scholarly journals Left ventricular dysfunction after open repair of simple congenital heart defects

1998 ◽  
Vol 116 (5) ◽  
pp. 881-883 ◽  
Keyword(s):  
Congenital Heart Defects ◽  
Left Ventricular Dysfunction ◽  
Congenital Heart ◽  
Ventricular Dysfunction ◽  
Open Repair ◽  
Heart Defects ◽  
Left Ventricular

Congenital heart defects and left ventricular non-compaction in males with loss-of-function variants inNONO

2016 ◽  
Vol 54 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Daryl A Scott ◽  
Andres Hernandez-Garcia ◽  
Mahshid S Azamian ◽  
Valerie K Jordan ◽  
Bum Jun Kim ◽  
...  
Keyword(s):  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Left Ventricular ◽  
Loss Of Function

scholarly journals Left Ventricular Noncompaction Is More Prevalent in Ventricular Septal Defect Than Other Congenital Heart Defects: A Morphological Study

2020 ◽  
Vol 7 (4) ◽  
pp. 39
Author(s):  
Laís Costa Marques ◽  
Gabriel Romero Liguori ◽  
Ana Carolina Amarante Amarante Souza ◽  
Vera Demarchi Aiello
Keyword(s):  
Ventricular Septal Defect ◽  
Congenital Heart Defects ◽  
Morphological Study ◽  
Congenital Heart ◽  
Septal Defect ◽  
Heart Defects ◽  
Atrioventricular Septal Defect ◽  
Left Ventricular ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction

Left ventricular noncompaction (LVNC) is a condition characterized by prominent ventricular trabeculae and deep intertrabecular recesses and has been described as a possible substrate for arrhythmias, thromboembolism, and heart failure. Herein, we explored the prevalence of LVNC morphology among hearts with congenital heart defects (CHD). We examined 259 postnatal hearts with one of the following CHD: isolated ventricular septal defect (VSD); isolated atrial septal defect (ASD); atrioventricular septal defect (AVSD); transposition of the great arteries (TGA); isomerism of the atrial appendages (ISOM); Ebstein’s malformation (EB); Tetralogy of Fallot (TF). Eleven hearts from children who died of non-cardiovascular causes were used as controls. The thickness of the compacted and non-compacted left ventricular myocardial wall was determined and the specimens classified as presenting or not LVNC morphology according to three criteria, as proposed by Chin, Jenni, and Petersen. Normal hearts did not present LVNC, but the CHD group presented different percentages of LVNC in at least one diagnostic criterium. The prevalence of LVNC was respectively, according to Chin’s, Jenni´s and Petersen´s methods: for VSD—54.2%, 35.4%, and 12.5%; ASD—8.3%, 8.3%, and 8.3%; AVSD—2.9%, 2.9%, and 0.0%; TGA—22.6%, 17%, and 5.7%; ISOM—7.1%, 7.1%, and 7.1%; EB—28.6%, 9.5%, and 0.0%; TF—5.9%. 2.9%, and 2.9%. VSD hearts showed a significantly greater risk of presenting LVNC when compared to controls (Chin and Jenni criteria). No other CHD presented similar risk. Current results show some agreement with previous studies, such as LVNC morphology being more prevalent in VSDs. Nonetheless, this is a morphological study and cannot be correlated with symptoms or severity of the CHD.

scholarly journals Impact of 3D Printing on Short-Term Outcomes of Biventricular Conversion From Single Ventricular Palliation for the Complex Congenital Heart Defects

2021 ◽  
Vol 8 ◽  
Author(s):  
Bozhong Shi ◽  
Yanjun Pan ◽  
Weiru Luo ◽  
Kai Luo ◽  
Qi Sun ◽  
...  
Keyword(s):  
3D Printing ◽  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Vena Cava ◽  
Left Ventricular ◽  
Long Term Results ◽  
Short Term ◽  
The Mean

Background: Although Fontan palliation seems to be inevitable for many patients with complex congenital heart defects (CHDs), candidates with appropriate conditions could be selected for biventricular conversion. We aimed to summarize our single-center experience in patient selection, surgical strategies, and early outcomes in biventricular conversion for the complex CHD.Methods: From April 2017 to June 2021, we reviewed 23 cases with complex CHD who underwent biventricular conversion. Patients were divided into two groups according to the development of the ventricles: balanced ventricular group (15 cases) and imbalanced ventricular group (8 cases). Early and short-term outcomes during the 30.2 months (range, 4.2–49.8 months) follow-up period were compared.Results: The overall mortality rate was 4.3% with one death case. In the balanced ventricular group, 6 cases received 3D printing for pre-operational evaluation. One case died because of heart failure in the early postoperative period. One case received reoperation due to the obstruction of the superior vena cava. In the imbalanced ventricular group, the mean left ventricular end-diastolic volume was (33.6 ± 2.1) ml/m2, the mean left ventricular end-diastolic pressure was 9.1 ± 1.9 mmHg, and 4 cases received 3D printing. No death occurred while one case implanted a pacemaker due to a third-degree atrioventricular block. The pre-operational evaluation and surgery simulation with a 3D printing model helped to reduce bypass time in the balanced group (p < 0.05), and reduced both bypass and aorta clamp time in the imbalanced group (p < 0.05). All patients presented great cardiac function in the follow-up period.Conclusion: Comprehensive evaluation, especially 3D printing technique, was conducive to finding the appropriate cases for biventricular conversion and significantly reduced surgery time. Biventricular conversion in selected patients led to promising clinical outcomes, albeit unverified long-term results.

Abstract 436: Maternal Pregestational Diabetes Alters Fetal Gene Regulatory Program to Cause Spectrum of Congenital Heart Defects

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Corrin Mansfield ◽  
Sathiyanarayanan Manivannan ◽  
Xinmin Zhang ◽  
Madhav K Kodigepalli ◽  
Vidu Garg ◽  
...  
Keyword(s):  
Congenital Heart Defects ◽  
Congenital Heart ◽  
Heart Defects ◽  
Neural Crest Cell ◽  
Left Ventricular ◽  
Fine Tuning ◽  
Endothelial Cell Proliferation ◽  
Left Ventricular Myocardium ◽  
Depth Analysis ◽  
Regulatory Program

Maternal pre-gestational diabetes results in range of congenital malformations with significantpreponderance of congenital heart defects (CHD). We and others have previously demonstratedthat maternal high glucose (HG) acts as primary teratogen in diabetes and in combination withgenetic susceptibility loci, it increases the incidence of CHD ranging from mild ventricular septaldefects (VSD) to complex outflow tract (OFT) abnormalities. However, the underlying cellularand molecular basis of maternal HG dose-response on fetal cardiac development remainselusive. In this study, we have utilized Streptozotocin-induced murine model of maternal type1diabetes and demonstrated that spectrum of CHD in HG exposed developing embryos in utero ,is dose-dependent. We have performed histological analysis of hearts at embryonic (E) day 9.5,11.5, 13.5 and 15.5 exposed to different levels of maternal HG and compared them withuntreated normoglycemic controls. Analysis of E9.5, E11.5 and E13.5 embryos displayedtrabeculation and touchdown defects, thinning of right and left ventricular myocardium, VSD,OFT misalignment, double outlet right ventricle with increasing levels of maternal glucose.Whereas, E15.5 embryos exposed to maternal HG exhibited VSD, cardiac hypertrophy andhyper-trabeculation phenotypes in comparison to normoglycemic controls. To test cell-specificgene-regulatory program in response to hyperglycemia stress, we performed in vivo 10X singlecell transcriptomics and in vitro global RNA-sequencing on murine embryonic cell-lines culturedin normal and increasing doses of HG. RNA-seq analysis revealed differential gene expressionchanges associated with metabolic dysfunction, oxidative stress response, endothelial tomesenchymal transition, cardiomyocytes proliferation and impaired neural crest cell migration.Cardiomyocytes and endothelial cell proliferation (PHH3) and apoptosis (TUNEL) weremeasured using immunohistochemical analysis at E9.5-E15.5 embryonic hearts exposed tomaternal HG. In summary, more in-depth analysis of this study is warranted to indicate howmaternal intrauterine hyperglycemic environment disrupts the fine tuning of fetal cardiogenicgene/epigenetic program to cause CHD.

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