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Differential effects of transcatheter edge-to-edge repair on forward stroke volume in atrial and ventricular secondary mitral regurgitation

  • Franziska Grewe,
  • Luise Ulrich,
  • Moritz Haus,
  • Philippe Felfeli,
  • Christian Schach,
  • Andreas Luchner,
  • Christoph Birner,
  • Lars S. Maier,
  • Bernhard Unsöld,
  • Christine Meindl,
  • Kurt Debl,
  • Michael Paulus

摘要

Introduction

Transcatheter edge-to-edge mitral valve repair (M-TEER) is an established treatment for secondary mitral regurgitation (MR). Forward stroke volume (FSV), reflecting left ventricular forward flow, is a prognostic marker in heart failure and valvular disease. However, its clinical relevance in secondary MR has not been clearly defined.

Objective

To assess the impact of M-TEER on FSV in atrial and ventricular secondary MR, identify predictors of FSV improvement, and evaluate its association with long-term outcomes.

Methods

In this retrospective single-center study, 103 patients with moderate-to-severe or severe secondary MR (ventricular MR: n = 60, atrial MR: n = 43) underwent M-TEER. FSV was quantified using left ventricular outflow tract measurements before and 4 weeks post-procedure. Clinical outcomes were assessed over a 2-year follow-up period.

Results

Procedural success (MR grade ≤ II) was high (ventricular MR: 95%, atrial MR: 100%). FSV remained unchanged in ventricular MR (49.4 ± 17.3 vs. 49.5 ± 16.5 ml, p = 0.960) but increased significantly in atrial MR (60.5 ± 21.7 vs. 66.8 ± 19.6 ml, p = 0.037). In multivariable analysis, atrial MR etiology (OR 5.12, p = 0.048) and lower baseline FSV (OR 0.36 per 10 ml/m2, p = 0.002) independently predicted FSV improvement > 10%. FSV responders and non-responders did not differ in functional status or residual MR grade. FSV improvement was not associated with reduced mortality or heart failure hospitalization.

Conclusion

M-TEER enhances FSV in atrial but not ventricular secondary MR. Atrial MR etiology and low baseline FSV independently predict FSV improvement. Early FSV improvement does not translate into improved clinical outcomes, suggesting that FSV response reflects hemodynamic adaptation rather than serving as a prognostic marker.

Graphical Abstract