(Circulation. 1997;95:1601-1610.)
© 1997 American Heart Association, Inc.
Articles |
Premorbid Determinants of Left Ventricular Dysfunction in a Novel Model of Gradually Induced Pressure Overload in the Adult Canine
From the Cardiology Division and Gazes Cardiac Research Institute (M.K., M.N., M.R.Z., G.D., H.T., G.C., B.A.C.) and the Department of Comparative Medicine (M.M.S., G.K.), Medical University of South Carolina, Charleston, and the Ralph H. Johnson Department of Veterans Affairs (M.R.Z., G.C., B.A.C.), Charleston, SC.
Correspondence to Blase A. Carabello, MD, Cardiology Division, Medical University of South Carolina, 171 Ashley Ave, Charleston, SC 29425-2221.
Background When a pressure overload is placed on the left ventricle, some patients develop relatively modest hypertrophy whereas others develop extensive hypertrophy. Likewise, the occurrence of contractile dysfunction also is variable. The cause of this heterogeneity is not well understood.
Methods and Results We recently developed a model of
gradual proximal aortic constriction in the adult canine that mimicked
the heterogeneity of the hypertrophic response seen in humans. We
hypothesized that differences in outcome were related to differences
present before banding. Fifteen animals were studied initially. Ten
developed left ventricular dysfunction (dys group). Five dogs
maintained normal function (nl group). At baseline, the nl group had a
lower mean systolic wall stress (96±9 kdyne/cm2; dys
group, 156±7 kdyne/cm2; P<.0002) and greater
relative left ventricular mass (left ventricular weight [g]/body wt
[kg], 5.1±0.36; dys group, 3.9±0.26; P<.02). On the
basis of differences in mean systolic wall stress at baseline, we
predicted outcome in the next 28 dogs by using a cutoff of 115
kdyne/cm2. Eighteen of 20 dogs with baseline mean systolic
stress >115 kdyne/cm2 developed dysfunction whereas 6 of 8
dogs with resting stress 
115 kdyne/cm2 maintained normal
function.
Conclusions We conclude that this canine model mimicked the heterogeneous hypertrophic response seen in humans. In the group that eventually developed dysfunction there was less cardiac mass despite 60% higher wall stress at baseline, suggesting a different set point for regulating myocardial growth in the two groups.
Key Words: hypertrophy • stenosis • ventricles • aorta • heart failure • valves
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