The Experts below are selected from a list of 4338 Experts worldwide ranked by ideXlab platform
Margaret L. Kirby - One of the best experts on this subject based on the ideXlab platform.
-
Cardiac neural crest is necessary for normal addition of the myocardium to the arterial pole from the secondary heart field
Developmental biology, 2005Co-Authors: Karen L. Waldo, Mary R. Hutson, Harriett A. Stadt, Marzena Zdanowicz, Jaroslaw Zdanowicz, Margaret L. KirbyAbstract:In cardiac neural-crest-ablated embryos, the secondary heart field fails to add myocardial cells to the outflow tract and elongation of the tube is deficient. Since that study, we have shown that the secondary heart field provides both myocardium and smooth muscle to the arterial pole. The present study was undertaken to determine whether addition of both cell types is disrupted after neural crest ablation. Marking experiments confirm that the myocardial component fails to be added to the outflow tract after neural crest ablation. The cells destined to go into the outflow myocardium fail to migrate and are left at the junction of the outflow myocardium with the nascent smooth muscle at the base of the arterial pole. In contrast, the vascular smooth muscle component is added to the arterial pole normally after neural crest ablation. When the myocardium is not added to the outflow tract, the point where the outflow joins the pharynx does not move caudally as it normally should, the Aortic Sac is smaller and fails to elongate resulting in abnormal connections of the outflow tract with the caudal Aortic arch arteries.
-
Connexin 43 Expression Reflects Neural Crest Patterns during Cardiovascular Development
Developmental biology, 1999Co-Authors: Karen L. Waldo, Margaret L. KirbyAbstract:We used transgenic mice in which the promoter sequence for connexin 43 linked to a lacZ reporter was expressed in neural crest but not myocardial cells to document the pattern of cardiac neural crest cells in the caudal pharyngeal arches and cardiac outflow tract. Expression of lacZ was strikingly similar to that of cardiac neural crest cells in quail-chick chimeras. By using this transgenic mouse line to compare cardiac neural crest involvement in cardiac outflow septation and Aortic arch artery development in mouse and chick, we were able to note differences and similarities in their cardiovascular development. Similar to neural crest cells in the chick, lacZ-positive cells formed a sheath around the persisting Aortic arch arteries, comprised the Aorticopulmonary septation complex, were located at the site of final fusion of the conal cushions, and populated the cardiac ganglia. In quail-chick chimeras generated for this study, neural crest cells entered the outflow tract by two pathways, submyocardially and subendocardially. In the mouse only the subendocardial population of lacZ-positive cells could be seen as the cells entered the outflow tract. In addition lacZ-positive cells completely surrounded the Aortic Sac prior to septation, while in the chick, neural crest cells were scattered around the Aortic Sac with the bulk of cells distributed in the bridging portion of the Aorticopulmonary septation complex. In the chick, submyocardial populations of neural crest cells assembled on opposite sides of the Aortic Sac and entered the conotruncal ridges. Even though the Aortic Sac in the mouse was initially surrounded by lacZ-positive cells, the two outflow vessels that resulted from its septation showed differential lacZ expression. The ascending aorta was invested by lacZ-positive cells while the pulmonary trunk was devoid of lacZ staining. In the chick, both of these vessels were invested by neural crest cells, but the cells arrived secondarily by displacement from the Aortic arch arteries during vessel elongation. This may indicate a difference in derivation of the pulmonary trunk in the mouse or a difference in distribution of cardiac neural crest cells. An independent mouse neural crest marker is needed to confirm whether the differences are indeed due to species differences in cardiovascular and/or neural crest development. Nevertheless, with the differences noted, we believe that this mouse model faithfully represents the location of cardiac neural crest cells. The similarities in location of lacZ-expressing cells in the mouse to that of cardiac neural crest cells in the chick suggest that this mouse is a good model for studying mammalian cardiac neural crest and that the mammalian cardiac neural crest performs functions similar to those shown for chick.
-
Cardiac neural crest cells provide new insight into septation of the cardiac outflow tract: Aortic Sac to ventricular septal closure.
Developmental biology, 1998Co-Authors: Karen L. Waldo, Sachiko Miyagawa-tomita, Donna Kumiski, Margaret L. KirbyAbstract:A great deal is unclear about the process of cardiac outflow septation. Much controversy exists regarding the precise details of tissue origins and movements of various components. The contribution of the cardiac neural crest to Aorticopulmonary and distal truncal septation has been described; however, the distribution of the neural crest in the proximal outflow and heart is unknown. The present study describes the movement of cardiac neural crest cells from the caudal pharyngeal arches into the outflow tract and base of the heart during the period of outflow septation. Using quail-chick chimeras we found that the cardiac neural crest was distributed to all levels of the outflow tract and into the base of the heart. Septation of the outflow tract lumen occurred by two different processes that involved the cardiac neural crest directly. Cardiac neural crest cells were also distributed to regions of the outflow tract that correlated with sites of remodeling, such as the Aortic Sac as it was remodeled into the base of the ascending aorta and pulmonary trunk, the distal truncus that was patterned into the two semilunar valves and in the proximal conotruncus where muscularization of the ridges and septum occurred. Additionally, cardiac neural crest cells were found at the site of closure of the ventricular septum, in the wall of the pulmonary infundibulum, and transiently in the wall of the Aortic vestibule. Contrary to current thinking, not all of the condensed mesenchyme in the outflow tract during septation was derived from neural crest.
-
The diverse roles of neural crest in cardiovascular development: myocardial function, Aortic arch repatterning and outflow septation
Progress in Pediatric Cardiology, 1998Co-Authors: Margaret L. Kirby, Michael FarrellAbstract:Abstract Ablation of the cardiac neural crest in chick embryos results in abnormal remodeling of the Aortic arch arteries and absence of the cardiac outflow septum. These traditional roles of neural crest were described more than a decade ago and with the advent of molecular and transgenic techniques, we are now beginning to unravel the molecular underpinnings of these processes. Recently, it has been shown that cardiac neural crest ablation also results in defects in myocardial development that can be observed as early as stage 14, a stage at which the cardiac neural crest has not yet entered the cardiac outflow tract. These defects, which include reduced contractility, deficient excitation–contraction coupling, as determined by lowered calcium transients, and disorganized contractile apparatus, are likely due to an absence of neural crest-derived cells in the pharyngeal arch region at this stage. In normal embryos, the cardiac neural crest provides a substantial cellular partition interposed between the pharyngeal endoderm, the endothelium of the Aortic arch arteries and the Aortic Sac and the myocardium of the outflow tract. In cardiac neural crest-ablated embryos, the geometry of these elements is disturbed such that the endoderm and endothelium are apposed leaving the myocardial cuff in much closer proximity to the pharyngeal endoderm than normal. New experimental evidence suggests that neural crest cells which normally interpose between the pharyngeal endoderm and the myocardium, suppress a signal, perhaps a growth factor, produced by the pharyngeal endoderm that deleteriously affects further myocardial development.
Gilles Soulez - One of the best experts on this subject based on the ideXlab platform.
-
Aortoduodenal fistula occurring after type II endoleak treatment with coil embolization of the Aortic Sac
Journal of vascular surgery, 2003Co-Authors: Stéphane Elkouri, Jean-françois Blair, Eric Therasse, Vincent L. Oliva, Luc Bruneau, Gilles SoulezAbstract:A bifurcated stent graft device was successfully deployed to exclude an asymptomatic abdominal Aortic aneurysm (AAA) with adequate proximal Aortic neck morphology. At 6 months, a type II endoleak was successfully embolized through a proximal perigraft channel with metallic coils. The patient was seen with upper gastrointestinal bleeding and a pulsatile abdominal mass 11 months later. Surgical exploration revealed an aortoduodenal fistula in the vicinity of the previous embolization. We discuss the possible causes of this complication and review the literature on the subject. We conclude that aortoduodenal fistula can occur after endovascular AAA repair despite the absence of endoleak or AAA diameter increase on follow-up computed tomographic scan.
Michel S. Makaroun - One of the best experts on this subject based on the ideXlab platform.
-
Occult type I or III endoleaks are a common cause of failure of type II endoleak treatment after endovascular Aortic repair.
Journal of vascular surgery, 2018Co-Authors: Michael C. Madigan, Michael J. Singh, Rabih A. Chaer, Georges E. Al-khoury, Michel S. MakarounAbstract:Most type II endoleaks have a benign natural history, but 6% to 8% are associated with Sac enlargement and respond poorly to treatment. Our aim was to evaluate whether these enlargements are associated with delayed or occult type I and III endoleaks. Patients with interventions for endoleak after endovascular Aortic repair from 2000 to 2016 were reviewed retrospectively. Patient demographics, comorbidities, endoleak type, secondary procedures, Aortic Sac growth (≥5 mm), and mortality were collected. Successful treatment was defined as endoleak resolution with no further Aortic Sac growth. Secondary procedures, ruptures, endograft explant, and death were captured. There were 130 patients diagnosed with a primary type II endoleak after endovascular Aortic repair at a median of 1.3 months (interquartile range, 1.0-13.3 months). One hundred eighteen had their initial treatment for a primary type II. Twelve of the 130 were initially stable and observed, but were treated for a delayed type I or III endoleak. The 130 patients underwent 279 procedures for endoleaks (mean of 2.2 ± 1.3) over 6.9 ± 3.8 years of follow-up. Of the 118 patients treated for primary type II endoleaks, 26 (22.0%) later required interventions for delayed type I and III endoleaks. The mean time to intervention for a delayed type I or III endoleak was 5.4 ± 2.8 years. Overall, there were 16 type IA, 11 type IB, 2 type III, 7 combined type IA/IB, and 2 type IA/III delayed endoleaks. The odds of harboring a delayed type I or III endoleak was 22.0% before the first attempt at type II endoleak treatment, 35.1% before the second, 44.8% before the third, and 66.6% before the fourth attempts. Rapid Aortic Sac growth of ≥5 mm/y before initial endoleak treatment was associated with increased risk for delayed type I or III endoleak (47.8 vs 14.1%; P = .003). Patients with delayed type I or III endoleaks had a lower successful treatment rate (8.3% vs 52.3%; P = .001) than those with only type II endoleaks. Late rupture was increased with delayed type I or III endoleak (P = .002), whereas mortality (P = .96) and Aortic-related mortality (P = .46) were similar. Graft explant (P = .06) trended toward an increase with a delayed type I or III endoleak, but was not statistically significant. Failed attempts treating type II endoleaks and/or a rapid Aortic Sac growth of 5 mm/y or greater should raise the suspicion of a delayed or occult type I or III endoleak. Occult endoleaks are associated with decreased chance of endoleak resolution. Copyright © 2018 Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Deborah J. Henderson - One of the best experts on this subject based on the ideXlab platform.
-
Development of the outflow tract
Oxford Medicine Online, 2018Co-Authors: Robert H. Anderson, Nigel A. Brown, Bill Chaudhry, Deborah J. Henderson, Simon D. Bamforth, Timothy J. MohunAbstract:The definitive cardiac outflow tracts have three components: the intra-pericardial arterial trunks, the arterial roots, and the ventricular outflow tracts. Improved correlations between normal development and cardiac malformations can be obtained by analysing the developing outflow tract in tripartite fashion with proximal, intermediate, and distal components. When first seen, the walls of the entire outflow tract express myocardial markers. With ongoing development, the distal border regresses away from the edges of the pericardial cavity. Subsequently, the distal outflow tract becomes the intra-pericardial arterial trunks, with a protrusion from the dorsal wall of the Aortic Sac forming the aortopulmonary septum. The arterial valves form in the intermediate part of the outflow tract. The proximal part eventually becomes transformed into the ventricular outflow tracts, with muscularization of the proximal cushions producing the right ventricular infundibulum. This approach provides rational explanations for the congenital lesions involving the different parts of the outflow tracts.
-
Normal and abnormal development of the intrapericardial arterial trunks in humans and mice.
Cardiovascular research, 2012Co-Authors: Robert H. Anderson, Nigel A. Brown, Antoon F.m. Moorman, Bill Chaudhry, Sandra Webb, Simon D. Bamforth, Timothy J. Mohun, Darren Hoyland, Helen M. Phillips, Deborah J. HendersonAbstract:The definitive cardiac outflow channels have three components: the intrapericardial arterial trunks; the arterial roots with valves; and the ventricular outflow tracts (OFTs). We studied the normal and abnormal development of the most distal of these, the arterial trunks, comparing findings in mice and humans. Using lineage tracing and three-dimensional visualization by episcopic reconstruction and scanning electron microscopy, we studied embryonic day 9.5-12.5 mouse hearts, clarifying the development of the OFTs distal to the primordia of the arterial valves. We characterize a transient aortopulmonary (AP) foramen, located between the leading edge of a protrusion from the dorsal wall of the Aortic Sac and the distal margins of the two outflow cushions. The foramen is closed by fusion of the protrusion, with its cap of neural crest cells (NCCs), with the NCC-filled cushions; the resulting structure then functioning transiently as an AP septum. Only subsequent to this closure is it possible to recognize, more proximally, the previously described AP septal complex. The adjacent walls of the intrapericardial trunks are derived from the protrusion and distal parts of the outflow cushions, whereas the lateral walls are formed from intrapericardial extensions of the pharyngeal mesenchyme derived from the second heart field. We provide, for the first time, objective evidence of the mechanisms of closure of an AP foramen that exists distally between the lumens of the developing intrapericardial arterial trunks. Our findings provide insights into the formation of AP windows and the variants of common arterial trunk.
-
Development of the outflow tracts with reference to aortopulmonary windows and aortoventricular tunnels.
Cardiology in the Young, 2010Co-Authors: Robert H. Anderson, Nigel A. Brown, Bill Chaudhry, Deborah J. Henderson, Andrew C. Cook, Timothy J. MohunAbstract:Although malformations involving the ventricular outflow tracts are often described as conotruncal malformations, there is no consensus as to the lesions included in, or excluded from, this category, reflecting, in part, the current lack of precise definitions of the embryonic truncus and conus. Analysis of development of the outflow tract in terms of proximal, intermediate, and distal components greatly facilitates understanding of the morphology of the aortopulmonary window and aortoventricular tunnels. The aortopulmonary windows reflect failure to close the embryonic aortopulmonary foramen, the space between the distal end of the cushions that divide the lumen of the outflow tract itself and the dorsal wall of the Aortic Sac. The aortopulmonary tunnels are produced subsequent to abnormal development of the cushions themselves. The distal ends of these cushions excavate to produce the sinuses and leaflets of the arterial valves. The proximal parts of the cushions muscularise to form the subpulmonary infundibulum. The middle part of the cushion mass disappears to provide a tissue plane between the infundibulum and the Aortic root. Abnormal formation of this area accounts for the various types of aortoventricular tunnel. In our brief review, we show how the anatomy of these lesions correlates with development of the outflow tract.
-
Dual role for neural crest cells during outflow tract septation in the neural crest-deficient mutant Splotch(2H).
Journal of anatomy, 2009Co-Authors: Lucy Bradshaw, Bill Chaudhry, Victoria Hildreth, Sandra Webb, Deborah J. HendersonAbstract:Splotch(2H) (Sp(2H)) is a well-recognized mouse model of neural crest cell (NCC) deficiency that develops a spectrum of cardiac outflow tract malformations including common arterial trunk, double outlet right ventricle, ventricular septal defects and pharyngeal arch artery patterning defects, as well as defects in other neural-crest derived organ systems. These defects have been ascribed to reduced NCC in the pharyngeal and outflow regions. Here we provide a detailed map of NCC within the pharyngeal arches and outflow tract of Sp(2H)/Sp(2H) embryos and fetuses, relating this to the development of the abnormal anatomy of these structures. In the majority of Sp(2H)/Sp(2H) embryos we show that deficiency of NCC in the pharyngeal region results in a failure to stabilize, and early loss of, posterior pharyngeal arch arteries. Furthermore, marked reduction in the NCC-derived mesenchyme in the dorsal wall of the Aortic Sac disrupts fusion with the distal outflow tract cushions, preventing the initiation of outflow tract septation and resulting in common arterial trunk. In around 25% of Sp(2H)/Sp(2H) embryos, posterior arch arteries are stabilized and fusion occurs between the dorsal wall of the Aortic Sac and the outflow cushions, initiating outflow tract septation; these embryos develop double outlet right ventricle. Thus, NCC are required in the pharyngeal region both for stabilization of posterior arch arteries and initiation of outflow tract septation. Loss of NCC also disrupts the distribution of second heart field cells in the pharyngeal and outflow regions. These secondary effects of NCC deficiency likely contribute to the overall outflow phenotype, suggesting that disrupted interactions between these two cell types may underlie many common outflow defects.
Nikolaos Tsilimparis - One of the best experts on this subject based on the ideXlab platform.
-
Reversed Frozen Elephant Trunk Technique to Treat a Type II Thoracoabdominal Aortic Aneurysm.
Journal of endovascular therapy : an official journal of the International Society of Endovascular Specialists, 2016Co-Authors: E. Sebastian Debus, Tilo Kölbel, Sabine Wipper, Holger Diener, B. Reiter, Christian Detter, Nikolaos TsilimparisAbstract:To describe a hybrid technique of reversed frozen elephant trunk to treat thoracoabdominal Aortic aneurysms (TAAA) through an abdominal only approach. The technique is demonstrated in a 29-year-old Marfan patient with a chronic type B Aortic dissection previously treated with a thoracic stent-graft who presented with a thoracoabdominal false lumen aneurysm. Through an open distal retroperitoneal approach to the abdominal aorta, a frozen elephant trunk graft was implanted over a super-stiff wire upside down with the stent-graft component in the thoracic aorta. Following deployment of the stent-graft proximally and preservation of renovisceral perfusion in a retrograde manner, the renovisceral vessels were sequentially anastomosed to the elephant trunk graft branches, thus reducing the ischemia time of the end organs. The Aortic Sac was then opened, and the distal part of the hybrid graft was anastomosed with a further bifurcated graft to the iliac vessels. The reversed frozen elephant trunk technique is feasible for hybrid treatment of TAAAs via an abdominal approach only. This has the benefit of substantially reducing the trauma of thoracic exposure, thus preserving major benefits of open thoracoabdominal surgery, such as the presence of short bypasses to the renovisceral vessels and reimplantation of lumbar arteries to reduce spinal cord ischemia.
-
Remodeling of Aortic aneurysm and Aortic neck on follow-up after endovascular repair with suprarenal fixation.
Journal of vascular surgery, 2014Co-Authors: Nikolaos Tsilimparis, Anand Dayama, Joseph J RicottaAbstract:The objective of this study was to evaluate the remodeling of abdominal Aortic aneurysms after endovascular Aortic aneurysm repair (EVAR) with the Zenith (Cook Medical, Bloomington, Ind) device. This was a retrospective study of anatomic data related to characteristics of the Aortic neck diameter, iliac artery diameter, and aneurysm Sac diameter collected during a clinical study of the Zenith device. In this study, 739 patients were observed for 2 years and 158 of them were observed for 5 years. The monthly rate of change for the neck diameter was more rapid in the early postoperative period (postoperative-30 days), with an expansion of 0.7 ± 0.09 mm/month, and during the third year of follow-up (24-36 months), with a monthly expansion rate of 0.10 ± 0.24 mm. The iliac arteries were also more prone to expansion during the first postoperative month (right iliac, 0.95 ± 0.08 mm/month; left iliac, 0.91 ± 0.08 mm/month) and in the next 6 months with a monthly expansion rate of 0.18 ± 0.02 mm and 0.21 ± 0.02 mm for the right and left iliac arteries, respectively. Remodeling of the aneurysm Sac occurred mainly in the first postoperative year with a regression rate of 0.89 ± 0.05 mm/month between 1 and 6 months and 0.44 ± 0.04 mm/month for the second half of the year. The aneurysm Sac regression rate dropped to 0.2 mm/month in the second postoperative year. Changes in the Aortic neck diameter were statistically significant (P < .001) only at the 24- to 36-month postoperative interval. Changes in the Aortic Sac diameter were statistically significant (P < .001) at the 30-day to 6-month, 6- to 12-month, and 12- to 24-month intervals. Among patients who underwent reintervention, Aortic Sac expansion occurred primarily in the 24- to 36-month interval. Expansion of the Aortic neck after EVAR for the Zenith endograft occurs mainly between 24 and 36 months; Aortic aneurysm Sac regression occurs more obviously at 1 to 12 months. Iliac arteries at the landing zone expand more rapidly in the first postoperative year. Late surveillance of EVAR patients is essential to avoid late complications after Aortic remodeling. Copyright © 2015. Published by Elsevier Inc.