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Congenital Heart Disease in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, Cardio-Obstetrics, 2020
Truncus arteriosus, also known as persistent truncus arteriosus, is an uncommon cyanotic congenital heart defect, accounting for 1%–4% of cardiac heart defects in a large autopsy series [15] and 0.6–1.4 per 10,000 live births [16]. In truncus arteriosus, the main pulmonary artery or branch pulmonary arteries arise from the aorta, typically the ascending aorta. Patients nearly always have a large nonrestrictive ventricular septal defect. The truncal (aortic) valve has normal trileaflet morphology in 69%, is quadricuspid in 22%, and bicuspid in 9%. The abnormality, as well as dilation of the aorta and valve annulus, predisposes patients with truncus arteriosus to aortic regurgitation.
The cardiovascular system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Mary N Sheppard, C. Simon Herrington
In persistent truncus arteriosus the aorta and pulmonary artery arise from a common stem vessel, the truncus arising from both ventricles and overriding a ventricular septal defect. If the septum fails to develop, a single ventricular cavity results. Interatrial septal defects are also common.
Multidetector Row CT Angiography of the Thoracic Aorta
Published in Phillip M. Boiselle, Charles S. White, New Techniques in Cardiothoracic Imaging, 2007
Curtis E. Green, Jeffrey S. Klein
Persistence of the right aortic arch with atresia of the left occurs in approximately 1/2200 persons without congenital heart disease. The incidence in certain congenital anomalies such as Tetralogy of Fallot and persistent truncus arteriosus can be as high as 50%. Most persons with right aortic arch are completely asymptomatic and come to medical attention because the right arch is misdiagnosed on chest radiographs as a mediastinal mass. There are two common types of right arch: those with mirror-image branching of the great vessels (Type 1) and those with aberrant origin of the left subclavian artery (Type 2).
An update on the use of sphingosine 1-phosphate receptor modulators for the treatment of relapsing multiple sclerosis
Published in Expert Opinion on Pharmacotherapy, 2023
Laura Dumitrescu, Athanasios Papathanasiou, Catalina Coclitu, Afagh Garjani, Nikos Evangelou, Cris S. Constantinescu, Bogdan Ovidiu Popescu, Radu Tanasescu
The contraindications for fingolimod overlap with those of the other approved S1PR modulators and include myocardial infarction in the previous 6 months, unstable angina pectoris, heart failure, heart arrhythmias requiring antiarrhythmic treatment, first and second degree atrioventricular block, sick sinus syndrome without pacemaker, prolonged baseline QTc interval, stroke and transient ischemic attack, ongoing cancers, severe active infections and active chronic infections, liver impairment, and macular edema [8–10,12–16]. Considering the increased risk of spontaneous abortion and malformations, fingolimod is contraindicated during pregnancy and in female patients of fertile age that do not use effective contraception methods [8–10]. Fingolimod can cross the placenta, and may have teratogenic effect in rats (persistent truncus arteriosus and ventricular septal defects) [56]. In the clinical development fingolimod program [57] which included 89 exposed pregnancies (i.e. fingolimod ongoing at conception or 6 weeks before), spontaneous abortion occurred in 24% of pregnancies and abnormal fetal development in 7.6% of cases (slightly higher, and borderline normal, respectively, when compared to the rate registered in the general population) [57]. In another 717 pregnancies exposed to fingolimod, the prevalence of major cardiac abnormalities and spontaneous and elective abortion was comparable with that in the general population [58].
MiR-23b targets GATA6 to down-regulate IGF-1 and promote the development of congenital heart disease
Published in Acta Cardiologica, 2022
Guo-Jin Huang, Xue-Liang Xie, Yong Zou
Numerous studies have corroborated that GATA6 is expressed during heart development [27,28]. At present, it has been found that GATA6 mutations in CHD include ASD, VSD, patent ductus arteriosus, pulmonary valve stenosis, persistent truncus arteriosus, and TOF [27,29]. GATA6 is indispensable to the normal expression of the transcription factor network during the development of cardiomyocytes. Kodo et al. [13] have confirmed that GATA6 can directly regulate the brain signal protein 3 C-plexus protein A2 signal pathway, affect the normal migration of cardiac neural crest cells, resulting in abnormal development of the cardiac outflow tract. Moreover, some studies have also confirmed that GATA6 may influence the development of the heart by regulating the signal of bone morphogenetic protein 4 [30,31]. In short, GATA6 can regulate downstream target genes, thus affecting cardiac development. In our research, we found that miR-23b can target the regulation of GATA6 in cardiomyocytes, thus affecting cell proliferation and apoptosis. As a growth hormone-dependent peptide, IGF-1 plays an indispensable role in tissue growth and differentiation. According to Carlos Stocco et al. [32] and Yvonne Y. Hui et al. [21], down-regulation of GATA6 can induce the decrease of IGF-1 expression. In this study, we also confirmed this regulatory mechanism in the CHD cells.
Wider intraoperative glycemic fluctuation increases risk of acute kidney injury after pediatric cardiac surgery
Published in Renal Failure, 2018
Guo-Huang Hu, Lian Duan, Meng Jiang, Cheng-Liang Zhang, Yan-Ying Duan
During four years, the incidence of AKI was 11.5% (118/1026) in our pediatric cardiac surgery center. Of those with AKI, 53.4% (63/118), 30.5% (36/118), and 16.1% (19/118) were categorized as AKIN stages I, II, and III, respectively. The patients’ perioperative characteristics are shown in Table 1; diseases included but were not limited to tetralogy of Fallot with/without atrial septal defect, pulmonary atresia, anomalous pulmonary veins drainage, endocardial cushion defect, transposition of the great arteries, coronary artery fistula, aorta-pulmonary window, atrioventricular canal malformation, persistent truncus arteriosus, single ventricle or atrium, hypoplastic or interrupted aortic arch, and Ebstein or other valve anomalies. Before matching, the entire sample who experienced AKI were younger and cyanotic, had a higher RACHS-1 score, and less preoperative LVEF (all p < .01) when compared with those who did not experience AKI. They also underwent CPB for a longer time, longer OA time, more frequency of multiple OA, ultrafiltration, DHCA or hypoperfusion (all p < .01) during surgery. They had higher mG, pG, intraGF, IS POD, and more transfusions during the perioperative period (all p < .01).