Increased circulating big endothelin-1, endothelin-1 and atrial natriuretic peptide in infants and children with heart failure secondary to congenital heart disease

Yeh, Jwu‐Lai; Hsu, Jong‐Hau; Dai, Zen‐Kong; Liou, Shwu-Fen; Chen, Ing‐Jun; Wu, Jiunn‐Ren

doi:10.1016/j.ijcard.2004.09.010

Cited by 12 publications

(12 citation statements)

References 27 publications

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“…[5][6][7][8] We have previously demonstrated the effects of increased pulmonary flow on ET-1 in animals with left to right shunt and in children with CHF caused by CHD. 17,18) The present study shows that plasma concentrations of CGRP are significantly elevated in relation to the clinical severity of CHF. Moreover, we have also demonstrated that increased pulmonary arterial pressure caused by left to right shunt correlates with increased plasma levels of CGRP.…”

Section: Discussionsupporting

confidence: 52%

Increased Circulating Calcitonin Gene-Related Peptide in Congestive Heart Failure Caused by Congenital Heart Disease

et al. 2005

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SUMMARYCalcitonin gene-related peptide has potent vasodilatory and inotropic actions. The aim of this study was to characterize the changes in this peptide in children with varying degrees of heart failure secondary to congenital heart disease with left to right shunt and to assess its relationship to systolic pulmonary arterial pressure.Plasma calcitonin gene-related peptide levels were measured in 131 children including 13 healthy ones, 43 with various degrees of heart failure secondary to congenital heart disease, and 75 with congenital heart disease without heart failure.In patients with heart failure, calcitonin gene-related peptide concentrations were markedly elevated (15.8 ± 2.1 pg/mL) as compared with healthy control subjects (7.0 ± 0.8 pg/mL, P < 0.05) or patients with congenital heart disease but without heart failure (18.6 ± 1.2 pg/mL, P < 0.01). Compared with the controls, there were highly significant stepwise increases in the calcitonin gene-related peptide levels in the mild (n = 15), moderate (n = 12), and severe (n = 16) heart failure subgroups by 1.5, 1.7 and 3.4 fold, respectively. The plasma calcitonin gene-related peptide levels also correlated directly with the pulmonary arterial systolic pressure (r = 0.515, P < 0.0001).The results of this study indicate that congestive heart failure secondary to congenital heart disease with increased pulmonary flow is associated with elevated levels of calcitonin gene-related peptide that are related to disease severity. Pulmonary overcirculation may play a role in upregulation of calcitonin gene-related peptide in congestive heart failure. (Int Heart J 2005; 46: 867-875)

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Section: Discussionsupporting

confidence: 52%

Increased Circulating Calcitonin Gene-Related Peptide in Congestive Heart Failure Caused by Congenital Heart Disease

et al. 2005

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“…ET-1 stimulates smooth muscle contraction via activation of ET A receptors. Previous studies have demonstrated an increase in plasma ET-1 in infants with PPHN (99), CDH (92), and congenital heart disease (197), suggesting that impaired ET-1 signaling contributes to pulmonary vasoconstriction in the neonatal period. Figure 2 shows the regulation of vascular tone by NO and ET-1.…”

Section: Pathogenesis Of Neonatal Pulmonary Vascular Diseasementioning

confidence: 97%

Role of Reactive Oxygen Species in Neonatal Pulmonary Vascular Disease

Wedgwood

Steinhorn

2014

Antioxidants & Redox Signaling

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Significance: Abnormal lung development in the perinatal period can result in severe neonatal complications, including persistent pulmonary hypertension (PH) of the newborn and bronchopulmonary dysplasia. Reactive oxygen species (ROS) play a substantive role in the development of PH associated with these diseases. ROS impair the normal pulmonary artery (PA) relaxation in response to vasodilators, and ROS are also implicated in pulmonary arterial remodeling, both of which can increase the severity of PH. Recent Advances: PA ROS levels are elevated when endogenous ROS-generating enzymes are activated and/or when endogenous ROS scavengers are inactivated. Animal models have provided valuable insights into ROS generators and scavengers that are dysregulated in different forms of neonatal PH, thus identifying potential therapeutic targets. Critical Issues: General antioxidant therapy has proved ineffective in reversing PH, suggesting that it is necessary to target specific signaling pathways for successful therapy. Future Directions: Development of novel selective pharmacologic inhibitors along with nonantioxidant therapies may improve the treatment outcomes of patients with PH, while further investigation of the underlying mechanisms may enable earlier detection of the disease.

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“…Of those, 38 (76%) had single morphologically right ventricles (RV), 11 (22%) had single morphologically left ventricles (LV), and one (2%) had a primitive ventricle of indeterminate morphology. Of the single RV patients, 19 had hypoplastic left heart syndrome (ten with mitral and aortic atresia, two with mitral stenosis and aortic atresia, and seven with mitral and aortic stenosis), 12 had a right dominant (unbalanced) atrioventricular canal defect, three had double-outlet RV, two had interrupted aortic arch with a large ventricular septal defect and small LV, and there was one patient each with aortic stenosis and severe LV dysfunction, or L-transposition of the great arteries with severe pulmonary stenosis and a small LV. Of the 11 patients with single LV, five had tricuspid atresia, three had pulmonary atresia with intact ventricular septum, two had double-inlet LV, and one had critical pulmonary stenosis with a small RV.…”

Section: Resultsmentioning

confidence: 99%

“…However, it has been utilized extensively in pediatric HF studies, 6 including the multicenter trials of carvedilol therapy for pediatric HF that included UVD patients, [17][18][19] and enalapril in infants with UVD. [17][18][19][20][21] As such, we considered it the most relevant outcome measure for this study.…”

Section: Discussionmentioning

confidence: 99%

High sensitivity C-reactive protein: a biomarker for heart failure in children with univentricular heart disease

Lowenthal¹,

Natal-Hernandez²,

Lowenthal³

et al. 2012

CBF

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Children with univentricular congenital heart disease are at increased risk for developing heart failure. However, detecting early heart failure in these patients is especially difficult because few objective measures have been validated in this cohort. The aim of this study is to determine the usefulness of high sensitivity C-reactive protein (hsCRP) as a biomarker for detecting heart failure in univentricular heart disease patients, and to define the impact of univentricular morphology and stage of palliation on its utility. A cross-sectional observational study of children with univentricular congenital heart disease aged 1 month to 7 years was conducted. The presence of heart failure was defined as a Ross score . 2. The association of hsCRP with heart failure was assessed using logistic regression and receiver operating characteristic curves. Of the 50 included children, 16 (32%) had clinical heart failure. A doubling of hsCRP resulted in a 0.31 unit increase in Ross score (95% confidence interval: -0.07, 0.56; P = 0.01) with a c-statistic of 68%. When stratified by ventricular morphology, the left univentricular morphology group exceeded the threshold of $75% (c-statistic = 81%) as did those at stage II of palliation (c-statistic = 85%). A cut point of $0.8 mg/mL correctly classified 75% of patients with left univentricular morphology, and 73% of patients regardless of morphology at stage II of palliation. From these results, we conclude that hsCRP is a useful biomarker of clinical heart failure in univentricular patients with left ventricular morphology at all stages of surgical palliation, and in all univentricular patients at stage II of palliation.

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Increased circulating big endothelin-1, endothelin-1 and atrial natriuretic peptide in infants and children with heart failure secondary to congenital heart disease

Cited by 12 publications

References 27 publications

Increased Circulating Calcitonin Gene-Related Peptide in Congestive Heart Failure Caused by Congenital Heart Disease

Increased Circulating Calcitonin Gene-Related Peptide in Congestive Heart Failure Caused by Congenital Heart Disease

Role of Reactive Oxygen Species in Neonatal Pulmonary Vascular Disease

High sensitivity C-reactive protein: a biomarker for heart failure in children with univentricular heart disease

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