Objective: Kawasaki disease (KD) is characterized as an acute systemic vasculitis predominantly affecting young children, with coronary artery lesions (CALs) representing the most serious complication. Therapeutic resistance to intravenous immunoglobulin (IVIG) remains a significant clinical challenge. Consequently, numerous investigations have sought to identify predictive risk factors for IVIG resistance (IVIGR) and CAL development. Limited research has systematically evaluated the prognostic utility of electrocardiographic (ECG) parameters in KD outcome prediction. This study was therefore undertaken to assess the contributory value of ECG analysis in determining KD prognosis and therapeutic responses. Methods: This prospective cohort study enrolled 255 hospitalized children diagnosed with KD at West China Second University Hospital between July 2022 and December 2024. Initially, univariate analysis was performed to identify risk factors differentiating IVIGR from non-IVIGR patients and CAL from non-CAL patients. Statistically significant parameters were subsequently incorporated into machine learning analyses. Random forest algorithms were employed to construct predictive models based on the following: (1) complete blood count parameters, (2) biochemical and metabolic profiles, (3) electrocardiographic features, and (4) a comprehensive multimodal model integrating all parameters. These models generated feature importance scores, providing hierarchical rankings that quantified the relative contribution of each predictor to outcome prediction. Results: Univariate analysis demonstrated that alterations in hematological parameters, biochemical and metabolic profiles, and electrocardiographic features were significantly associated with therapeutic responses to IVIG and CAL development. Machine learning analysis revealed that ECG parameters individually contributed modest predictive weight for KD prognosis. However, the integration of ECG features into the comprehensive model substantially enhanced the discriminatory capacity, elevating the area under the curve (AUC) to 0.92 for CAL prediction. For IVIGR prediction, ECG-exclusive models demonstrated suboptimal performance in early disease management. Nevertheless, the multimodal integration of ECG with inflammatory and metabolic biomarkers achieved a comparable AUC of 0.92 for IVIGR prediction. Conclusions: This study establishes that ECG parameter alterations are significantly associated with CAL development and IVIGR in KD patients. Although ECG features demonstrate a limited independent predictive capacity compared to inflammatory and metabolic biomarkers, their integration into comprehensive predictive models substantially enhances discriminatory performance. These findings underscore the complementary value of electrocardiographic assessment in multimodal risk stratification strategies for KD management, supporting the clinical utility of ECG analysis as an adjunctive prognostic tool when combined with conventional laboratory parameters.

Isolated congenital heart block (iCHB) is defined as atrioventricular block without structural cardiac defects, characterized by irreversible fibrosis of the cardiac conduction system. Maternal autoantibodies may elicit systemic exaggerated immune responses involving type I interferon (IFN) signalling cascade, yet peripheral circulating immunity in CHB pathogenesis remains poorly understood. To investigate this, we performed single-cell RNA sequencing (scRNA-seq), followed by differential expression gene (DEG) analysis, SCENIC analysis, pseudotime analysis and cell communication analysis, to characterize systemic immune alterations in foetuses with CHB treated with dexamethasone and validated key findings by real-time quantitative PCR (qPCR) and flow cytometry. Compared with controls, CHB foetuses exhibited a markedly activated inflammatory response involving both IFN and NF-κB pathways. Although monocytes showed significant changes in cellular proportions, upregulated DEGs and interferon-stimulated genes, prioritized cellular responses and enhanced intercellular interactions. Notably, THBS1+CD14+ monocytes had a pro-inflammatory phenotype with upregulated NLRP3 inflammasome-related genes and maturation toward a pro-inflammatory state, and Thbs1 conditional knockout mice showed reduced IL-1β levels in BMDMs. Additionally, dexamethasone-treated monocytes had downregulated SOD2 (anti-apoptotic) levels compared to controls, confirmed by qPCR, and flow cytometry verified that dexamethasone promoted monocyte apoptosis. In conclusion, the peripheral immune system in CHB is characterized by innate immune activation driven mainly by monocytes, along with systemic inflammation including IFN signalling. THBS1+/CD14+ monocytes represent a distinct proinflammatory phenotype potentially linked to NLRP3-mediated inflammatory responses.

We report a case of a 12-year-old male patient presenting with paroxysmal atrial fibrillation (AF). Catheter ablation was indicated for symptomatic paroxysmal AF. The procedure was conducted utilizing a cardiac pulsed-field ablation technology (LEAD-PFA, JJET). Lesion creation followed a systematic protocol comprising two sets of four consecutive applications at 1800 V targeting pulmonary veins, plus fifteen applications in inter-pulmonary vein regions and pulmonary venous vestibule. AF was induced during left inferior pulmonary vein ablation and terminated post-procedure. This case represents a documented successful ablation of paroxysmal AF utilizing PFA technology in a pediatric patient. These findings suggest that PFA may constitute a viable and potentially superior therapeutic modality for young patients with AF.

BackgroundHigh-quality pediatric clinical research depends on effective and ethically robust recruitment, yet participation can be difficult for families of children with congenital heart disease (CHD), particularly in resource-constrained and culturally diverse settings. In western China, long-distance care-seeking, financial strain, family-centered decision-making, and evolving pediatric research protections may shape how caregivers understand and negotiate research participation.MethodsWe conducted a qualitative descriptive study at a tertiary pediatric referral center in western China between June and December 2025. Caregivers of children with CHD participated in one-to-one semi-structured interviews. Interviews explored practical burden, perceptions of research and treatment, therapeutic misconception, trust, child assent, and strategies to improve recruitment. Audio-recordings were transcribed verbatim, anonymized, and analyzed using qualitative content analysis.ResultsThematic saturation was reached after 22 interviews. Four overarching themes were identified: (1) families' real-world constraints and the costs of research participation; (2) cognitive biases and tensions surrounding therapeutic misconception; (3) trust anchors and views on assent, insurance, and institutional protection under a changing policy context; and (4) strategies for optimizing recruitment. Caregivers commonly weighed research participation against treatment-related burdens, especially travel distance, accommodation costs, wage loss, and repeated hospital visits. Decisions were further shaped by collective family decision-making, culturally mediated concerns about bodily integrity, confusion between research and individualized treatment, and strong reliance on physician recommendation. Participation was generally more acceptable when procedures were non-invasive or integrated into routine care, whereas extra venipuncture was often resisted. Caregivers also emphasized the value of plain-language, visual, dialect-adapted, and child-friendly communication.ConclusionsCaregivers' decisions about pediatric clinical research participation in western China are shaped by structural disadvantage, family-centered norms, therapeutic misconception, and trust in physicians and institutions. Recruitment should reduce burden, improve comprehension, support family communication, and accommodate children's developing role in research decisions.

Kawasaki disease shock syndrome (KDSS) is a severe phenotype of Kawasaki disease (KD) characterized by hemodynamic instability and systemic inflammation. Early identification of children at risk for KDSS remains challenging. N-terminal pro-B-type natriuretic peptide (NT-proBNP) reflects cardiovascular stress and has been associated with severe manifestations of KD; however, its interpretation in children is complicated by age dependency. This study aimed to evaluate the predictive utility of baseline NT-proBNP, compare raw NT-proBNP concentrations with age-adjusted NT-proBNP z-scores, and assess their performance relative to other routinely available laboratory biomarkers for KDSS prediction. A total of 588 KD patients were finally enrolled in this prospective cohort study between January 2015 and March 2021. The demographic/clinical characteristics and laboratory data were compared between the patients with KDSS (KDSS group, n = 35) and those without (KD group, n = 553). NT-proBNP concentrations were analyzed as both raw values and age-adjusted z-scores calculated using established pediatric reference ranges. Multivariable logistic regression models were constructed using baseline variables, with log10-transformed NT-proBNP and NT-proBNP z-score evaluated in separate models. Receiver operating characteristic (ROC) analyses were performed to compare predictive performance among NT-proBNP-related parameters and other candidate biomarkers. Children in the KDSS group were older than those in the non-KDSS group (66.11 ± 47.06 vs. 31.36 ± 23.57 months, P < 0.001). KDSS patients had significantly higher rates of coronary artery lesions (40.0

Children with giant coronary artery aneurysms (gCAA) after Kawasaki disease (KD) are at high risk of coronary artery thrombosis (CAT), associated with adverse cardiovascular events (ACEs). Long-term anticoagulation is the standard regimen, but evidence comparing rivaroxaban with warfarin in gCAA after KD remains limited. We performed a retrospective observational study at 2 pediatric centers from 2020 to 2025, enrolling children with gCAA after KD. Participants received rivaroxaban or warfarin. The primary efficacy assessment included ACEs and CAT outcomes within 6 months. CAA changes and safety outcomes were assessed. The final cohort included 30 patients, 14 treated with rivaroxaban and 16 with warfarin. ACEs were infrequent, occurring in 1 patient (7.1

Background:Titin (TTN) variants have been implicated in various types of cardiomyopathy. Allelic variant heterogeneity results in variable clinical phenotypes, which remains a major barrier for effective disease management. We aim to investigate the relationship between TTN variants and their associated cardiomyopathies and clinical outcomes. Methods:A retrospective observational study was performed to evaluate patients with cardiomyopathy and TTN variants confirmed by whole-exome sequencing (WES) from January 2015 to December 2024. Univariable Cox regression analysis was conducted to identify independent risk factors for major adverse cardiovascular events (MACEs), and receiver operating characteristic analysis was used to determine its capability. In addition, the contribution of combined pathogenic variants with the TTN gene was assessed. Results:A total of 53 patients were identified with TTN variants, with a median onset age of 42.3 months (IQR 18.5-76.1), while 48 of 53 (90.50%) individuals had other genetic variants. Among them, 47.17% of patients presented with recurrent heart failure, while late gadolinium enhancement (LGE) was identified in 56.67% of cases that underwent magnetic resonance imaging (MRI) assessment. The variants in the A-band of TTN were most frequently recorded among the patients. Notably, early age-onset disease (HR = 1.008; 95% CI = 1.000-1.016; p = 0.037) served as a predictor of MACE in pediatrics with TTN-associated cardiomyopathy, and the optimal cutoff value was calculated as 75.50 months (specificity 57.1% and sensitivity 75.0%). Unfortunately, the combined genetic disorders failed to establish an association with worse outcomes in the general cohort. However, the presence of multiple genetic variants was associated with more severe adverse outcomes specifically in patients with dilated cardiomyopathy (DCM), with a higher prevalence of MACE occurrence. Conclusion:In our cohort, early age-onset disease was a predictor of MACE in pediatrics with TTN-associated cardiomyopathy. In addition, the early age of disease onset revealed a higher likelihood of MACE in the first year after diagnosis. Multiple genetic variants with TTN presented more severe adverse outcomes in DCM assessment.

Idiopathic pulmonary fibrosis (IPF) is characterized by progressive fibrotic remodeling accompanied by persistent endothelial activation and leukocyte infiltration. Although endothelial dysfunction is increasingly recognized as a key contributor to fibrogenesis, the intracellular signaling pathways that couple inflammatory cues to endothelial-immune interactions remain incompletely defined. Ras-related protein Rap2a (RAP2A), a small GTPase implicated in stress and inflammatory signaling, has not been systematically investigated in pulmonary endothelial cells during fibrotic lung injury. Here, using a bleomycin-induced experimental lung fibrosis model, we observed that RAP2A expression was markedly upregulated in pulmonary endothelial cells and correlated with disease severity. Endothelium-enriched knockdown of Rap2a via AAV9-Cdh5-shRNA attenuated inflammatory cell adhesion to the pulmonary endothelium, reduced fibrotic remodeling, and improved lung function. Mechanistically, RAP2A promoted endothelial activation by enhancing MAP4K4-dependent signaling and upregulating vascular cell adhesion molecule 1 (VCAM1) in response to pro-inflammatory stimulation, thereby facilitating leukocyte-endothelial interactions. In vitro assays further demonstrated that RAP2A deficiency impaired tumor necrosis factor-α-induced endothelial adhesiveness without affecting basal endothelial integrity. Collectively, our findings identify endothelial RAP2A as a regulator of inflammatory endothelial activation in experimental lung fibrosis and suggest that targeting RAP2A-mediated signaling may represent a potential strategy to modulate endothelial-immune crosstalk during fibrotic lung injury.

BACKGROUND:P-glycoprotein (P-gp), the most extensively studied ATP-binding cassette (ABC) transporter, is expressed in the apical membrane of syncytiotrophoblast cells and plays a crucial role in placental drug transport. However, the roles of the vitamin D receptor (VDR) and steroid receptor coactivators (SRCs) family members in VDR-mediated transcriptional regulation of the ABCB1 gene in response to 1,25-dihydroxyvitamin D3 in the placenta remain unclear. METHODS:VDR-mediated drug efflux was first examined using VDR-deficient mice. Subsequently, the roles of VDR and SRCs in regulating placental P-gp were investigated via specific deletion of VDR and SRCs in mouse trophoblast cells in vivo, and further validated using transfection assays in placental trophoblast cells in vitro. Additionally, the mechanisms underlying VDR-regulated ABCB1 expression were explored. RESULTS:In this study, we first knocked out the Vdr gene in C57BL/6J mice and observed a significant downregulation of P-gp in the placenta. Furthermore, both gain-of-function and loss-of-function assays demonstrated that VDR promotes P-gp expression in human trophoblast cells. Mechanistically, VDR induces ABCB1 gene transcription by binding to the region 2026-2031 bp upstream of the transcriptional start site in the ABCB1 gene promoter in human trophoblast cells. Moreover, we found that SRCs interact with VDR in trophoblast cell lines, and both in vivo and in vitro studies showed that SRC-1 enhances placental ABCB1 expression. Further investigations confirmed that SRC-1 is an essential transcriptional coactivator for VDR-mediated ABCB1 transactivation in human trophoblast cells. CONCLUSIONS:Our findings reveal a novel mechanism regulating placental P-gp expression, which may assist clinicians in ensuring the safety of drug therapy during pregnancy.

INTRODUCTION:Atrial standstill represents a rare cardiac arrhythmia characterised by the complete absence of atrial electrical and mechanical activity. Early diagnostic recognition coupled with comprehensive genetic counselling assumes paramount importance. Herein, we report a rare case of a patient who presented with bradycardia at an early age and demonstrated aggressive atrial standstill during a pacemaker upgrade, which challenged the therapeutic strategy. CASE PRESENTATION:A 5-year-old girl was initially diagnosed with bradycardia. Holter monitoring confirmed severe bradycardia with prolonged sinus arrest episodes. Subsequently, the patient underwent single-chamber pacemaker implantation. During a planned dual-chamber upgrade at age 11, despite systematic exploration of multiple anatomical sites within the right atrium, adequate atrial capture could not be achieved. Intracardiac electrophysiological assessment demonstrated a complete absence of electrical activity in the bi-atrium. While speckle-tracking echocardiography revealed mildly reduced global longitudinal strain with impairment noted in the lateral myocardial segments, indicating potential injuries from ventricular demand pacing. Genetic test identified a compound heterozygous variant of SCN5A c.2431C>T and c.2893C>T. The protein structure of SCN5A has been built and named AF-P21333-F1, and the molecular function of the variant site has been annotated. Additionally, murine scRNA-seq data (GSE132658) revealed cardiac Scn5a expression is confined to the conductive bundles and fibres rather than cardiomyocytes, and the loss-of-function caused aggressive atrial standstill. CONCLUSION:This case provides valuable insights into genotype-phenotype correlations in SCN5A-associated atrial standstill, emphasises the importance of comprehensive electrophysiological assessment during device implantation, and underscores considerations for physiological pacing strategies in paediatric patients requiring lifelong device dependency.

BACKGROUND AND AIMS:Paediatric myocardial strain analysis through echocardiography is often characterized by high variance and limited precision, highlighting the need for a standardized and vendor-agnostic approach applicable for diverse image qualities and populations, which could enhance cardiac function evaluation and enable early detection of cardiac impairment. METHODS:The Motion-Echo system was proposed, a semi-supervised deep learning framework built on 11 096 paediatric and 11 297 adult echocardiograms spanning diverse image qualities and vendors. It integrated context compensation and motion estimation modules for temporally coherent segmentation, myocardial motion estimation, and global strain assessment with minimal manual annotations. Clinical utility was further evaluated through downstream applications. RESULTS:Motion-Echo achieved mean absolute errors of 2.099% [95% confidence interval (CI) 1.803-2.401] and 2.665% (95% CI 2.339-3.026) for global longitudinal and circumferential strain assessments, with Pearson correlation coefficients of 0.799 (95% CI 0.715-0.871) and 0.781 (95% CI 0.687-0.844), respectively. To validate the clinical utility, automated strain values achieved an area under the curve (AUC) of 0.906 (95% CI 0.816-0.981) for cancer therapy-related cardiac dysfunction risk prediction. For late gadolinium enhancement detection, automated global longitudinal strain reached an AUC of 0.782 (95% CI 0.666-0.885). For left ventricular ejection fraction decline forecasting, the system outperformed manual strain values (DeLong P < .001). In addition, incorporating estimated motion flows yielded a remarkable AUC improvement to 0.952 (95% CI 0.917-0.980) for myocardial infarction detection. CONCLUSIONS:Leveraging a large-scale paediatric dataset, Motion-Echo provided a reliable and generalizable framework for myocardial strain analysis, demonstrating potential to facilitate earlier detection of cardiac dysfunction and generate digital cardiac function profiles of children.

Background Kawasaki disease shock syndrome (KDSS) is a severe form of Kawasaki disease (KD). The serum lipid has been proposed to be valuable in predicting shock syndrome in clinical circumstances; however, limited data is available in KDSS patients. Therefore, we prospectively evaluated the ability of serum lipid in predicting KDSS. Methods A total of 1009 KD patients aged 2 months to 139 months were enrolled in this prospective cohort study between June 2017 and April 2022. The demographic/clinical characteristics and laboratory data were compared between the patients with KDSS (KDSS group) and those without (KD group). Multivariate logistic regression analysis was utilized to determine the correlation between serum lipid and KDSS. Receiver operating characteristic (ROC) curve analysis was subsequently performed to assess the validity of serum lipids in predicting KDSS. Results Except for triglyceride (TG), almost all the levels of detected lipid profiles were significantly lower in the KDSS subjects compared to non-KDSS patients. In terms of KDSS prediction, the cut-off values of 2.845 mmol/L, 0.355 mmol/L, 1.405 mmol/L, 0.595 g/L, and 0.805 g/L for total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A (Apo A) and apolipoprotein B (Apo B), yielded sensitivities of 80

Di-(2-ethylhexyl)-phthalate (DEHP) is a common endocrine disruptor that causes very serious environmental pollution. Recent studies have described that DEHP exerts detrimental effects on key processes of placental development, including implantation, differentiation, invasion, and angiogenesis. However, its effects on the proliferation of placental trophoblasts and related regulatory mechanisms remain elusive. This study demonstrated that maternal DEHP exposure significantly disrupted placental growth. Similarly, transcriptomic and proteomic analyses of DEHP-treated placental tissues revealed that DEHP may disrupt placental growth by affecting the cell cycle of placental trophoblasts. Further analyses validated that DEHP inhibited the growth of mouse placental trophoblasts by significantly upregulating the expression of the p53 protein, which arrests the cell cycle. Mechanistically, Tripartite motif protein 38 (Trim38) was identified as a target protein of MEHP, with Trim38 binding to p53 and downregulating p53 expression by promoting its ubiquitination-proteasomal degradation. Interestingly, MEHP could inhibit the Trim38-regulated ubiquitination degradation of p53 and up-regulate p53 protein expression, which in turn inhibited the cell cycle and, ultimately, mouse placental trophoblast growth. In conclusion, DEHP disrupted mouse placental growth by inhibiting the cell cycle of mouse placental trophoblasts via the Trim38-p53 signaling axis. Overall, this study provides a theoretical reference for elucidating the mechanism underlying DEHP-induced placental toxicity.

Background:Kawasaki disease (KD) is an acute pediatric vasculitis with significant implications for coronary arteries and myocardium, potentially leading to long-term myocardial fibrosis. With the advancements in speckle tracking echocardiography (STE), ultrasound parameters have been shown to be reliable in the early detection of structural and functional myocardial abnormalities, thus mitigating some limitations of cardiac magnetic resonance imaging (MRI). Despite its gold standard status for assessing myocardial fibrosis, the application of cardiac magnetic resonance (CMR) with late gadolinium enhancement (LGE) in pediatrics is restricted. Therefore, this study aimed to investigate the correlation between myocardial strain parameters and LGE in children with KD. Methods:We prospectively recruited 100 children with KD and 25 healthy control (HC) children. Left ventricular (LV) function and LGE in the children were evaluated concurrently using echocardiography and CMR. Results:Of the 55 KD children (11 LGE-positive, 44 LGE-negative) and 22 HCs, LGE positivity was higher among those with giant coronary aneurysms (GCAs) and medium coronary aneurysms (MCAs). LGE-positive patients exhibited significantly reduced LV global longitudinal strain (GLS) and strain rates, including 4-chamber GLS [mid-myocardial layer (Mid): 16.82%±5.50% vs. 20.45%±2.43%, subepicardial myocardial layer (Subepi): 14.71%±4.76% vs. 17.67%±2.18%, subendocardial myocardial layer (Subendo): 19.33%±6.49% vs. 23.74%±2.84%] and 4-chamber early diastolic strain rate (SRe: 1.92±0.73 vs. 2.33±0.46 s-1), compared to LGE-negative patients and HCs. Conclusions:In the chronic phase, patients with KD may be at risk of myocardial fibrosis, underscoring the importance of evaluating myocardial function and LGE. Our study indicates that STE could be a valuable tool for assessing focal fibrosis in children with chronic-phase KD. However, due to limitations such as a small sample size, high dropout rate of CMR, and differences in LGE distribution, future studies with larger sample sizes are needed to validate these findings and their predictive efficacy.

The objective of this study is to determine whether the data of blood profiles before and after therapy can be useful for predicting medium-giant coronary artery aneurysms (CAA) in patients with KD. In total, 1856 KD children from 2013 to 2022 were prospectively recruited. Serial blood samples on the day of initial IVIG infusion and 36–48 h thereafter were collected. The clinical and laboratory parameters were compared between the medium-giant CAA (n = 95) group and the non-CAA group (n = 1761). Multivariate analysis was performed to explore the independent risk factors for medium-giant CAA and the receiver operating characteristic (ROC) curve was used to evaluate and assess the prediction validities. Fever duration prior to initial IVIG infusion, IVIG resistance, cardiac enlargement, white blood cells prior to initial IVIG treatment, albumin levels, and the percentage of △neutrophils were independent risk factors for predicting medium-giant CAA. The predictive value of △neutrophil percentage (≤ 30.2

Background:The study of mid- and long-term myocardial function in myocarditis survivors was limited, which cannot fully reflect their clinical prognosis. The present study was carried out to prospectively evaluate the left atrial (LA) and ventricular (LV) function of pediatric myocarditis survivors by speckle tracking echocardiography (STE) combined with stress echocardiography and to uncover its potential risk factors regarding myocardial impairment during follow-up. Methods:Fifteen consecutive asymptomatic pediatric myocarditis survivors and fifteen age- and sex-matched healthy controls were prospectively enrolled. LA and LV deformations at rest and after stress tests were evaluated by conventional echocardiography and STE. The cardiac function reserve reflected as the differences in systolic/diastolic indices between at rest and peak-exercise was also explored. After Shapiro-Wilk and homogeneity test, the Chi-squared test, independent-sample t-test, or Mann-Whitney U test was applied to compare the differences between the two groups. Spearman's correlation analysis was used to explore the relationships between different indices. Results:Basic clinical data were comparable between two groups. As for the echocardiographic indices at rest, asymptomatic pediatric myocarditis survivors displayed worse resting LA function [reservoir strain (εR) (34.33±5.93 vs. 40.72±6.71, P=0.01), conduit strain (εCD) (25.42±4.88 vs. 30.41±5.52 P=0.014)]. After the exercise stress test, pediatric myocarditis survivors displayed worse LV function in comparison with controls as evidenced by lower peak-systolic myocardial velocity (s) of mitral (10.23±1.75 vs. 12.08±1.84, P=0.012), septal s' (8.35±0.48 vs. 9.07±0.94, P=0.021), global longitudinal strain (GLS) (19.39±1.08 vs. 21.18±1.44, P=0.001), global circumferential strain (GCS) (18.88±1.34 vs. 20.89±1.59, P=0.001) and impaired systolic function reserve. Additionally, both resting LA εR and εCD displayed moderate correlations with post-exercise LV lateral s, septal s, and GLS as well as changes before and after exercise (Δ) of lateral s, Δseptal s, and ΔGLS. Conclusions:Regular STE-based LA functional assessment is recommended for asymptomatic pediatric myocarditis survivors to detect early myocardial impairment and probably improve risk prediction.

Background:Kawasaki disease (KD) is a pediatric acute vasculitis affecting the coronary arteries and cardiac tissues. Research has been conducted on the assessment of acute cardiac function in KD; however, chronic cardiac dysfunction remains understudied, particularly in terms of coronary artery lesion (CAL) grading and acute-phase inflammatory markers. This study aimed to assess the effect of CAL grading on chronic cardiac function in KD patients, and explore the association between CAL grading and acute-phase inflammatory markers. Methods:A prospective study was conducted on 25 children with giant coronary aneurysms (GCAs) and gender-, height-, and weight-matched subgroups. Chronic cardiac function and inflammatory markers were assessed using echocardiography and laboratory tests. Results:The KD group showed significantly impaired left ventricular function compared to the healthy control group, including reduced global longitudinal strain (19.94%±3.42% vs. 21.27%±1.69%, P=0.001) and circumferential strain (20.85%±4.01% vs. 23.14%±5.37%, P=0.002). Most systolic/diastolic parameters demonstrated similar statistical significance (KD vs. healthy control group, all P<0.05). Notably, no association was found between CAL severity gradation and cardiac dysfunction (P>0.05 across CAL subgroups). Surprisingly, a considerable proportion of patients with GCAs (61.11%) and medium-sized coronary artery aneurysms (69.57%) had normalized cardiac function. Acute-phase C-reactive protein levels emerged as a predictor for chronic cardiac dysfunction (cut-off value: 127.79 mg/L). Conclusions:Chronic cardiac dysfunction in KD patients is affected by CAL grading and acute-phase inflammatory markers. Integrating inflammatory indicators into CAL risk stratification could enhance clinical management strategies. Further research with larger cohorts needs to be conducted to validate these findings and establish longitudinal monitoring protocols.