Researchers found modest 1-month changes in left ventricular diameters across mitral regurgitation mechanisms following mitral transcatheter edge-to-edge repair, while pulmonary artery systolic pressure responses varied by subtype.
Results from the study, conducted by Medha Biswas, MD, of the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, and colleagues, were presented as poster P1-01 at the American Society of Echocardiography 2026 Scientific Sessions and published in the Journal of the American Society of Echocardiography.
The researchers evaluated 442 patients assessed for mitral transcatheter edge-to-edge repair, or M-TEER, between 2014 and 2024. Of those patients, 411 received at least one clip. Postprocedural changes in left ventricular diameters and hemodynamics were evaluated among patients with atrial functional, ventricular functional, and degenerative mitral regurgitation. Outcomes were also examined in patients who did not undergo clip implantation.
Medical records were used to abstract clinical data. Researchers reviewed preprocedural and postprocedural transthoracic echocardiograms and intraprocedural transesophageal echocardiograms. Mitral regurgitation mechanism was classified using intraprocedural imaging findings. Outcomes reflected postprocedural minus preprocedural changes in left ventricular end-diastolic diameter, left ventricular end-systolic diameter, and pulmonary artery systolic pressure.
Among treated patients with paired mitral regurgitation grade data, the average change in mitral regurgitation grade was −2.42 at 1 month, with a median change of −3 grades.
Paired echocardiographic data were available for 279 patients for left ventricular end-diastolic diameter, 280 patients for left ventricular end-systolic diameter, and 235 patients for pulmonary artery systolic pressure. No statistically significant differences in left ventricular diameter changes were observed across mitral regurgitation subtypes. Median changes in left ventricular end-diastolic diameter were −0.20 cm in atrial functional mitral regurgitation, −0.10 cm in ventricular functional mitral regurgitation, and −0.10 cm in degenerative mitral regurgitation. Median changes in left ventricular end-systolic diameter were 0.20 cm, −0.10 cm, and 0.05 cm, respectively.
Pulmonary artery systolic pressure changes differed by mitral regurgitation subtype. Median pulmonary artery systolic pressure changes were 4 mm Hg in atrial functional mitral regurgitation, −5.5 mm Hg in ventricular functional mitral regurgitation, and −3 mm Hg in degenerative mitral regurgitation.
In a very small no-clip reference cohort, median changes were −0.30 cm for left ventricular end-diastolic diameter among 4 patients, −0.45 cm for left ventricular end-systolic diameter among 4 patients, and −18 mm Hg for pulmonary artery systolic pressure among 3 patients.
In an exclusive interview with Conexiant, Dr. Biswas said the pulmonary artery systolic pressure findings should be interpreted cautiously.
“I think the one thing I will caveat is: I don’t think we can pull clinical data from this yet,” Dr. Biswas said. “When I look at this, what I wonder is, is there a phenotypic difference in our atrial functional and ventricular functional patients? And do the atrial functional patients that we looked at have irreversible remodeling of their left atrium that has caused some group 2 pulmonary hypertension that is being underdiagnosed, which has led to the PASP to then get worse in the atrial functional group, as opposed to really not having much of a change, or maybe improving even in the ventricular functional group?”
She emphasized that the analysis was limited by small subgroup sizes and should be viewed as an early signal rather than a basis for clinical decision-making.
“With this study, I think I would limit it by saying we have small numbers,” Dr. Biswas said. “This was just a proof of concept, and we would really need to look further before we call any clinical limitations.”
Dr. Biswas said the next step will be to evaluate whether the pulmonary artery systolic pressure changes persist beyond the early postprocedural period.
“The things that I would want to do next are look at: is this change sustained over time?” she said. “The next step that we’ll do is look at our 1-year data to see: is this truly something that sustains, or is it a temporary change from the procedure?”
She added that larger cohorts would be needed before drawing conclusions about which patients may be more or less likely to benefit from M-TEER.
“The other thing that I think we would have to do is really bump up those numbers,” Dr. Biswas said. “Instead of looking at groups that are about 13, 14, 15 patients, really look at 100 patients to make sure that this is a true change we’re seeing overall.”
If the findings are sustained and replicated in larger groups, Dr. Biswas said future work could help identify which patients with atrial functional mitral regurgitation may still have reversible remodeling and may be more likely to benefit from M-TEER.
“Maybe what that would mean, if we still see that, and we see it sustained and in larger groups, then we could figure out which ones could benefit from M-TEER and have a chance of having reversible remodeling because of the procedure versus who’s had this for too long that their heart is not going to respond to it,” she said.
The researchers concluded that mechanism-based phenotyping may help contextualize early remodeling signals after M-TEER, but Dr. Biswas emphasized that the findings remain hypothesis-generating and limited by power.
Asked whether the lack of statistically significant differences in left ventricular diameter change should be viewed as evidence of similar remodeling across subtypes, Dr. Biswas again cautioned against overinterpretation.
“I would use this purely as a hypothesis that is limited by power,” she said. “At this point, we have two small groups to be able to pull a true hypothesis. So really, just a proof of concept and hopefully more to come as we go further into our data and we pull more of these patients.”
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