Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean ± standard deviation segmental thallium-201 defect score (22 ± 7 vs 12 ± 8, p < 0.0001), tower ejection fraction (35 ± 14 vs 49 ± 14%, p < 0.002), higher peak creatine kinase levels (2,410 ± 1,247 vs 1,496 ± 1,228 IU/liter, p < 0.01), higher wall motion abnormality score (25 ± 13 vs 13 ± 12, p < 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p < 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p < 0.02) compared to those without increased lung thallium-201 uptake. On stepwise discriminant function analysis, congestive heart failure emerged to be the most important determinant (F = 33.3) and thallium-201 defect score to be the most important correlate (F = 20.07) of abnormal lung thallium-201 uptake. The finding of increased lung thallium-201 uptake may complement the clinical information derived from rest thallium-201 imaging during AMI and may be used for the assessment of acute infarction-limiting interventions. © 1990.