EXERCISE CAPACITY AND INCIDENCE OF MYOCARDIAL PERFUSION DEFECTS AFTERKAWASAKI-DISEASE IN CHILDREN AND ADOLESCENTS

Citation
Sm. Paridon et al., EXERCISE CAPACITY AND INCIDENCE OF MYOCARDIAL PERFUSION DEFECTS AFTERKAWASAKI-DISEASE IN CHILDREN AND ADOLESCENTS, Journal of the American College of Cardiology, 25(6), 1995, pp. 1420-1424
Citations number
13
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
25
Issue
6
Year of publication
1995
Pages
1420 - 1424
Database
ISI
SICI code
0735-1097(1995)25:6<1420:ECAIOM>2.0.ZU;2-B
Abstract
Objectives. This study evaluated exercise performance and myocardial p erfusion during exercise in patients with Kawasaki disease who had a b road 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 directl y correlating exercise performance, electrocardiographic (ECG) changes and myocardial perfusion imaging. Methods. Forty-six patients were cl assified into three groups on the basis of coronary artery status: gro up 1 (n = 27) had no objective evidence of coronary artery lesions; gr oup 2 (n = 11) had resolved aneurysms; group 3 (n = 8) had persistent coronary aneurysms. All patients underwent exercise testing with monit oring of ECG changes and oxygen consumption. Single-photon emission co mputed tomographic imaging was performed at rest and during peak exerc ise using technetium-99m sestamibi. Results. Maximal oxygen consumptio n was within normal Limits and was similar for all three groups. Five patients had mild ST segment changes at peak exercise. Two of these pa tients had stress-induced perfusion defects. Myocardial perfusion defe cts 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 le sion site in all but three patients. Conclusions. Maximal oxygen consu mption is normal after Kawasaki disease regardless of coronary artery status. Stress-induced perfusion defects are frequent even in the abse nce of coronary abnormalities and are common in the absence of ST segm ent changes suggestive of ischemia.