Chinese cases of early infantile epileptic encephalopathy: a novel mutation in the PCDH19 gene was proved in a mosaic male- case report.

BACKGROUND: The link between the protocadherin-19 (PCDH19) gene and epilepsy suggests that an unusual form of X-linked inheritance affects females but is transmitted through asymptomatic males. Individuals with epilepsy associated with mutations in the PCDH19 gene display generalized or focal seizures with or without fever sensitivity. The clinical manifestation of the condition ranges from mild to severe, resulting in intellectual disability and behavioural disturbance. In the present study, we assessed mutations in the PCDH19 gene and the clinical features of a group of Chinese patients with early infantile epileptic encephalopathy and aimed to provide further insight into the understanding of epilepsy and mental retardation limited to females (EFMR; MIM 300088). CASE PRESENTATION: We described three variations in the PCDH19 gene in Chinese patients with epilepsy who developed generalized seizures occurring in clusters with or without triggering by fever. Candidate genes were screened for mutations that cause epilepsy and related paroxysmal or nervous system diseases in the coding exons and intron-exon boundaries using polymerase chain reaction (PCR) of genomic deoxyribonucleic acid (DNA) followed by sequencing. The variations were sequenced using next-generation sequencing technology and verified with first-generation sequencing. Exome sequencing of a multigene epilepsy panel revealed three mutations in the PCDH19 gene in a mosaic male and two unrelated females. These included a frameshift mutation c.1508_1509insT (p.Thr504HisfsTer19), a missense mutation c.1681C > T (p.Pro561Ser) and a nonsense mutation c.918C > G (p.Tyr306Ter). Of the three mutations in the PCDH19 gene associated with early infantile epileptic encephalopathy, the frameshift variation in a mosaic male is novel and de novo, the missense variation is de novo and is the second ever reported in females, and the nonsense variation was inherited from the paternal line and is the first example discovered in a female. CONCLUSIONS: The results from our current study provide new insight into and perspectives for the molecular genetic link between epilepsy and PCDH19 alterations. Moreover, our new findings of the male mosaic variant broaden the spectrum of PCDH19-related epilepsy and provide a new understanding of this complex genetic disorder.

Effect of Selective Thrombus Aspiration on Serum Lipoprotein-Associated Phospholipase A2 in Patients with ST-Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention with High Thrombus Burden.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a potential therapeutic target in acute coronary syndromes. Although recent evidence does not support the routine use of manual thrombus aspiration (TA) in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI), the use of TA is associated with a significant improvement in myocardial reperfusion, especially in patients with high thrombus burden (HTB). We hypothesized that TA would reduce the serum Lp-PLA2 levels in STEMI patients undergoing PPCI with HTB. METHODS AND RESULTS: Our study cohort included 320 consecutive STEMI patients undergoing PPCI with HTB who were randomly assigned to receive either TA before PPCI (TA group, n = 160) or PPCI alone (standard PPCI group, n = 160). The baseline characteristics of study participants were well-matched. After 30 ± 2 days, serum Lp-PLA2 levels decreased by 53.9% in the TA group (152.9 ± 58.1 ng/mL) and decreased by 31.2% in the standard PPCI group (84.2 ± 86.6 ng/mL, p < 0.001). The TA group had a significantly lower prevalence of balloon predilatation, number of stents used, total stent length and corrected thrombolysis in myocardial infarction frame count, and a higher percentage of myocardial blush grade ≥ 2 compared with the standard PPCI group (all p < 0.001). No significant difference between the groups was observed in 30 ± 2 days for major adverse cardiovascular and cerebrovascular events (p = 0.702). CONCLUSIONS: After 30 ± 2 days of treatment, TA may significantly reduce serum levels of Lp-PLA2 in STEMI patients undergoing PPCI with HTB.

Effect of Carvedilol on Serum Heart-type Fatty Acid-binding Protein, Brain Natriuretic Peptide, and Cardiac Function in Patients With Chronic Heart Failure.

OBJECTIVE: To observe the changes of serum heart-type fatty acid-binding protein (h-FABP) and brain natriuretic peptide (BNP) in children with chronic heart failure (CHF) and evaluate the effects of carvedilol. METHODS: A total of 36 patients with CHF, including 17 of endocardial fibroelastosis and 19 of dilated cardiomyopathy, were enrolled and were randomly divided into a carvedilol treatment group (group A) and a conventional treatment group (group B). Group A (n = 16) was treated with carvedilol and conventional treatment and group B (n = 20) was managed with conventional treatment only. Thirty healthy children were enrolled as controls. The concentrations of serum h-FABP and BNP were measured by enzyme-linked immunosorbent assay, and the left ventricular end-systolic diameter, left ventricular end-diastolic diameter, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), and cardiac index (CI) were measured by echocardiography. RESULTS: The concentrations of serum h-FABP and BNP in patients with CHF were significantly higher than in the control group (21.7 ± 4.3 ng/mL vs. 6.3 ± 1.7 ng/mL, 582.4 ± 180.6 pg/mL vs.31.2 ± 9.8 pg/mL, all P < 0.01), positively correlated with the degree of heart failure (all P < 0.01), and were both higher in groups endocardial fibroelastosis and dilated cardiomyopathy than in the control group (all P < 0.01), but there was no statistically significant difference between the 2 groups (P > 0.05). h-FABP concentration in patients with CHF was positively correlated with BNP (r = 0.78, P < 0.01) but negatively correlated with LVEF, LVFS, and CI (r = -0.65, -0.64, and -0.71, respectively; all P < 0.01). BNP concentration was also negatively correlated with LVEF, LVFS, and CI (r = -0.75, -0.61, and -0.79, respectively; all P<0.01). After treatment with carvedilol, the serum concentrations of h-FABP and BNP in group A were lower than in group B, and the magnitude of heart rate reduction, improvement of LVEF, LVFS, and CI, and reduction of left ventricular end-systolic diameter and left ventricular end-diastolic diameter in group A were all greater than in group B (all P < 0.01). Treatment with carvedilol had no adverse events. CONCLUSIONS: Serum concentrations of h-FABP and BNP can be used as biomarkers to evaluate the severity of heart failure, and carvedilol can significantly improve heart function in children with CHF.

Relationship between Helicobacter pylori infection and serum interleukin-18 in patients with carotid atherosclerosis.

BACKGROUND: Helicobacter pylori (H. pylori) infection stimulates the production of proinflammatory cytokines associated with the development of atherosclerosis. Levels of circulating interleukin-18 (IL-18) have been positively correlated with carotid intima-media thickness (IMT) and coronary plaque area and have identified IL-18 levels as important predictors of coronary events and cardiovascular mortality. This study aimed to examine the relationship between serum IL-18 and H. pylori-IgG antibody as a sign of H. pylori infection in patients with carotid atherosclerosis. METHODS: The carotid IMT, traditional atherosclerotic risk factors, levels of serum H. pylori-IgG and IL-18 were measured in 573 health checkup examinees. RESULTS: Serum IL-18 and H. pylori-IgG levels were significantly increased in subjects with increased IMT in comparison with those with normal IMT. In subjects with increased IMT, serum H. pylori-IgG was positively correlated with serum IL-18 (r = .402, p = .002), and the association was independent of traditional atherosclerotic risk factors (ß = 0.310, p < .001). CONCLUSIONS: In health checkup examinees with increased IMT, serum IL-18 and H. pylori-IgG were independently correlated and were significantly higher than in subjects with normal IMT.

[Changes of heart-type fatty acid-binding protein in children with chronic heart failure and its significance].

OBJECTIVE: To study serum levels of heart-type fatty acid-binding protein (h-FABP) in children with chronic heart failure (CHF), and the correlation between heart function and the level of h-FABP, with the aim of studying the significance of h-FABP in CHF. METHODS: Thirty-six children with CHF, including 16 cases of endocardial fibroelastosis (EFE) and 20 cases of dilated cardiomyopathy (DCM) were enrolled in the study. Thirty healthy children sevred as the control group. Serum levels of h-FABP were determined using ELISA, and left ventricular ejection fraction (LVEF), cardiac index (CI) and fractional shortening of the left ventricle (LVSF) were measured by two-dimensional echocardiography in the CHF group. RESULTS: Mean levels of h-FABP in the CHF group were significantly higher than in the control group (21.7±4.3 ng/mL vs 6.2±1.7 ng/mL; P<0.01). The worse the heart function, the higher the h-FABP levels (P<0.01). Mean levels of h-FABP in both the EFE and DCM groups were significantly higher than in the control group (P<0.01). Serum h-FABP concentrations were negatively correlated with LVEF, CI and LVSF (r=-0.65, -0.64 and -0.71 respectively; P<0.01) in the CHF group. CONCLUSIONS: Serum h-FABP levels increase in children with CHF and are closely related to the severity of the condition. Serum h-FABP levels can be used as a biomarker for the diagnosis of heart failure and the evaluation of its severity.

Experimental study on the properties of modern blue clay brick for Kaifeng People's Conference Hall.

This article presents building assessment research comprising on-site inspections, indoor scientific tests, and material performance studies on the wall blue clay bricks in the Kaifeng People's Conference Hall, objectively developing an enhanced scientific understanding to renovate modern buildings. Using X-ray diffraction (XRD), scanning electron microscopy (SEM), alongside a parametric study of density, moisture content, water absorption, void ratio, frosting, compressive strength, and softening coefficient in assessing the material health of the blue clay bricks and it's non-key parts, in developing "appropriate and compatible renovation" to repair contemporaneous buildings. The composition, pore characteristics, weathering degree, and mechanical properties of the blue clay brick samples were analyzed. These parameters showed that blue clay brick fired at less than 1000 °C; the main mineral composition as quartz, followed by albite, mica, and anorthite. Its density was 1.573 g/cm3, less than the 1.70 g/cm3 of ordinary clay brick. According to the standards, the water absorption was greater than that of regular sintered bricks by more than 18% and was slightly frosted. Compressive strength being less than MU10 did not meet the current design specifications for masonry. Its softening coefficient was between 0.70 and 0.85, but its water resistance was relatively good. The research results provide an essential reference for judging the health and longevity of modern buildings to achieve scientific guidelines for practical protection.

Novel variants in TBC1D24 associated with epilepsy and deafness: Report of two cases.

PURPOSE: To identify the causative variants in two unrelated Chinese patients presenting with epilepsy and deafness. METHODS: The two patients underwent a thorough examination, including brain MRI, EEG and metabolic studies. Next-generation sequencing (NGS) was performed on genomic DNA samples from the siblings and parents. Sanger sequencing was used to confirm the variants. RESULTS: Gene sequencing revealed that they carried two novel compound heterozygous missense variants of the TBC1D24: c.116 C > T (p.Ala39Val) and c.827 T > C (p.Ile276Thr) in patient 1; c.404 C > T (p.Pro135Leu) and c.679 T > C (p.Arg227Trp) in patient 2. Audiologic examination showed bilateral sensorineural hearing loss in both patients. CONCLUSION: We have found novel variants in the TBC1D24 in two Chinese unrelated patients. They result in a rare phenotype, characterized by drug-resistant epilepsy and deafness.

A case of TSC2-PKD1 contiguous deletion syndrome: Clinical features and effective treatment for epilepsy.

Polycystic kidney disease with Tuberous sclerosis is a disease caused by the deletions of the TSC2-PKD1 gene. The disease is rarely reported and the characterized manifestation is severe polycystic kidney growth. The diagnosis can be made by molecular analysis. We report the first case of PKDTS discovered in infancy in China with typical neurological and renal manifestations. The patient has infantile spasm, polycystic kidney, skin damage, hypertension, and hematuria after infection. After effective treatment of Rapamycin, the seizures were completely controlled. There was not been any renal function damage in the patient. At the same time, we review the related literature and further elaborate on the variety of clinical manifestations, treatment, and prognosis.

[Levels of serum brain natriuretic peptide and the correlation to heart function in children with Kawasaki disease].

OBJECTIVE: To study serum levels of brain natriuretic peptide (BNP) in children with Kawasaki disease (KD) and the correlation between BNP levels and the heart function. METHODS: Forty-three children with KD and thirty healthy children were enrolled. Serum levels of BNP were measured using ELISA. KD children received an echocardiographic examination, including measurements of left ventricular ejection fraction (LVEF), left ventricular shorten fraction (LVSF), cardiac index (CI) and left ventricular inflow velocity through the mitral annulus. RESULTS: Mean serum level of BNP at the acute stage in children with KD was significantly higher than that at the recovery stage as well as the control group (p<0.01). The LVEF, LVSF and CI levels at the acute stage were significantly lower than those at the recovery stage in children with KD (p<0.05). The linear regression analysis showed that the BNP level was negatively correlated with the levels of LVEF, LVSF and CI (r=-0.63, -0.52, -0.53, p<0.05). CONCLUSIONS: The serum BNP levels increase significantly in KD children at the acute stage, and are negatively correlated with the levels of LVEF, LVSF and CI. Measurement of serum BNP level is useful for the early diagnosis of KD.

Reappraisal of the role of the DRD3 gene in essential tremor.

OBJECTIVES: Analyze the distribution of polymorphism in the dopamine receptor D3 (DRD3) gene, which was previously reported as a susceptibility risk for essential tremor (ET), in a large cohort of ET. METHODS: The role of 312G>A DRD3 polymorphism was analyzed using linkage analysis, association study and transmission disequilibrium test in a group of 433 ET patients, and two unrelated control groups with 121 and 151 individuals. RESULTS: Allelic frequencies of glycine and serine forms of the DRD3 gene did not differ between patients and both control groups, and were in Hardy-Weinberg equilibrium. Linkage analysis identified obligatory recombinants in every large pedigree, even in those with relatively high frequency of glycine allele, thus excluding the linkage to this locus. Both alleles were transmitted with an equal likelihood to affected offspring. We also failed to replicate the relationship between glycine homozygosity and an earlier age of onset or more severe tremor course. CONCLUSIONS: Our comprehensive genetic analysis in a large ET cohort strongly argues against the role of the DRD3 gene in ET pathogenesis.

Retraction Note: Oxidized Low-density Lipoprotein (ox-LDL) Cholesterol Induces the Expression of miRNA-223 and L-type Calcium Channel Protein in Atrial Fibrillation.

This Article has been retracted.

Mutations in GABRA1, GABRA5, GABRG2 and GABRD receptor genes are not a major factor in the pathogenesis of familial focal epilepsy preceded by febrile seizures.

GABA(A) receptors mutations have been reported in few epilepsy families with febrile seizures (FS) followed by generalized epilepsy. It is not known if such mutations may underlie FS followed by partial epilepsy, which is a more common type of epilepsy. We searched for disease-causing mutations in the genes of the alpha1, alpha5, gamma2 and delta subunits of the GABA-A receptor that were previously shown to contain epilepsy-causing mutations or epilepsy susceptibility polymorphisms. All coding and untranslated exons of these four GABA(A) subunit genes were screened in 74 unrelated patients with familial partial epilepsy preceded by FS. Most patients had temporal lobe epilepsy (TLE). We did not detect any disease-causing mutations that would be consistent with missense, nonsense or splice site mutations in any of the four analyzed genes. We conclude that these genes are not a major genetic factor in familial TLE preceded by FS.

Mutations in the GABRA1 and EFHC1 genes are rare in familial juvenile myoclonic epilepsy.

Juvenile myoclonic epilepsy (JME), accounting for approximately 25% of idiopathic generalized epilepsies, is genetically heterogeneous. Mutations in the alpha-1 subunit of the GABAA receptor (GABRA1) and EFHC1 genes have been reported in a few families with autosomal dominant (AD) JME. We have investigated the contribution of these two genes to familial JME in our cohort of 54 JME Caucasian families. Syndromic classification of JME was based on previously published criteria. We considered kindreds with at least one affected first-degree relative and the evidence of a vertical transmission as definite AD JME, and families with at least one affected second-degree relative as probable AD JME. We included 33 families meeting criteria for definitive AD JME and 21 that were classified as probable AD JME. None of these families were considered informative enough to analyze candidate loci for JME using linkage analysis. We have systematically screened coding exons of these two genes using temperature gradient capillary electrophoresis. Every heteroduplex with an abnormal mobility was sequenced. No disease-causing mutations in the GABRA1 gene were identified. Analysis of EFHC1 gene found one putative disease-causing mutation R221H that was previously reported as a tandem mutation. Several synonymous and non-synonymous coding polymorphisms were identified but the allelic frequency did not differ between controls and affected individuals. Our data suggests that the majority of familial AD JME is not caused by mutations in the GABRA1 and EFHC1 genes.

Oxidized Low-density Lipoprotein (ox-LDL) Cholesterol Induces the Expression of miRNA-223 and L-type Calcium Channel Protein in Atrial Fibrillation.

Atrial fibrillation (AF) is the most common sustained arrhythmia causing high morbidity and mortality. While changing of the cellular calcium homeostasis plays a critical role in AF, the L-type calcium channel α1c protein has suggested as an important regulator of reentrant spiral dynamics and is a major component of AF-related electrical remodeling. Our computational modeling predicted that miRNA-223 may regulate the CACNA1C gene which encodes the cardiac L-type calcium channel α1c subunit. We found that oxidized low-density lipoprotein (ox-LDL) cholesterol significantly up-regulates both the expression of miRNA-223 and L-type calcium channel protein. In contrast, knockdown of miRNA-223 reduced L-type calcium channel protein expression, while genetic knockdown of endogenous miRNA-223 dampened AF vulnerability. Transfection of miRNA-223 by adenovirus-mediated expression enhanced L-type calcium currents and promoted AF in mice while co-injection of a CACNA1C-specific miR-mimic counteracted the effect. Taken together, ox-LDL, as a known factor in AF-associated remodeling, positively regulates miRNA-223 transcription and L-type calcium channel protein expression. Our results implicate a new molecular mechanism for AF in which miRNA-223 can be used as an biomarker of AF rheumatic heart disease.

The GABBR1 locus and the G1465A variant is not associated with temporal lobe epilepsy preceded by febrile seizures.

BACKGROUND: Polymorphism G1465A in the GABBR1 gene has been suggested as a risk factor for non-lesional temporal lobe epilepsy (TLE); however, this genetic association study has not been independently replicated. We attempted to replicate this study in our cohort of patients with TLE. Furthermore, we also analyzed the coding sequence of this gene and searched for disease-causing mutations. METHODS: We included 120 unrelated individuals with TLE that was preceded by febrile seizures (FS) who did not have any evidence of structural lesions suggesting secondary epilepsy. 66 individuals had positive family history of TLE epilepsy and 54 were sporadic. Each patient was genotyped for the presence of G1465A polymorphism. All exons of the GABBR1 gene were screened by single strand confirmation polymorphism method. Genotypes were compared with two independent matched control groups. RESULTS: We detected two A alleles of the G1465A polymorphism in one homozygous control subject (0.87% of all alleles) and one A allele in a patient with TLE (0.45%, not significant). Other detected polymorphisms in coding regions had similar frequencies in epilepsy patients and control groups. No disease causing mutations in the GABBR1 gene were detected in patients with sporadic or familial TLE. CONCLUSION: Our results indicate that TLE preceded by FS is not associated with the polymorphisms or mutations in the GABBR1 gene, including the G1465A polymorphism. The proportion of TLE patients with FS in the original study, reporting this positive association, did not differ between allele A negative and positive cases. Thus, our failure to reproduce this result is likely applicable to all non-lesional TLE epilepsies.

[Comparative study on effects of puerarin and granulocyte colony-stimulating factor in treating acute myocardial infarction].

OBJECTIVE: To compare the effects of puerarin and granulocyte colony-stimulating factor (G-CSF) in treating acute myocardial infarction (AMI) and on the size of infarcted area and cytokines. METHODS: Seventy-nine patients with anterior AMI were randomly divided into three groups, they were treated with conventional Western medical treatment, but to the puerarin group (PG) and the G-CSF group (GCG) puerarin and G-CSF was given additionally, respectively. The infarcted size, plasma G-CSF, matrix metalloproteinase-9 (MMP-9), serum interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were detected before and after treatment. RESULTS: The infarcted size was positively correlated to the levels of G-CSF, MMP-9, IL-6 and TNF-alpha before treatment ( r = 0.45, 0.42, 0.44 and 0.42, P<0.01 ). The infarcted size in the PG and the GCG decreased on the 28th day (P<0.01), the level of G-CSF, MMP-9, IL-6 and TNF-alpha in the PG on the 7th day all decreased (P<0.05), but these indexes in the GCG increased (P<0.05), while those in the control group were unchanged (P>0.05). CONCLUSION: Puerarin and G-CSF are effective in decreasing infarcted size, but their effects on cytokines are different entirely.

Simplified Calculation Model and Experimental Study of Latticed Concrete-Gypsum Composite Panels.

In order to address the performance complexity of the various constituent materials of (dense-column) latticed concrete-gypsum composite panels and the difficulty in the determination of the various elastic constants, this paper presented a detailed structural analysis of the (dense-column) latticed concrete-gypsum composite panel and proposed a feasible technical solution to simplified calculation. In conformity with mechanical rules, a typical panel element was selected and divided into two homogenous composite sub-elements and a secondary homogenous element, respectively for solution, thus establishing an equivalence of the composite panel to a simple homogenous panel and obtaining the effective formulas for calculating the various elastic constants. Finally, the calculation results and the experimental results were compared, which revealed that the calculation method was correct and reliable and could meet the calculation needs of practical engineering and provide a theoretical basis for simplified calculation for studies on composite panel elements and structures as well as a reference for calculations of other panels.

[Study on the effect and mechanism of puerarin on the size of infarction in patients with acute myocardial infarction].

OBJECTIVE: To observe the effect of puerarin on infarction size, fatty acids metabolism, inflammatory response and atherosclerotic plaque stability in patients with acute myocardial infarction (AMI). METHODS: Sixty-one patients with AMI were randomly divided into two groups, the control group (n = 30) and the treated group (n = 31). All were treated with conventional treatment, but to the treated group, puerarin injection was given additionally by injecting 500 mg per day for 2 weeks. Before and after treatment, blood levels of free fatty acids (FFA), matrix metalloproteinases-9 (MMP-9) and C-reactive protein (CRP) were assayed, and the size of infarction was determined by Ideker QRS scoring method. RESULTS: Before treatment, the size of infarction was positively correlated to the levels of FFA, MMP-9 and CRP (r = 0.43, 0.42 and 0.39, respectively, all P<0.01). As compared with those before treatment, after treatment, the three parameters lowered by 30%, 41% and 23%, respectively and the size of infarction significantly reduced in the treated group (P<0.01), while in the control group, no significant change was found (P>0.05). CONCLUSION: Puerarin treatment could significantly reduce the size of infarction in patients with AMI, the mechanism is possibly related with its effects in lowering plasma levels of FFA, inhibiting inflammation and stabilizing atherosclerotic plaque.

Serum brain natriuretic peptide in children with Kawasaki disease.

BACKGROUND: Kawasaki disease (KD) is a common cause of acquired heart disease in children. Recent studies have focused on the biochemical markers of the myocardium, their high sensitivity and specificity and significance in the diagnosis of KD. This study aimed to determine the serum level of brain natriuretic peptide (BNP) and its relation with the heart function of children with KD and to explore its clinical value in diagnosis of KD. METHODS: Forty-three KD children, aged from 5 months to 8 years (mean 2.3±0.6 years), were admitted to Qingdao Children's Hospital from February 2007 to April 2009. Among them 27 were male, and 16 female. The 43 patients served as a KD group. Patients with myocarditis, cardiomyopathy, congenital heart disease and other primary heart diseases were excluded. Thirty healthy children, aged from 3 months to 15 years (mean 2.5±0.8 years) or 17 males and 13 females served as a control group. There were no significant differences in age and gender between the two groups (P>0.05). In the KD group, ELISA was used to measure the levels of serum BNP in acute and convalescent stages; and in the control group, the levels of serum BNP were measured once randomly. Left ventricular ejection fraction (LVEF), left ventricular shorten fraction (LVSF), cardiac index (CI) and left ventricular inflow velocity through the mitral annulus (including E-velocity and A-velocity) were measured by two-dimensional echocardiography in the acute and convalescent stages in the KD group. All data were expressed as mean±SD. The methods of analysis included Student's t test and the linear regression analysis test. P<0.05 was considered statistically significant. RESULTS: The level of serum BNP in the acute stage (517.26±213.40) ng/ml was significantly higher than that in the convalescent stage (91.56±47.97) ng/ml in the control group (37.55±7.56) ng/ml (P<0.01). The levels of LVEF, LVSF and CI in the acute stage were significantly lower than those in the convalescent stage (P<0.05), but the E/A level was not significantly different between the acute and convalescent stages (P>0.05). Linear regression analysis showed that the BNP level was negatively correlated with the levels of LVEF, LVSF and CI(r=-0.63, -0.52, -0.53, P<0.05), but not significantly correlated with the E/A level (r=-0.18, P>0.05). CONCLUSION: The levels of serum BNP are significantly increased in KD patients, and are negatively correlated with the levels of LVEF, LVSF, and CI. The detection of serum BNP level is of clinical significance in the diagnosis of KD.