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At least 55 records · Page 3Linked to original sources
PubMed2002

[Transcatheter treatment of patent ductus arteriosus].

Isolated patent ductus arteriosus accounts for 10 to 18% of all cardiovascular malformations. Transcatheter closure of the patent ductus arteriosus has now become established practice with a high success rate and a low incidence of complications. Many devices have been proposed during the last 20 years. The use of some of these devices has largely been abandoned for different reasons: high costs, the need of large transvenous sheaths and the high incidence of late residual shunts. The devices currently available (Amplatzer duct occluder, buttoned device, DuctOcclud coil, Gianturco-Grifka vascular occlusion device, detachable coils) render the embolization of a patent ductus arteriosus relatively easy, with a short hospital stay. We feel that this is the treatment of choice for the majority of patients with a patent ductus arteriosus. The aim of this article was to review our experience and report the state-of-the-art in transcatheter patent ductus arteriosus therapy.

Balloon Occlusion↗
PubMed2005

Rupture of fetal ductus arteriosus aneurysm.

BACKGROUND: Ductus arteriosus aneurysm is a rare fetal disorder. CASE: A 35-year-old primigravida had an uneventful antenatal course. Ultrasound examination at 30 weeks of gestation revealed hydramnios. The fetal ductus arteriosus became saccular and dilated with turbulent flow and diameter of 2.5 cm. It was located at the left upper thorax, just distal to the pulmonic valve and extended to the thoracic aorta. A ductus arteriosus aneurysm was diagnosed prenatally. Five days after diagnosis, preterm labor occurred, and dexamethasone and terbutaline were administered. Six hours after initiation of terbutaline, the fetal heart rate suddenly dropped to 90 beats per minute (bpm). A bedside ultrasound examination performed immediately showed profound bradycardia. The aneurysm became a heterogeneous hypoechoic mass with no pulsation, and the fetal heart rate suddenly disappeared. CONCLUSION: Ductus arteriosus aneurysm can be diagnosed prenatally, and terbutaline or dexamethasone may be associated with a risk for rupture.

Adult↗
PubMed1988

Hyaluronic acid accumulation and endothelial cell detachment in intimal thickening of the vessel wall. The normal and genetically defective ductus arteriosus.

The closing ductus arteriosus (DA) was studied as a model for the development of intimal thickening of vessel walls using ultrastructural and immunohistochemical techniques. The material consisted of DA from neonatal dogs of three types: normal beagles, DA-defective pups from a line of mixed poodles with a genetic defect in the closure of the DA leading to persistent ductus arteriosus (PDA line), and normal litter-mates of DA-defective pups in the PDA line. The DA of the normal litter-mates of DA-defective pups did not differ from those of normal beagles. In the DA of normal beagles and normal PDA-line pups, closure is preceded by intimal thickening characterized by formation of a widened subendothelial region (SR), detachment of endothelial cells, invagination of endothelial cells, and migration of smooth muscle cells into the SR. It was observed that immediately before and after endothelial cell detachment, there was an increase in hyaluronic acid (HA) in the SR and inner media. In the DA-defective pups, the increase in hyaluronic acid failed to occur and there was no intimal thickening. The SR failed to expand, endothelium remained attached to the internal elastic membrane, and there was no invagination of endothelium or migration of smooth muscle cells. It is hypothesized that the increased synthesis of HA is an important early event leading to intimal thickening in the normal DA and perhaps to abnormal intimal thickening of other vessels. By its hygroscopic properties, HA may be directly involved in the formation of a wide SR, inducing endothelial cell detachment and favoring smooth muscle cell migration. In affected pups of the PDA line, there is a genetically-determined "block" in the normal process of intimal thickening at or before the initiation of increased HA synthesis.

Animals↗
PubMed1978

Histopathology of the ductus arteriosus after prostaglandin E1 administration in ductus dependent cardiac anomalies.

The histology of the ductus arteriosus was studied after prostaglandin E1 (PGE1) administration in 4 infants with ductus dependent cardiac malformations. Pronounced pathological changes were found in each instance. The changes consisted of oedema of the media with separation of medial components by clear spaces, pathological interruptions of the internal elastic lamina, and intimal lacerations, some of which extended into the media. The findings suggest that PGE1 administration has a profound weakening effect on the structure of the wall of the ductus arteriosus, rendering the vessel prone to laceration.

Ductus Arteriosus↗
PubMed2006

Mechanisms regulating the ductus arteriosus.

A patent ductus arteriosus (PDA) results in increased pulmonary blood flow and redistribution of flow to other organs. Several co-morbidities (i.e., necrotizing enterocolitis, intracranial hemorrhage, pulmonary edema/hemorrhage, bronchopulmonary dysplasia, and retinopathy) are associated with the presence of a PDA, but whether or not a PDA is responsible for their development is still unclear. In this review, comparative physiology between the full term and preterm newborn and the barriers preventing the necessary cascade of events leading to permanent constriction of the PDA are reviewed.

Animals↗