The Circulating Level of Endothelial Progenitor Cells After Transcatheter Closure of Congenital Heart Disease in Children

2013 ◽  
Vol 34 (6) ◽  
pp. 1344-1349 ◽  
Author(s):  
Ming-Guo Xu ◽  
Xiang-Chun Meng ◽  
Bo-Ning Li ◽  
Cong Liu
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Congenital Heart ◽  
Transcatheter Closure ◽  
Endothelial Progenitor

scholarly journals The relationship between endothelial progenitor cells and pulmonary hypertension in children with congenital heart disease

2019 ◽  
Author(s):  
Hong-Xiao Sun ◽  
Guo-Ju Li ◽  
Zhan-Hui Du ◽  
Zhen Bing ◽  
Zhi-Xian Ji ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Pulmonary Hypertension ◽  
Heart Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Peripheral Blood ◽  
Congenital Heart ◽  
Endothelial Progenitor ◽  
High Ph ◽  
The Relationship

Abstract Background: To assess the relationship between endothelial progenitor cells (EPCs) in peripheral blood and pulmonary hypertension (PH) in children with congenital heart disease (CHD) and explore the possibility of applying EPCs to treatment of PH in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the right heart catheterization of mean pulmonary arterial pressure (mPAP) results, these cases were divided into PH groups (including high PH group, n=32, and the middle PH group, n=30) and non-PH group (n=111). We took their peripheral blood for flow cytometry, and counted the number of EPCs(CD133+/KDR+ cells). The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PH group, middle PH group and high PH group are 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the EPCs was significantly associated with a decreased risk of high PH (OR=0.37, 95%CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PH (P>0.05). Conclusion: The findings revealed that the EPCs and high PH in CHD patients correlate significantly and EPCs may become an effective treatment for PH in CHD patients.EPCs may be a protective factor of high PH for children with CHD.

Widespread endotheliopathy in adults with cyanotic congenital heart disease

2014 ◽  
Vol 25 (3) ◽  
pp. 511-519 ◽  
Author(s):  
Rachael L. Cordina ◽  
Shirley Nakhla ◽  
Shamus O’Meagher ◽  
John Leaney ◽  
Stuart Graham ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Congenital Heart ◽  
Asymmetric Dimethylarginine ◽  
Cyanotic Congenital Heart Disease ◽  
Endothelial Progenitor ◽  
Flow Mediated Dilatation

AbstractIntroduction: Cyanotic congenital heart disease is associated with functional limitation and vascular events. The nature and extent of endothelial dysfunction in cyanotic adults is poorly understood. We sought to characterise endothelial function in this setting. Methods: A total of fourteen adults with cyanotic congenital heart disease (40±3 years) together with age- and sex-matched healthy controls underwent assessment of nitric oxide-dependent vascular responses, including flow-mediated dilatation of the brachial artery and dynamic vessel analysis of the retina in response to flickering light. Plasma levels of the endothelium-derived vasoconstrictor endothelin-1 and the nitric oxide antagonist, asymmetric dimethylarginine, were measured. Circulating endothelial progenitor cells were assessed by flow cytometry. Results: Flow-mediated dilatation was significantly lower in cyanosed adults than controls (4.0±0.8 versus 7.2±1.0%, p=0.019, n=11 per group). Retinal arterial and venous dilatory responses were also impaired (2.9±0.8 versus 5.0±0.6%, p=0.05 and 3.4±0.3 versus 5.2±0.7%, p=0.04, n=13). Serum levels of endothelin-1 and asymmetric dimethylarginine were higher in cyanosed adults (3.0±0.6 versus 1.1±0.1 pg/ml, p=0.004 and 0.68±0.05 versus 0.52±0.02 μmol/L, p=0.03, n=11). Endothelial progenitor cells (CD34+CD45dimCD133+KDR+) were reduced in those with chronic cyanosis (17±4 versus 40±6 per million white blood cells, p=0.005, n=11). Conclusions: Endothelial function is impaired in the systemic arteries and retinal vessels in adults with cyanotic congenital heart disease, suggesting a widespread endotheliopathy. Diminished numbers of endothelial progenitor cells might potentially contribute to these observations.

scholarly journals The relationship between endothelial progenitor cells and pulmonary arterial hypertension in children with congenital heart disease

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Hong-Xiao Sun ◽  
Guo-Ju Li ◽  
Zhan-Hui Du ◽  
Zhen Bing ◽  
Zhi-Xian Ji ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Peripheral Blood ◽  
Congenital Heart ◽  
Pulmonary Arterial ◽  
The Relationship

Abstract Background Pulmonary arterial hypertension (PAH) caused by congenital heart disease (CHD) is very common in clinics. Some studies have shown that PAH is related to the number of endothelial progenitor cells (EPCs), but there is no report on the relationship between PAH and the number of EPCs in children with CHD. Methods In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the mean pulmonary arterial pressure (mPAP) measured by right heart catheterization, these cases were divided into PAH groups (including high PAH group, mPAP> 25 mmHg, n = 32, and the middle PAH group, 20 mmHg ≤ mPAP≤25 mmHg, n = 30) and non-PAH group (mPAP< 20 mmHg, n = 111). Peripheral blood was taken for flow cytometry, and the number of EPCs (CD133+/KDR+ cells) was counted. The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL = WBC /L × lymphocytes % × EPCs % × 10− 6. Results The median EPCs of the non-PAH group, middle PAH group and high PAH group is 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P < 0.05). After adjustment of gender, age and BMI, the number of EPCs was significantly associated with a decreased risk of high PAH (OR = 0.37, 95% CI: 0.16–0.87, P < 0.05). However, EPCs was not significantly associated with middle PAH (P > 0.05). Conclusion The findings revealed that the EPCs and high PAH in patients with CHD correlate significantly and EPCs may become an effective treatment for PAH in patients with CHD. EPCs may be a protective factor of high PAH for children with CHD.

scholarly journals The relationship between endothelial progenitor cells and pulmonary arterial hypertension in children with congenital heart disease

2019 ◽  
Author(s):  
Hong-Xiao Sun ◽  
Guo-Ju Li ◽  
Zhan-Hui Du ◽  
Zhen Bing ◽  
Zhi-Xian Ji ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Peripheral Blood ◽  
Congenital Heart ◽  
Pulmonary Arterial ◽  
The Relationship

Abstract Background: Pulmonary arterial hypertension (PAH) caused by congenital heart disease (CHD) is very common in clinics. Some studies have shown that PAH is related to the number of endothelial progenitor cells (EPCs), but there is no report on the relationship between PAH and the number of EPCs in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the mean pulmonary arterial pressure (mPAP) measured by right heart catheterization, these cases were divided into PAH groups (including high PAH group, mPAP>25mmHg, n=32, and the middle PAH group, 20mmHg≤mPAP≤25mmHg, n=30) and non-PAH group (mPAP<20mmHg, n=111). Peripheral blood was taken for flow cytometry, and the number of EPCs (CD133+/KDR+ cells) was counted. The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PAH group, middle PAH group and high PAH group is 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the number of EPCs was significantly associated with a decreased risk of high PAH (OR=0.37, 95% CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PAH (P>0.05). Conclusion: The findings revealed that the EPCs and high PAH in patients with CHD correlate significantly and EPCs may become an effective treatment for PAH in patients with CHD. EPCs may be a protective factor of high PAH for children with CHD.

scholarly journals The relationship between endothelial progenitor cells and pulmonary arterial hypertension in children with congenital heart disease

2019 ◽  
Author(s):  
Hong-Xiao Sun ◽  
Guo-Ju Li ◽  
Zhan-Hui Du ◽  
Zhen Bing ◽  
Zhi-Xian Ji ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Peripheral Blood ◽  
Congenital Heart ◽  
Pulmonary Arterial ◽  
The Relationship

Abstract Background: Pulmonary arterial hypertension (PAH) caused by congenital heart disease (CHD) is very common in clinical. Some studies have shown that PAH is related to the number of endothelial progenitor cells (EPCs), but there is no report on the relationship between PAH and the number of EPCs in children with CHD. Methods: In this study, a total of 173 cases with CHD (from 0 to 6 years old) were collected. According to the mean pulmonary arterial pressure (mPAP) measured by right heart catheterization, these cases were divided into PAH groups (including high PAH group, mPAP>25mmHg, n=32, and the middle PAH group, 20mmHg≤mPAP≤25mmHg, n=30) and non-PAH group (mPAP<20mmHg, n=111). Peripheral blood was taken for flow cytometry, and the number of EPCs(CD133+/KDR+ cells) was counted. The number of EPCs /μL of peripheral blood was calculated using the following formula: EPCs /μL =WBC /L × lymphocytes % × EPCs % × 10-6. Results: The median EPCs of the non-PAH group, middle PAH group and high PAH group is 1.86/μL, 1.30 /μL and 0.98/μL, respectively. The mPAP decreases steadily as the level of EPCs increases (P<0.05). After adjustment of gender, age and BMI, the number of EPCs was significantly associated with a decreased risk of high PAH (OR=0.37, 95% CI: 0.16-0.87, P<0.05). However, EPCs was not significantly associated with middle PAH (P>0.05). Conclusion: The findings revealed that the EPCs and high PAH in patients with CHD correlate significantly and EPCs may become an effective treatment for PAH in patients with CHD. EPCs may be a protective factor of high PAH for children with CHD

Abstract 42: In Vivo Differentiation of Epigenetically Reprogrammed Human Endothelial Progenitor Cells into Cardiomyocytes Enhances Functional and Anatomical Postinfarct Myocardial Repair

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Melissa A Thal ◽  
Prasanna Krishnamurthy ◽  
Alexander R Mackie ◽  
Eneda Hoxha ◽  
Erin Lambers ◽  
...  
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Ischemic Heart ◽  
Specific Gene ◽  
Myocardial Repair ◽  
Endothelial Progenitor ◽  
Human Cd34 ◽  
Cd34 Cells

Currently, bone marrow derived endothelial progenitor cells (human CD34+ cells, EPC) are being used clinically to improve vascularization in patients with ischemic heart disease. While it is generally accepted that CD34+ cells predominantly work through a paracrine mechanism, there exists no convincing evidence that these cells trans-differentiate into functional cardiomyocytes (CMC). Since ischemic heart disease leads to substantial loss of CMC, improving cardiomyogenic plasticity of an existing autologous cell therapy is of obvious import. EPC and CMC both differentiate from a common mesodermal progenitor however; during EC-specific lineage differentiation, CMC specific genes are epigenetically silenced. We hypothesized that reprogramming of CD34+ cells using small molecules targeting key epigenetic repressive marks may recapitulate their cardiomyogenic potential. Human CD34+ EPCs were treated with inhibitors of histone deacetylases (valproic acid) for 24 hours followed by an additional 24 hours with the DNA methyltransferase inhibitor (5-Azacytidine). This forty-eight hour treatment led to the reactivation of pluripotency associated and CMC specific mRNA expression while EC specific gene expression was maintained. Intra-myocardial transplantation of a sub-therapeutic dose of reprogrammed CD34+ cells in an acute myocardial infarction mouse model showed significant improvement in LV function compared to the same number of control CD34+ cells that are therapeutically equivalent to no treatment at all. This was histologically supported by de novo CMC differentiation. In addition to increased cardiomyogenic plasticity, drug treatment also enhanced the inherent therapeutic capacity of the CD34+ cells as shown by reduced fibrosis, increased capillary density, increased proliferation, increased cell survival and increased secretion of angiogenic factors. Taken together, our results suggest that epigenetically reprogrammed CD34+ cells are “super-CD34+ cells” that have an enhanced paracrine effect, display a more plastic phenotype and improve post-infarct cardiac repair by both neo-cardiomyogenesis and neovascularization.

Transcatheter Treatment of Aortopulmonary Window with a Symmetrical Membranous Ventricular Septal Occluder

Cardiology ◽  
2017 ◽  
Vol 138 (2) ◽  
pp. 76-79 ◽  
Author(s):  
Hai-Xia Xu ◽  
Dong-Dong Zheng ◽  
Min Pan ◽  
Xiao-Fei Li
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Congenital Heart ◽  
Surgical Intervention ◽  
Transcatheter Closure ◽  
Aortopulmonary Window ◽  
Transcatheter Device

Aortopulmonary window (APW), the presence of a communication between aorta and pulmonary artery, is a rare congenital heart disease, and surgical intervention is the standard for closure. Recently, several cases have been treated with transcatheter device occluders. Here, we report an APW patient treated successfully using a transcatheter closure with a symmetrical membranous ventricular septal occluder. We are the first to report on a case treated with this type of occluder for APW.

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