Wolfgang Bothe1, Tomasz A Timek2, Frederick A Tibayan3, Mario Walther4, George T Daughters5, Neil B Ingels6, D Craig Miller7. 1. Department of Cardiovascular Surgery, Heart Center Freiburg-Bad Krozingen, Faculty of Medicine, University of Freiburg, Freiburg, Germany; Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif. 2. Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif; Division of Cardiothoracic Surgery Spectrum Health, Grand Rapids, Mich. 3. Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif; Department of Cardiothoracic Surgery, Oregon Health and Science University, Portland, Ore. 4. Department of Mathematics and Applied Statistics, University of Applied Sciences, Jena, Germany. 5. Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif. 6. Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif; Laboratory of Cardiovascular Physiology and Biophysics, Research Institute of the Palo Alto Medical Foundation, Palo Alto, Calif. 7. Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif. Electronic address: dcm@stanford.edu.
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Experimental in vivo ovine models suggest posterolateral PPM displacement as a predominant pathomechanism leading to apical leaflet tethering during IMR/FMR.
OBJECTIVE: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. METHODS: 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. RESULTS: 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. CONCLUSIONS: Experimental in vivo ovine models suggest posterolateral PPM displacement as a predominant pathomechanism leading to apical leaflet tethering during IMR/FMR.
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