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Original research
Association of pulmonary hypertension with the outcome in patients undergoing edge-to-edge mitral valve repair
  1. Timm Ubben1,
  2. Christian Frerker2,3,
  3. Buntaro Fujita4,
  4. Stephan Rosenkranz5,
  5. Roman Pfister5,
  6. Stephan Baldus5,
  7. Hannes Alessandrini2,3,
  8. Karl-Heinz Kuck6,
  9. Stephan Willems1,
  10. Ingo Eitel2,3,
  11. Tobias Schmidt2,3
  1. 1 Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany
  2. 2 Department of Cardiology, University Heart Center Lübeck, Lübeck, Germany
  3. 3 German Center for Cardiovascular Research, Lübeck, Germany
  4. 4 Department of Cardiac and Thoracic Vascular Surgery, University Heart Center Lübeck, Lübeck, Germany
  5. 5 Department of Cardiology, University Heart Center Cologne, Cologne, Germany
  6. 6 Lans Cardio, Lanserhof, Hamburg, Germany
  1. Correspondence to Dr Timm Ubben, Cardiology, Asklepios Klinik St. Georg, Hamburg, Germany; t.ubben{at}asklepios.com

Abstract

Objectives The association of pulmonary hypertension (PH) with the outcome after mitral transcatheter edge-to-edge repair (M-TEER) focusing on the new ESC/ERS guidelines definition for PH.

Background PH is frequently found in patients with mitral regurgitation and is associated with lower survival rates. Recent studies were based on echocardiographic parameters, but results based on invasive haemodynamics differentiating distinct types of PH using the new definition for PH are missing.

Methods 449 consecutive M-TEER-treated patients from December 2009 to February 2015 were included in this retrospective analysis. All patients were stratified by the distinct types of PH (no PH, precapillary PH, isolated postcapillary PH, combined post-PH and precapillary PH) according to the definitions of the ESC/ERS guidelines for the diagnosis of PH from 2015 (meanPA cut-off <25 mm Hg, pulmonary capillary wedge pressure (PCWP) cut-off ≤15 mm Hg, diastolic pulmonary gradient cut-off ≥7 mm Hg or pulmonary vascular resistance (PVR) >3 WU) and 2022 (meanPA cut-off ≤20 mm Hg, PCWP cut-off ≤15 mm Hg, PVR cut-off ≥3 WU).

Results Patients with any type of PH (2015: meanPA cut-off 25 mm Hg; 2022: meanPA cut-off >20 mm Hg) showed a higher risk of death after M-TEER compared with patients with no PH (2015: HR 1.61 (95% CI 1.25 to 2.07); p<0.001 and 2022: HR 2.09 (95% CI 1.54 to 2.83); p<0.001). Based on the new PH definition, each PH subgroup showed a lower survival after M-TEER compared with patients with no PH. Echocardiographic estimated systolic PAP showed a correlation with invasively measured mean pulmonary artery pressure (mPAP) (r=0.29, p<0.001) and systolic pulmonary arterial pressure (r=0.34,p<0.001). Cox-regression analysis showed higher invasive diastolic, systolic and mean pulmonary pressures were associated with higher all-cause mortality (p<0.001). In addition, invasive measured higher right atrial pressure, lower pulmonary arterial compliance, higher PVR and higher wedge pressure were identified as predictors of all-cause mortality after M-TEER.

Conclusions The new PH definition discriminates PH groups and mortality better than the old definition. The lower threshold of mPAP of 20mmHg improved prognostication in this cohort of patients.

  • Mitral regurgitation
  • Heart Failure, Systolic
  • Mitral Valve Insufficiency
  • Pulmonary Arterial Hypertension
  • Hypertension, Pulmonary

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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Footnotes

  • TU and CF are joint first authors.

  • X @tbubben

  • Contributors TU, BF, K-HK and SR declare the full disclosure of any relationship with industry. IE received lecture honoraria and research grants by Abbott and lecture honoraria by Edwards. HA received travel support by Abbott. T. Schmidt, S. Willems, CF received lecture honoraria and travel support from Abbott Vascular and Edwards Lifesciences. RP received lecture honoraria from Abbott Vascular and Edwards and is a consultant for Edwards. SB received lecture honoraria and research grants from Edwards and Abbott.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests TU, BF, K-HK and SR declare the full disclosure of any relationship with industry. IE received lecture honoraria and research grants by Abbott and lecture honoraria by Edwards. HA received travel support by Abbott. T. Schmidt, S. Willems, CF received lecture honoraria and travel support from Abbott Vascular and Edwards Lifesciences. RP received lecture honoraria from Abbott Vascular and Edwards and is a consultant for Edwards. SB received lecture honoraria and research grants from Edwards and Abbott.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer-reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.