Author + information
- Received July 10, 1989
- Revision received October 12, 1989
- Accepted November 2, 1989
- Published online April 1, 1990.
- Robert J. Bache, MD, FACC∗ and
- Xue Zheng Dai, MD
- ↵∗Address for reprints: Robert J. Bache, MD, Division of Cardiology, University of Minnesota, Box 338 UMHC, 420 Delaware Street Southeast, Minneapolis, Minnesota 55455.
The hypothesis that abnormally increased myocardial oxygen demands may contribute to increased vulnerability to ischemia during exercise in the chronically pressureoverloaded 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.
☆ This work was supported by U.S. Public Health Services Grant HL21872 and Program Project Grant HL32427 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland.
- Received July 10, 1989.
- Revision received October 12, 1989.
- Accepted November 2, 1989.