Abstract 2706: Persistent Reduction of Ischemic Mitral Regurgitation by Papillary Muscle Repositioning: Stabilization of the Papillary Muscle-Ventricular Wall Complex
Background: Recurrent ischemic mitral regurgitation (IMR) is frequent despite initial reduction by annuloplasty because continued LV remodeling increases tethering to the infarcted papillary muscle (PM). We have previously shown that PM repositioning by an external device can acutely reduce IMR. In this study, we tested the hypothesis that IMR reduction persists despite possible continued remodeling.
Methods: In 6 sheep, we used a chronic ischemic posterior infarct model that produces LV dilatation and MR over 8 weeks. An epicardial patch device was adjusted under echo guidance to reduce MR, with follow-up over a further 8 weeks and evaluation by 3D echo and sonomicrometry.
Results: In all 6 sheep, moderate IMR resolved with acute patch application and PM repositioning (6.5±1.8mm to 0.6±1.3mm proximal jet width, see table⇓) without decrease in EF (46±5% to 47±7%). Eight weeks after PM repositioning, MR was not significantly greater (0.6±1.3 vs1.0±1.0mm,P=ns) despite LV volumes that increased by 50±15% in 2 sheep. On average, LV volumes did not change significantly (ESV: 46±8 vs 49± 15 mL; p=ns and EDV: 85±16 vs 89±30 mL; p=ns). EF was unchanged from acute to chronic patch (47± 7vs 47± 6%). End-systolic elastance did not decrease from the chronic MI to the chronic patch stages, nor did segmental systolic strain in the non-infarcted zone; the diastolic stiffness constant showed a borderline decrease over time (table⇓).
Conclusion: PM repositioning is persistently effective in reducing moderate chronic IMR, even when LV volume increases. This may reflect stabilization of the papillary muscle-LV wall complex (Komeda and Miller) that controls mitral valve tethering.