Evaluation of echogenicity of the heart in Kawasaki disease
Hazumu Nagata1, Kenichiro Yamamura, Kiyoshi Uike
1Department of Pediatrics, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka City 812-8582, Japan. dadan@pediatr.med.kyushu-u.ac.jp
Insights
Echogenicity of the heart increases in Kawasaki disease (KD) patients during the acute phase. Higher coronary artery wall echogenicity in KD patients may predict non-response to intravenous immunoglobulin (IVIG) treatment.
Area of Science:
- Cardiology
- Pediatric Cardiology
- Medical Imaging
Background:
- Kawasaki disease (KD) is known to cause cardiac inflammation, including vasculitis, myocarditis, and pericarditis.
- Quantitative assessment of multi-site cardiac echogenicity in KD patients and its correlation with treatment response remains understudied.
Purpose of the Study:
- To quantitatively measure multi-site cardiac echogenicity in KD patients during the acute phase.
- To investigate the relationship between cardiac echogenicity and response to intravenous immunoglobulin (IVIG) treatment in KD.
Main Methods:
- Prospective analysis of cardiac echogenicity using calibrated integrated backscatters (cIBs) in 81 KD patients and 30 controls.
- Echogenicity measurements were taken at four sites: coronary artery wall (CAW), mitral valve (MV), papillary muscle (PM), and ascending aortic wall (AAo wall).
Main Results:
- KD patients exhibited significantly higher cIB values across all measured cardiac sites compared to controls.
- Specifically, CAW, MV, PM, and AAo wall showed significant increases in echogenicity in KD patients.
- Higher CAW echogenicity at the acute phase was observed in IVIG non-responders compared to responders.
Conclusions:
- Cardiac echogenicity is elevated in multiple heart sites during the acute phase of Kawasaki disease.
- Coronary artery wall echogenicity may serve as a potential biomarker for predicting unresponsiveness to IVIG treatment in KD patients.
Abstract:
Pathologic studies of the heart in patients with Kawasaki disease (KD) revealed vasculitis, valvulitis, myocarditis, and pericarditis. However, there have been no studies on the quantitative determination of multi-site echogenicity of the heart in KD patients. It is also undetermined whether the degree of echogenicity of each site of the heart in patients with KD might be related to the response to intravenous immunoglobulin (IVIG) treatment. In 81 KD patients and 30 control subjects, we prospectively analyzed echogenicity of the heart. Echogenicity was measured in four sites: coronary artery wall (CAW), mitral valve (MV), papillary muscle (PM), and ascending aortic wall (AAo wall) by the calibrated integrated backscatters (cIBs). The cIB values of all measurement sites at acute phase in KD patients were significantly higher than those in control subjects (KD patients vs control subjects; CAW, 19.8 ± 6.2 dB vs 14.5 ± 2.0 dB, p < 0.05; MV, 23.3 ± 5.3 dB vs 16.0 ± 3.3 dB, p < 0.05; PM, 22.4 ± 5.1 dB vs 12.7 ± 1.9 dB, p < 0.05; AAo wall, 25.3 ± 5.6 dB vs 18.3 ± 3.4 dB, p < 0.05). The cIB values of CAW at the acute phase in IVIG nonresponders were significantly higher than those in responders. Conclusion: Echogenicity of the heart in KD patients at the acute phase increased not only in the coronary artery wall but also in other parts of the heart. Echogenicity of CAW might be helpful in determining the unresponsiveness of IVIG treatment.
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