Long term consequences of regressed coronary aneurysms after Kawasaki disease: vascular wall morphology and function

Abstract

Objectives-To investigate the long term consequences of regressed aneurysms after Kawasaki disease, using follow up coronary angiography; to assess the vascular wall morphology at the site of the aneurysms by intravascular ultrasound imaging; and to evaluate the function of the aVected vessels using intracoronary infusions of acetylcholine and isosorbide dinitrate. Design-33 patients were studied, 27 with previous Kawasaki disease and six with congenital heart disease. All Kawasaki disease patients were followed for more than 10 years from disease onset. The 33 patients comprised four groups: group 1 included 13 Kawasaki disease patients with a total of 23 sites of regressed large sized (> 4 mm) coronary aneurysms; group 2 included 13 Kawasaki disease patients with 22 sites of regressed small sized (< 4 mm) coronary aneurysms (four patients had sites of both large and small sized aneurysms); group 3 included a further five Kawasaki disease patients with 25 normal coronary angiography sites in the acute stage of Kawasaki disease; and group 4 comprised the six patients with congenital heart disease as controls, with a total of 27 normal coronary angiography sites. During coronary angiography, 15 µg of acetylcholine and 0.5 mg isosorbide dinitrate were infused into the coronary artery. The luminal diameter at the sites was measured using a cine-videodensitometric analyser, to assess the distensibility of the coronary artery wall. Results-Coronary angiography in all 22 patients in groups 1 and 2 and in all the patients in group 3 was normal, with no stenoses and no irregularity of the arterial wall. However, the intravascular ultrasound imaging in groups 1 and 2 showed various degrees of the intimal thickening. In groups 1 and 2, there was significantly more vascular constriction with acetylcholine, and poorer dilatation with isosorbide dinitrate than in groups 3 or 4 (each p < 0.05, respectively). There was no diVerence between group 3 and group 4 in response to either acetylcholine or isosorbide dinitrate, Conclusions-There is evidence of persisting abnormal vascular wall morphology and vascular dysfunction at the site of regressed coronary aneurysms in patients with previous Kawasaki disease. These patients should be counselled to avoid potential risk factors for atherosclerosis, and long term follow up is needed into adult life. (Heart 2000;83:307-311)

Sequential Follow-Up Results of Catheter Intervention for Coronary Artery Lesions After Kawasaki Disease

“…The minimal lumen diameter (MLD) was measured before and after the catheter intervention and on follow-up studies with the use of the image analyzing system (CARDIO 500, Kontron Elektronic Corp), according to our previous studies. 12,14 …”

“…11,12 The IVUS examination was performed by use of 30-MHz catheters (3.5F, Boston Scientific Corp). We then measured the thickness of the intima-media complex and calculated the calcification index by use of the following formula: Calcification index (%)ϭ(calcification area/area of intima-media complex)ϫ100.…”

“…11,12 Whenever possible, we used IVUS imaging for this evaluation before catheter intervention and then used these results to select a suitable device for catheter intervention. Furthermore, we used IVUS imaging to confirm therapeutic effects and to observe the vascular wall structure during the follow-up period.…”

Noninvasive Determination of Endothelial Cell Function in the Microcirculation in Kawasaki Syndrome

“…There were no adverse effects from the ACh or any This study addresses for the first time the EC function in the microvasculature of KS patients. EC dysfunction in medium-size muscular arteries in children after recovery from KS has been documented invasively by angiography with ACh infusion and arterial input impedance [3] as well as noninvasively by measurement of brachial artery flow-mediated dilation [5][6][7]10]. Studies have demonstrated elevated levels of von Willebrand factor, selectins (both E and P), and cellular adhesion molecules (ICAM-1, VCAM-1) as potential biomarkers of EC activation or damage during acute KS [17].…”

“…Intracoronary injection of acetylcholine (ACh) in children with both persistent and regressed coronary artery aneurysms has demonstrated EC dysfunction with paradoxical vasoconstriction [5][6][7]. However, EC function after recovery from KS in children without coronary artery abnormalities in the acute stage is less clear.…”