Abstract

The contribution of anterior mitral leaflet second-order ("strut") chordae tendineae to left ventricular (LV) systolic mechanics is debated; we measured the in vivo contribution of anterior chordae tendineae (ACT) and posterior chordae tendineae (PCT) to regional and global LV contractile function. Eight sheep had radiopaque markers implanted in the LV epicardium, partitioning the ventricle into 12 regions. Microminiature force transducers and snares were sutured to anterior leaflet "strut" chordae originating from ACT and PCT papillary muscles. Chordal tension, marker images, and hemodynamic data were acquired before and after (CUT) severing ACT and PCT. Fractional area shrinkage and slope of the regional end-diastolic area-regional stroke work relation (r-PRSW) were computed for each LV region. CUT did not affect global LV systolic function but reduced FAS in LV segments near the PCT insertion site: equatorial posterior lateral (19+/-2% versus 16+/-2%, P<0.05), apical posterior lateral (23+/-4% versus 19+/-4%, P<0.05), and posterior medial LV segments (16+/-2% versus 13+/-2%, P<0.05). r-PRSW fell near both the ACT (equatorial anterior medial [84+/-8 versus 62+/-11 mm Hg, P<0.05] and lateral [73+/-7 versus 53+/-9 mm Hg, P<0.05]) and PCT (apical posterior medial [91+/-12 versus 67+/-17 mm Hg, P<0.05] and lateral [72+/-8 versus 59+/-9 mm Hg, P<0.05]) LV insertion sites. Maximum tension in PCT was higher than in ACT (0.81+/-0.1 versus 0.52+/-0.08N, P<0.01). Dividing anterior leaflet strut chordae in sheep was associated acutely with regional LV systolic dysfunction near the chordal insertion sites. Caution is necessary when embarking on procedures that cut second-order chordae to treat ischemic mitral regurgitation, since this may compromise LV systolic function in ventricles that are already impaired.

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