Perfusion imaging with N13 Ammonia demonstrates a large perfusion defect in the inferior wall (extending from base to apex) and moderate perfusion defect in the basal anterolateral wall. Perfusion abnormalities are primary fixed, but there is worsened stress perfusion around the defects, compatible with surrounding ischemia. These finding are easily shown on the polar map images of the entire left ventricle:

At this point, the images available so far may suggest myocardial infarcts with peri-infarct ischemia. But the basal anteroseptal defect is an atypical pattern for coronary disease. Furthermore, this patient had no risk factors for coronary disease, and in fact underwent a cardiac catheterization less than one year previously which demonstrated normal coronary arteries.

Perfusion imaging was followed by metabolic imaging with F18 FDG:

Metabolic imaging shows increased FDG activity exactly correlating to the perfusion abnormalities, indicating glucose metabolism in these regions.

This is a patient with cardiac sarcoidosis, proven with myocardial biospy. The study was performed after a non-carbohydrate diet for 24 hours, which enables fatty acid metabolism of normal myocardium, ensuring that any myocardial FDG uptake is due to an abnormal inflammatory process.

This patient also underwent cardiac MR imaging:

MR images show mid-myocardial and subepicardial delayed enhancement (atypical pattern for coronary disease), right ventricle involvement, and susceptibility in the right ventricle lumen due to the pacemaker lead. Delayed post-contrast enhancement on MRI may represent inflammation or scar tissue, but in this case the enhancement closely matches the distribution of FDG uptake, compatible with active inflammation.

Although sarcoidosis is described to result in primarily fixed perfusion defects, small areas of reversibility can be seen at the periphery of actively inflamed myocardium.

See topic discussion on Uses of Cardiac PET/CT.