Circulation, Vol 84, 2167-2180, Copyright © 1991 by American Heart Association
S Kaul, WD Spotnitz, WP Glasheen and DA Touchstone
BACKGROUND. Papillary muscle dysfunction (PMD) has been implicated in the
pathogenesis of ischemic mitral regurgitation (MR). We hypothesized that
ischemic MR is not caused by PMD and/or dysfunction of the myocardial
regions from where the papillary muscles arise but is related to reduction
in global left ventricular (LV) function. To test this hypothesis, three
groups of dogs were studied. METHODS AND RESULTS. In group 1 dogs (n = 8),
varying degrees of regional and global LV dysfunction were produced. In
group 2 dogs (n = 7), the circulation to the papillary muscles was isolated
from that of the rest of the LV. Dysfunction of one or both papillary
muscles was produced without producing global LV dysfunction. Global LV
dysfunction was also produced while keeping papillary muscle function
intact. The degree of MR (assessed using contrast echocardiography) was
correlated in both groups of dogs with thickening of the papillary muscles
and regional and global LV function. In the group 3 dogs (n = 6), the
spatial distribution of blood flow within each papillary muscle was
determined during ischemia by using radiolabeled microspheres. Thickening
of the papillary muscles was assessed at three different levels along their
lengths and was correlated with average blood flow at these levels. In
group 1 dogs, MR was noted only when global LV function was affected and
its severity correlated inversely with global LV function (r = - 0.84 with
peak positive LV dP/dt and r = -0.95 with global LV thickening,
respectively). In comparison, there was poor correlation between MR and
anterior and posterior papillary muscle thickening (r = - 0.38 and r =
-0.49, respectively). In group 2 dogs, MR did not occur in the presence of
either PMD or akinesia of the immediately adjacent LV myocardium. MR
occurred only when global LV dysfunction was produced (with the papillary
muscle function intact), and its severity correlated inversely with global
LV function (r = -0.92 with LV dP/dt and r = -0.86 with global LV
thickening, respectively). There was poor correlation between the degree of
MR and thickening of the anterior and posterior papillary muscles (r =
-0.24 and r = -0.38, respectively). In both groups of dogs, MR was
associated with incomplete mitral leaflet closure (IMLC), and the severity
of MR correlated linearly with the degree of IMLC (r = 0.98). MR was never
associated with mitral valve prolapse. In the group 3 dogs, despite more
inhomogeneous flow during ischemia to the anterior compared with the
posterior papillary muscle, mean thickening of these muscles was similar (3
+/- 10% and 3 +/- 4%, respectively). Furthermore, there was minimal
variability in thickening between different parts of the muscles (3 +/- 2%
and 5 +/- 3%, respectively). CONCLUSIONS. It is concluded that PMD and/or
dysfunction of the immediately adjacent LV myocardium does not result in
MR. MR occurs during ischemia only when global LV function is affected,
even when thickening of the papillary muscles and the immediately adjacent
LV remains intact. MR in this situation is related to IMLC; the greater the
degree of IMLC, the greater the MR. These findings suggest that the
mechanism of ischemic MR is not related to PMD. There may also be important
therapeutic implications of these findings.
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Mechanism of ischemic mitral regurgitation. An experimental evaluation
Department of Medicine, University of Virginia School of Medicine, Charlottesville 22908.
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