Infarct restraint attenuates remodeling and reduces chronic ischemic mitral regurgitation after postero-lateral infarction.

Abstract

Chronic ischemic mitral regurgitation (IMR) is produced by adverse postinfarction ventricular remodeling. We hypothesize that restraining infarct expansion reduces left-ventricular (LV) dilatation and the severity of mitral regurgitation. Two groups of 6 sheep had coronary snares placed around the second and third obtuse marginal coronary arteries and four piezoelectric transducers sutured within myocardium across the mid short axis of the LV. In one group, a patch of Marlex mesh was precisely fitted and lightly sutured to myocardium destined for infarction (determined by temporary snare occlusion). Two weeks after instrumentation, coronary snares were tied tight to infarct approximately 24% of the posterolateral LV mass. Transdiaphragmatic echocardiograms were obtained in all animals at baseline, and 30 minutes, and 2, 5, and 8 weeks after infarction. Echocardiograms confirmed similar infarct sizes and locations in both groups. Eight weeks after infarction, IMR grade averaged 3.6+ (scale: 0, no MR; 4, severe MR) in control sheep and 1.9+ in mesh-restrained animals (p = 0.0001). LV end-diastolic and end-systolic volumes at the eighth week were less in mesh-treated sheep (87 +/- 11.3 vs 113 +/- 18.3; 61 +/- 10.6 vs 77 +/- 14.1, respectively), but differences were not significant. Data from mid short axis piezoelectric transducers indicated significantly less strain in the infarcted myocardium in mesh-restrained sheep than in control. Early restraint of postero-lateral infarct expansion attenuates the severity of ischemic mitral regurgitation and slows ventricular dilatation. However, the remodeling process is not arrested 8 weeks after infarction.