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  • Title: Geometric distribution of chordae tendineae: an important anatomic feature in mitral valve function.
    Author: He S, Weston MW, Lemmon J, Jensen M, Levine RA, Yoganathan AP.
    Journal: J Heart Valve Dis; 2000 Jul; 9(4):495-501; discussion 502-3. PubMed ID: 10947041.
    Abstract:
    BACKGROUND AND AIM OF THE STUDY: This study examined the geometric distribution of chordae tendineae and their importance in compensating for papillary muscle (PM) displacement. METHODS: Anatomic, chordal mechanics and hemodynamic measurements were performed with porcine mitral valves. For hemodynamic measurements, physiological pulsatile flow conditions were maintained, and PM positions varied. Leaflet coaptation was documented by 2-D echocardiography, and regurgitation measured directly. RESULTS: Anatomic measurements showed the sum of marginal leaflet and marginal chordal lengths to exceed basal chordal length (1.8+/-0.4 versus 2.8+/-0.7 cm for anterior leaflets; 1.6+/-0.3 versus 2.5+/-0.6 cm for posterior leaflets). Triangular structures existed between basal chordae and marginal chordae with the marginal leaflet as the third side. Basal chordae resisted apical PM displacement in static experiments, while marginal chordae governed leaflet closure in hemodynamic experiments. Under pulsatile flow conditions, apical PM displacement decreased leaflet coaptation length and increased regurgitation (9.4+/-2.1 versus 4.0+/-1.6 ml). When marginal chordae were fused to the basal chordae, eliminating the role of the marginal chordae, severe regurgitation resulted (28.5+/-5.0 ml with apical PM displacement). CONCLUSION: Based on triangular structures involving the basal and marginal chordae, a compensatory mechanism was described which explains how the severity of mitral regurgitation can vary following PM displacement. Basal chordae provide a constant connection between the annulus and papillary muscles, while marginal chordae maintain marginal leaflet flexibility, governing proper valve closure. This study relates chordal distribution to normal valve function, and provides a better understanding of breakdown in valve function under pathophysiological conditions.
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