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Abstract
The hypothesis that abnormally increased myocardial oxygen demands may contribute
to increased vulnerability to ischemia during exercise in the chronically pressure-overloaded
hypertrophied left ventricle was tested. Myocardial oxygen consumption was measured
during a five stage graded treadmill exercise protocol in eight normal dogs and nine
adult dogs in which a 90% increase in left ventricular mass was produced by banding
the ascending aorta at 8 weeks of age. Heart rate increased progressively during exercise
in both groups of dogs, but was significantly faster than normal in the group with
aortic banding. Coronary blood flow increased progressively with exercise in both
groups, but was significantly greater than normal in dogs with aortic banding during
each exercise stage. Coronary sinus oxygen tension decreased significantly and similarly
during exercise in normal and hypertrophied hearts. In dogs with hypertrophy, oxygen
consumption per gram of myocardium averaged 52% greater than normal during exercise.
This excess myocardial oxygen consumption in dogs with aortic banding resulted from
an abnormally large increase in oxygen consumption per beat during exercise and from
the faster heart rate in this group of dogs. Measurements of myocardial blood flow
with microspheres demonstrated a lower subendocardial/subepicardial blood flow ratio
in dogs with hypertrophy; this ratio decreased significantly during exercise in dogs
with hypertrophy, but not in normal dogs. These data are consistent with the hypothesis
that increased vulnerability to ischemia in the pressure-overloaded hypertrophied
left ventricle is the result of both increased myocardial oxygen demands during exercise
and abnormalities of myocardial perfusion.