AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Background

The ductus arteriosus is a normal fetal anatomic structure that connects the systemic and pulmonary circulations. It usually closes shortly after birth; if it remains patent, the ductus arteriosus may cause heart failure that results from a large shunt into the lungs, the development of pulmonary hypertension, or endocarditis. In its isolated form, patients with patent ductus arteriosus (PDA) are frequently asymptomatic. PDA has been described in combination with virtually every other congenital heart disease, especially those that are characterized by cyanosis, in which this condition may be essential for survival. Patient age at diagnosis can vary from infancy to old age.

The diagnosis is usually made clinically and confirmed echocardiographically, although magnetic resonance imaging (MRI) can also demonstrate a PDA. Conventional treatment has been with indomethacin or similar prostaglandin synthetase inhibitors in infants or with surgical ligation or transection. In older children and adults, an increasing number of patients are treated using percutaneous techniques. Surgical treatment is very safe in children and adults unless other defects are associated.¹

For excellent patient education resources, visit eMedicine's Heart Center. Also, see eMedicine's patient education articles Coronary Heart Disease, Congestive Heart Failure, Ventricular Septal Defect, Atrial Fibrillation, and Atrial Flutter.

Pathophysiology

Normal fetal circulation has 2 major vascular shunts that connect the systemic and pulmonary circulations: the ductus arteriosus and the ductus venosus. The ductus arteriosus is the portion of the sixth aortic arch that connects the left pulmonary artery with the descending portion of the aortic arch. As a result of the high resistance of the pulmonary arteries in the unexpanded fetal lungs, most of the right ventricular output is shunted away from the lungs, through the ductus arteriosus, to the descending aorta. Reversal of flow is associated with severe congenital heart disease and a poor outcome.²

The ductus venosus connects the portal sinus with the inferior vena cava and allows oxygenated umbilical vein blood to bypass the liver and reach the central circulation. Both blood vessels lose this function after birth and usually undergo permanent closure. Prenatal patency of the ductus arteriosus is sustained by E series prostaglandins.³

After birth, changes in oxygen tension lead to ductal constriction (by smooth muscle), which starts at the pulmonary artery end of the ductus. This explains the usual conical shape of the PDA. Functional closure usually occurs within a few days of birth, even in preterm infants.⁴ During embryonic development, apoptosis regulates tissue remodeling by eliminating unwanted cells and structures and then appears to play a part in the remodeling and absorption of the ductus tissue.⁵ As closure progresses, the ductus is replaced by fibrous tissue to form the ligamentum arteriosum. Both the PDA and the ligamentum arteriosum can form part of a vascular ring.⁶ The aortic end of the ductus arteriosus may persist as a small outpouching, the ductus diverticulum. The importance of the ductus diverticulum is that it may mimic a false aortic aneurysm caused by trauma.

Persistence of a PDA may be related to persisting hypoxia in infants with cyanotic congenital heart disease or severe respiratory disease (eg, hyaline membrane disease). Although, in some situations, persistence of the PDA may be beneficial (eg, pulmonary atresia, transposition of the great arteries), it often contributes a degree of heart failure to an already severe illness.

Persistence of ductal tissue in the aorta may be related to the development of coarctation or aortic stenosis after PDA repair.⁷

A ductus arteriosus aneurysm is a rare but potentially lethal complication of PDA and may develop in children or adults.⁸ The reported incidence of such aneurysms may be rising because of better investigative methods and newer technology.⁹ In childhood, a ductus arteriosus aneurysm is often unrecognized until complications (endocarditis, thrombus, embolism, rupture, pressure effects) develop. The aneurysm may also present in adults, and the diagnosis can be made by echocardiography (especially in children), computed tomography (CT) scanning, MRI, and angiography.¹⁰ Increasingly, other conditions are associated with ductus arteriosus aneurysm, including connective tissue disorders.¹¹

Frequency

United States

The reported incidence depends on the population that is under study and the diagnostic methods.

The incidence of isolated PDA is generally believed to be in the range of 1 case per 2000 births, or approximately 10% of all congenital heart defects at birth.¹² The incidence of PDA varies substantially and may be increasing.

Cases of PDA reported to the Centers for Disease Control and Prevention rose from 686 in 1970-1971 to 2804 in 1976-1977, increasing the incidence from 3.96 to 13.25 per 10,000 total births, or an annual percentage increase of 22.3%.¹³ Whether this represented a true increase in incidence, a change in reporting practice, or improved survival of preterm infants is unclear.

PDA occurs in variable combination with virtually every other congenital heart defect. A female predominance is seen, and the incidence is increased in the offspring of mothers who contracted rubella in the first trimester of pregnancy. The incidence of PDA is as much as 30 times greater in populations that live at high altitudes (especially >5000 m), reflecting lower oxygen tensions at high altitude.

International

The incidence and associations are similar to those in the United States.

Mortality/Morbidity

• In the first year of life, mortality rates that result from large DPAs are high in patients who are not treated surgically. If the child survives the first year of life, few symptoms may be evident until adult life, when symptoms of heart failure as a result of left ventricular volume overload may develop. Symptoms may take the form of dyspnea, arrhythmias, and poor exercise tolerance. Death occurs as a consequence of heart failure, pulmonary hypertension, and endocarditis. Mortality rates in adults with PDA who remain untreated may be as high as 4% per year, with two thirds of patients dying by age 60 years. The mortality rate for ductus arteriosus aneurysm is high.
• In patients with PDA who are not treated, pulmonary hypertension develops in approximately 5%. Pulmonary hypertension eventually leads to shunt reversal with hypoxemia in the lower extremities.
• For patients with a small PDA, the risk of heart failure or pulmonary hypertension is small. The primary risk is related to endocarditis, with an annual incidence of approximately 0.5%. Endocarditis may cause up to one third of deaths in untreated PDA patients. Antibiotic prophylaxis is recommended, although this may be unnecessary after closure of the PDA.¹⁴ Inaudible PDA that is detected on echocardiography may not require treatment or antibiotic prophylaxis.

Race

No definite racial predilection exists, but PDA occurs more commonly in populations that live at high altitudes. The incidence is as much as 30 times greater in populations that live higher than 5000 m, reflecting lower oxygen tensions at high altitude.

Sex

A female predominance is seen, with a female-to-male incidence rate as high as 2:1.

Age

PDA is present at birth, but if left untreated, patients may not present with symptoms and/or signs until late in adult life, when a murmur is heard on physical examination. Other presentations in adult life can be associated with endocarditis, heart failure, or pulmonary hypertension. Occasionally, the first diagnosis is made when a calcified PDA is detected on chest radiographs.

Anatomy

The ductus arteriosus is the portion of the sixth aortic arch that connects the left pulmonary artery with the descending portion of the aortic arch. The pulmonary artery end of the PDA is usually immediately to the left of the pulmonary artery bifurcation. The aortic connection is just distal to the origin of the left subclavian artery. The normal direction of flow in the ductus determines its orientation, and its size (along with pressure differences) determines the amount of flow. Closure of the PDA usually starts at the pulmonary end, accounting for the funnel-shaped configuration seen in approximately two thirds of patients.

Several other configurations include the following:

• Short duct with narrow aortic end
• Tubular connection without narrowing
• Tubular connection with multiple narrowings
• Calcified PDA
• Aneurysm of the aortic end of the PDA
• Long PDA with unusual orientation (may occur with cyanotic congenital heart disease because of in utero flow from the aorta to the pulmonary arteries)

Clinical Details

Patients of any age may present with a PDA. The condition is a common cause of heart failure in premature infants, often occurring with other complications of prematurity, such as hyaline membrane disease. Younger patients usually present with heart failure or with more complex congenital heart disease. Once the age of early presentation with heart failure has been passed, patients with PDA seldom experience symptoms until the second or third decade of life.

Patients can also be asymptomatic. However, even if patients are asymptomatic, the general recommendation is that patients with an audible PDA should receive antibiotic prophylaxis for procedures that are likely to cause bacteremia. A PDA that is detected only on a Doppler ultrasound study but occurs in patients without a murmur or symptoms may not require antibiotic prophylaxis, although the evidence for this is limited.

In older patients with PDA, the presentation may be with changes related to pulmonary hypertension or other complications such as endocarditis. On physical examination, characteristic findings include a continuous systolic/diastolic or machinery-type murmur. The pulse may be collapsing because of rapid flow into the low-resistance pulmonary circulation.

The early symptoms of PDA are related to the increased pulmonary blood flow that is caused by shunting from the high-pressure aorta, through the PDA, to the low-pressure pulmonary arteries. The degree of shunting depends on the size of the ductus and the difference in the aortic and pulmonary arterial pressures.

Early presentations that result from large shunts occur with heart failure. Later presentations, usually in adulthood, may involve an asymptomatic continuous murmur, heart failure, or pulmonary hypertension, with the eventual reversal of shunt flow as pulmonary vascular resistance rises to exceed systemic vascular resistance. The mortality rate associated with ductus arteriosus aneurysm is high.

PDAs occur in variable combination with virtually every other congenital heart defect. A female preponderance is seen, and a strong association exists between PDA and maternal rubella. The incidence rate is increased in the offspring of mothers who contracted rubella in the first trimester of pregnancy. PDA is also associated with trisomy 13 and trisomy 18.

Preferred Examination

The preferred imaging method for diagnosing PDA is 2-dimensional echocardiography with color flow Doppler ultrasound study. Although characteristic chest radiograph changes have been identified, in many patients, chest radiographic findings are normal. In situations in which echocardiography is inadequate, cine magnetic resonance angiography (MRA) can demonstrate the PDA and, with even more sensitivity, the flow void that results from ductus flow into the pulmonary artery.

Limitations of Techniques

The usefulness of chest radiographs is limited by a lack of specificity and sensitivity. Radiographic features of a shunt are nonspecific. Filling in of the aortopulmonary window is a good sign, but other causes of mediastinal masses can mimic this appearance. Demonstration of this sign also requires good-quality radiography. The most reliable but least common finding on chest radiographs is of a calcified PDA in the aortopulmonary window.

Echocardiography is a reliable method for making the diagnosis of PDA, and it may detect the flow from PDA in patients with no clinical signs. The primary limitation of echocardiography is the restriction imposed by limited acoustic access. In situations in which echocardiography is inadequate (eg, chest deformity, airway disease), cine MRA is a sensitive technique that can detect ductal flow in the left pulmonary artery, even when the PDA is too small to be visualized.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Left-to-right shunts (acyanotic)

Endocardial cushion (arteriovenous canal)
Partial anomalous pulmonary venous return
Aortopulmonary window
Sinus Valsalva aneurysm
Coronary artery fistula
Coronary artery from pulmonary artery (must be at least 1 from pulmonary artery, 1 from aorta)
Left ventricle-to-right atrium shunt (Gerbode defect)

Continuous murmur

Aortopulmonary window
Sinus Valsalva aneurysm
Coronary artery fistula
Venous hum

RADIOGRAPH

Section 4 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
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• Intervention
• Multimedia
• References

Findings

Chest radiographs may demonstrate a large heart, depending on the size of the ductus shunt, with features of pulmonary plethora, heart failure (especially in neonates), or pulmonary hypertension. Filling in of the aortopulmonary window may be seen on good-quality radiographs (see Image 1). In elderly patients, a calcified duct may be demonstrated in this position. In patients with a significant shunt, the ascending and arch aortas are dilated, and the left atrium and left ventricle are enlarged.

Although a calcified PDA may be visible on lateral chest radiographs, a noncalcified PDA is not profiled and cannot be separated from other vascular structures in the mediastinum.

Degree of Confidence

The degree of confidence for radiographs is moderate. The value of the chest radiograph is limited by a lack of specificity and sensitivity. Findings in a shunt are nonspecific, although filling in of the aortopulmonary window is a good sign. However, this is seldom appreciated prospectively and requires good-quality radiographs (see Image 1).

Other causes of mediastinal masses can mimic this appearance. However, identifying a calcified PDA in the aortopulmonary window is a reliable sign.

False Positives/Negatives

False-positive findings may occur as a result of the other causes of left-to-right (acyanotic) shunts, including ventricular septal defect, atrial septal defect, endocardial cushion defect (arteriovenous canal), partial anomalous pulmonary venous return, aortopulmonary window, sinus Valsalva aneurysm, coronary artery fistula, and left ventricle-to-right atrium shunt (Gerbode defect).

Filling in of the aortopulmonary bay may also occur as a result of mediastinal masses (eg, lymphoma, thymoma) and mediastinal lipomatosis. In patients with a small patent PDA, chest radiographic findings may be normal. In patients who were in a rotated position during imaging or who did not take a deep breath, the mediastinal contour may be sufficiently distorted that the filling in of the aortopulmonary window cannot be appreciated.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

Although a large PDA may be visible on CT scanning or CT angiography, CT scan studies have only limited value because of the need to use ionizing radiation and, usually, contrast agents. Occasionally, calcification in the PDA is demonstrated in a characteristic position. CT scanning may be used to image the aorta in an evaluation of the chest for possible aneurysms; this is when ductus arteriosus aneurysm may be detected.

Degree of Confidence

The degree of confidence is high in detecting complications of PDA, such as ductus arteriosus aneurysm. CT scanning is less applicable for detecting a PDA.

MRI

Section 6 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

The value of MRI is limited in children, in whom echocardiography is almost always adequate to evaluate for PDA. However, in adults with restricted acoustic access, echocardiography may not be possible. Larger PDA can be seen on spin-echo images (see Image 2), breath-hold MRA (see Image 3), or cine MRA. The flow disturbance produced by even small PDA in the pulmonary artery is visible as signal loss on cine MRA.¹⁵ Flow disturbance is demonstrated best using sagittal cine MRA through the distal aortic arch and left pulmonary artery (see Image 4).

Although a PDA can be calcified, spin-echo MRI does not demonstrate calcification in this position. Filling in of the aortopulmonary window is a sign in adults. In the first year of life, thymus tissue often obliterates the aortopulmonary window, which makes this an unhelpful sign. Ductus arteriosus aneurysm is a rare finding on echocardiography or any other imaging technique.

Degree of Confidence

Although a PDA must be fairly large to be visualized on MRI or conventional MRA, detection of the flow void caused by turbulent flow passing through the ductus into the pulmonary artery is a sensitive and reliable method for diagnosis. The only realistic circumstance in which this may not occur is in patients with pulmonary hypertension in whom the pulmonary artery pressure equals the aortic pressure and no shunt is present.

False Positives/Negatives

False-positive and false-negative findings are unlikely with cine MRA unless a suitable sequence (ie, one that is sensitive to the flow-dephasing effects of high-velocity turbulent flow) is used. Newer segmented breath-hold sequences are less sensitive to these effects and may not show a signal void due to the turbulent flow from the PDA. In addition, the use of an imaging section that is too thick or the use of an MRI contrast agent may reduce the signal loss due to the PDA.

ULTRASOUND

Section 7 of 12  

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• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

On M-mode echocardiography, the findings demonstrate normal-sized right heart chambers unless pulmonary hypertension is present. As a result of increased left heart output, both the left atrium and left ventricle are dilated, with an increased stroke volume. The same findings are seen on 2-dimensional echocardiography.

In suitable patients, especially the young, the PDA can be visualized directly between the distal arch aorta and pulmonary artery at the origin of the left pulmonary artery (see Image 5). A left-to-right shunt is demonstrated using contrast echocardiography.

Continuous-wave or pulsed Doppler echocardiography usually demonstrates continuous flow at the origin of the left pulmonary artery. On color flow imaging, a continuous or diastolic jet of flow from the PDA is demonstrated. Continuous flow on continuous-wave Doppler imaging is a hallmark of PDA.

Degree of Confidence

Doppler echocardiography is an extremely reliable method for the diagnosis of PDA. Its sensitivity is high, and echocardiography may detect PDA in patients being evaluated for innocent murmurs in whom specific clinical features suggesting the condition are absent.

False Positives/Negatives

False-positive findings are rare and may result from misinterpretation of the Doppler signal from pulmonary regurgitation as diastolic flow from a PDA. False-negative findings are rare in children. In adults, false-negative findings may occur as a result of acoustic shadowing that obscures the pulmonary artery, preventing adequate imaging of the area of the PDA or of the main pulmonary artery to detect the characteristic flow abnormalities found on Doppler imaging.

NUCLEAR MEDICINE

Section 8 of 12  

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• Introduction
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• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Findings

In patients with reversal of flow through a PDA, a nuclear medicine shunt study shows early activity in the distal systemic circulation. In practice, this study is of little value, and echocardiography is the preferred examination.

ANGIOGRAPHY

Section 9 of 12  

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• Nuclear Medicine
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• Intervention
• Multimedia
• References

Findings

Contrast angiography is seldom required for the diagnosis of PDA, but it may be needed before surgery or during percutaneous interventions. Angiography may also be required to evaluate any coexistent congenital heart lesions or to exclude a differential diagnosis, such as a coronary artery fistula or aortopulmonary window.

The PDA is profiled best in a steep (60º) left anterior oblique orientation. After contrast material is injected into the descending aorta, the pulmonary artery fills rapidly (see Image 6). A true lateral aortogram may be the best view for sizing devices before percutaneous interventions because this view profiles the PDA well between the aorta and pulmonary artery.

The presence of a PDA can be confirmed with the passage of a catheter from the pulmonary artery (low pressure, low oxygen saturations) through the ductus to the aorta (high pressure, high oxygen saturations) below the diaphragm (see Image 7). This approach allows an aortogram to be obtained without risk of arterial puncture, an especially important consideration in younger patients.

At cardiac catheterization, changes occur in oxygen saturation and in the pulmonary artery and pulmonary artery pressures, which are dependent on the size of the PDA and the differences between pulmonary artery and aortic pressures. For a small PDA, the increase in oxygen saturation from the right ventricle to the pulmonary artery is small. The systolic pulmonary artery pressure is increased, but diastolic pressure remains low unless pulmonary vascular resistance is increased.

In some patients, pulmonary regurgitation may cause an increase in oxygen saturation in the right ventricle, necessitating excluding the diagnosis of a ventricular septal defect. Stretching of a patent foramen ovale by dilatation of the left atrium may also cause an increase in oxygen saturation in the right atrium. Coexistent congenital heart lesions should be evaluated at the same time (see Image 8).

In patients with pulmonary hypertension, pressure measurements should be repeated with administration of 100% oxygen to assess the lability of the increased pulmonary vascular resistance. In patients in whom intervention is planned, test occlusion of the PDA indicates which changes in pulmonary artery pressure may occur and how this may affect other cardiac lesions.

Degree of Confidence

Angiography and cardiac catheterization findings are generally regarded as diagnostically accurate if PDA is under consideration in the differential diagnosis.

False Positives/Negatives

Few false-negative findings occur with good angiographic technique. If a double PDA exists, one of the two may be missed if it is not sought consciously.

INTERVENTION

Section 10 of 12  

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• Differentials
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• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

In premature infants with PDA, medical treatment with indomethacin or a similar prostaglandin synthetase inhibitor is usually the first treatment. Prostaglandin E₂ is used to maintain ductal patency. Closure may be achieved surgically or with prostaglandin synthetase inhibitors. Surgical ligation or resection is performed if closure of the PDA fails. Early closure reduces the incidence of major complications in small infants.^{16, 17} In older patients, surgery may be the preferred option and is indicated in patients who have heart failure or a shunt ratio greater than 2:1. Risk of endocarditis means that closure eventually is required for almost all patients. Current catheter-based techniques are usually more suitable for larger infants or children.

An alternative to surgical closure is to use one of a variety of closure devices, such as the Porstmann plug, Rashkind umbrella, Botallo occluder, or embolization coil, which may be introduced by using a percutaneous approach.^{18, 19} Good results have been reported with use of the Rashkind umbrella, which has primary closure rates of 72-100% (see Images 9-10). A low risk of complications exists when skilled physicians perform the procedure (>90% primary success rate). Coils are effective, especially in PDA of less than 7 mm in diameter,²⁰ and they may be more effective than other devices.²¹

In cyanotic congenital heart disease, prostacyclin infusion or stenting of the ductus to maintain patency until the time of shunt surgery or repair may be required. The results of stenting are variable and often disappointing, and repeated intervention may be required to maintain patency.²²

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Frontal chest radiograph in a patient with patent ductus arteriosus. This image shows filling in of the aortopulmonary window (arrow).
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Media type:  X-RAY

Media file 2:  Axial electrocardiograph-gated, spin-echo magnetic resonance image. This study shows a large patent ductus arteriosus (arrow) running between the aorta and the pulmonary artery (same patient as in Images 3 and 4). AAo = ascending aorta; DAo = descending aorta.
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Media type:  MRI

Media file 3:  Coronal breath-hold magnetic resonance angiogram. This study shows the position of the patent ductus arteriosus (arrow) filling in the aortopulmonary bay, as would be viewed on a frontal chest radiograph (same patient as in Images 2 and 4). Ao = aorta; LA = left atrium; RPA = right pulmonary artery.
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Media type:  MRI

Media file 4:  Left anterior oblique cine magnetic resonance angiogram. This study shows a large area of signal loss (arrow) that results from turbulent flow extending into the pulmonary artery (PA) from a patent ductus arteriosus (PDA). Although the PDA is not visualized directly on this image, the presence and orientation of the jet makes the diagnosis, even if the PDA is not visible on other images (same patient as in Images 2-3). Ao = aorta; LA = left atrium; RA = right atrium.
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Media type:  MRI

Media file 5:  Two-dimensional echocardiogram (suprasternal view). This image shows a large patent ductus arteriosus (arrow) that runs above the left atrium (LA) between the aorta (Ao) and the pulmonary artery (PA).
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Media type:  Image

Media file 6:  Lateral aortogram. This image demonstrates the conventional configuration of a short-segment patent ductus arteriosus (arrow) that tapers from a narrow segment at the pulmonary artery (PA) to a wider lumen at the aortic end (same patient as in Images 9 and 10). DAo = descending aorta.
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Media type:  X-RAY

Media file 7:  Left anterior oblique balloon-occlusion aortogram. This image depicts a balloon angiographic catheter that has been passed from the pulmonary artery through the patent ductus arteriosus (PDA). The balloon (white open arrow) has been inflated in the descending aorta (DAo). Contrast material fills the aortic arch and DAo but not the PDA, which is almost occluded by the catheter (solid black arrow).
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Media type:  X-RAY

Media file 8:  Lateral left ventriculogram in a patient with tetralogy of Fallot. This image shows opacification of both the right ventricle (RV) and the left ventricle (LV). The pulmonary artery (white open arrow) is small and partly fills from a long-segment, downward-pointing patent ductus arteriosus (solid black arrow). DAo = descending aorta.
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Media type:  X-RAY

Media file 9:  Lateral aortogram. This image was obtained during deployment of a Rashkind duct occluder in a patient with patent ductus arteriosus (arrow) (same patient as in Images 6 and 10). DAo = descending aorta.
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Media type:  X-RAY

Media file 10:  Lateral aortogram. This image was taken following closure of a patent ductus arteriosus with use of the Rashkind duct occluder (arrow) (same patient as in Images 6 and 9). DAo = descending aorta.
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Media type:  X-RAY

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Nuclear Medicine
• Angiography
• Intervention
• Multimedia
• References

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2. Berning RA, Silverman NH, Villegas M, et al. Reversed shunting across the ductus arteriosus or atrial septum in utero heralds severe congenital heart disease. J Am Coll Cardiol. Feb 1996;27(2):481-6. [Medline]. [Full Text].
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8. Mitchell RS, Seifert FC, Miller DC, Jamieson SW, Shumway NE. Aneurysm of the diverticulum of the ductus arteriosus in the adult. Successful surgical treatment in five patients and review of the literature. J Thorac Cardiovasc Surg. Sep 1983;86(3):400-8. [Medline].
9. Acherman RJ, Siassi B, Wells W, et al. Aneurysm of the ductus arteriosus: a congenital lesion. Am J Perinatol. 1998;15(12):653-9. [Medline].
10. Laurin S, Sandström S, Ivancev K, et al. Ductus arteriosus aneurysm imaging using modern diagnostic methods. Acta Radiol. Jul 1992;33(4):285-91. [Medline].
11. Dyamenahalli U, Smallhorn JF, Geva T, et al. Isolated ductus arteriosus aneurysm in the fetus and infant: a multi-institutional experience. J Am Coll Cardiol. Jul 2000;36(1):262-9. [Medline]. [Full Text].
12. Perloff JK. Patent ductus arteriosus. Clinical Recognition of Congenital Heart Disease. 4^th ed. Philadelphia, Pa: WB Saunders Co; 1994:510-45.
13. Anderson CE, Edmonds LD, Erickson JD. Patent ductus arteriosus and ventricular septal defect: trends in reported frequency. Am J Epidemiol. Apr 1978;107(4):281-9. [Medline].
14. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Circulation. Jul 1 1997;96(1):358-66. [Medline]. [Full Text].
15. Hartnell GG, Cohen MC, Meier RA, Finn JP. Magnetic resonance angiography demonstration of congenital heart disease in adults. Clin Radiol. Dec 1996;51(12):851-7. [Medline].
16. Cassady G, Crouse DT, Kirklin JW, et al. A randomized, controlled trial of very early prophylactic ligation of the ductus arteriosus in babies who weighed 1000 g or less at birth. N Engl J Med. Jun 8 1989;320(23):1511-6. [Medline].
17. Pongiglione G, Marasini M, Silvestri G, et al. Early treatment of patent ductus arteriosus in premature infants with severe respiratory distress syndrome. Pediatr Cardiol. 1988;9(2):91-4. [Medline].
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Article Last Updated: Aug 2, 2007