Relevant bibliographies by topics / Aortic override

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Academic literature on the topic 'Aortic override'

Author: Grafiati
Published: 5 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Aortic override"

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Anderson, Robert H., Diane E. Spicer, G. William Henry, Cynthia Rigsby, Anthony M. Hlavacek, and Timothy J. Mohun. "What is aortic overriding?" Cardiology in the Young 25, no. 4 (2014): 612–25. http://dx.doi.org/10.1017/s1047951114001139.

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AbstractBackground: Disagreement currently exists regarding the definition of aortic dextroposition. It is suggested that the term be used interchangeably with aortic overriding, along with suggestions that the aortic valve overrides in the normal heart. The dextroposed aorta, however, does not always override the crest of the muscular ventricular septum. It is incorrect to argue that the normal aortic valve overrides. It is the cavity of the right aortic valvar sinus, rather than the valvar orifice, that sits above the muscular septum when the septum itself is intact. Therefore, to circumvent
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2

Khan, Saad M., Nigel E. Drury, John Stickley, et al. "Tetralogy of Fallot: morphological variations and implications for surgical repair." European Journal of Cardio-Thoracic Surgery 56, no. 1 (2019): 101–9. http://dx.doi.org/10.1093/ejcts/ezy474.

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AbstractOBJECTIVESTetralogy of Fallot is characterized by anterocephalad deviation of the outlet septum, along with abnormal septoparietal trabeculations, which lead to subpulmonary infundibular stenosis. Archives of retained hearts are an important resource for improving our understanding of congenital heart defects and their morphological variability. This study aims to define variations in aortic override, coronary arterial patterns and ventricular septal defects in tetralogy of Fallot as observed in a morphological archive, highlighting implications for surgical management.METHODSThe Birmi
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3

Elsaka, O., M. A. Noureldean, Gamil M. Adel, M. T. Ghazali, Al-Razik A. H. Abd, and D. Hisham. "Tetralogy of Fallot: Diagnosis and Management." Asian Journal of Research in Medicine and Medical Science 4, no. 1 (2022): 18–31. https://doi.org/10.5281/zenodo.7636348.

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Tetralogy of Fallot is a complex heart defect characterized by the presence of a multilevel right ventricular outflow pathway, resulting in right ventricular hypertrophy and misalignment of the ventricular septal defect with aortic overlap. The pulmonary valve is usually small and dysplastic, as is the pulmonary artery. In Tetralogy of Fallot with pulmonary atresia, it represents the most advanced form of Tetralogy of Fallot, the pulmonary stress valve. Tetralogy of Fallot with the absence of a pulmonary valve is a rare form of the disease, in which only inactive remains of the pulmonary valve
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4

YEN, Chia-Hung, та Ying-Tung LAU. "17β-Oestradiol enhances aortic endothelium function and smooth muscle contraction in male spontaneously hypertensive rats". Clinical Science 106, № 5 (2004): 541–46. http://dx.doi.org/10.1042/cs20030334.

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17β-Oestradiol (E2; oestrogen) is known to increase endothelium-dependent vasodilatation and NO (nitric oxide) production. It is also known to decrease the response of VSMCs (vascular smooth muscle cells) to vasoconstrictors in vitro. E2 induces a decrease in age-related BP (blood pressure) development in MSHR (male spontaneously hypertensive rats). Whether this decrease is due to an effect on the endothelium or smooth muscle is unknown. To determine this effect, we examined the role of E2 on vascular endothelium and smooth muscle separately. We treated MSHR with E2 (2 mg·kg-1 of body weight·w
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5

Silverman, Norman H. "The essential echocardiographic features of tetralogy of Fallot." Cardiology in the Young 23, no. 6 (2013): 871–82. http://dx.doi.org/10.1017/s1047951113001704.

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AbstractThis presentation will demonstrate the essential features of tetralogy of Fallot in the infant and child before surgery, as well as some noteworthy features in the foetus. The four features, namely, subpulmonary stenosis, ventricular septal defect, aortic override, and right ventricular hypertrophy, can all be easily demonstrated by echocardiography. In addition, morphology of the pulmonary valve and the main and branch pulmonary arteries can be seen. The position of the coronary arteries and the major variants of proximal coronary anatomy can be defined. The arch anatomy and the prese
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6

Pump, Bettina, Tsutomu Kamo, Anders Gabrielsen, Peter Bie, Niels Juel Christensen, and Peter Norsk. "Central volume expansion is pivotal for sustained decrease in heart rate during seated to supine posture change." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (2001): H1274—H1279. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1274.

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During prolonged, static carotid baroreceptor stimulation by neck suction (NS) in seated humans, heart rate (HR) decreases acutely and thereafter gradually increases. This increase has been explained by carotid baroreceptor adaptation and/or buffering by aortic reflexes. During a posture change from seated to supine (Sup) with similar carotid stimulation, however, the decrease in HR is sustained. To investigate whether this discrepancy is caused by changes in central blood volume, we compared ( n = 10 subjects) the effects of 10 min of seated NS (adjusted to simulate carotid stimulation of a p
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7

Pitra, Dian Ayu Hamama, and Lydia Susanti. "Ischemic Stroke In infant With Tetralogy of Fallot." Health & Medical Journal 1, no. 1 (2019): 64–70. http://dx.doi.org/10.33854/heme.v1i1.221.

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Objectives: Although stroke is often viewed as occurring primarily in the elderly, it also strikes infants, children, young adults. Stroke in children are rare but increasingly important conditions due to the severity of their complications and diverse diagnostic differentials. It is not yet clearly understood and with multifactorial etiologies. When it comes to stroke, children are not just little adults. Stroke risk factors, symptoms, prevention efforts, and treatment are often different in children than in adults. Up to 80 % of children with ischemic stroke have cardiovascular disease. Case
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8

Hinson, Jeremiah S., Matthew D. Medlin, Kashelle Lockman, Joan M. Taylor, and Christopher P. Mack. "Smooth muscle cell-specific transcription is regulated by nuclear localization of the myocardin-related transcription factors." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 2 (2007): H1170—H1180. http://dx.doi.org/10.1152/ajpheart.00864.2006.

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On the basis of our previous studies on RhoA signaling in smooth muscle cells (SMC), we hypothesized that RhoA-mediated nuclear translocalization of the myocardin-related transcription factors (MRTFs) was important for regulating SMC phenotype. MRTF-A protein and MRTF-B message were detected in aortic SMC and in many adult mouse organs that contain a large SMC component. Both MRTFs upregulated SMC-specific promoter activity as well as endogenous SM22α expression in multipotential 10T1/2 cells, although to a lesser extent than myocardin. We used enhanced green fluorescent protein (EGFP) fusion
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9

Schmit, Bradley M., Pu Yang, Chunhua Fu, Kenneth DeSart, Scott A. Berceli, and Zhihua Jiang. "Hypertension overrides the protective effect of female hormones on the development of aortic aneurysm secondary to Alk5 deficiency via ERK activation." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 2 (2015): H115—H125. http://dx.doi.org/10.1152/ajpheart.00521.2014.

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The prevalence of aortic aneurysm is five times higher in men than women among the general population. Similar sexual dimorphism also exists in syndromic aortic aneurysms triggered by TGF-β signaling disorders. To understand the responsible mechanisms, we developed an animal model where inducible deletion of the type I TGF-β receptor, Alk5, specifically in smooth muscle cells ( Alk5 iko) causes spontaneous aortic aneurysm formation. This model recapitulated an extreme scenario of the dimorphism in aortic aneurysm development between genders. In a comparative experiment, all Alk5 iko males ( n
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10

Bowler, Meghan A., Matthew R. Bersi, Larisa M. Ryzhova, Rachel J. Jerrell, Aron Parekh, and W. David Merryman. "Cadherin-11 as a regulator of valve myofibroblast mechanobiology." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 6 (2018): H1614—H1626. http://dx.doi.org/10.1152/ajpheart.00277.2018.

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Cadherin-11 (CDH11) is upregulated in a variety of fibrotic diseases, including arthritis and calcific aortic valve disease. Our recent work has identified CDH11 as a potential therapeutic target and shown that treatment with a CDH11 functional blocking antibody can prevent hallmarks of calcific aortic valve disease in mice. The present study investigated the role of CDH11 in regulating the mechanobiological behavior of valvular interstitial cells believed to cause calcification. Aortic valve interstitial cells were harvested from Cdh11+/+, Cdh11+/−, and Cdh11−/− immortomice. Cells were subjec
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Book chapters on the topic "Aortic override"

1

Daly, M. de Burgh. "Reflex effects on the cardiovascular system: role of changes in respiration." In Peripheral Arterial Chemoreceptors and Respiratory-Cardiovascular Integration. Oxford University PressOxford, 1997. http://dx.doi.org/10.1093/oso/9780198576754.003.0006.

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Abstract In the spontaneously breathing animal, selective stimulation of the carotid bodies causes hyperventilation but often has variable effects on heart rate and systemic vascular resistance. The evidence indicates that the variable cardiovascular responses are due, at least in part, to mechanisms initiated by this hyperventilation and that when these are controlled, bradycardia and vasoconstriction in most vascular beds invariably occur. These latter responses have been designated the primary cardiac and vascular responses of carotid body stimulation. Hyperventilation modulates these responses through various mechanisms and may completely override them, although there are species differences in the extent to which this occurs. Stimulation of the aortic bodies also causes hyperventilation but the size of the response is much smaller than that resulting from the same excitatory stimulus applied to the carotid bodies.
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