Cardiac Positron Emission Tomography

Published on 23/05/2015 by admin

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Last modified 22/04/2025

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Chapter 11

Cardiac Positron Emission Tomography

1. What is positron emission tomography (PET)?

    A positron, as its name implies, is a positively charged particle that is ejected from the nucleus of an unstable atom. It is identical in mass to an electron. Strictly speaking, it is “antimatter” and very shortly after leaving the nucleus it collides with an electron in what is called an annihilation reaction. This reaction generates two 511 keV gamma photons that are emitted almost diametrically opposite from each other. The energy of these photons is captured by a special (PET) scanner and through a sophisticated network of electronics as well as computer software and hardware, it is transformed into an image.

2. Which are the two most common PET radiopharmaceuticals used for myocardial perfusion imaging (MPI)?

    Rubidium-82 (Rb-82) and nitrogen-13 (N-13) ammonia.

3. What are the characteristics of Rb-82?

    Rb-82 is a monovalent cation analog of potassium. It is commercially available as a strontium-82 generator. Its physical half-life is 75 seconds. It is extracted with high efficiency by myocardial cells through the Na+,K+-ATPase pump. The adult radiation dose from a Rb-82 MPI varies from 1.75 to 7.5 mSv (Fig. 11-1).

4. What are the characteristics of N-13 ammonia?

    N-13 Ammonia is an extractable myocardial perfusion tracer which, due to its 10 minute half-life, requires an on-site cyclotron. It is retained in myocardial tissue as N-13 glutamine by the action of glutamine synthetase. The adult radiation dose from an N-13 ammonia MPI is approximately 1.4 mSv.

5. What are the advantages of PET MPI over single-photon emission computed tomography (SPECT)?

6. My patient’s PET myocardial perfusion study was reported as demonstrating severe ischemia, but the coronary angiogram showed only nonobstructive coronary artery disease (CAD). How can this be?

    This can happen because the correlation between stenosis severity and coronary flow reserve (CFR) is weak and non-linear. Therefore, angiographically mild stenoses can cause severe derangement of CFR whereas severe coronary atherosclerosis can result in little to no alteration in myocardial perfusion.

7. What is the radiopharmaceutical used in cardiac PET for the assessment of myocardial viability?

    Fluorine-18 (F-18) fluorodeoxyglucose (FDG).

8. What is meant by “glucose loading” when a viability F-18 FDG cardiac PET is being performed?

    Under fasting nonischemic conditions, the myocardium preferentially oxidizes fatty acids. Under ischemic conditions, the myocardium switches to oxidation of glucose, as it can do this with a lower oxygen requirement. In order to promote accumulation of F-18 FDG (a glucose analog) within viable myocardial tissue, an oral or intravenous “glucose load” is administered to the patient prior to the injection of F-18 FDG. Under fasting conditions, the relative abundance of circulating glucose will cause the myocardium to switch to glucose oxidation and thus enhance the uptake of F-18 FDG into viable hibernating myocardial tissue.

9. What is meant by perfusion-metabolism (P-M) “match” or “mismatch” on cardiac PET viability imaging?

    A P-M match is present when there is markedly decreased FDG uptake that corresponds to the area of decreased perfusion. This finding would be consistent with a myocardial scar.

    A P-M mismatch would be present if the area of decreased perfusion demonstrates normal or increased FDG uptake (Fig. 11-2). This finding would be consistent with an area of viable hibernating myocardium.

10. Are there any other tracers that can be used for PET cardiac imaging?

    Yes. There are many other useful radiopharmaceuticals that can be used to interrogate different aspects of myocardial metabolism, innervation, ATP generation, etc. Some of these include:

Additionally, there are several tracers currently under development for imaging of α- and β-adrenergic cardiac receptors.