Pediatric Cardiology Journal Impact Factor & Information

Publisher: Springer Verlag

Journal description

The editor of Pediatric Cardiology welcomes original manuscripts concerning all aspects of heart disease in infants, children, and adolescents, including embryology and anatomy, physiology and pharmacology, biochemistry, pathology, genetics, radiology, clinical aspects, investigative cardiology, electrophysiology and echocardiography, and cardiac surgery. Articles which may include original articles, case reports, letters to the editor etc., must be written in English and must be submitted solely to Pediatric Cardiology.

Current impact factor: 1.55

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.55
2012 Impact Factor 1.197
2011 Impact Factor 1.298
2010 Impact Factor 1.237
2009 Impact Factor 1.151
2008 Impact Factor 1.03
2007 Impact Factor 0.868
2006 Impact Factor 0.826
2005 Impact Factor 0.986
2004 Impact Factor 0.694
2003 Impact Factor 0.581
2002 Impact Factor 0.771
2001 Impact Factor 0.72
2000 Impact Factor 0.863
1999 Impact Factor 0.835
1998 Impact Factor 0.582
1997 Impact Factor 0.39
1996 Impact Factor 0.363
1995 Impact Factor 0.278
1994 Impact Factor 0.302
1993 Impact Factor 0.443
1992 Impact Factor 0.396

Impact factor over time

Impact factor

Additional details

5-year impact 1.26
Cited half-life 6.40
Immediacy index 0.30
Eigenfactor 0.01
Article influence 0.44
Website Pediatric Cardiology website
Other titles Pediatric cardiology (Online)
ISSN 1432-1971
OCLC 41903795
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

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    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The pathogenesis of congenital heart disease (CHD) is unclear. There is a high incidence of CHD in Down syndrome, in which RCAN1 (regulator of calcineurin 1) overexpression is observed. However, whether RCAN1 plays an important role in non-syndromic CHD is unknown. This study investigates the relationship between sequence variations in the RCAN1 promoter and sporadic CHD. This was a case-control study in which the RCAN1 promoter was cloned and sequenced in 128 CHD patients (median age 1.1 year) and 150 normal controls (median age 3.0 year). No mutation sites had been identified in this research. Three single-nucleotide (C to T) polymorphisms were detected: rs193289374, rs149048873 and rs143081213. The polymorphisms were not associated with CHD risk according to a logistic regression analysis. Functional assays in vitro showed that compared with the wild-type genotype, the rs149048873 polymorphism decreased, and the rs143081213 increased, the RCAN1 promoter activity, though the rs193289374 polymorphism had no effect. In conclusion, the sequence variations in RCAN1 promoter are not major genetic factors involved in sporadic CHD, at least in the current research population.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1172-y
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    ABSTRACT: Congenital heart disease (CHD) is the most prevalent type of birth defect in humans and is the leading non-infectious cause of infant death worldwide. There is a growing body of evidence demonstrating that genetic defects play an important role in the pathogenesis of CHD. However, CHD is a genetically heterogeneous disease and the genetic basis underpinning CHD in an overwhelming majority of patients remains unclear. In this study, the coding exons and splice junction sites of the TBX1 gene, which encodes a T-box homeodomain transcription factor essential for proper cardiovascular morphogenesis, were sequenced in 230 unrelated children with CHD. The available family members of the index patient carrying an identified mutation and 200 unrelated ethnically matched healthy individuals used as controls were subsequently genotyped for TBX1. The functional effect of the TBX1 mutation was predicted by online program MutationTaster and characterized by using a dual-luciferase reporter assay system. As a result, a novel heterozygous TBX1 mutation, p.Q277X, was identified in an index patient with double outlet right ventricle (DORV) and ventricular septal defect (VSD). Genetic analysis of the proband's available relatives showed that the mutation co-segregated with CHD transmitted in an autosomal dominant pattern with complete penetrance. The nonsense mutation, which was absent in 400 control chromosomes, altered the amino acid that was completely conserved evolutionarily across species and was predicted to be disease-causing by MutationTaster. Biochemical analysis revealed that Q277X-mutant TBX1 lost transcriptional activating function when compared with its wild-type counterpart. This study firstly associates TBX1 loss-of-function mutation with enhanced susceptibility to DORV and VSD in humans, which provides novel insight into the molecular mechanism underlying CHD and suggests potential implications for the development of new preventive and therapeutic strategies for CHD.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1173-x
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    ABSTRACT: Prematurity is a recognized risk factor for morbidity and mortality following cardiac surgery. Postoperative and long-term outcomes after cardiac surgery performed in the preterm period are poorly described. The aim of this study was to analyze a population of preterm neonates operated on for critical congenital heart disease (CHD) before 37 weeks of gestational age (wGA) with special attention given to early and late mortality and morbidity. Between 2000 and 2013, 28 preterm neonates (median gestational age (GA) 34.3 weeks) underwent cardiopulmonary bypass (CPB) surgery for critical CHD before 37 wGA; records were retrospectively reviewed. All patients except three with single ventricle physiology had a single-stage anatomic repair. Overall mortality was 43 % (95 % CI 25-62). Risk factors for death were birth weight (p = 0.032) and weight at surgery (p = 0.037), independently of GA, preoperative status, CPB and aortic clamp time. Seven patients, including those with univentricular hearts, died during the postoperative period, and five in the first year after surgery. Median follow-up was 5.9 years (range 1 month-12.8 years). Kaplan-Meier survival rate was 75 % (95 % CI 59-91) at 1 month, and 57 % (95 % CI 39-75) at 1 and 5 years. Eight patients required reoperations after a delay of 2.8 ± 1.3 months; eight had bronchopulmonary dysplasia. At the end of follow-up, nine patients were asymptomatic. One-stage biventricular repair for critical CHD on preterm neonates was feasible. Mortality remained high but acceptable, mainly confined to the first postoperative year and related to small weight. Despite reoperations, long-term clinical status was good in most survivors. Further long-term prospective investigations are necessary to evaluate neurodevelopmental outcomes.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1158-9
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    ABSTRACT: We report a rare case of hypoplastic left heart syndrome coexisting in a patient with Ebstein anomaly of the tricuspid valve, which has previously been described only in pathological studies. A fetal echocardiogram at 27-weeks gestation showed severe aortic stenosis with evolving hypoplastic left heart syndrome, significant endocardial fibroelastosis, a dysplastic tricuspid valve with moderate regurgitation, right atrial and ventricular dilation, and signs of fetal congestive heart failure. Due to inadequate left heart size, the patient was not a candidate for fetal intervention for critical aortic stenosis, and repeat studies showed progression of the lesion through the pregnancy. The infant was delivered at 36-weeks gestation with signs of hydrops, and a postnatal echocardiogram confirmed hypoplastic left heart syndrome as well as severe Ebstein anomaly of the tricuspid valve. The infant did not survive to intervention.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1171-z
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    ABSTRACT: Antenatal diagnosis of right heart enlargement has a wide spectrum of differential diagnosis from maternal, placental and fetal causes, and outcomes of all are not known. Coarctation of the aorta is in the differential diagnosis of right heart enlargement. In our study, we focused to measure multiple cardiac dimensions in fetuses with right heart enlargement to identify the fetus with coarctation of the aorta utilizing echocardiographic measurements. Ten cardiovascular dimensions were measured from fetal studies between 20- and 34-week gestation, and six were measured on postnatal echocardiograms. Z-scores for the cardiac dimensions were calculated, and each variable for fetuses and infants was tested using a two-sample t test between patients with and without coarctation. We excluded fetuses with TAPVR, Shone complex, interrupted aortic arch, Ebstein anomaly or HLHS. Of the 31 fetuses with in utero right heart enlargement, 11 had coarctation postnatally and 20 did not have coarctation. We compared the fetal and newborn cardiac dimensions between the groups. The mean fetal carotid-subclavian index (CS Index) was 0.7 mm with coarctation compared with 1.1 mm without coarctation (p < 0.0001). The mean difference in diameter z-scores for fetal aortic isthmus (p < 0.0001), mitral valve (<0.001) and aortic valve (p < 0.009) was also significantly different. Similar significant differences were noted postnatally in the diameters of the cardiac dimensions between the coarctation and no-coarctation group: CS index (p < 0.0001), aortic isthmus (p < 0.0002) and aortic valve annulus (p < 0.007). A spectrum of diagnoses was found postnatally in fetuses with right heart enlargement, including a normal heart. The likelihood of identifying fetuses with coarctation of the aorta and planning for postnatal management can be refined by noninvasive screening measurements. A smaller CS index and smaller diameters of the aortic isthmus, mitral valve and aortic valve were significantly associated prenatally (p < 0.05) with coarctation of the aorta versus without coarctation and might be useful in prenatally diagnosing coarctation of the aorta. Postnatally, these measurements are reproducible. This is the first study utilizing these specific measurements to diagnose coarctation prenatally.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1168-7
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    ABSTRACT: QT prolongation is an independent risk factor for cardiovascular mortality in adults. However, there is little information available on pediatric patients with QT prolongation and their outcomes. Herein, we evaluated the prevalence of QT prolongation in pediatric patients identified by an institution-wide QT alert system, and the spectrum of their phenotype. Patients with documented QT prolongation on an ECG obtained between November 2010 and June 2011 were included. There were 1303 pediatric ECGs, and 68 children had electrographically isolated QT prolongation. Comprehensive review of medical records was performed with particular attention to QT-prolonging clinical, laboratory, and medication data, which were summarized into a pro-QTc score. Overall, 68 (5 %) pediatric patients had isolated QT prolongation. The mean age of this pediatric cohort was 9 ± 6 years, and the average QTc was 494 ± 42 ms. All children had 1 or more QT-prolonging risk factor(s), most commonly QT-prolonging medications. One patient was identified with congenital long QT syndrome (LQTS), which was not previously diagnosed. In one-year follow-up, only one pediatric death (non-cardiac) occurred (1.5 %). Potentially QT-offending/pro-arrhythmic medications were changed in 80 % of pediatric patients after the physician received the QT alert. Children with QT prolongation had very low mortality and minimal polypharmacy. Still, medications and other modifiable conditions were the most common causes of QT prolongation. Children with a prolonged QTc should be evaluated for modifiable QT-prolonging factors. However, if no risk factors are present or the QTc does not attenuate after risk factor modification/removal, the child should be evaluated for congenital LQTS.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1164-y
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    ABSTRACT: Sinus node disease is a problem encountered in patients after the Mustard surgery, requiring a pacemaker implantation. The knowledge of the complexity anatomy is crucial because of the possible challenges associated with this procedure. We report a case of a 24-year-old woman presented with symptomatic bradycardia, in which a bicameral stimulation using a single-lead VDD pacing system was successfully performed.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1155-z
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    ABSTRACT: The aim is to compare tricuspid valve (TV) atrioventricular junction (AVJ) annular motion parameters in unrepaired atrial septal defect (ASD) and repaired Tetralogy of Fallot (TOF) by cardiac magnetic resonance (CMR) imaging. We retrospectively reviewed CMR studies performed between November 2007 and November 2013 in patients 16-45 years of age with unrepaired ASD (with or without partial anomalous pulmonary venous return) and with repaired TOF, who had previous infundibulotomy, but have not undergone pulmonary valve replacement. Longitudinal motion of lateral TV in four-chamber view cine image was tracked through the cardiac cycle with custom software. Twenty TOF patients and 12 ASD patients were included, and values were compared with 80 controls. Right ventricular end-diastolic volume index and right ventricular end-systolic volume index were similar in the ASD and TOF groups and were significantly higher in both groups than in controls. Maximum displacement of the TV in systole, velocity at half-maximal displacement during systole, and velocity at half-maximal displacement during early diastole were all significantly lower in the TOF group than the ASD group [1.39 ± 0.47 vs. 2.21 ± 0.46 (cm, p < 0.01), 5.9 ± 2.1 vs. 10.1 ± 2.3 (cm/s, p < 0.01), and 7.7 ± 2.6 vs. 10.9 ± 3.1 (cm/s, p < 0.05)]. TOF patients have diminished early diastolic TV AVJ velocity compared to patients with an unrepaired ASD, despite similar RV volumes. This observation could suggest diastolic dysfunction or cardiac mechanics unique to the postoperative, volume-overloaded right ventricle in patients with repaired TOF.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1160-2
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    ABSTRACT: Pulmonary vein stenosis (PVS) carries significant morbidity and mortality for affected children, and its management often requires multiple angioplasty procedures. PVS angioplasty can be complicated by systemic embolic events such as stroke, but incidence and risk factors are poorly understood. We reviewed pediatric catheterizations involving PVS angioplasty and/or stent placement performed at Boston Children's Hospital between July 2005 and February 2014. A total of 406 cases were performed in 144 distinct patients. Patients underwent a median of two catheterizations, at median age 1 year and weight 6.9 kg. Eleven (2.7 %) catheterizations were complicated by clinically apparent systemic embolic events, comprising 10 strokes (one with associated hepatic embolism) and 1 renal infarct. Prevalence of clinically evident stroke among this cohort was 7.6 %. Using a prior (uncomplicated) catheterization to allow each patient to serve as their own control, we sought to identify potentially modifiable risk factors for systemic embolic events. Although this analysis was limited by low power, complicated and uncomplicated angioplasties did not appear to differ in case time, contrast dose, anticoagulation management, use of cutting balloons, number of catheter exchanges, or size of long sheath used. Significant non-embolic adverse events were common, occurring in 25 % of catheterizations. Systemic embolism appears to complicate PVS angioplasty at a rate much higher than that described for other congenital catheterizations. This risk may be inherent to the procedure rather than related to any modifiable or operator-dependent factors.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1165-x
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    ABSTRACT: Vitamin D has anti-inflammatory properties, and deficiency is prevalent in children. There is a paucity of data regarding vitamin D status and its correlation with low-grade inflammation and vasculature. We prospectively enrolled 25 children, 9-11 years old (13 male); 21 obese. Eight atherosclerosis-promoting risk factors were scored as categorical variables with the following thresholds defining abnormality: body mass index Z score ≥1.5; systolic blood pressure ≥95th percentile (for age, sex, and height); triglyceride ≥100 mg/dL; low-density lipoprotein cholesterol (LDL-C) ≥110 mg/dL; high-density lipoprotein cholesterol ≤45 mg/dL; hemoglobin A1C (HBA1C) ≥5.5; 25-hydroxyvitamin D [25(OH) D] ≤30 ng/mL, and tobacco smoke exposure. High-sensitivity C-reactive protein (hsCRP) was measured to assess low-grade inflammation and classified as low- (<1 mg/L), average- (1-3 mg/L), and high-risk (>3 to <10 mg/L) groups. The proportion of children within each hsCRP group who had above threshold risk factors was calculated. Carotid artery ultrasound was performed to measure carotid artery intima-media thickness (CIMT). Median (range) for 25(OH) D was 24 (17-45) ng/mL. Eighteen were either 25 (OH) D deficient (<20 ng/mL) or insufficient (20-30 ng/mL), and seven were sufficient (>30 ng/mL). hsCRP was 1.7 (0.2-9.1) mg/L, with 11 being <1.0 mg/L, 8 between 1.0-3.0 and 6 > 3.0 to < 10.0 mg/L. Risk factor score was 3.9 ± 1.7 out of eight. 25(OH) D levels did not correlate with hsCRP or CIMT. While vitamin D deficiency, inflammation, and risk factors coexist at a very young age, causative mechanisms remain unclear.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1162-0
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    ABSTRACT: Cardiac examination has evolved over centuries. The goal of cardiac evaluation, regardless the era, is to "see" inside the heart to diagnose congenital and acquired intra-cardiac structural and functional abnormalities. This article briefly reviews the history of cardiac examination and discusses contemporary best, evidence-based methods of cardiac inspection.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1161-1
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    ABSTRACT: We reviewed our experience of surgical repair of Tetralogy of Fallot (TOF) in children weighing less than or equal to 4 kg to compare outcome of early palliation versus complete repair as the initial surgical approach. Seventy-six patients, weighing ≤4 kg, with TOF surgery between January 2005 and September 2013 were included in this single-center retrospective study. Twenty-five patients who underwent initial shunt procedure followed by later full repair were compared to 51 patients who had primary full repair for differences in baseline characteristics and outcomes. Shunt group patients had lower body weight, 2.76 ± 0.69 versus 3.11 ± 0.65 (kg), p = 0.03, and lower preoperative oxygen saturations, 82 ± 7 versus 90 ± 6 (%), p = 0.0001, than full repair group. A higher number of surgical procedures per patient was recorded in shunt patients, 2.29 ± 0.59 versus 1.27 ± 0.49, p = 0.00002. Thirteen of 51 patients in the full repair group required a repeat surgery. Catheterization procedures were performed in 12 patients in shunt and in 15 patients in full repair group, with interventional angioplasty in three and 11, respectively, p ≥ 0.05. Two patients, both in the shunt group, died after the surgery. Early full repair had longer hospital stay but significantly less hospitalizations 1.95 ± 1.3 versus 2.5 ± 1.4, p = 0.03. Initial complete repair of TOF in small children yielded favorable outcome with significantly less surgical procedures and subsequent hospitalizations. Cath laboratory re-interventions for residual defects were similar after both surgical approaches, and type of initial surgery does not predict freedom from re-intervention.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1163-z
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    ABSTRACT: Increasingly, more patients with univentricular heart reach adulthood. Therefore, long-term psychological features are an important concern. The aim of this study was to evaluate the clinical and psychological profile of post-Fontan adult patients and to identify the most significant determinants of quality of life. In this retrospective cross-sectional study, we reviewed the surgical and medical history of post-Fontan adult patients. Patients underwent a 24-h electrocardiogram, echocardiography and exercise testing. Self-report questionnaires were used to assess the Work Ability Index, quality of life (Satisfaction with Life Scale), perceived health status (SF-36 questionnaire), coping strategies (Brief Cope questionnaire) and presence of mood disorders (Hospital Anxiety and Depression Scale). Thirty-nine patients aged between 18 and 48 years (mean 27.5 years) were enrolled. The mean follow-up was 21.5 years. Most patients were unmarried (82.9 %), had a high school diploma (62.9 %) and were employed (62.9 %). Twenty-nine patients (82.3 %) had at least one long-term complication. The median single ventricle ejection fraction was 57 %, and the median maximal oxygen consumption was 26.8 ml/min/kg. This population tended to be anxious and to use adaptive coping strategies. Quality of life was perceived as excellent or good in 57.2 % of cases and was not related to either cardiac function or exercise capacity. Both quality of life and SF-36 domains were related to the Work Ability Index. This cohort of post-Fontan adult patients enjoyed a good quality of life irrespective of disease severity.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1156-y
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    ABSTRACT: Children born with a functional single ventricle who undergo Fontan palliation are prone to early pump failure. Whether they develop early arterial stiffness with resultant increase in afterload is not well known. We hypothesized that the aortic stiffness is higher in pediatric Fontan patients when compared to healthy controls. A prospective study was conducted at the Children's Hospital of Michigan. Twenty-two Fontan patients (aged 6-21 years) were compared with 22 healthy controls (aged 9-17 years) selected from children referred to our clinic who had normal cardiac anatomy and function on the echocardiogram. Aortic stiffness was assessed noninvasively by measuring the aortic augmentation index (AAI) using applanation tonometry (Sphygmocor, Atcor, IL). AAI was calculated as AP/PP where augmentation pressure (AP) is the increase in aortic systolic blood pressure (BP) and pulse pressure (PP) is the difference between aortic systolic and diastolic BP. Ten patients (45 %) had hypoplastic left ventricle, and 11 (50 %) had undergone aortic arch surgery. The median AAI was significantly higher in Fontan patients when compared to controls (12.5, IQR 4.8, 17.3 vs 0, IQR -6.3, 5.8; p = 0.0003). History of aortic arch surgery and single ventricle morphology did not have a significant impact on AAI. Pediatric patients who undergo Fontan palliation have significantly higher AAI, a marker of aortic stiffness and increased afterload, compared to healthy controls. Larger longitudinal studies are warranted to elucidate the possible contribution of elevated AAI on pump failure in these patients.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1151-3
  • Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1166-9
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    ABSTRACT: Sildenafil, a phosphodiesterase-5 inhibitor, is a controversial treatment option for pulmonary arterial hypertension (PAH), a significant complication of bronchopulmonary dysplasia (BPD). The objective of this study was to evaluate the use of sildenafil in infants with PAH secondary to BPD. This was a retrospective review of medical records of all premature infants with PAH associated with BPD treated with sildenafil between January 2009 and May 2013 in a level 3 neonatal intensive care unit. The primary outcomes were clinical response (20 % decreases in respiratory support score or oxygen requirements) and echocardiographic response (20 % decrease in tricuspid regurgitation gradient or change of at least 1° of septal flattening). Twenty-three infants were included in the study. Significant echocardiographic and clinical responses were, respectively, observed in 71 and 35 % of cases. Most clinical responses were observed in the first 48 h of treatment, and the median time to an echocardiographic response was of 19 days. The median dose of sildenafil used was 4.4 mg/kg/day, with a median time to reach the maximum dose of 9 days. Transient hypotension was the primary reported side effect, and it was observed in 44 % of our study population. Sildenafil treatment in patients with PAH secondary to BPD was associated with an echocardiographic improvement in the majority of patients, whereas clinical improvement was observed in a minority of patients. Many infants presented with transient hypotension during the course of the treatment. Further prospective studies are required to better assess safety and efficacy of this treatment in this population.
    Pediatric Cardiology 04/2015; DOI:10.1007/s00246-015-1154-0
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    ABSTRACT: Products of hemeoxygenase (HO)-1 have anti-inflammatory and antioxidant functions. The HO-1 promoter has a variable number of GT(n) repeats: A low number (n < 23) is associated with high transcriptional activity in response to oxidative stress. We hypothesized that the frequency of GT(n) repeats in pediatric heart failure (HF) reflects plasma biomarkers of different disease processes: the soluble receptor for advance glycation end products (sRAGE, marking cellular activation), oxLDL (oxidative stress), NGAL (impaired renal function), HIF-1α (hypoxia) and hsCRP (inflammation). Sixty HF children [aged 4-14 years, 30 with HF due to idiopathic dilated cardiomyopathy (IDCM), 30 due to chronic renal failure (CRF)] were compared to 20 healthy controls (HC). Leukocyte HO-1 GT(n) repeats were determined by PCR, plasma markers by ELISA or nephelometry. The number of GT(n) repeats in the HF patients was higher than the number of repeats in the controls, with no difference between the patient groups (p < 0.001). sRAGE, oxLDL, HIF-1α, NGAL and hsCRP were higher in both HF groups compared to HC (all p < 0.01). IDCM had higher sRAGEs and HIF-1α compared to CRF patients (p < 0.01). NGAL was higher in CRF compared to IDCM (p < 0.01). None of the plasma/serum markers correlated with the number of GT(n) repeats in any group. The number of HO-1 promoter GT(n) polymorphism is increased in both IDCM and CRF children with HF, but is unrelated to plasma markers of different pathological processes. This casts doubts on the clinical value of the number of GT(n) repeats in pediatric HF.
    Pediatric Cardiology 03/2015; DOI:10.1007/s00246-015-1146-0
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    ABSTRACT: To investigate the relationship between the risk factors associated with intravenous immunoglobulin (IVIG) non-response and the incidence of coronary artery lesions (CAL) in patients with Kawasaki disease (KD). A retrospective study was performed on clinical records of 1953 KD patients who were admitted to hospitals in Shanghai, China, between 1998 and 2007. Related clinical and laboratory findings were studied using univariate and multivariate statistical analyses. Of the 1953 KD patients, 133 (6.8 %) were unresponsive to IVIG therapy, and 356 (18.6 %) developed CAL. The incidence of CAL in the non-responsive IVIG group was significantly different from that in the responsive IVIG group (31.3 vs. 17.6 %). The incidence of IVIG non-response was significantly lower in the patients who received sufficient doses of IVIG than in the patients who received insufficient doses (5.2 vs. 18.1 %). A logistic regression analysis of 1295 patients who received sufficient IVIG doses indicated that cervical lymph node enlargement, CAL, erythrocyte sedimentation rate (ESR) ≥75 mm/h, and platelet count (PLT) ≥530 × 10(9)/L were independent risk factors of IVIG non-response. IVIG non-responders are prone to develop CAL. Initiation of therapy with sufficient IVIG doses at the early stage of the disease is crucial for preventing IVIG non-response. Lymph node enlargement, ESR ≥75 mm/h, and PLT count ≥530 × 10(9)/L are independent risk factors for predicting non-response to sufficient IVIG doses. For patients with the tendency of being unresponsive to IVIG therapy, treatment using sufficient IVIG doses combined with hormones or immunosuppressive agents should be considered to reduce the incidence of IVIG non-response and CAL.
    Pediatric Cardiology 03/2015; DOI:10.1007/s00246-015-1138-0