severity and New York Heart Association (NYHA) functional class at 1 year.
Statistical Analysis
Categorical variables were reported as frequencies and percentages, while continuous variables were presented as means with SDs or medians with interquartile ranges, as appropriate. The Kolmogorov–Smirnov test was used to assess the normality of continuous variables. Categorical variables were compared using the chi-squared test or Fisher exact test, as appropriate.
The primary outcome was 2-year all-cause mortality, HFH, and the composite of mortality at HFH at 2 years. Time-to-event outcomes were analyzed using Cox proportional hazards regression models. Univariate Cox regression was first conducted to evaluate the association between individual variables and mortality. Variables with a p value <0.1 in the univariate analysis were subsequently included in a multivariable Cox regression model using a stepwise forward selection method to identify independent predictors of mortality. The proportional hazards assumption was verified for each covariate. Results were reported as hazard ratios (HRs) with 95% CIs.
The variables evaluated in the univariate analysis included age, baseline MVA, MVA indexed to BSA, gender, baseline NYHA class III–IV, baseline left ventricular ejection fraction (LVEF), preprocedural creatinine, preprocedural hemoglobin, baseline pulmonary artery systolic pressure, tricuspid regurgitation severity, atrial fibrillation/flutter, number of clips used, coronary artery disease, and diabetes.
Survival outcomes were visualized using Kaplan–Meier curves, with comparisons between groups assessed using the log-rank test.
We evaluated the discriminative ability of MVA indexed to BSA to predict mortality and post-M-TEER TMPG > 5 mmHg using receiver-operating characteristic curve analysis. The area under the curve (AUC) and 95% CIs were reported to assess the performance of the predictor.
A two-sided p value < 0.05 was considered statistically significant. All analyses were performed using STATA version 17.0 (StataCorp, College Station, Texas, USA).
Results
Baseline Clinical and Echocardiographic Characteristics
Among the 305 patients included, 66 (21.6%) had MVA <4.0 cm2 and 239 (78.3%) had MVA ≥4.0 cm2 (Table 1). Mean age was similar between the 2 groups (77.8 ± 1.1 vs. 76.8 ± 0.7 years; p = 0.52). There was a higher proportion of women in the small MVA group (57.6 vs. 42.7%; p = 0.03). NYHA functional class was comparable, with nearly 75% of patients in both groups presenting with class III or IV symptoms (p = 0.08). While there were no significant differences in most baseline comorbidities, patients with small MVA had significantly higher Society of Thoracic Surgeons-predicted risk scores for both MV repair (17.9% ± 11.0% vs. 4.8% ± 0.3%; p = 0.02) and replacement (10.4% ± 1.4% vs. 6.5% ± 0.3%; p < 0.001).
Table 1.
Baseline characteristics of the study population
| Total N = 305 | MVA <4.0 cm2 (n = 66) | MVA ≥4.0 cm2 (n = 239) | p value | |
|---|---|---|---|---|
| Baseline characteristics | ||||
| Age, y (mean ± SD) | 77.0 ± 0.6 | 77.8 ± 1.1 | 76.8 ± 0.7 | 0.52 |
| Female, n (%) | 140 (45.6) | 38 (57.6) | 102 (42.7) | 0.03 |
| Race, n (%) | ||||
| White | 232 (78.4) | 47 (74.6) | 185 (79.4) | 0.21 |
| Black | 33 (11.1) | 6 (9.5) | 27 (11.6) | |
| Asian | 14 (4.7) | 5 (7.9) | 9 (3.9) | |
| Other | 17 (5.7) | 5 (7.9) | 12 (5.2) | |
| Body mass index, kg/m2 (mean ± SD) | 28.4 ± 0.5 | 28.3 ± 1.2 | 28.4 ± 0.6 | 0.91 |
| Body surface area, m2 (mean ± SD) | 1.9 ± 0.02 | 1.8 ± 0.03 | 1.9 ± 0.02 | 0.01 |
| MVA indexed to BSA∗, cm2/m2 (mean ± SD) | 2.8 ± 0.05 | 1.9 ± 0.04 | 3.1 ± 0.05 | <0.001 |
| STS risk MV repair, % (mean ± SD) | 7.5 ± 2.31 | 17.9 ± 11.0 | 4.8 ± 0.3 | 0.02 |
| STS risk MV replacement, % (mean ± SD) | 7.3 ± 0.4 | 10.4 ± 1.4 | 6.5 ± 0.3 | <0.001 |
| Frailty, n (%) | 210 (68.4) | 48 (72.7) | 162 (67.8) | 0.44 |
| Hypertension, n (%) | 223 (73.1) | 46 (69.7) | 177 (74.1) | 0.48 |
| Diabetes, n (%) | 86 (28.1) | 25 (37.9) | 61 (25.5) | 0.05 |
| Smoking, n (%) | 61 (28.2) | 9 (13.6) | 52 (25.5) | 0.14 |
| Coronary artery disease, n (%) | 111 (36.4) | 27 (40.9) | 83 (34.7) | 0.36 |
| Atrial fibrillation/flutter, n (%) | 182 (59.9) | 33 (50.0) | 149 (62.6) | 0.07 |
| Pacemaker use, n (%) | 54 (15.2) | 10 (18.4) | 44 (17.85) | 0.54 |
| Prior ICD use, n (%) | 49 (16.1) | 11 (16.7) | 38 (15.9) | 0.88 |
| Prior stroke, n (%) | 46 (15.1) | 10 (15.2) | 36 (15.1) | 0.99 |
| Prior PCI, n (%) | 63 (20.7) | 21 (31.8) | 42 (17.6) | 0.01 |
| Prior CABG, n (%) | 69 (22.5) | 13 (17.6) | 56 (24.0) | 0.52 |
| Prior surgical ring, n (%) | 21 (6.9) | 6 (9.1) | 15 (6.3) | 0.40 |
| Prior myocardial infarction, n (%) | 55 (18.0) | 12 (18.2) | 43 (18.0) | 0.87 |
| Chronic kidney disease, n (%) | 235 (77.0) | 51 (77.3) | 184 (77.0) | 0.80 |
| Dialysis, n (%) | 19 (6.2) | 8 (12.1) | 11 (4.6) | 0.03 |
| KCCQ12 (mean ± SD) | 42.1 ± 1.6 | 35.2 ± 2.8 | 43.9 ± 1.9 | 0.03 |
| Prior 2-wk New York Heart Association class, n (%) | ||||
| Class I | 10 (3.3) | 2 (3.0) | 8 (3.4) | 0.39 |
| Class II | 57 (18.7) | 8 (12.1) | 49 (20.9) | |
| Class III | 193 (63.3) | 45 (68.2) | 148 (63.2) | |
| Class IV | 40 (13.1) | 11 (16.7) | 29 (12.4) | |
| Preprocedural hemoglobin, g/L (mean ± SD) | 11.6 ± 0.1 | 11.3 ± 0.3 | 11.6 ± 0.1 | 0.30 |
| Preprocedural creatinine, mg/dL, (mean ± SD) | 1.6 ± 0.08 | 1.7 ± 0.2 | 1.6 ± 0.1 | 0.44 |
| Medications prescribed | ||||
| Aspirin use, n (%) | 118 (38.7) | 26 (39.4) | 92 (38.5) | 0.89 |
| Beta-blockers, n (%) | 208 (67.8) | 46 (69.7) | 162 (67.8) | 0.77 |
| ACEi or ARB, n (%) | 123 (40.3) | 29 (43.9) | 94 (39.3) | 0.50 |
| Aldosterone antagonists, n (%) | 47 (15.4) | 7 (10.6) | 40 (16.7) | 0.22 |
| Loop diuretics, n (%) | 222 (72.8) | 49 (74.2) | 173 (72.6) | 0.76 |
| Thiazide, n (%) | 27 (8.9) | 7 (10.6) | 20 (8.4) | 0.57 |
| Echocardiographic parameters | ||||
| MR etiology, n (%) | ||||
| Primary | 160 (54.2) | 35 (55.6) | 125 (53.9) | 0.51 |
| Secondary | 107 (36.3) | 20 (31.7) | 87 (37.5) | |
| Mixed | 28 (9.5) | 8 (12.7) | 20 (8.6) | |
| Mean MVA, cm2 (mean ± SD) | 5.3 ± 0.1 | 3.4 ± 0.1 | 5.9 ± 0.1 | <0.001 |
| LVEF, %, mean ± SD | 51.3 ± 0.8 | 53.0 ± 1.8 | 50.9 ± 1.0 | 0.84 |
| LVEDV, mL (mean ± SD) | 174.5 ± 6.2 | 162.4 ± 15.7 | 177.4 ± 6.6 | 0.17 |
| LVESV, mL (mean ± SD) | 88.9 ± 4.9 | 97.8 ± 13.2 | 86.7 ± 5.2 | 0.82 |
| LVIDs, cm (mean ± SD) | 3.7 ± 0.1 | 3.5 ± 0.2 | 3.8 ± 0.1 | 0.07 |
| LVIDd, cm (mean ± SD) | 5.3 ± 0.1 | 5.0 ± 0.1 | 5.4 ± 0.1 | 0.004 |
| LA volume, mL (mean +SD) | 120.8 ± 3.5 | 104.8 ± 5.1 | 125.0 ± 4.1 | 0.008 |
| LA volume index, mL/m2 (mean +SD) | 56.3 ± 3.0 | 62.5 ± 2.1 | 61.2 ± 1.8 | 0.07 |
| PA systolic pressure, mm Hg (mean ± SD) | 52.7 ± 1.2 | 48.1 ± 2.4 | 52.6 ± 1.4 | 0.55 |
| Mean RAP, mm Hg (mean ± SD) | 11.5 ± 0.4 | 12.3 ± 0.9 | 11.3 ± 0.5 | 0.84 |
| Baseline MR severity, n (%) | ||||
| Mild | 1 (0.3) | 0 (0.0) | 1 (0.4) | 0.20 |
| Moderate | 7 (2.3) | 4 (6.2) | 3 (1.3) | |
| Moderate to severe | 54 (17.8) | 11 (16.9) | 43 (18.1) | |
| Severe | 241 (79.5) | 50 (76.9) | 191 (80.3) | |
| Baseline TMPG, mm Hg (mean ± SD) | 3.3 ± 0.1 | 3.5 ± 0.2 | 3.3 ± 0.1 | 0.72 |
| Baseline TR severity, n (%) | ||||
| None/trace | 164 (53.8) | 39 (59.1) | 125 (52.3) | 0.58 |
| Mild | 87 (28.5) | 17 (25.8) | 70 (29.3) | |
| Moderate | 21 (6.9) | 4 (6.1) | 17 (7.1) | |
| Severe | 33 (10.8) | 6 (9.1) | 27 (11.3) | |
| Mitral annular calcification, n (%) (≥mild) | 96 (31.6) | 30 (45.5) | 66 (27.7) | 0.006 |
Notes. Values are represented as n (%) or mean ± SD. Bold represents significant values (“p < 0.05”).
Abbreviations: ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin II receptor blocker; BSA, body surface area; CABG, coronary artery bypass grafting; ICD, implantable cardioverter defibrillator; KCCQ-12, Kansas City Cardiomyopathy Questionnaire; LA, left atrium; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection fraction; LVESV, left ventricular end-systolic volume; LVIDd, left ventricular internal diameter in diastole; LVIDs/d, left ventricular internal diameter (systole/diastole); MR, mitral regurgitation; MV, mitral valve; MVA ,mitral valve area; PA, pulmonary artery; PCI, percutaneous coronary intervention; RAP, right atrial pressure; STS, Society of Thoracic Surgeons; TMPG, transmitral pressure gradient; TR, tricuspid regurgitation.
MVA was indexed to BSA and expressed in cm2/m2 by dividing the absolute MVA by the corresponding BSA.
In the MVA <4.0 cm2 group, the MV area ranged from 2.5 to 3.98 cm2 (3.4 ± 0.05 cm2), while in the MVA ≥4.0 cm2 group, it ranged from 4 to 11.6 cm2 (5.9 ± 0.1 cm2). The distribution of baseline MR severity was similar between groups, with most patients presenting with severe MR (76.9 vs. 80.3%; p = 0.20). Baseline TMPG did not differ significantly (3.5 ± 0.2 vs. 3.3 ± 0.1 mmHg; p = 0.56). Primary MR was the predominant etiology in both cohorts (55.6 vs. 53.9%; p = 0.51), and left ventricular function and volumes were generally similar. However, patients with smaller MVA had significantly smaller left ventricular internal diameter in diastole (5.0 ± 0.2 vs. 5.4 ± 0.1 cm; p = 0.008) and lower left atrial volume (104.8 ± 5.1 vs. 125.0 ± 4.1 mL; p = 0.02). Importantly, moderate or greater MAC was more prevalent in the small MVA group (45.5 vs. 27.7%; p = 0.006).
Procedural Characteristics
Procedural characteristics are detailed in Table 2. The MVA <4.0 cm2 group had significantly fewer implanted clips (1.3 ± 0.06 vs. 1.5 ± 0.04; p = 0.03). A greater proportion of patients in the smaller MVA group received only one clip (68.2 vs. 53.8%), while fewer received 2 clips (27.3 vs. 39.4%). M-TEER was aborted in 3 patients due to anatomical or procedural challenges. In 2 cases, despite adequate transeptal access and clip positioning at A2-P2, the posterior leaflet was too short to ensure effective grasping—one patient had a baseline MVA of 2.7 cm2 with an attempted narrow tissue wide clip, and the other had an MVA of 6.5 cm2 with an attempted extended tissue wide clip. In the third patient, the procedure was aborted due to pericardial effusion.
Table 2.
Procedural details of the study population
| Total N = 305 | MVA <4.0 cm2 (n = 66) | MVA ≥4.0 cm2 (n = 239) | p value | |
|---|---|---|---|---|
| Type of clip used, n (%) | ||||
| Old gen | 100 (32.8) | 25 (37.9) | 75 (31.4) | 0.47 |
| NT classic | 20 (6.6) | 5 (7.6) | 15 (6.3) | 0.77 |
| NTW | 52 (17.0) | 10 (15.2) | 42 (17.6) | 0.49 |
| NTR | 24 (7.9) | 9 (13.6) | 15 (6.3) | 0.09 |
| XT | 16 (5.2) | 4 (6.1) | 12 (5.0) | 0.78 |
| XTW | 92 (30.2) | 11 (16.7) | 83 (34.7) | 0.10 |
| XTR | 42 (13.8) | 9 (13.6) | 33 (13.8) | 0.96 |
| Mean number of clips implanted (mean ± SD) | 1.5 ± 0.04 | 1.3 ± 0.07 | 1.5 ± 0.04 | 0.03 |
| Number of clips implanted, n (%) | ||||
| 0 | 3 (1.0) | 1 (1.5) | 2 (0.8) | 0.28 |
| 1 | 172 (57.0) | 45 (68.2) | 127 (53.8) | |
| 2 | 111 (36.8) | 18 (27.3) | 93 (39.4) | |
| ≥3 | 16 (5.3) | 2 (3.0) | 14 (5.9) | |
| Location of regurgitant jet, n (%) | ||||
| A2-P2 | 262 (87.0) | 62 (95.4) | 202 (85.6) | 0.76 |
| A3-P3 | 17 (5.6) | 4 (6.2) | 13 (5.5) | |
| A1-P1 | 11 (3.7) | 0 (0.0) | 11 (4.7) | |
| A2-P3 | 8 (2.7) | 2 (3.1) | 6 (2.5) | |
| A2-P1 | 3 (1.0) | 0 (0.0) | 3 (1.3) | |
| Fluoroscopy time, min (mean ± SD) | 22.7 ± 1.0 | 21.7 ± 1.7 | 22.9 ± 1.2 | 0.60 |
Notes. Values are represented as n (%); mean ± SD. Bold represents significant values (“p < 0.05”).
Abbreviations: MVA, mitral valve area; NT, narrow tissue clip; NTR, narrow tissue repair; NTW, narrow tissue wide clip; XT, extended tissue clip; XTR, extended tissue repair; XTW, extended tissue wide clip.
In-Hospital Outcomes and Postprocedural Echocardiographic Findings
In-hospital outcomes and echocardiographic characteristics at discharge are summarized in Table 3. In-hospital mortality was 0% in both groups. Rates of postprocedural complications were low and comparable between groups.
Table 3.
In-hospital complications and echocardiographic characteristics at discharge of the study population
| Total N = 305 | MVA <4.0 cm2 (n = 66) | MVA ≥4.0 cm2 (n = 239) | p value | |
|---|---|---|---|---|
| In-hospital complications | ||||
| Length of stay, d (mean ± SD) | 3.4 ± 0.3 | 4.6 ± 0.7 | 3.1 ± 0.4 | 0.06 |
| In-hospital mortality, n (%) | 0 (0.0) | 0 (0.0) | 0 (0.0) | - |
| Vascular complications, n (%) | 12 (3.9) | 5 (7.6) | 7 (2.9) | 0.09 |
| Perforation/tamponade, n (%) | 5 (1.6) | 3 (4.5) | 2 (0.8) | 0.04 |
| New-onset dialysis, n (%) | 6 (2.0) | 1 (1.5) | 5 (2.1) | 0.77 |
| Atrial fibrillation, n (%) | 4 (1.3) | 1 (1.5) | 3 (1.3) | 0.87 |
| Valve reintervention, n (%) | 4 (1.3) | 2 (3.0) | 2 (0.8) | 0.17 |
| Endocarditis, n (%) | 3 (1.0) | 1 (1.5) | 2 (0.8) | 0.62 |
| Single leaflet device attachment, n (%) | 2 (0.9) | 0 (0.0) | 2 (1.1) | 0.47 |
| Leaflet tear, n (%) | 2 (0.9) | 1 (2.1) | 1 (0.5) | 0.30 |
| Echocardiographic characteristics at discharge | ||||
| Discharge LVEF, mm Hg (mean ± SD) | 48.5 ± 1.0 | 50.9 ± 2.1 | 47.8 ± 1.1 | 0.19 |
| Residual MR at discharge, n (%) | ||||
| None/trace | 43 (14.3) | 9 (13.8) | 34 (14.5) | 0.78 |
| Mild | 158 (52.7) | 35 (53.8) | 123 (52.3) | |
| Moderate | 84 (28.0) | 19 (29.2) | 65 (27.7) | |
| Moderate-severe | 9 (3.0) | 1 (1.5) | 8 (3.4) | |
| Severe | 6 (2.0) | 1 (1.5) | 5 (2.1) | |
| Mean TMPG, mm Hg (mean ± SD) | 3.4 ± 0.1 | 3.9 ± 0.2 | 3.3 ± 0.1 | 0.006 |
| TMPG ≥5 mm Hg (mean ± SD) | 23 (9.0) | 9 (15.5) | 14 (7.1) | 0.13 |
| Residual TR at discharge, n (%) | ||||
| None/trace | 160 (62.5) | 35 (61.4) | 125 (62.8) | 0.68 |
| Mild | 11 (4.3) | 3 (5.3) | 8 (4.0) | |
| Moderate | 54 (21.1) | 14 (24.6) | 40 (20.1) | |
| Moderate-severe | 16 (6.3) | 1 (1.8) | 15 (7.6) | |
| Severe | 15 (5.9) | 4 (7.0) | 11 (5.5) | |
| LA volume, mL (mean ± SD) | 122.3 ± 3.8 | 121.1 ± 8.7 | 122.5 ± 4.2 | 0.88 |
| LA volume index, mL/m2 (mean +SD) | 66.3 ± 2.1 | 68.6 ± 5.4 | 65.7 ± 2.2 | 0.58 |
| LAP, mm Hg (mean ± SD) | 14.7 ± 0.4 | 14.0 ± 0.9 | 14.8 ± 0.5 | 0.40 |
| V-wave, mm Hg (mean ± SD) | 21.3 ± 0.7 | 19.4 ± 1.4 | 21.8 ± 0.8 | 0.12 |
| NYHA class at discharge, n (%) | ||||
| Class I | 75 (40.5) | 13 (38.2) | 62 (41.1) | 0.52 |
| Class II | 84 (45.4) | 14 (41.2) | 70 (46.4) | |
| Class III | 24 (13.0) | 6 (17.6) | 18 (11.9) | |
| Class IV | 2 (1.1) | 1 (2.9) | 1 (0.7) | |
| Difference pre and post | ||||
| MR reduction (mean +SD) | 2.6 ± 0.1 | 2.6 ± 0.1 | 2.6 ± 0.1 | 0.90 |
| Mean LAP reduction, mm (Hg) (mean +SD) | 5.1 ± 0.5 | 2.8 ± 1.0 | 5.6 ± 0.5 | 0.01 |
| V-wave reduction, mm Hg (mean +SD) | 13.2 ± 1.1 | 10.4 ± 2.3 | 13.9 ± 1.2 | 0.21 |
Notes. Values are represented as n (%); mean ± SD. Bold represents significant values (“p < 0.05”).
Abbreviations: LA, left atrium; LAP, left atrial pressure; LVEF, left ventricular ejection fraction; MR, mitral regurgitation; MVA, mitral valve area; NYHA, New York Heart Association; TMPG, transmitral pressure gradient; TR, tricuspid regurgitation.
At discharge, residual MR severity was similar between groups. None or mild MR was observed in 67.7% of patients in the MVA <4.0 cm2 group and 66.8% in the MVA ≥4.0 cm2 group, while ≤ moderate MR was present in 96.9 and 94.5% of patients, respectively (p = 0.85). Notably, the mean TMPG was significantly higher in the MVA <4.0 cm2 group (3.9 ± 0.2 vs. 3.3 ± 0.1 mmHg; p = 0.006), although the proportion of patients with elevated TMPG (>5 mmHg), despite being numerically higher, was not significantly different (15.5 vs. 7.1%; p = 0.13).
NYHA functional class at discharge was comparable (79.4 vs. 87.4% achieving NYHA class I or II; p = 0.52). Improvements in hemodynamic parameters, including MR reduction (2.6 ± 0.1 vs. 2.6 ± 0.1 grades; p = 0.90), LAP reduction (2.8 ± 1.0 vs. 5.6 ± 0.5 mmHg; p = 0.01), and V-wave reduction (10.4 ± 2.3 vs. 13.9 ± 1.2 mmHg; p = 0.21), were comparable between groups.
Follow-Up Outcomes
Table 4 summarizes the 30-day, 1-year, 2-year, and last follow-up outcomes for patients undergoing M-TEER stratified by baseline MVA.
Table 4.
Clinical outcomes post-M-TEER at 1-year, 2-year, and final follow-up stratified by baseline MVA
| Total N = 305 | MVA <4.0 cm2 (n = 66) | MVA ≥4.0 cm2 (n = 239) | p value | |
|---|---|---|---|---|
| 30-d outcomes | ||||
| All-cause mortality, n (%) | 8 (2.6) | 4 (5.4) | 4 (1.7) | 1.00 |
| HFH, n (%) | 7 (2.3) | 1 (1.4) | 6 (2.6) | 0.14 |
| Composite, n (%) | 59 (19.2) | 20 (27.0) | 39 (16.7) | 0.45 |
| MV reintervention, n (%) | 0 (0.0) | 0 (0.0) | 0 (0.0) | - |
| LVEF, mm Hg (mean ± SD) | 50.4 ± 1.1 | 52.4 ± 2.1 | 49.8 ± 1.3 | 0.31 |
| LA volume, mL (mean ± SD) | 111.4 ± 3.3 | 111.6 ± 9.6 | 111.4 ± 3.5 | 0.98 |
| LAVI, mL/m2 (mean ± SD) | 69.7 ± 3.9 | 76.3 ± 9.3 | 68.0 ± 4.4 | 0.41 |
| LVIDs, cm (mean ± SD) | 3.6 ± 0.1 | 3.3 ± 0.2 | 3.7 ± 0.1 | 0.1 |
| LVIDd, cm (mean ± SD) | 5.1 ± 0.1 | 4.9 ± 0.2 | 5.1 ± 0.1 | 0.37 |
| TMPG, mm Hg (mean ± SD) | 4.4 ± 0.2 | 4.3 ± 0.5 | 4.4 ± 0.2 | 0.91 |
| Residual MR, n (%) | ||||
| None/trace | 41 (19.0) | 10 (19.6) | 31 (18.8) | 0.05 |
| Mild | 105 (48.6) | 24 (47.1) | 81 (49.1) | |
| Moderate | 63 (29.2) | 13 (25.5) | 50 (30.3) | |
| Severe | 7 (3.2) | 4 (7.8) | 3 (1.8) | |
| Residual TR, n (%) | ||||
| None/trace | 33 (22.4) | 7 (21.2) | 26 (22.8) | 0.36 |
| Mild | 66 (44.9) | 13 (39.4) | 53 (46.5) | |
| Moderate | 38 (25.9) | 9 (75.8) | 29 (25.4) | |
| Severe | 10 (6.8) | 4 (3.0) | 6 (5.3) | |
| Estimated PASP, mm Hg (mean ± SD) | 43.9 ± 1.8 | 39.5 ± 3.9 | 45.2 ± 2.0 | 0.19 |
| Estimated RAP, mm Hg (mean ± SD) | 10.4 ± 1.2 | 9.2 ± 2.4 | 10.8 ± 1.4 | 0.55 |
| One-year outcomes | ||||
| All-cause mortality, n (%) | 50 (19.0) | 15 (25.0) | 35 (17.2) | 0.16 |
| HFH, n (%) | 36 (13.7) | 10 (16.7) | 26 (12.8) | 0.45 |
| Composite, n (%) | 77 (29.3) | 23 (39.7) | 54 (27.1) | 0.08 |
| MV reintervention, n (%) | 7 (2.3) | 1 (1.5) | 6 (2.5) | 0.28 |
| One-year NYHA class, n (%) | ||||
| Class I | 90 (47.9) | 11 (29.8) | 79 (52.3) | 0.09 |
| Class II | 88 (46.8) | 24 (64.9) | 64 (42.4) | |
| Class III | 10 (5.3) | 2 (5.4) | 8 (5.3) | |
| Class IV | 0 (0.0) | 0 (0.0) | 0 (0.0) | |
| LVEF, mm Hg (mean ± SD) | 50.9 ± 2.1 | 51.1 ± 4.4 | 50.9 ± 2.3 | 0.98 |
| LA volume, mL (mean ± SD) | 121.8 ± 4.3 | 129.2 ± 11.2 | 119.7 ± 4.6 | 0.36 |
| LAVI, mL/m2 (mean ± SD) | 65.2 ± 2.4 | 70.5 ± 6.5 | 63.7 ± 2.4 | 0.23 |
| LVIDs, cm (mean ± SD) | 3.5 ± 0.1 | 3.6 ± 0.2 | 3.5 ± 0.1 | 0.77 |
| LVIDd, cm (mean ± SD) | 5.1 ± 0.1 | 5.2 ± 0.2 | 5.0 ± 0.1 | 0.50 |
| TMPG, mm Hg (mean ± SD) | 4.3 ± 0.3 | 3.8 ± 0.6 | 4.3 ± 0.3 | 0.50 |
| Residual MR grade, n (%) | ||||
| None/trace | 81 (60.7) | 17 (60.7) | 64 (56.6) | 0.76 |
| Mild | 49 (28.6) | 8 (28.6) | 41 (36.3) | |
| Moderate | 7 (7.1) | 2 (7.1) | 5 (4.4) | |
| Severe | 4 (2.8) | 1 (3.6) | 3 (2.7) | |
| Residual TR, n (%) | ||||
| None/trace | 84 (65.6) | 18 (66.7) | 66 (65.3) | 0.65 |
| Mild | 36 (28.1) | 7 (25.9) | 29 (28.7) | |
| Moderate | 4 (3.1) | 1 (3.7) | 3 (3.0) | |
| Severe | 4 (3.1) | 1 (3.7) | 3 (3.0) | |
| Estimated PASP, mm Hg (mean ± SD) | 46.3 ± 1.3 | 44.8 ± 2.7 | 46.6 ± 1.5 | 0.60 |
| Estimated RAP, mm Hg (mean ± SD) | 9.6 ± 0.4 | 7.4 ± 0.9 | 9.6 ± 0.5 | 0.05 |
| Two-year outcomes | ||||
| All-cause mortality, n (%) | 72 (27.4) | 21 (35.0) | 51 (25.1) | 0.13 |
| HFH, n (%) | 46 (17.5) | 11 (18.3) | 35 (17.2) | 0.85 |
| Composite, n (%) | 101 (38.4) | 27 (45.0) | 74 (36.5) | 0.23 |
| MV reintervention, n (%) | 8 (3.0) | 1 (1.7) | 7 (3.4) | 0.05 |
| Last follow-up | ||||
| Mean follow-up, d, mean ± SD | 803.4 ± 37.0 | 844.9 ± 96.5 | 792.1 ± 39.2 | 0.56 |
| All-cause mortality, n (%) | 131 (43.1) | 33 (50.8) | 98 (41.0) | 0.16 |
| HFH, n (%) | 68 (22.4) | 16 (24.6) | 52 (21.8) | 0.62 |
| Composite, n (%) | 155 (59.4) | 38 (65.5) | 117 (57.6) | 0.16 |
| MV reintervention, n (%) | 10 (3.3) | 3 (4.5) | 7 (2.9) | 0.51 |
Notes. Values are represented as n (%); mean ± SD.
Abbreviations: HFH, heart failure hospitalization; LA, left atrium; LAVI, left atrial volume index; LVEF, left ventricular ejection fraction; LVIDd, left ventricular internal diameter in diastole; LVIDs/d, left ventricular internal diameter (systolic/diastolic); MR, mitral regurgitation; M-TEER, mitral transcatheter edge-to-edge repair; MV, mitral valve; MVA, mitral valve area; NYHA, New York Heart Association; PASP, pulmonary artery systolic pressure; RAP, right atrial pressure; TMPG, transmitral pressure gradient; TR, tricuspid regurgitation.
Thirty-Day Outcomes
At 30 days, all-cause mortality, HFH, and the composite of mortality and HFH rates were similar in both groups (all p > 0.05). The proportion of patients with ≤moderate residual MR (92.2 vs. 98.2%; p = 0.05) was similar in the 2 groups. TMPG (mean of 4.4 ± 0.2 mm Hg) and other echocardiographic measures (LVEF, left atrium volume, LVID) did not differ significantly between groups (all p > 0.05).
One-Year Outcomes
At 1 year, the rates of all-cause mortality, HFH, and the composite outcome (mortality + HFH) were similar between the 2 groups. The proportion of patients with ≤moderate residual MR (96.4 vs. 97.3%; p = 0.76) was similar in the 2 groups. Moderate to severe residual MR remained low at 1 year, with 3.4% of the MVA <4.0 cm2 group and 7.2% of the MVA >4.0 cm2 group (p = 0.76) (Figure 2). TMPG (mean of 4.3 ± 0.3 mm Hg) did not differ significantly between the groups (p = 0.50) (Figure 3). For NYHA class at 1 year, most patients in both groups were in class I or II (p = 0.09); the NYHA distribution is detailed in Figure 3.
Figure 2.
Changes in MR severity.
Abbreviations: MR, mitral regurgitation; MVA, mitral valve area.
Figure 3.
Changes in NYHA severity.
Abbreviations: MVA, mitral valve area; NYHA, New York Heart Association.
Two-Year Outcomes
At 2 years, there was no significant difference in all-cause mortality between patients with MVA <4.0 cm2 and those with MVA ≥4.0 cm2 (35.0 vs. 25.1%; p = 0.13). HFH and the composite outcome were also not significantly different between the 2 groups. Kaplan–Meier analysis showed no significant differences in all-cause mortality (HR: 0.89; 95% CI: [0.60–1.33]; p = 0.59), HFH (HR: 0.85; 95% CI: [0.49–1.50]; p = 0.58) and composite outcome (HR: 0.89; 95% CI: 0.62–1.27; p = 0.53) (Figure 4).
Figure 4.
Kaplan-Meier curve survival estimates for (a) all-cause mortality, (b) heart failure hospitalization, and (c) composite, stratified by mitral valve area group.
Abbreviations: HFH, heart failure hospitalization; HR, hazard ratio; MVA, mitral valve area.
Last Follow-Up
At the last follow-up, all-cause mortality (50.8 vs. 41.0%; p = 0.16), HFH (24.6 vs. 21.8%; p = 0.62), and the composite outcome of mortality and HFH (65.5 vs. 57.6%; p = 0.16) did not reach statistical significance.
Multivariable Analysis
In the multivariate Cox regression analysis for all-cause mortality, only age (HR: 1.03; 95% CI: [1.01-1.05]; p = 0.001), preprocedural hemoglobin (HR: 0.88; 95% CI: [0.81-0.95]; p = 0.002), and preprocedural creatinine (HR: 1.10; 95% CI: [1.10-1.19]; p = 0.03) emerged as independent predictors of all-cause mortality (Figure 5). Regarding the composite outcome of mortality and HFH, older age (HR: 1.02; 95% CI: 1.01-1.04; p = 0.003), lower LVEF (HR: 0.98; 95% CI: 0.97-0.99; p < 0.001) and a low preprocedural hemoglobin (HR: 0.90; 95% CI: 0.83-0.97; p = 0.005) at baseline were associated with a higher risk of both mortality and HFH (Figure 6). Baseline MVA and NYHA class did not predict mortality nor composite outcomes at follow-up (Supplemental Tables 1 and 2).
Figure 5.
Forest plot for all-cause mortality predictors at follow-up following M-TEER.
Abbreviations: HR, hazard ratio; M-TEER, mitral transcatheter edge-to-edge repair; TR, tricuspid regurgitation.
Figure 6.
Forest plot for all-cause mortality +and heart failure hospitalization predictors at follow-up following M-TEER.
Abbreviations: Hb, hemoglobin; HFH, heart failure hospitalization; HR, hazard ratio; LVEF, left ventricular ejection fraction; M-TEER, mitral transcatheter edge-to-edge repair; NYHA, New York Heart Association; TR, tricuspid regurgitation.
Subgroup Analyses
A Kaplan-Meier analysis comparing overall survival in patients with baseline MVA < 3.5 cm2 versus 3.5 ≤ MVA <4.0 cm2 showed no difference at 2 years (p = 0.83) (Figure 7).
Figure 7.
Kaplan-Meier survival estimates by mitral valve area (MVA <3.5 cm2 vs. 3.5<MVA<4.0 cm2).
Abbreviation: HR, hazard ratio; MVA, mitral valve area.
In a subanalysis of patients with MVA <4.0 cm2, the presence of MAC was not associated with increased mortality (HR: 1.29; 95% CI [0.94-1.76]; p = 0.12) (Supplemental Figure 1).
Among female patients, there was no difference in 2-year survival between patients with small vs. large MVA (HR: 0.90; 95% CI [0.60-1.33]; p = 0.59). In addition, within the MVA <4.0 cm2 group, survival was similar between men and women (HR: 0.99; 95% CI [0.73-1.35]; p = 0.97) (Supplemental Figure 2).
We also evaluated whether baseline MVA indexed to BSA could predict adverse postprocedural outcomes. The receiver-operating characteristic curve evaluating the predictive value of indexed MVA for all-cause mortality at follow-up yielded an AUC of 0.48 (95% CI: 0.42-0.56), indicating no significant discriminative capacity. Similarly, indexed MVA demonstrated poor performance in predicting elevated TMPG (>5 mmHg) at discharge, with an AUC of 0.41 (Figure 8).
Figure 8.
ROC curve: predictive value of indexed mitral valve area (MVA) for (a) mortality and (b) TMPG >5 mm Hg at discharge.
Abbreviations: MVA, mitral valve area; ROC, receiver-operating characteristic; TMPG, transmitral pressure gradient.
Discussion
This study evaluated the impact of baseline MVA on procedural and clinical outcomes following M-TEER. The key findings are as follows:
-
1.
Baseline MVA (<4.0 cm2 vs. ≥4.0 cm2) was not significantly associated with 2-year all-cause mortality, HFH, or the composite outcome.
-
2.
Residual MR and NYHA functional class at 1 year were comparable between both groups.
-
3.
Patients with MVA <4.0 cm2 had higher postprocedural TMPG at discharge, despite receiving fewer clips.
-
4.
Two-year survival and HFH are comparable between patients with MVA <3.5 cm2 and 3.5 to 4.0 cm2.
-
5.
Very small MVA, MAC, and female sex were not associated with increased 2-year all-cause mortality.
-
6.
Age, preprocedural creatinine, and preprocedural hemoglobin were independently associated with all-cause mortality at follow-up. Additionally, older age, reduced LVEF, and lower preprocedural hemoglobin independently predicted the composite outcome.
-
7.
In our cohort, no meaningful cutoff for MVA indexed to BSA was identified to predict either all-cause mortality at follow-up or an elevated TMPG (>5 mmHg) at discharge.
Our findings indicate that a small baseline MVA does not independently predict adverse clinical outcomes following M-TEER. This challenges the longstanding concern that smaller MVAs predispose patients to postprocedural mitral stenosis,19 often defined by an effective orifice area <1.5 cm2 or TMPG ≥5 mmHg and potentially worse clinical outcomes.20,21 Notably, our data align with those of Mushiake et al.,22 who similarly found no association between small baseline MVA and adverse outcomes over 2 years in a large Japanese cohort undergoing M-TEER.
Although the small MVA group exhibited higher postprocedural TMPG at discharge, these gradients remained below clinically significant thresholds and did not correlate with worse outcomes. These differences likely reflect the anatomical constraints in small MVAs, where even modest reductions in orifice area can lead to elevated gradients. Nevertheless, the clinical relevance appears limited, as both groups achieved comparable MR reduction and symptom improvement at follow-up.
Small MVAs are often associated with anatomical challenges such as MAC or restricted leaflet motion, which can limit clip placement and increase post-clip gradients.7 Alkady et al. demonstrated that small left ventricular cavities and mitral annuli are associated with more technically challenging surgical repairs.23 Similarly, Kagawa et al.24 reported worse outcomes in cases of degenerative MR with an MVA ≤1.5 cm2 post M-TEER. In patients with smaller MVA, the operator may choose to implant fewer clips and accept somewhat greater residual MR in order to avoid a higher TMPG and thus creating significant iatrogenic mitral stenosis. This is the likely cause of fewer clips in our small MVA cohort—most likely reflecting anatomical limitations rather than undertreatment.
Importantly, our data reinforce that M-TEER is not only feasible but also safe and effective in patients with small MVAs, particularly in high-surgical-risk populations. Surgical MV repair or replacement in the setting of small annuli or extensive MAC is technically complex and has been associated with increased morbidity and mortality.25,26 In contrast, M-TEER offers a viable alternative, especially when performed in experienced high-volume centers.
In a subanalysis, we explored whether indexing MVA to BSA could better predict outcomes, especially considering clinical observations suggesting that obese patients with small MVAs tend to do worse. However, MVA indexed to BSA demonstrated poor discriminatory ability in predicting either all-cause mortality at follow-up (AUC = 0.48) or elevated TMPG >5 mmHg at discharge (AUC = 0.41). This lack of predictive value may be explained by the well-selected nature of our cohort, where patients undergoing M-TEER were carefully screened and managed in a high-volume center with tailored procedural strategies. Such individualized approaches, including limiting clip number to avoid excessive gradients, might have mitigated the impact of anatomical factors like indexed MVA. Therefore, while indexed MVA did not enhance prognostic accuracy in our study, its role in broader, less-selected patient populations remains uncertain. Larger, more inclusive trials or registries may be required to clarify whether indexing MVA to BSA can meaningfully contribute to risk stratification and procedural planning in M-TEER.
Importantly, our multivariate analysis confirmed that traditional clinical parameters—older age, lower preprocedural hemoglobin, elevated creatinine, and reduced LVEF—remain the strongest independent predictors of adverse outcomes,27 underscoring the importance of holistic patient assessment beyond anatomical metrics.
Collectively, our findings support a more individualized approach to patient selection for M-TEER. The results from Sorajja et al.28 complement our multivariate analysis and highlight the need to consider the broader interplay between anatomical characteristics, hemodynamics, and clinical status. While elevated post-clip gradients are a valid concern, a small MVA should not, in isolation, preclude M-TEER in otherwise suitable candidates. Given the reassuring safety profile in our small MVA cohort, current guideline-based contraindications based solely on valve area may warrant reconsideration.
Our subanalysis comparing patients with baseline MVA <3.5 cm2 versus 3.5 to 4.0 cm2 further supports that M-TEER can be safely performed in anatomically suitable patients even with smaller valve areas, suggesting that the historical 4.0 cm2 threshold, initially established from early trial exclusion criteria, may no longer represent a rigid boundary in contemporary practice. However, patients with MVA <3.0 cm2 remain particularly challenging, as this anatomy is still regarded as unsuitable for M-TEER according to the 2025 European Society of Cardiology/European Association of Cardiothoracic Surgery Valvular Heart Disease Guidelines.29 Given the very limited number of such cases in our cohort, a separate analysis was not feasible. Future larger multicenter studies should specifically evaluate outcomes in this subgroup to better delineate the procedural and clinical limits of M-TEER feasibility in extremely small valve areas.
Study Limitations
This study has several limitations. First, the retrospective, single-center nature introduces the possibility of selection bias and limits generalizability. Second, group assignment based on MVA was not randomized; while baseline demographics were largely balanced, residual confounding may exist. Third, echocardiographic data, including MVA and TMPG, were derived from clinical reports and may be subject to interobserver variability. Fourth, the relatively small size of subgroups—especially female patients and those with MVA <3.5 cm2—limits statistical power for subgroup analysis. Finally, postprocedural MVA was not consistently reported, preventing comprehensive evaluation of changes in valve area after repair.
Future multicenter, prospective studies with standardized imaging protocols and longer follow-up are necessary to validate these findings and explore thresholds for MVA and TMPG that may influence outcomes in broader populations.
Conclusion
In conclusion, this study demonstrates that M-TEER can be safely and effectively performed in patients with baseline MVA <4.0 cm2 with similar degrees of MR reduction and NYHA functional class improvement compared to those with MVA ≥4.0 cm2 despite higher postprocedural TMPG without an adverse impact on clinical outcomes such as mortality, HFH, or the composite outcome out to 2 years. Importantly, 2-year survival and HFH rates were comparable between patients with MVA<3.5 cm2 and those with MVA 3.5 to 4.0 cm2.
Ethics Statement
This study was conducted in accordance with the ethical standards of the institutional research committee and with the 1964 Declaration of Helsinki and its later amendments. The study was approved by the Houston Methodist Institutional Review Board, and the requirement for informed consent was waived due to the retrospective nature of the study.
Funding
This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Disclosure Statement
M.D. Atkins is a consultant for W. L. Gore & Associates. M. Reardon is a consultant for Medtronic, Boston Scientific, Abbott, and W. L. Gore & Associates. N.S. Kleiman is a local principal investigator in trials sponsored by Boston Scientific, Medtronic, Abbott, and Edwards Lifesciences. S.S. Goel is a consultant for Medtronic, W. L. Gore & Associates, and JC Medical and is on the Speakers Bureau for Abbott Structural Heart. The other authors had no conflicts to declare.
Footnotes
Supplemental data for this article can be accessed on the publisher’s website.
Supplementary Material
Tables 1 to 3
Supplement 1.
Kaplan-Meier Curve Survival Estimates in MVA<4cm2 stratified by MAC
Supplement 2.
Kaplan-Meier Curve Survival Estimates in (a) Female patients stratified by MVA and (b) in MVA<4.0 cm2 stratified by Gender
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Supplementary Materials
Tables 1 to 3