Characterization of 3-dimensional papillary muscle displacement in in vivo ovine models of ischemic/functional mitral regurgitation

Papillary muscle (PM) displacement contributes to ischemic/functional mitral regurgitation (IMR/FMR). The displaced PMs pull the mitral leaflets into the left ventricle (ie, toward the apex) thus hampering leaflet coaptation. Intuitively apical leaflet tethering results from apical PM displacement. The 3-dimensional directions of PM displacement are, however, incompletely characterized. Data from in vivo ovine models of IMR (6-8 weeks of posterolateral infarction, n = 12) and FMR (9-21 days of rapid left ventricular pacing, n = 11) were analyzed. All sheep had radiopaque markers implanted on the anterior and posterior PM (PPM) tips, around the mitral annulus, and on the left ventricular apex. To explore 3-dimensional PM displacement directions, differences in marker coordinates were calculated at end-systole before and during IMR/FMR using a right-handed coordinate system centered on the mitral annular “saddle horn” with the y-axis passing through the apical marker. No apical PM displacement was observed during either IMR or FMR. The anterior PM displaced laterally during FMR. Posterolateral PPM displacement was observed during IMR and FMR. Experimental in vivo ovine models suggest posterolateral PPM displacement as a predominant pathomechanism leading to apical leaflet tethering during IMR/FMR. Consistent posterolateral, but not apical dislocation of the posterior papillary muscle was observed with experimental IMR/FMR: data from studies using ovine models of IMR and FMR and radiopaque marker tracking of anterior and posterior papillary muscle tips (APM and PPM, respectively) suggest posterolateral PPM displacement as a predominant pathomechanism leading to apical leaflet tethering during IMR and FMR. IMR, Ischemic mitral regurgitation; FMR, functional mitral regurgitation; LV, left ventricle. [Display omitted]