Key result
Cutting second-order mitral chordae in sheep caused global left ventricular dysfunction, significantly decreasing end-systolic elastance (0.98 vs 1.48 mm Hg/mL, P=0.04).
Why the study?
Does cutting second-order mitral chordae alter LV geometry and systolic function in a sheep model?
Does cutting second-order mitral chordae alter LV geometry and systolic function in a sheep model?
Absolute Event Rate: 0.98% vs 1.48%
p-value: p=0.04
Cutting second-order mitral chordae causes global LV systolic dysfunction and alters LV geometry and local strain patterns, highlighting their importance for maintaining LV structure and function.
Strut chordae transection impairs LV function in sheep; leaves open whether preservation during repair improves human outcomes.
BACKGROUND: Mitral valvular-ventricular continuity is important for left ventricular (LV) systolic function, but the specific contributions of the anterior leaflet second-order "strut" chordae are unknown. METHODS AND RESULTS: Eight sheep had radiopaque markers implanted to silhouette the LV, annulus, and papillary muscles (PMs); 3 transmural bead columns were inserted into the mid-lateral wall between the PMs. The strut chordae were encircled with exteriorized wire snares. Three-dimensional marker images and hemodynamic data were acquired before and after chordal cutting. Preload recruitable stroke work (PRSW) and end-systolic elastance (E(es)) were calculated to assess global LV systolic function (n=7). Transmural strains were measured from bead displacements (n=4). Chordal cutting caused global LV dysfunction: E(es) (1.48+/-1.12 versus 0.98+/-1.30 mm Hg/mL, P=0.04) and PRSW (69+/-16 versus 60+/-15 mm Hg, P=0.03) decreased. Although heart rate and time from ED to ES were unchanged, time of mid-ejection was delayed (125+/-18 versus 136+/-19 ms, P=0.01). Globally, the LV apex and posterior PM tip were displaced away from the fibrous annulus and LV base-apex length increased at end-diastole and end-systole (all +1 mm, P<0.05). Locally, subendocardial end-diastolic strains occurred: Longitudinal strain (E22) 0.030+/-0.013 and radial thickening (E33) 0.081+/-0.041 (both P<0.05 versus zero). Subendocardial systolic shear strains were also perturbed: Circumferential-longitudinal "micro-torsion" (E12) (0.099+/-0.035 versus 0.075+/-0.025) and circumferential radial shear (E13) (0.084+/-0.023 versus 0.039+/-0.008, both P<0.05). CONCLUSIONS: Cutting second-order chords altered LV geometry, remodeled the myocardium between the PMs, perturbed local systolic strain patterns affecting micro-torsion and wall-thickening, and caused global systolic dysfunction, demonstrating the importance of these chordae for LV structure and function.
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Rodriguez et al. (2004) studied Left ventricular systolic function and mitral valvular-ventricular continuity (n=8). Cutting second-order "strut" chordae vs. Before chordal cutting (baseline) was evaluated on Global LV systolic function assessed by end-systolic elastance (E(es)) and preload recruitable stroke work (PRSW) (p=0.04). Cutting second-order mitral chordae in sheep caused global left ventricular dysfunction, significantly decreasing end-systolic elastance (0.98 vs 1.48 mm Hg/mL, P=0.04).
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