Bingham J B, McKusick K A, Strauss H W, Boucher C A, Pohost G M
Am J Cardiol. 1980 Nov;46(5):821-6. doi: 10.1016/0002-9149(80)90434-8.
An increased pulmonary thallium-201 concentration has been observed in exercise stress thallium perfusion imaging in patients with coronary artery disease. To understand the cause of this lung uptake, studies were performed in experimental animals and in patients undergoing stress thallium perfusion imaging. The extraction fraction of thallium-201 by the lungs was measured in a group of eight dogs using a dual isotope technique. Basal thallium-201 extraction fraction at rest was 0.09 +/- 0.009. After administration of isoproterenol, it decreased to 0.06 +/- 0.02 (difference not significant). After balloon obstruction of the left atrium (which increased mean left atrial pressure and pulmonary transit time) and after administration of acetylcholine as a bolus injection (which prolonged pulmonary transit time only) it increased to 0.19 +/- 0.02 (p < 0.01). Lung thallium-201 activity was measured in 86 patients who had undergone cardiac catheterization and stress-redistribution myocardial perfusion imaging. The initial/final lung activity ratio was 1.41 +/- 0.03 in patients with no significant coronary artery disease, 1.52 +/- 0.03 (difference not significant) in patients with single vessel coronary disease, 1.60 +/- 0.05 (p < 0.05) in those with two vessel disease and 1.59 +/- 0.05 (p < 0.05) in those with triple vessel disease. Quantitation of lung activity in 30 of these patients indicated that the increased ratio in patients with multivessel coronary artery disease was due to a transient absolute increase in the thallium-201 concentration immediately after maximal exercise. The data imply that increased pulmonary concentration of thallium-201 during exercise is a consequence of left ventricular failure.
