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Myocardial bioenergetic abnormalities in a canine model of left ventricular dysfunction
K M McDonald1, M Yoshiyama, G S Francis
1Department of Medicine, University of Minnesota, Minneapolis.
Journal of the American College of Cardiology
|March 1, 1994
Summary
Remodeled heart muscle shows altered high-energy phosphate metabolism, indicated by a reduced creatine phosphate/adenosine triphosphate (CP/ATP) ratio. This abnormality may stem from an imbalance between oxygen supply and demand in the heart.
Area of Science:
- Cardiovascular Physiology
- Biochemistry
- Medical Imaging
Background:
- Heart failure development post-myocardial infarction is often unexplained.
- Remodeled myocardium may exhibit structural changes contributing to later heart failure.
- The impact of these changes on myocardial metabolism and ventricular function is unknown.
Purpose of the Study:
- To assess high-energy phosphate compound metabolism in remodeled left ventricular myocardium.
- To investigate metabolic alterations in viable myocardium after myocardial damage.
Main Methods:
- Utilized phosphorus-31 nuclear magnetic resonance spectroscopy for assessing high-energy phosphate metabolism.
- Compared eleven dogs with left ventricular dysfunction (post-infarction) to eight normal dogs.
- Measured myocardial blood flow using radioactive microspheres during coronary hyperperfusion induced by adenosine.
Main Results:
- Significantly reduced creatine phosphate/adenosine triphosphate (CP/ATP) ratio in subepicardium and subendocardium of dogs with left ventricular dysfunction.
- Coronary hyperemia induced by adenosine was less pronounced in the dysfunction group.
- Increased subendocardial CP/ATP ratio observed with improved myocardial perfusion in the dysfunction group.
Conclusions:
- Abnormal transmural distribution of high-energy phosphate compounds is present in remodeled myocardium.
- This metabolic abnormality may be partly due to a mismatch between oxygen delivery and demand.
- Suggests a link between altered metabolism and ventricular dysfunction in post-infarction remodeling.