Mechanism underlying the absence of ischemic changes on the exercise electrocardiogram in patients with abnormal exercise thallium‐201 imaging and coronary artery disease

• Published in: Clinical cardiology (Mahwah, N.J.) Vol. 8; no. 7; pp. 399 - 405
• Main Authors: Coplan, N. L., Horowitz, S. F., Hoffman, D. P., Goldman, M. E., Machac, J.
• Format: Journal Article
• Language: English
• Published: New York Wiley Periodicals, Inc 01.07.1985; Wiley
• Subjects: Biological and medical sciences; Cardiac Catheterization; Cardiology. Vascular system; Coronary Circulation; Coronary Disease - diagnostic imaging; Coronary heart disease; Electrocardiography; exercise electrocardiogram‐thallim discordance; exercise stress test; Exercise Test; Female; Heart; Humans; Male; Medical sciences; Middle Aged; Radioisotopes; Radionuclide Imaging; Thallium; thallium myocardial perfusion scan; Physical exercise; Radionuclide study; Human; Electrodiagnosis; Electrocardiography; Myocardium; Cardiovascular disease; Exercise tolerance test; Radioisotope; Scintigraphy; Coronary heart disease
• ISSN: 0160-9289; 1932-8737
• DOI: 10.1002/clc.4960080705

Patients with coronary artery disease may have reversible abnormalities on a thallium myocardial perfusion study without simultaneous ischemic changes on the exercise electrocardiogram, but the mechanisms responsible for this disparity have not been fully elucidated. A group of 37 patients with angiographically demonstrated coronary artery disease and abnormal thallium perfusion imaging were divided into two groups on the basis of their exercise electrocardiographic ST segment response. Thirteen patients (Group A) had no significant electrocardiographic changes with exercise, while 24 patients (Group B) had ST changes consistent with ischemia during the test. There were no significant differences in clinical or angiographic characteristics between the two groups. Stress test results showed a similar mean duration of exercise in the two groups (6.2 ± 1.8 versus 6.7 ± 2.5 min, p=NS), but the patients in Group A achieved a significantly lower mean maximal heart rate (117 ± 26 versus 132 ± 21 beats/min, p<0.05) and mean maximal double product (19,650 ± 5116 versus 22,650 ± 4871, p<0.05). There was no consistent pattern of thallium perfusion abnormality noted in Group A to suggest that a particular region of electrically silent myocardium was responsible for ischemia in the absence of electrocardiographic changes. These results suggest that exercise thalliumelectrocardiogram discordance is mediated by the level of myocardial workload achieved. An abnormal perfusion scan accompanying an exercise electrocardiogram which does not demonstrate any ischemic ST change may occur when there is sufficient increase in myocardial oxygen demand to result in differential augmentation of myocardial blood flow, but insufficient imbalance of supply and demand to result in signs of ischemia on the surface electrocardiogram.