Pulmonary artery systolic pressure moved in opposite directions depending on the mechanism of mitral regurgitation after mitral transcatheter edge-to-edge repair (M-TEER), even as left ventricular diameters changed only modestly—and similarly—across subtypes at 1 month, according to a study presented at the American Society of Echocardiography 2026 Scientific Sessions.
The findings, reported as poster P1-01 by Medha Biswas, MD, of the University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, and colleagues, and published as an abstract in the Journal of the American Society of Echocardiography, suggest that mechanism-based phenotyping may help contextualize early remodeling after M-TEER. But Dr. Biswas repeatedly cautioned that the analysis is hypothesis-generating and limited by small subgroups.
The researchers reviewed 442 patients assessed for M-TEER between 2014 and 2024, of whom 411 received at least one clip. Drawing on clinical data abstracted from medical records, preprocedural and postprocedural transthoracic echocardiograms, and intraprocedural transesophageal imaging—which was also used to classify the mitral regurgitation (MR) mechanism—they compared postprocedural with preprocedural left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), and pulmonary artery systolic pressure (PASP). Outcomes were assessed across atrial functional, ventricular functional, and degenerative MR, as well as in a small reference group that did not receive a clip.
Among treated patients with paired grading data, MR severity fell by a mean of 2.42 grades (median, 3 grades) at 1 month. Paired echocardiographic data were available for 279 patients for LVEDD, 280 for LVESD, and 235 for PASP.
Left ventricular diameter changes were small and did not differ significantly across subtypes. Median LVEDD changes were −0.20 cm in atrial functional MR, −0.10 cm in ventricular functional MR, and −0.10 cm in degenerative MR; median LVESD changes were 0.20 cm, −0.10 cm, and 0.05 cm, respectively.
PASP, by contrast, diverged. The median change was +4 mm Hg in atrial functional MR but −5.5 mm Hg in ventricular functional MR and −3 mm Hg in degenerative MR. In the very small no-clip cohort, median changes were −0.30 cm for LVEDD (n = 4), −0.45 cm for LVESD (n = 4), and −18 mm Hg for PASP (n = 3).
That divergence is what most interested Dr. Biswas, and Dr. Biswas cautioned against overinterpreting it. "When I look at this, what I wonder is, is there a phenotypic difference in our atrial functional and ventricular functional patients?" she said in an interview with Conexiant. She raised the possibility that atrial functional patients may have irreversible left atrial remodeling and underdiagnosed group 2 pulmonary hypertension, which could explain why their PASP worsened while it held steady or improved in the ventricular functional group. Even so, she added, "I don't think we can pull clinical data from this yet."
Her next step is to test whether the signal lasts. The team plans to examine its 1-year data to determine whether the change is sustained or simply a temporary effect of the procedure. Larger cohorts will also be needed—closer to 100 patients in key subgroups rather than subgroups as small as 13 to 15 patients—before concluding that the PASP differences are real, she said.
If the pattern holds, Dr. Biswas said, it could eventually help distinguish atrial functional patients who retain reversible remodeling, and stand to benefit from M-TEER, from those whose hearts have been remodeled too long to respond.
For now, she framed both the PASP divergence and the absence of LV differences the same way. "I would use this purely as a hypothesis that is limited by power," she said. "Really, just a proof of concept, and hopefully more to come."
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