摘要
Kawasaki disease (KD) is a leading cause of CAD in children. The impairment of cardiac sympathetic nerve function (CSNF)- in the adult patients with coronary artery disease (CAD) could often be seen. However, little is known concerning the impairment of CSNF in KD patients. We investigated CSNF and its relationship with myocardial perfusion in KD patients. Eleven children with KD and 4 controls were studied with 123I- metaiodobenzylguanidine (MIBG) and stressed 201T1 single photon emission computed tomography. By the findings on coronary artery angiography (CAG), the patients were divided into 2 groups: A, without stenosis; B, with significant stenosis and/or old myocardial infarction. CSNF was evaluated from the uptake of 123I- MIBG.While myocardial perfusion was evaluated from 201T1 uptake. The numbers of patients in the groups A and B were 7 and 4. Perfusion defect was found in 0, and 2 patients in group A(0% ), and B (50% ). 123I- MIBG defects were found in 1 and 4 patients in the group A (14% ) and B (100% ). There were excellent concordances between the finding of 201Tl and 123I- MIBG in group A. While in group B, the coronary territories with 123I- MIBG defects were significantly more than those with perfusion defects (p < 0.05). In KD patients, the impairment of CSNF might be subsequent to coronary artery stenosis and was more severe than the injury of myocardial perfusion.
Kawasaki disease (KD) is a leading cause of CAD in children. The impairment of cardiac sympathetic nerve function (CSNF)- in the adult patients with coronary artery disease (CAD) could often be seen. However, little is known concerning the impairment of CSNF in KD patients. We investigated CSNF and its relationship with myocardial perfusion in KD patients. Eleven children with KD and 4 controls were studied with 123I- metaiodobenzylguanidine (MIBG) and stressed 201T1 single photon emission computed tomography. By the findings on coronary artery angiography (CAG), the patients were divided into 2 groups: A, without stenosis; B, with significant stenosis and/or old myocardial infarction. CSNF was evaluated from the uptake of 123I- MIBG.While myocardial perfusion was evaluated from 201T1 uptake. The numbers of patients in the groups A and B were 7 and 4. Perfusion defect was found in 0, and 2 patients in group A(0% ), and B (50% ). 123I- MIBG defects were found in 1 and 4 patients in the group A (14% ) and B (100% ). There were excellent concordances between the finding of 201Tl and 123I- MIBG in group A. While in group B, the coronary territories with 123I- MIBG defects were significantly more than those with perfusion defects (p < 0.05). In KD patients, the impairment of CSNF might be subsequent to coronary artery stenosis and was more severe than the injury of myocardial perfusion.
