The effect of regional ischemia on mitral valve annular saddle shape.
Publication/Presentation Date
2-1-2004
Abstract
BACKGROUND: The mitral valve annulus has a distinctive saddle shape. Recent finite element analysis indicates this shape may contribute to normal valve function by increasing leaflet curvature and reducing leaflet stress. This study tests the hypothesis that acute ischemic mitral regurgitation (AIMR) is associated with loss of annular saddle shape.
METHODS: Sonomicrometry array localization (SAL) measured the three-dimensional geometry of the mitral annulus in 6 sheep before and after 30 min of posterior ischemia that produced severe AIMR. Using this SAL data the annular height to commissural width ratio (AHCWR), a measure of annular saddle shape, was calculated throughout the cardiac cycle and reported as a percentage.
RESULTS: The normal mitral annulus accentuated its saddle shape rapidly during isovolemic contraction: AHCWR increased from 11.6% +/- 1.1%-13.9% +/- 1.6% (p < 0.001). During ejection AHCWR remained relatively constant ranging from a minimum of 14.1% +/- 1.5% to a maximum of 14.9% +/- 1.3%. During ischemia AHCWR was found to be significantly smaller (p < 0.05) during isovolemic contraction, ejection, and isovolemic relaxation, but not during diastolic filling. Whereas ischemia did not affect AHCWR at end diastole (11.6% +/- 2.8%), the isovolemic accentuation of the saddle shape was lost.
CONCLUSIONS: The normal mitral annulus accentuates its saddle shape during systole. This accentuation is eliminated during ischemia that causes AIMR. These data suggest an association between annular saddle shape and valve competency.
Volume
77
Issue
2
First Page
544
Last Page
548
ISSN
0003-4975
Published In/Presented At
Gorman, J. H., 3rd, Jackson, B. M., Enomoto, Y., & Gorman, R. C. (2004). The effect of regional ischemia on mitral valve annular saddle shape. The Annals of thoracic surgery, 77(2), 544–548. https://doi.org/10.1016/S0003-4975(03)01354-7
Disciplines
Medicine and Health Sciences
PubMedID
14759435
Department(s)
Department of Medicine, Cardiology Division
Document Type
Article