Association of Toll-like receptor 2-positive monocytes with coronary artery lesions and treatment nonresponse in Kawasaki disease

Kang, Soo Jung; Kim, Nam Su

Thirtyone children diagnosed with KD at CHA University Bundang Medical Center, between November 2007 and November 2008, were enrolled in this study. All enrolled patients met the following criteria for complete KD: fever and at least 4 of the fol lowing 5 clinical symptoms-rash, conjunctival injection, cervical lymphadenopathy, changes in the oral mucosa, and changes in the extremities; or fever and 3 of the above clinical symptoms plus coronary artery abnormalities (dilatation or aneurysm) documented by echocardiography 4) . Children who presented with incomplete KD were excluded from our study. To exclude other febrile illnesses resembling KD, we determined the serum titers of antistreptolysin O, antiEpsteinBarr vi ral, anti mumps viral, and antimycoplasma antibodies in all samples from patients with KD. Furthermore, we performed multiplex polymerase chain reaction on nasopharyngeal aspirates taken from patients with KD, for common respiratory viruses (adenovirus, respiratory syncytial virus, parainfluenza virus, influ enza virus, metapneumovirus, coronavirus, and rhinovirus). We also perform ed neck ultrasonography on these patients to rule out suppurative lymphadenitis. All patients received 2 g/kg IVIG in a single dose at the time of diagnosis and were treated with high doses of oral aspirin (80 mg/kg/day), until they became afebrile for 3 to 4 days, as specified in the 2004 American Heart Associa tion guidelines 4) . Afterwards, they were given low doses of aspirin (5 mg/kg/day). Serial echocardiography was performed on all patients with KD at the time of diagnosis and 1 month later, to study CAL development in the acute stage of KD. Echocardiography was conducted on all patients by a single cardiologist to evaluate the pre sence of structural heart diseases as well as to obtain M mode echocardiographic parameters, in cluding left ventricular enddiastolic dimensions (LVEDD), left ventricular endsystolic dimensions (LVESD), and fractional shortening (FS). We measured the internal diameter of the proxi mal right coronary artery (RCA) and proximal left anterior des cending coronary artery (LAD) to classify patients with CAL development (CAL (+)) and those who without CAL development (CAL (−)). We did not include the measu rements of the left main coronary arteries (LMCAs), as normal anatomic variations in LMCAs have been reported to be frequent, and the probability of isolated dilatation of LMCA without accom panying dilatation of LAD has been reported to be low 22) . The z scores of coronary arteries were obtained using RCA and LAD measurements as well as the nonlinear regression equations based on the body surface area (BSA) 22) . To calculate the z scores of RCA and LAD measurements, we derived the predicted values of RCA and LAD measurements for a patient with a given BSA using the following regression equations, reported by McCrindle et al. 22 The z scores were calculated by dividing the differences between the actual measurements of RCA and LAD and the cor responding predicted values by the corresponding standard devi ations, as described by McCrindle et al. 22) . CAL (+) patients had dilated (2.5 ≤z score<4.0) or aneurysmal (focal or diffuse dilatation of a coronary artery segment with z score ≥4.0) coronary arteries, based on the maximal internal diameters of the RCA and LAD one month after the initial diagnosis. CAL (−) patients had normal (z score <2.5) coronary arteries one month after the initial diagnosis 4) .