Background and aim of the study: Mitral insufficiency, a common and morbid pathology, has been related to topological changes in the left ventricle. These changes may affect mitral leaflet coaptation by displacing the tips of the papillary muscles (PMs), subsequently changing the tension distribution on the chordae tendineae. Therefore, further understanding of the effects of PM displacement on chordal force i distribution is required. Methods: Six human and five porcine mitral valves were studied in a physiological left heart simulator. Cardiac output and transmitral pressure were recorded online and maintained within physiological ranges. Force transducers were placed on six chordae tendineae to measure chordal force distribution. Tension on individual chordae tendineae was recorded online during the cardiac cycle. The experiment was conducted for eight different PM positions, which were constructed from 5-mm vectorial displacements from the normal PM position. Results: The anterior strut chord showed significant (p <0.05) variations in peak systolic tension (PST) for those positions associated with apical motion of the PMs. The posterior intermediate chord also showed significant variations in PST for positions associated with apical displacement of the PMs, whereas posterior displacement of the PMs resulted in a reduction in tension. In contrast, both the anterior marginal and posterior marginal chords showed a relatively uniform PST for the eight different PM positions. The posterior basal and commissural chords were the most sensitive to tension variations due to PM displacement. These chords showed relatively large and significant (p <0.05) variations in PST for most of the different PM displacements. Conclusion: The effects of PM relocation on chordal tension depended on chordal type. Chords which insert closer to the annulus were more sensitive to PM displacement, whereas those further from the annulus, the marginal chords, were the least sensitive to PM displacement.
|Number of pages||8|
|Journal||Journal of Heart Valve Disease|
|State||Published - 2005|