Pediatric Cardiology and Cardiovascular Surgery: 1950-2000

Freedom, Robert M.; Lock, James E.; Bricker, J. Timothy

doi:10.1161/01.cir.102.suppl_4.iv-58

Cited by 40 publications

(34 citation statements)

References 154 publications

(88 reference statements)

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“…Indeed, the Bethesda Conference task force document on educational requirements for the care of adults with congenital heart disease reported similar estimates of formal ACHD training (b20%) for the physician workforce caring for ACHD patients [22]. The taskforce suggests ascending levels [1][2][3] of ACHD training and associated required competencies [22]. Although funded ACHD training Fellowships are available in Canada, there has been no systematic assessment of ACHD training throughout the country.…”

Section: Discussionmentioning

confidence: 99%

Structure and process measures of quality of care in adult congenital heart disease patients: A pan-Canadian study

Beauchesne

Therrien

Alvarez

et al. 2012

International Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Structure and process measures of quality of care in adult congenital heart disease patients: A pan-Canadian study

Beauchesne

Therrien

Alvarez

et al. 2012

International Journal of Cardiology

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“…M) and diethylamine NONOate (10 Ϫ7 -10 Ϫ5 M) induced dosedependent relaxation of oxygen-constricted DA (Ϫ52 Ϯ 4% and Ϫ51 Ϯ 6%, respectively) that was inhibited by the soluble guanylyl-cyclase inhibitor, 1H- [1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one (5 ϫ 10 Ϫ5 M). Sildenafil increased cyclic GMP levels.…”

Section: ϫ4mentioning

confidence: 99%

“…This has resulted in successful pharmacological manipulation of the DA (3). To date, PGE1 is the only available therapy to maintain DA patency (4). Although effective, numerous side effects are associated with PGE1 infusions (respiratory depression, fever, lethargy, irritability, myoclonic jerks, flushing, edema, pyloric stenosis, hyperostosis, necrotizing enterocolitis, and structural remodeling of the DA and the pulmonary vessels) (5,6).…”

Section: ϫ4mentioning

confidence: 99%

Sildenafil Reverses O2 Constriction of the Rabbit Ductus Arteriosus by Inhibiting Type 5 Phosphodiesterase and Activating BKCa Channels

Thébaud

Michelakis

et al. 2002

Pediatr Res

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Oxygen constriction causes functional closure of the ductus arteriosus (DA) at birth. Although DA closure is crucial for postnatal adaptation, patency of the DA is critical for survival of newborns with duct-dependent cardiac malformations. In these cases, DA patency is achieved by i.v. infusion of prostaglandin E1, which, though effective, is often associated with complications. We hypothesized that sildenafil, a specific phosphodiesterase type 5 inhibitor, is an effective DA vasodilator. In isolated DA rings from term (d 30) fetal rabbits, sildenafil (10 Ϫ6 -10 Ϫ4 M) and diethylamine NONOate (10 Ϫ7 -10 Ϫ5 M) induced dosedependent relaxation of oxygen-constricted DA (Ϫ52 Ϯ 4% and Ϫ51 Ϯ 6%, respectively) that was inhibited by the soluble guanylyl-cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (5 ϫ 10 Ϫ5 M). Sildenafil increased cyclic GMP levels. Iberiotoxin (200 nM), an inhibitor of calcium-sensitive potassium channels, decreased the vasodilatory effect of sildenafil and diethylamine NONOate (Ϫ30 Ϯ 2% and Ϫ27 Ϯ 4%, respectively). Oxygen inhibition of whole-cell K ϩ current and membrane depolarization were partially restored by sildenafil, and this was inhibited by iberiotoxin. Immunohistochemistry and immunoblotting confirmed the presence of phosphodiesterase type 5 and calcium-sensitive potassium channels in the DA smooth muscle cells. This is the first study to demonstrate that sildenafil dilates the DA by increasing soluble guanylyl-cyclase-derived cGMP levels and thereby activating calcium-sensitive potassium channels, causing membrane hyperpolarization. Sildenafil, already approved for human usage, might be an alternative or a useful adjunct to prostaglandin E1 as a bridge to cardiac surgery. The DA is a vital fetal structure that connects the pulmonary artery to the descending aorta. During fetal life, the DA shunts over half of the blood flow away from the lung into the umbilico-placental circulation, where gas exchange takes place (1). At birth, closure of the DA, essential for postnatal adaptation, is initiated by an increase in O 2 . In full-term newborns, the DA closes 24 -48 h after delivery (1). However, in newborns with duct-dependent cyanotic cardiac malformations (e.g. transposition of the great vessels) or duct-dependent aortic obstructions (including hypoplastic left heart syndrome and coarctation of the aorta), patency of the DA is critical for survival until surgery. The paramount importance of PG in the regulation of ductal tone is well established [reviewed in (2)]. This has resulted in successful pharmacological manipulation of the DA (3). To date, PGE1 is the only available therapy to maintain DA patency (4). Although effective, numerous side effects are associated with PGE1 infusions (respiratory depression, fever, lethargy, irritability, myoclonic jerks, flushing, edema, pyloric stenosis, hyperostosis, necrotizing enterocolitis,

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“…Over the past 20 years, techniques for percutaneous device placement in the management of congenital heart disease have gradually replaced many open surgical procedures, significantly increasing interventional catheterization procedures performed in the pediatric catheterization laboratory [1,2]. Compared with diagnostic catheterization procedures, interventional procedures use larger sheaths and increase the time and complexity of cases, which increase the incidence of postprocedural thrombosis in pediatric patients [3][4][5].…”

Section: Introductionmentioning

confidence: 99%