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Published on: October 15, 2010
Assessment of Endothelial Dysfunction in Patients with Kawasaki Disease: A Meta-Analysis
Xiaona Yu1, Dan Wu1, Guang Song1
1Department of Ultrasound, Shengjing Hospital of China Medical University, 110004 Shenyang, Liaoning, China.
Insights
Kawasaki disease (KD) causes endothelial dysfunction, evident from reduced flow-mediated dilation (FMD) and elevated inflammatory biomarkers. This dysfunction persists long-term, potentially worsening with coronary artery lesion severity.
Area of Science:
- Cardiovascular Research
- Pediatric Rheumatology
- Vascular Biology
Background:
- Kawasaki disease (KD) is a systemic inflammatory vasculitis.
- Endothelial dysfunction is a significant, often overlooked, non-coronary complication of KD.
- Previous studies on endothelial dysfunction in KD using flow-mediated dilation (FMD), nitroglycerin-mediated dilation (NMD), and biomarkers yielded inconsistent results.
Purpose of the Study:
- To comprehensively assess endothelial dysfunction in children with Kawasaki disease.
- To evaluate FMD, NMD, and specific adhesion molecule biomarkers (E-selectin, P-selectin, ICAM-1, VCAM-1) in KD patients across different disease phases.
- To investigate the relationship between endothelial dysfunction and coronary artery lesion (CAL) severity in KD.
Main Methods:
- A systematic literature search was conducted across five databases up to March 8, 2022.
- A meta-analysis was performed to pool data from 40 studies involving 2670 children (1665 KD patients, 1005 controls).
- Weighted mean differences (WMDs) with 95% confidence intervals (CIs) were calculated for FMD, NMD, and biomarker levels; subgroup analyses were performed.
Main Results:
- KD patients exhibited significantly lower FMD during acute, subacute, and convalescent phases compared to controls.
- During the convalescent phase, FMD impairment was more severe in KD patients with coronary artery lesions (CAL) and aneurysms.
- Elevated levels of E-selectin, P-selectin, and ICAM-1 were observed in KD patients across phases, while VCAM-1 was elevated during the acute phase.
Conclusions:
- Endothelial dysfunction is a persistent complication of Kawasaki disease, present from the acute phase and lasting for years.
- FMD measurements and elevated biomarkers confirm endothelial dysfunction in KD patients.
- The severity of endothelial dysfunction, indicated by FMD impairment, may correlate positively with the severity of coronary artery lesions in the convalescent phase of KD.
Background:
Kawasaki disease (KD) is a well-known systemic inflammatory vasculitis. Endothelial dysfunction is one of most easily overlooked non-coronary complications of KD. Several studies have assessed endothelial dysfunction using flow-mediated dilatation (FMD), nitroglycerin-mediated dilation (NMD), and biomarkers (E-selectin, P-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cellular adhesion molecule-1 (VCAM-1)). However, the results were inconsistent and incomplete.
Methods:
We searched five databases for eligible studies until March 8, 2022. The summarized weighted mean difference (WMD) with 95% confidence intervals (CIs) were estimated for FMD, NMD, and four biomarkers level between KD and healthy children. A meta-analysis with subgroup analysis was conducted.
Results:
40 studies with a total of 2670 children (1665 KD patients and 1005 healthy children) were identified. During the acute phase, KD patients had lower FMD compared to the control group (WMD = -10.39, 95% CI: -13.80- -6.98). During the subacute phase, KD patients had lower FMD compared to the control group (WMD = -15.07, 95% CI: -17.61- -12.52). During the convalescence phase, KD patients had lower FMD and similar NMD compared to the control group (WMD = -4.95, 95% CI: -6.32- -3.58; WMD = -0.92, 95% CI: -2.39-0.55, respectively). During the convalescence phase, those KD patients without coronary artery lesion (CAL), with CAL, even with coronary artery aneurysm, had progressively lower FMD compared to healthy children (WMD = -3.82, 95% CI: -7.30- -0.34; WMD = -6.32, 95% CI: -7.60- -5.04; and WMD = -6.97, 95% CI: -7.99- -5.95, respectively). Compared to KD patients without CAL, those with CAL had lower FMD (WMD = -1.65, 95% CI: -2.92- -0.37). KD patients had higher levels of E-selectin, P-selectin, and ICAM-1 compared to healthy controls during different phases. KD patients had a higher level of VCAM-1 compared to healthy controls only during the acute phase (WMD = 61.62, 95% CI: 21.38-101.86).
Conclusions:
Endothelial dysfunction is present since the onset of KD and persists for years, confirmed by the measurement of FMD and biomarkers from different phases. An assumption is advanced that FMD impairment (the severity of endothelial dysfunction) may be positively correlated with CAL severity during the convalescence phase.
