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The Journal of Thoracic and Cardiovascular Surgery, Vol 97, 521-533, Copyright © 1989 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
DE Hansen, GE Sarris, MA Niczyporuk, GC Derby, PD Cahill and DC Miller
In animal models, severing the chordae tendineae of the mitral valve
reduces the maximum global left ventricular elastance (Emax,g), a load-
independent measure of left ventricular systolic performance; moreover,
chamber geometry is altered with systolic bulging in the region of the
papillary muscle insertions. This suggests that forces transmitted by the
mitral apparatus increase the regional volume elastance (Emax,r) of
segments subtending the insertions of the papillary muscles, and these
regions contribute substantially to overall left ventricular systolic
function (Emax,g). To test this hypothesis, we developed a method to
evaluate changes in the magnitude and uniformity of Emax,r as quantitated
by the slopes (E'max,i) of regional left ventricular isovolumetric
pressure-dimension relations. Such measurements were obtained before and
after all chordal attachments of the mitral valve were surgically divided
in seven open-chest swine preparations. Significant declines in E'max,i
were limited to the region of the posteromedial papillary muscle insertion.
Although the mean E'max,i of all ventricular regions (E'max,ave) was
unchanged, regional left ventricular elastances were less uniform after the
mitral chordae tendineae were severed, which indicated a less synergistic
contraction, and Emax,g fell by 21% from 7.1 +/- 2.0 to 5.6 +/- 1.2 mm
Hg/ml (p less than 0.05). These data demonstrate that the mitral apparatus
contributes importantly to the magnitude and uniformity of regional left
ventricular elastances and suggest that such alterations in regional
mechanics underlie the deterioration in global left ventricular systolic
performance (Emax,g) after excision of the mitral apparatus.
ARTICLES
Physiologic role of the mitral apparatus in left ventricular regional mechanics, contraction synergy, and global systolic performance
Division of Cardiology, Stanford University School of Medicine, Calif.
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