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J Am Coll Cardiol, 1995; 25:1420-1424
© 1995 by the American College of Cardiology Foundation
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Exercise capacity and incidence of myocardial perfusion defects after Kawasaki disease in children and adolescents

SM Paridon, FM Galioto, JA Vincent, TL Tomassoni, NM Sullivan, and JT Bricker

Division of Cardiology, Georgetown University Children's Medical Center, Georgetown University School of Medicine, Washington, D.C., USA.

OBJECTIVES. This study evaluated exercise performance and myocardial perfusion during exercise in patients with Kawasaki disease who had a broad spectrum of residual coronary abnormalities. BACKGROUND. Reports of exercise performance after Kawasaki disease have generally included a small number of patients evaluated by various protocols, frequently with incomplete data. Myocardial perfusion studies have usually been limited to those using pharmacologically induced coronary vasodilation. Therefore, to our knowledge there has not been a large study directly correlating exercise performance, electrocardiographic (ECG) changes and myocardial perfusion imaging. METHODS. Forty-six patients were classified into three groups on the basis of coronary artery status: group 1 (n = 27) had no objective evidence of coronary artery lesions; group 2 (n = 11) had resolved aneurysms; group 3 (n = 8) had persistent coronary aneurysms. All patients underwent exercise testing with monitoring of ECG changes and oxygen consumption. Single-photon emission computed tomographic imaging was performed at rest and during peak exercise using technetium-99m sestamibi. RESULTS. Maximal oxygen consumption was within normal limits and was similar for all three groups. Five patients had mild ST segment changes at peak exercise. Two of these patients had stress-induced perfusion defects. Myocardial perfusion defects were present in 37% of patients in group 1, 63% in group 2 and 100% in group 3. Perfusion defects corresponded to the coronary artery lesion site in all but three patients. CONCLUSIONS. Maximal oxygen consumption is normal after Kawasaki disease regardless of coronary artery status. Stress-induced perfusion defects are frequent even in the absence of coronary abnormalities and are common in the absence of ST segment changes suggestive of ischemia.


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