By Barry L. Zaret MD, George A. Beller MD
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Extra info for Clinical Nuclear Cardiology: State of the Art and Future Directions: Expert Consult: Online and Print, 4 Edition
In such cases, the ability to detect discrete lesions by observing defects in relative blood flow may be reduced or eliminated. The cause of this is simply that while stress does not cause increased flow in vessels with discrete flow-limiting lesions, neither does it cause increased flow to other parts of the heart served by vessels without discrete flow-limiting lesions. Thus, the flow differential that we use as indicator of a flow-limiting lesion is reduced or eliminated. Another possible failure to detect CAD is the case of balanced multivessel disease, often noted as balanced ischemia.
Malonyl-CoA is an inhibitor of CPT-1, the enzyme that regulates the entry of fatty acids into the mitochondria, thereby regulating fatty acid oxidation. Therefore, inactivation of ACC by AMPK relieves malonyl-CoA inhibition of CPT-1 to increase fatty acid oxidation. 23 This increase in fatty acid oxidation in the reperfused myocardium has been hypothesized to increase the production of lipid-derived free radicals and uncouple glucose uptake from glucose oxidation. Another target of regulation by AMPK is PFK-1, one of the enzymes regulating glycolytic flux.
Now suppose further that the normal segment (the solid line) was not visible. This could happen in a case of diffuse multiple-vessel disease so severe that there is no normally perfused segment for reference. The tracer then redistributes into the ischemic segments so that they have more uptake than the partly infarcted segments. This can create the appearance of a defect (the infarct) in the delayed or rest images that was not apparent in the stress images. When there is no physiologically reasonable explanation for the appearance of reverse redistribution, our experience has been that it is one of the several artifacts mentioned.