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(Circulation. 2005;111:2119-2125.)
© 2005 American Heart Association, Inc.

Pediatric Cardiology

Arterial Hemodynamics in Patients After Kawasaki Disease

Hideaki Senzaki, MD; Chen-Huan Chen, MD; Hirotaka Ishido, MD; Satoshi Masutani, MD; Tamotsu Matsunaga, MD; Mio Taketazu, MD; Toshiki Kobayashi, MD; Nozomu Sasaki, MD; Shunei Kyo, MD; Yuji Yokote, MD

From the Department of Pediatric Cardiology and Pediatrics (H.S., H.I., S.M., T.M., M.T., T.K., N.S., S.K., Y.Y.), Saitama Heart Institute, Saitama Medical School Hospital, Saitama, Japan, and Cardiovascular Research Center (C.-H.C.), National Yang-Ming University Taipei Veterans General Hospital, Taiwan.

Correspondence to Hideaki Senzaki, MD, Department of Pediatric Cardiology, Saitama Heart Institute, Saitama Medical School Hospital, 38 Morohongo, Moroyama, Saitama 350-0495, Japan. E-mail hsenzaki{at}saitama-med.ac.jp

Received June 21, 2004; revision received January 8, 2005; accepted January 11, 2005.

Background— Histopathological findings in the acute stage of Kawasaki disease (KD) indicate widespread vascular inflammation that involves not only coronary arteries but also systemic arteries. This may cause changes in systemic arterial wall properties after KD, which could have adverse effects on arterial hemodynamics (an important predictor of cardiovascular morbidity and mortality).

Methods and Results— Systemic arterial hemodynamics were investigated by measuring aortic input impedance during cardiac catheterization in 42 KD patients who had developed coronary artery lesions (CALs) in the acute stage of KD. The KD patients were subdivided into 2 groups according to the angiographic findings (group 1A, 26 patients with persistent CALs; group 1B, 16 patients with regressed CALs), and results were compared with those of 36 referents (group 2). Compared with referents, characteristic impedance was significantly higher for KD patients (137.0±5.1, 125.7±8.2, and 97.9±4.1 dyne · s · cm^–5 · m² for group 1A, group 1B, and group 2, respectively), and total peripheral arterial compliance indexed to age-specific values was significantly lower for KD patients (group 1A 72.9±4.2% of normal; group 1B 70.6±5.9% of normal; group 2 97.7±4.0% of normal; for both variables, P<0.05 for each KD group versus group 2; P=NS between KD groups), which suggests that both central and peripheral arterial wall stiffness increase after KD regardless of persistence of CALs. Also, indices of arterial wave reflection (reflection coefficient, reflection factor, and augmentation index) were all significantly higher in KD patients than in referents (P<0.05), with the result that the aortic pressure waveforms of the present KD patients resembled those generally observed in the elderly. In addition, levels of circulating markers of endothelial dysfunction (ACE and von Willebrand factor) were associated with increased vascular stiffening in KD patients but not in referents.

Conclusions— These results indicating abnormal arterial hemodynamics after KD highlight the importance of regular monitoring of the systemic arterial bed and potentially relevant cardiovascular events in long-term follow-up of KD.

Key Words: arteries • coronary disease • Fourier analysis • hemodynamics • risk factors

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