Immunohistochemical study of apparently intact coronary artery in a child after Kawasaki disease.
BACKGROUND
Coronary arterial lesions (CAL) due to Kawasaki disease (KD) often show progressive intimal hyperplasia even many years after the disease. However, most patients have no CAL after the acute phase, and it is an important issue whether or not coronary arteries without CAL have significant intimal hyperplasia, and whether or not there is the potential for this to progress to stenosis and/or atherosclerosis.


METHODS
The authors examined formalin-fixed specimens of the coronary arteries immunohistochemically, using antibodies against vascular growth factors (GFs), the receptors of transforming growth factor-beta (TbetaRs) and inducible nitric oxid synthesis (iNOS) in a KD patient without CAL, and also in four control patients: two with CAL due to KD and two without a history of KD.


RESULTS
Vascular endothelial GFs, Platelet-derived growth factor-A (PDGF-A) and TbetaRs were expressed in the vascular smooth muscle cells of all patients. PDGF-A, transforming Gfbeta1 and iNOS were expressed in the intimal smooth muscle cells of the KD but not the normal coronary artery without a history of KD. The number of TbetaR-II-positive cells were fewer than TbetaR-I-positive cells in the intima of CAL due to KD, but the number was of both almost same in the intima of coronary artery without CAL after KD and in the normal coronary.


CONCLUSIONS
The intact coronary artery 13 months after KD still showed the influence of the inflammation of KD. Although the authors speculate that the intimal proliferation will not continue beyond the acute phase, those patients may have a risk factor for atherosclerosis.
Suzuki
Atsuko
A
Department of Pediatrics, Tokyo Postal Services Agency Hospital, Tokyo, Japan. asuzuki@tth-japanpost.jp
Miyagawa-Tomita
Sachiko
S
Komatsu
Keiko
K
Nakazawa
Makoto
M
Fukaya
Takashi
T
Baba
Kunizou
K
Yutani
Chikao
C
D002675:Child, Preschool; D003324:Coronary Artery Disease / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism; D003331:Coronary Vessels / Q000737:chemistry / Q000473:pathology*; D006801:Humans; D007150:Immunohistochemistry / Q000379:methods; D007223:Infant; D009080:Mucocutaneous Lymph Node Syndrome / Q000150:complications*; D019001:Nitric Oxide Synthase / Q000032:analysis; D052247:Nitric Oxide Synthase Type II; D010982:Platelet-Derived Growth Factor / Q000032:analysis; D018125:Receptors, Transforming Growth Factor beta / Q000032:analysis; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000032:analysis; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
D010982:Platelet-Derived Growth Factor; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D042461:Vascular Endothelial Growth Factor A; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II