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PubMed1984

Urinary excretion rates of 6-keto-PGF1 alpha in preterm infants recovering from respiratory distress with and without patent ductus arteriosus.

Patency of the ductus arteriosus in preterm infants is mediated by vasodilating prostanoids; however, reliable methods to monitor prostanoid activity or production in preterm infants are lacking. We measured the excretion rates of major and characteristic urinary metabolites of prostacyclin (PGI2), PGE1, and PGE2, 6-keto-PGF1 alpha, and 7 alpha-hydroxy-5,11-diketotetranorprostane-1,16-dioic acid (PGE-M), respectively. Besides these parameters which reflect total body prostanoid turnover and production, the urinary levels of PGE2 and PGF2 alpha, the primary prostaglandins, were measured as an index of renal prostanoid synthesis. There were four study groups. One contained 11 thriving preterm infants; a second, six preterm infants with respiratory distress syndrome (RDS); a third, 30 preterm infants with RDS and patent ductus arteriosus (PDA); and a fourth, nine fullterm infants. All infants with RDS required artificial ventilation. There were no significant differences in PGE-M, PGE2, and PGF2 alpha excretion rates among the various groups; however, a significant increase of the 6-keto-PGF1 alpha excretion rates was observed in the groups of infants with RDS and with and without PDA (P less than 0.01 and P less than 0.02, respectively). Spontaneous (n = 2) or indomethacin-induced (n = 6) closure of PDA was associated with weaning from the respirator and a concomitant drop into the normal and subnormal range of the excretion rates of 6-keto-PGF1 alpha (P less than 0.01) and PGE-M (P less than 0.02).

6-Ketoprostaglandin F1 alpha↗
PubMed2006

CD44-v6 expression in smooth muscle cells in the postnatal remodeling process of ductus arteriosus.

Closure of the ductus arteriosus (DA) is due to functional constriction followed by wall remodeling, with neointimal formation caused by proliferation and migration of smooth muscle cells (SMCs) from the media to subendothelium. CD44 is a surface cell proteoglycan family. Its isoform, CD44-v6, is only minimally expressed in SMCs in the media of normal arteries, but is highly expressed in SMCs in the intima and media of injured arteries (e.g., atherosclerosis). Twenty-two autopsy DA specimens, 11 from full-term babies (age range 2 days to 5 months) and 11 from premature babies (age range 3 days to 5 months), with varying degrees of ductal wall remodeling, were evaluated by immunohistochemistry using antiactin, antifibronectin-extradomain A, anti-leukocyte common antigen, anti-CD44, and anti-CD44-v6. In DA with wall remodeling, synthetic antifibronectin-extradomain A-positive SMCs were evident at the neointimal mounds, and the SMCs were highly positive for the CD44-v6 isoform, irrespective of gestational age at birth. Conversely, SMCs of either closed DAs or persistently patent DAs were CD44-v6 negative. In conclusion, the present data provide evidence that closure of DA involves synthetic SMCs highly positive for CD44-v6, and patent or closed DAs are populated by CD44-v6-negative SMCs.

Ductus Arteriosus↗
PubMed1996

Endogenous retinoic acid signaling colocalizes with advanced expression of the adult smooth muscle myosin heavy chain isoform during development of the ductus arteriosus.

During fetal development, a specialized vessel the ductus arteriosus, shunts blood from the pulmonary artery to the aorta, thus bypassing the lungs. The ductus differs primarily from the great vessels in that it is a muscular rather than an elastic artery, and the etiology of this differential development remains controversial. We present evidence that retinoic acid (RA) may contribute to the unique muscle phenotype of the ductus arteriosus. Using a transgenic mouse carrying an RA response element-lacZ transgene that expresses beta-galactosidase (beta-gal) in response to endogenous RA signals during embryonic and fetal development, we observe a strong beta-gal signal in the ductus arteriosus. By immunofluorescence, this signal colocalizes with the expression of the adult-specific smooth muscle myosin heavy chain isoform, SM2. The beta-gal signal is present throughout fetal development and persists in the neonate until the ductus arteriosus is completely closed. beta-Gal-positive cells are first detected by immunofluorescence at 13.5 days postcoitum (dpc) in the mesenchyme surrounding the ductus. By 15.5 dpc, very intense beta-gal staining localizes to the ductus arteriosus but is absent or minimal in the pulmonary trunk and aortic arch; by 17.5 dpc, the smooth muscle layers of the tunica media in the ductus arteriosus exhibit positive beta-gal staining. Immunostaining with antibodies against smooth muscle myosins shows that, while SM1 is expressed in all embryonic vessels, SM2 is precociously expressed in the ductus arteriosus. Furthermore, SM2 expression can be detected in the ductus as early as 15.5 dpc. In the neonate, the beta-gal signal persists in the smooth muscle layer of the ductus and immunostaining colocalizes with SM2 expression. These data suggest that RA may play a role in inducing and maintaining smooth muscle differentiation in the developing ductus arteriosus and may promote precocious expression of the adult vascular phenotype.

Animals↗
PubMed2002

Silent and audible persistent ductus arteriosus: an angiographic study.

Persistent ductus arteriosus (PDA) murmurs become silent probably due to the direction of the jet across the ductus arteriosus when entering the pulmonary artery. Out of 15 children with silent PDA, 14 demonstrated a ductal flow not contacting and away from the anterior wall of the main pulmonary artery. In 15 children with a continuous murmur caused by a PDA, 12 exhibited a ductal flow toward and reaching the anterior wall of the MPA. There was no correlation between the presence of a murmur and the size of the arterial duct in this study.

Angiography↗
PubMed1988

Patent ductus arteriosus in the elderly.

Patent ductus arteriosus presenting in an elderly patient is unusual. This report describes the oldest patient (72 years) to undergo successful surgical interruption of a patent ductus arteriosus with a unique clinical presentation of typical angina pectoris with normal coronary anatomy. A possible pathophysiologic mechanism for this previously unreported presenting symptom is proposed. The natural history of patent ductus arteriosus and the role of surgery in the elderly patient are discussed.

Aged↗
PubMed1991

Doppler ultrasound and the silent ductus arteriosus.

A clinically undetectable, small ductus arteriosus was identified by Doppler ultrasonography in 21 individuals. Infants were excluded from the study and no patient had pulmonary hypertension. Persistence of the ductus arteriosus is likely to be more common than shown by less sensitive diagnostic methods. Some patients considered to have infective endocarditis with a normal heart may have a silent ductus arteriosus. Evidence of such an association would justify ligation or antibiotic cover as prophylactic measures.

Adolescent↗
PubMed1981

Prostaglandins and the ductus arteriosus.

Fetal patency of the ductus arteriosus is an active state maintained by the relaxant action of a prostaglandin, most probably prostaglandin E2. This PG mechanism is most active in the immature ductus and decreases toward term. The ductus closes when this prostaglandin effect if withdrawn. Indomethacin may induce closure of the patent ductus arteriosus of prematurity. It is most likely to be successful if given intravenously and early in postnatal life. Prostaglandin E1, to maintain patency of the ductus, is now established in the emergency management of several congenital heart defects causing problems in the newborn.

Animals↗
PubMedDate not supplied

Patent ductus arteriosus in neonates.

Patency of the ductus arteriosus is one of the more common problems of the neonate. Although the ductus arteriosus usually closes within the first days of life, persistent patency can complicate the clinical status of a newborn. The ductus arteriosus also may play a role in the pathophysiology of persistent pulmonary hypertension of the newborn and in some forms of congenital heart disease. Diagnosis of patent ductus arteriosus can be suspected clinically but should be verified by echocardiography before treatment. Accurate diagnosis, early intervention and proper treatment are necessary to decrease the immediate risks and minimize the potential for long-term complications.

Contraindications↗
PubMed1994

Thoracoscopic clipping and ligation of a patent ductus arteriosus.

Several techniques of patent ductus arteriosus occlusion primarily by thoracotomy have been practiced. They have shown to be more reliable than nonsurgical procedures. Videothoracoscopy has been useful in several intrathoracic surgical procedures with faster recovery and minimal mortality and morbidity. We report 2 patients with clipping and ligation of a patent ductus arteriosus by a thoracoscopic approach. This technique may be useful in children with a noncomplicated patent ductus arteriosus. It allows an easier recovery and causes less pain.

Child↗
PubMed2003

[False aneurysm complicating ligation of patent ductus arteriosus operated on successfully].

Postoperative aneurysm of ductus arteriosus is a rare complication but may be lethal without treatment. It is less frequent than spontaneous aneurysm of ductus arteriosus. We report the case of 5 years-old girl who underwent a ligation of patent ductus arteriosus complicated, 6 months later, with a false aneurysm of ductus arteriosus and endocarditis of the ductus and the aortic valve. The diagnosis of the aneurysm was suspected on the anteroposterior chest X-ray which showed a left superior mediastinal opacity and confirmed by echocardiography. Through bilateral thoracotomy, an anevrismorraphy and aortic repair was carried out without problem. The postoperative course was unremarkable.

Aneurysm, False↗
PubMed2000

Historical Aspects of Transcatheter Closure of the Patent Ductus Arteriosus.

The patent ductus arteriosus was the first congenital cardiac lesion to undergo successful closure in the cardiac catheterization laboratory. Porstmann in 1966 reported the successful closure of the ductus with an Ivalon foam plug. Since then numerous devices have been used to close the ductus. For the smaller ductus (< 4 mm in diameter), the Gianturco coil is now routinely used. For a ductus more than 4 mm in diameter, the devices used are currently undergoing clinical trials.

Journal Article↗
PubMed2000

Molecular determinants of atrial and ventricular septal defects and patent ductus arteriosus.

Septation defects and patent ductus arteriosus are the most common human cardiovascular malformations (CVMs). Genetic factors play a major part in the origin of these malformations. Recent molecular analyses have shed light on several mendelian forms. In the autosomal dominant Holt-Oram syndrome, both atrial and ventricular septal defects are inherited in association with limb deformity as a result of mutations in the gene encoding the TBX5 transcription factor. Mutations in the NKX2.5 transcription factor gene cause autosomal dominant familial atrial septal defects in association with progressive atrioventricular block as well as complex congenital heart disease. Common atrial syndromes in autosomal dominant Ellis-van Creveld syndrome arise in the context of axial skeletal and limb malformation as a result of mutations in the EVC gene, whose function is unknown. Patent ductus arteriosus occurs in several syndromic forms of congenital heart disease, including Holt-Oram syndrome. Recent analyses of autosomal dominant Char syndrome, which includes, with variable penetrance, patent ductus arteriosus as well as craniofacial and hand malformations, have shown that the syndrome is caused by mutations in the TFAP2B transcription factor gene. Ongoing analyses are poised to determine the contribution of these genes as well as others yet to be identified to common, sporadic forms of congenital heart disease.

Abnormalities, Multiple↗
PubMed1985

Histologic studies on normal and persistent ductus arteriosus in the dog.

The process of anatomic closure of the ductus arteriosus was studied at the ultrastructural level in 15 normal beagles (age 0 hour to 13 days) and in 18 specimens from a strain of dogs with hereditary persistent ductus arteriosus (age 4 hours to 27 days). Normal ductal closure takes place from the pulmonary artery to the aortic end. It is accompanied by a series of histologic changes: 1) separation of the endothelial cells from the internal elastic lamina resulting in a wide region of subendothelial edema; 2) ingrowth and infolding of endothelial cells and migration of undifferentiated smooth muscle cells from the inner media into the subendothelial region; 3) apposition of endothelial cells bordering the lumen; and 4) degenerative changes. In persistent ductus arteriosus, these changes do not occur. The endothelial cells remain closely adhered to the internal elastic lamina and the underlying media is abnormal in structure. In the case of partial persistent ductus arteriosus (ductus diverticulum), both the normal and the abnormal type of wall are found in a single ductus arteriosus. The histologic features of the normal and the persistent ductus arteriosus in the dog resemble those of the normal and the persistent ductus arteriosus in humans, suggesting a similar pathogenesis.

Animals↗
PubMed1982

Indomethacin and the preterm infant with a patent ductus arteriosus: relationship between plasma concentration and ductus closure.

The relationship of indomethacin pharmacokinetics to clinical and echocardiographic evidence of closure of the patient ductus arteriosus (PDA) is described in 9 preterm infants. PDA closures occurred in 4 infants when peak indomethacin plasma concentrations were 0.71-1.10 micrograms/ml, mean 0.93 +/- 0.16 microgram/ml. With partial or no PDA response to oral treatment, the peak concentrations were 0.20-0.69 microgram/ml, mean 0.57 +/- 0.08 microgram/ml, p less than 0.01. The left atrial size in the study infants correlated inversely with the indomethacin peak concentrations, r = 0.75. The plasma apparent terminal half-life correlated with postnatal age, r = 0.75. All patients with peak concentrations greater than 0.50 microgram/ml had transient oliguria. This study suggests that a minimum indomethacin concentration may be needed to promote PDA constriction.

Bacterial Infections↗
PubMed1984

Decreased contractility of the ductus arteriosus in experimental pulmonic stenosis.

Delayed closure of the ductus arteriosus after birth has been observed in newborn infants with critical pulmonic stenosis and in newborn lambs with experimental pulmonic stenosis. This delayed ductal closure may be caused by a decreased ability of the muscle to contract when exposed to oxygen or to an increased production of or sensitivity to prostaglandin (PG) E2, the endogenous ductus arteriosus vasodilator. To determine whether the abnormal hemodynamic pattern during fetal life associated with pulmonic stenosis alters the responsiveness of the ductus arteriosus, we operated on 10 fetal lambs of gestational ages 70 to 77 days (term is 148 days) and placed a band around the pulmonary artery. Catheterization at 137 to 142 days showed severe pulmonic stenosis. We then studied isolated rings of ductus arteriosus from these lambs. The oxygen-induced increase in tension in rings of ductus arteriosus from lambs with pulmonic stenosis was significantly decreased (2.55 +/- 0.38; n = 10) compared with rings from control lambs (4.03 +/- 0.51; n = 6, p less than .03). There was no difference between the two groups in either the amount of PGE2 released by the rings or in the sensitivity (expressed as median effective dose) of the rings to PGE2. There was also no difference in the increase in tension when endogenous PGE2 was inhibited by indomethacin. We conclude that delayed closure of the ductus arteriosus in lambs with experimental pulmonic stenosis is not caused by increased sensitivity to or production of PGE2 in the ductus arteriosus (as it is in premature lambs) but rather is the result of a diminished ability of the ductus arteriosus to contract when exposed to oxygen.

Animals↗
PubMed1994

Percutaneous closure of the small patent ductus arteriosus using occluding spring coils.

OBJECTIVES: This report summarizes our experience with the use of occluding spring coils to close the small patent ductus arteriosus. BACKGROUND: Several patent ductus arteriosus occluders (most notably the Rashkind device) have been developed and studied. Occluding spring coils have been used to close abnormal vessels and vascular connections. We previously reported the use of occluding spring coils to close the small patent ductus arteriosus in a small group of patients. This report describes our series of patients having patent ductus arteriosus closure with occluding spring coils. METHODS: Between June 1990 and June 1993, 30 patients underwent cardiac catheterization to have patent ductus arteriosus closure by occluding spring coils. Selection criteria were age > 6 months and narrowest patent ductus arteriosus internal dimension < or = 3.0 mm by color flow imaging. Definitive selection was based on review of aortograms performed at catheterization. A 5.2F coronary catheter was used to deliver one or two standard occluding spring coils. A loop was delivered in the main pulmonary artery, and the remainder of the coil was delivered across the patent ductus arteriosus and into the aortic diverticulum. Patent ductus arteriosus closure was confirmed by aortography or color flow imaging, or both. Follow-up after coil placement occurred at 6 weeks and 6 months and included two-view chest radiography, echocardiography and color flow imaging. RESULTS: Of the 30 patients, 29 had successful implantation by one (27 patients) or two (2 patients) occluding spring coils. Of these 29 patients, 19 had a clinically apparent and 10 had a silent patent ductus arteriosus. Average ductus minimal internal dimension was 1.7 mm (range 1.0 to 3.0). Complete closure of the ductus was confirmed in 27 patients by aortography or color flow imaging or both (in 24 within 4 h, in 2 after 6 weeks and in 1 after 6 months). Six weeks after implantation, two patients had a tiny residual patent ductus arteriosus noted on color flow imaging. One patient did not have successful implantation. This patient had a 3.2-mm ductus, and two coils migrated to the distal left pulmonary artery and could not be retrieved. There were no deaths or any significant complications noted during early or late follow-up in these patients. CONCLUSIONS: Occluding spring coils may have additional application in closing the small patent ductus arteriosus.

Aortography↗
PubMed2006

Consequences of delayed surgical closure of patent ductus arteriosus in very premature infants.

BACKGROUND: Surgical closure of ductus arteriosus is commonly indicated in premature newborns. The aim of this study was to assess short-term and mid-term effects of delayed surgical closure of the ductus arteriosus on respiratory and digestive outcome in extremely preterm infants. METHODS: We retrospectively studied 58 infants less than 28 weeks gestational age who underwent surgical closure of ductus arteriosus between January 1997 and December 2002. Nine infants with intrauterine growth restriction and major congenital malformation were excluded from the study. Criteria for surgical closure of ductus arteriosus were: (1) medical treatment failure (ie, indomethacin or ibuprofen) and (2) hemodynamically patent ductus arteriosus: systemic arterial pressure less than gestational age in mm Hg, heart failure, left atrial-aortic root ratio greater than 1.6, mean velocity in the left pulmonary artery greater than 0.6 m/s, and ductus arteriosus diameter greater than 3 mm. Infants were divided into two groups: (1) the early group who had surgery before 21 days of life (n = 31), and (2) the late group who had surgery after 21 days of life (n = 27). Preoperative and postoperative criteria were compared between the two groups (ie, gestational age, birth weight, hemodynamic, ventilatory, and echographic [left atrial-aortic root ratio, mean velocity in the left pulmonary artery] parameters). RESULTS: Preoperative gestational age and birth weight did not differ between the two groups. In the early group, gestational age was 26 weeks (range, 23 to 28 weeks and birth weight was 800 g (range, 630 to 1,240 g). In the late group, gestational age was 26 weeks (range, 24 to 28 weeks) and birth weight was 840 g (530 to 1,130 g). Hemodynamic, ventilatory, and echographic parameters were similar in both groups. Rate of bronchopulmonary dysplasia was similar in both groups. However, at 24 hours post surgery, median FiO2 was higher in the late group (28% [range, 21% to 65%]) than in early group (21% [range, 21% to 60%]) (p < 0.05). Furthermore, full oral feeding was acquired later in the late group (57 days of life [range, 30 to 136 days]) than in the early group (37 days of life [range, 27 to 84 days]) (p < 0.01), and body weight at 36 weeks of post-conceptional age was higher in the early group at 1,800 g (range, 1,250 to 2,750 g) than in the late group at 1,607 g (1,274 to 2,200 g) (p < 0.05). CONCLUSIONS: Our findings show that early surgical closure of the ductus arteriosus (< 3 weeks of life) is associated with shortened delay for full oral feeding and improved body growth when compared with late surgical closure (> 3 weeks of life).

Combined Modality Therapy↗