Persistent reduction of ischemic mitral regurgitation by papillary muscle repositioning: structural stabilization of the papillary muscle-ventricular wall complex

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 patch device can acutely reduce IMR. In this study, we tested the hypothesis that IMR reduction persists despite possible continued LV remodeling.

In 7 sheep, we used a chronic ischemic posterior infarct model that produces LV dilatation and MR over 10 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. In all 7 sheep, moderate IMR resolved with acute patch application and PM repositioning (6.5+/-1.8 mm to 0.6+/-1.3 mm proximal jet width, P<0.001) without decrease in LVEF (43+/-3% to 44+/-8%). Eight weeks after PM repositioning, MR was not significantly greater (0.6+/-1.3 mm versus 1.0+/-1.0 mm, P=NS) despite an increase in LV volumes in 3 animals (2 had increases of 50+/-15%). On average, LV volumes did not change significantly (ESV: 46+/-8 mL versus 49+/-15 mL; P=NS and EDV: 85+/-16 mL versus 89+/-30 mL; P=NS). LVEF was unchanged from acute to chronic patch (44+/-8% versus 43+/-8%). Contractility as end-systolic elastance did not decrease from the chronic MI to the acute and chronic patch stages, nor were there any significant changes in dP/dt, LV stiffness constant, or time constant of LV relaxation (Tau).

PM repositioning is persistently effective in reducing moderate chronic IMR, even when LV volume increases. This may reflect structural stabilization by an external patch device of the papillary muscle-LV wall complex that controls mitral valve tethering.