Abstract
Infarct (MI) patching has been shown to reduce mitral regurgitation (MR) in chronic MI models, but its local and global effects on the LV require further study. We tested the hypothesis that MI patching with papillary muscle (PM)repositioning not only reduces MR but also limits infarct expansion and progression of global LV dysfunction. Methods. Fourteen sheep with MIs created in a standard vascular territory as confirmed by first-pass gadolinium (Gd) MRI were studied at baseline, acutely post-MI and at 3 months by sonomicrometry, 3D echo and MRI. Animals were randomized to control versus treatment with an adjustable patch device to reposition the inferior PM (n=7 each). MI size was assessed by Gd-enhanced MRI and local wall motion by echo-derived tissue velocities. Results. MR was reduced chronically in all patch animals (vena contracta=0.08 vs 0.5 cm, p<0.001). At 3 months, despite end-diastolic dilatation in both groups (127±20 vs 128±16 mL, p=0.91, 1.4±0.1 x baseline), end-systolic volumes were smaller (71±9 vs 100±21 mL, p=0.05) and EF higher (43±11 vs 24±10%, p=0.02) in the treated group, with better maintained preload recruitable stroke work (41±5 vs 33±3, p=0.01). Infarct expansion at 3 months was reduced by patching (infarct/LV surface area=22±5 vs 41±6%, p=0.001; figure ). Remote zone contractile function was also improved by patching (strain=20±5 vs 11±4%, p=0.03; tissue velocity=3.5±0.7 vs 1.8±0.6 cm/s, p=0.05). Conclusion. Despite continued LV remodeling, inferior infarct patching leads to long-term decreased MR and better preserved global LV function, with both diminished expansion of the restrained infarct and preserved contractility of the remote myocardium.
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