Key result
Transcatheter mitral valve repair decreased pulmonary vascular resistance from 3.5 to 2.3 wood units (p=0.02) in patients with end-stage HFrEF and severe secondary mitral regurgitation.
Why the study?
Elevated pulmonary vascular resistance in HFrEF patients with secondary mitral regurgitation limits eligibility for heart transplantation, but whether TMVr improves pulmonary circulatory hemodynamics and transplant eligibility was unknown.
Does transcatheter mitral valve repair improve pulmonary hemodynamics and increase eligibility for heart transplantation in patients with end-stage HFrEF and severe secondary mitral regurgitation?
Cohort (n=17)
Does transcatheter mitral valve repair improve pulmonary hemodynamics and increase eligibility for heart transplantation in patients with end-stage HFrEF and severe secondary mitral regurgitation?
Absolute Event Rate: 2.3% vs 3.5%
p-value: p=0.02
TMVr may improve pulmonary hemodynamics and reduce PVR in end-stage HFrEF patients with severe secondary mitral regurgitation, potentially increasing their eligibility for heart transplantation.
May support hemodynamic assessment in end-stage HFrEF; hypothesis-generating and requires prospective trials before practice change.
BACKGROUND: Heart transplantation remains the gold standard for treatment of patients with end-stage heart failure and severely reduced ejection fraction (HFrEF). An increased pulmonary vascular resistance (PVR), which is often prevalent in HFrEF patients with secondary mitral regurgitation (SMR), limits the eligibility for transplantation. Therefore, we evaluated whether transcatheter mitral valve repair (TMVr) improves pulmonary circulatory hemodynamics and increases the eligibility for transplantation in end-stage HFrEF patients with severe SMR. METHODS: We retrospectively analysed the hemodynamics by right heart catheterization (RHC) as well as laboratory and clinical outcomes of end-stage HFrEF patients with SMR that underwent TMVr. RESULTS: Seventeen patients (age: 55 ± 10 yrs) underwent TMVr and repeat RHC at a mean follow-up of 5.7 ± 7.9 months. TMVr decreased PVR (3.5 ± 2.2 to 2.3 ± 1.2 wood units, p = 0.02) and systolic pulmonary artery pressure (55.4 ± 15 mmHg to 45.6 ± 9.8 mmHg, p = 0.02) from baseline to follow-up, respectively, while cardiac output was increased (3.7 ± 0.9 l/min to 4.6 ± 1.3 l/min, p = 0.02). In addition, transpulmonary gradient decreased significantly (12.0 ± 7.5 mmHg to 9.7 ± 5.3 mmHg, p = 0.04). The prevalence of New York Heart Association functional class ≥III at follow-up was reduced from 88% (15/17 patients) to 47% (8/17 patients, p = 0.01). All five patients with initially too high PVR (>3.5 WU) showed a significant decrease in PVR and three of them became potential candidates for heart transplantation after TMVr. CONCLUSION: TMVr is associated with reduction in PVR which may increase eligibility for transplantation in some HFrEF patients with severe SMR.
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Doldi et al. (2021) conducted a cohort in End-stage heart failure with severely reduced ejection fraction and severe secondary mitral regurgitation (n=17). Transcatheter mitral valve repair (TMVr) vs. Baseline was evaluated on Pulmonary vascular resistance (p=0.02). Transcatheter mitral valve repair decreased pulmonary vascular resistance from 3.5 to 2.3 wood units (p=0.02) in patients with end-stage HFrEF and severe secondary mitral regurgitation.
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