Glenn Procedure in a Baby with Single Pulmonary Artery and Single Lung.
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ABSTRACT:
SUBMITTER: Ugurlucan M
PROVIDER: S-EPMC6448474 | biostudies-literature | 2018 Jul-Sep
REPOSITORIES: biostudies-literature
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Project description:BackgroundLongevity of the superior cavopulmonary connection (SCPC) is limited by the development of pulmonary arteriovenous malformations (PAVM). The goal of this study was to determine whether phenotypic changes in pulmonary artery endothelial cells (PAEC) that favor angiogenesis occur with PAVM formation.MethodsA superior vena cava to right pulmonary artery connection was constructed in 5 pigs. Pulmonary arteries were harvested at 6 to 8 weeks after surgery to establish cultures of PAEC and smooth muscle cells, to determine cell proliferation, gene expression, and tubule formation. Abundance of proteins related to angiogenesis was measured in lung tissue.ResultsContrast echocardiography revealed right-to-left shunting, consistent with PAVM formation. While the proliferation of smooth muscle cells from the right pulmonary artery (shunted side) and left pulmonary artery (nonshunted side) were similar, right PAEC proliferation was significantly higher. Expression profiles of genes encoding cellular signaling proteins were higher in PAECs from the right pulmonary artery versus left pulmonary artery. Protein abundance of angiopoietin-1, and Tie-2 (angiopoietin receptor) were increased in the right lung (both p < 0.05). Tubule formation was increased in endothelial cells from the right pulmonary artery compared with the left pulmonary artery (404 ± 16 versus 199 ± 71 tubules/mm(2), respectively; p < 0.05).ConclusionsThese findings demonstrate that PAVMs developed in a clinically relevant animal model of SCPC concomitantly with differential changes in PAEC proliferative ability and phenotype. Moreover, there was a significant increase in the angiopoietin/Tie-2 complex in the right lung, which may provide novel therapeutic targets to attenuate PAVM formation after a SCPC.
| S-EPMC3934798 | biostudies-literature
Project description:ObjectivesSevere hypoxemia in the early postoperative period after bidirectional cavopulmonary shunt (BCPS) is a critical complication. We aimed to evaluate patients who underwent additional systemic to pulmonary shunt and septation of central pulmonary artery (partial takedown) after BCPS.MethodsThe medical records of all patients who underwent BCPS between 2007 and 2020 were reviewed. Patients who underwent partial takedown were extracted and their outcomes were analyzed.ResultsOf 441 BCPS patients, 27 patients (6%) required partial takedown. Most frequent diagnosis was hypoplastic left heart syndrome (n = 14; 52%). Additional complicating factors included pulmonary artery hypoplasia (n = 12) and pulmonary venous obstruction (n = 3). Thirteen patients (48%) underwent partial takedown on the same day of BCPS, and all of them survived the procedure. The remaining 14 patients (52%) underwent partial takedown between postoperative 1 to 64 days. The reasons for partial takedown were: postoperative high pulmonary vascular resistance (n = 4), early BCPS (<90 days) with PA hypoplasia (n = 3), mediastinitis/pneumonia (n = 3), pulmonary venous obstruction (n = 2), ventricular dysfunction (n = 1), and recurrent pneumothorax (n = 1). Four patients experienced hospital deaths. Six patients died after discharge, 10 achieved Fontan completion, and 6 were alive and waiting for Fontan. Overall survival after partial takedown was 54% at 3 years. The pulmonary venous obstruction (P = .041) and genetic/extracardiac anomalies (P = .085) were identified as risks for mortality after partial takedown.ConclusionsThe partial takedown resulted in a 3-year survival rate of more than 50%. Of these patients, a significant number underwent successful Fontan completion who would exhibit potential early death with conservative treatment.
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Project description:A potential advantage of the right ventricle to pulmonary artery versus modified Blalock-Taussig shunt in patients undergoing the Norwood procedure is limitation of diastolic runoff from the systemic to pulmonary circulation. We evaluated mesenteric flow patterns and gastrointestinal outcomes following the Norwood procedure associated with either shunt type. Patients randomized to a right ventricle to pulmonary artery versus modified Blalock-Taussig shunt in the Pediatric Heart Network Single Ventricle Reconstruction Trial at centers participating in this ancillary study were eligible for inclusion; those with active necrotizing enterocolitis, sepsis, or end-organ dysfunction were excluded. Celiac artery flow characteristics and gastrointestinal outcomes were collected at discharge. Forty-four patients (five centers) were included. Median age at surgery was 5 days [interquartile range (IQR) = 4-8 days]. Median celiac artery resistive index (an indicator of resistance to perfusion) was higher in the modified Blalock-Taussig shunt group (n = 19) versus the right ventricle to pulmonary artery shunt group (n = 25) [1.00 (IQR = 0.84-1.14) vs. 0.82 (IQR = 0.74-1.00), p = 0.02]. There was no difference in interstage weight gain, necrotizing enterocolitis, or feeding intolerance episodes between the groups. The celiac artery resistive index was higher in patients with the modified Blalock-Taussig shunt versus the right ventricle to pulmonary artery shunt but was not associated with measured gastrointestinal outcomes.
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Project description:To improve the single-procedural success and long-term outcomes of catheter ablation techniques for AF, there is a need for durable, contiguous and transmural lesions encircling the pulmonary veins (PV). Measurement of contact force (CF) between the catheter tip and the target tissue can optimise ablation procedures. A new approach to obtain single-procedure durable PV isolation (PVI) using the latest CF technology combined with the CARTO VISITAG™ Module with Ablation Index (Biosense Webster) has been shown in small studies to almost eliminate recurrence of paroxysmal AF at 1-year follow up and to make PVI procedures more reproducible. The use of a standardised workflow is expected to increase the reproducibility of results and to increase the efficiency of PVI procedures.
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Project description:Cardiac catheterization associated with central vein cannulation can involve potential thrombotic and infectious complications due to multiple cannulation trials or improper placement. To minimize the risks, medical simulators are used for training. Simulators are also employed to test medical devices such as catheters before performing animal tests because they are more cost-effective and still reveal necessary improvements. However, commercial simulators are expensive, simplified for their purpose, and provide limited access sites. Inexpensive and anatomical cardiovascular simulators with central venous access for cannulation are sparse. Here, we developed an anatomically and physiologically accurate cardiovascular flow simulator to help train medical professionals and test medical devices. Our simulator includes an anatomical right atrium/ventricle, femoral and radial access sites, and considers the variability of arm position. It simulates physiological pulsatile blood flow with a setting for constant flow from 3 to 6 L/min and mimics physiological temperature (37°C). We demonstrated simulation by inserting a catheter into the system at radial/femoral access sites, passing it through the vasculature, and advancing it into the heart. We expect that our simulator can be used as an educational tool for cardiac catheterization as well as a testing tool that will allow for design iteration before moving to animal trials.
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Project description:The mechanisms responsible for thromboembolic events in children with congenital heart disease have not yet been fully elucidated. Furthermore, establishment of long-term anticoagulation therapy in Fontan patients remains controversial. Here, we report the case of a 9-year-old boy who presented with hemiparesis due to a thromboembolic stroke; the boy had previously undergone staged pulmonary artery banding and Fontan procedure. Cardiac multidetector-row computed tomography (MDCT) clearly showed the supravalvular thrombus at the roofed (blind) pulmonary valve and circulatory stasis, which could be considered a possible source of the thrombus. Follow-up CT examination showed that the thrombus disappeared, but the circulatory stasis remained. Therefore, because the risk of thrombus formation was not eliminated, anticoagulation therapy was continued for the patient. Our case indicates the possible application of cardiac MDCT for providing insight into the hemodynamic mechanisms responsible for the thromboembolic events in children with congenital heart disease.
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Project description:NFU1 is an iron-sulfur (Fe-S) scaffold protein, involved in Fe-S assembly and transfer to a range of mitochondrial metalloproteins. Patients with the NFU1G208C mutation develop pulmonary arterial hypertension (PAH) with 70% penetrance. Rats with NFU1G206C homozygous mutation demonstrated the PAH phenotype showing increased pulmonary vasculature remodeling, right ventricular (RV) hypertrophy, and RV pressure. In the present study, we discovered phenotypic metabolic changes in pulmonary arterial smooth muscle cells (PASMC) from NFU1G206C homozygous mutant rats associated with alterations in the mitochondrial proteome. Quantitative analysis of the mitochondrial proteome showed significant changes in the abundance of 208 proteins involved in various metabolic and antioxidant functions in response to the NFU1 mutation. Our data indicates that the NFU1G206C homozygous mutant rats have decreased expression of complex I and II, which are known to depend on iron-sulfur clusters, and increased expression of complexes III to V, accompanied with a significant decrease in mitochondrial function, pyruvate dehydrogenase (PDH) activity and amplified glycolysis and anabolism in PASMC. The NFU1 mutation produced a dysregulated antioxidant system in the mitochondria which leads to increased levels of reactive oxygen species. Due to alterations in apoptosis regulating proteins, the NFU1G206C cells were found to exhibit high proliferation rates and resistance to apoptosis as compared with the wild type (WT). Finally, the NFU1G206C mitochondrial proteome showed significant abundance changes in proteins that regulate fatty acid (FA) metabolism and exhibited increased FA oxidation compared to WT, suggesting increased FA oxidation compensates for the decreased PDH activity. In conclusion, our data indicates that the NFU1G206C mutation induces a metabolic shift in the PASMC, which results in a hyper-proliferative and apoptosis resistant phenotype and presents a novel cellular model to study PAH.
2021-09-08 | PXD015022 | Pride
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