Implications of Unexpected Diffuse Lung Uptake on a ^99mTc-Sestimibi Parathyroid Scan

DISCUSSION

The possible mechanism for uptake of ^99mTc-sestamibi uptake in the lungs can be explained by the chemical characteristics of ^99mTc-sestamibi. The radiotracer is a positively charged ligand that has natural affinity for negative transmembrane potentials, specifically the mitochondria (1). Patients with chronic heart failure have an increased predisposition for pleural effusions and consequent pulmonary injury. Lung uptake of ^99mTc-sestamibi can also occur as a result of left ventricular failure, which causes the radiotracer to persist in the lung arterioles rather than reaching the systemic circulation and physiologic distribution (2). However, the differential diagnosis includes many other serious conditions, such as systemic lupus erythematosus, pulmonary embolism, amyloidosis, sarcoidosis, and cancer. In view of these etiologies for diffuse lung uptake, it is vital to definitively establish the exact cause.

This patient’s history pointed to a cardiac etiology, specifically systolic dysfunction, which was confirmed by the subsequent work-up. Previous studies, such as the one by Bacher-Stier et al., found that postexercise lung uptake of ^99mTc-sestamibi correlated with severe coronary artery disease and reduced left ventricular function (3). An interesting finding in our patient was that he lacked severe coronary artery disease despite having end-stage restrictive cardiomyopathy. A study by Giubbini et al. showed that ^99mTc-sestamibi lung uptake was significantly higher in patients with left ventricular dysfunction than in healthy subjects. Moreover, severely compromised left ventricular function and an ejection fraction lower than 40% demonstrated an increase in lung uptake (4). However, a marked delay in lung clearance, as evident on the 2-h image (Fig. 1B), cannot always be explained by simple association between systolic heart failure and ^99mTc-sestamibi lung uptake. Other causes should be considered as well.