AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Background

Coarctation of the aorta is a common congenital cardiovascular defect characterized by upper-body hypertension resulting from constriction of the aorta. Constrictions vary in degree; they may occur at any point from the transverse arch to the iliac bifurcation.¹

Related eMedicine topics:
Aortic Coarctation (from Cardiology)
Coarctation of the Aorta (from Pediatrics: Cardiac Disease and Critical Care Medicine)
Coarctation of the Aorta and Interrupted Aortic Arch: Surgical Perspective

Related Medscape topics:
Specialty Site Radiology
Specialty Site Cardiology
Resource Center Pediatrics/Neonatal Care Nursing
Resource Center Cardiometabolic Risk Factor Management
CME Which Drugs, When, for the Hypertensive Patient With Risk Factors?
CME The Hemodynamics of Hypertension -- The Importance of Pathophysiology and Pharmacology

Pathophysiology

Coarctation of the aorta may occur as a discrete juxtaductal obstruction or as tubular hypoplasia of the transverse aorta. Hypoplasia may start at one of the head or neck vessels and extend to the ductal area (preductal or infantile-type coarctation. Often, both components are present.

Aortic coarctation is most likely related to an abnormality in the pattern of ductus arteriosus blood flow in utero, which, in turn, may be the result of associated intracardiac anomalies.

In fetal life, blood flow through the aortic isthmus constitutes only 12-17% of the total cardiac output, whereas blood flow through the ductus arteriosus exceeds that across the aortic valve. Coarctation is initiated when a cardiac abnormality causes a decrease in blood flow anterograde through the aortic valve; abnormalities that may lead to coarctation include a bicuspid aortic valve and a ventricular septal defect (VSD).

In the first few days of life, the patent ductus arteriosus may serve to widen the juxtaductal area of the aorta and provide temporary relief from the obstruction. In these acyanotic infants, net left-to-right ductal shunting occurs. In contrast, with more severe juxtaductal coarctation or in cases involving transverse arch hypoplasia, right ventricular blood is ejected through the ductus to supply the descending aorta, as it does during fetal life. Perfusion of the lower body then depends on right ventricular output. In this situation, the femoral pulses are palpable, and differential blood pressures may not be helpful in making the diagnosis.

The ductal right-to-left shunting is manifested as differential cyanosis, with the upper extremities being pink and the lower extremities being blue. In such cases, severe pulmonary hypertension and high pulmonary vascular resistance may be present. Signs of heart failure are prominent. Occasionally, severely hypoplastic segments of the aortic isthmus become completely atretic, resulting in an interrupted aortic arch, with the left subclavian artery arising either proximal or distal to the interruption.

Coarctation associated with arch hypoplasia is referred to as infantile type coarctation because it usually manifests itself in early infancy, owing to its severity. The adult type is isolated juxtaductal coarctation; if mild, such coarctation usually does not manifest itself until later in childhood.

Blood pressure is elevated in the vessels that arise proximal to the coarctation; blood pressure and pulse pressure below the constriction are lower. Hypertension is not the result of the mechanical obstruction alone; rather, neurohumoral mechanisms are also involved. Unless operated on in infancy, patients with coarctation of the aorta usually develop an extensive collateral circulation, chiefly from the branches of the subclavian, the superior intercostal, and the internal mammary arteries, which create channels for arterial blood to bypass the area of coarctation.

The vessels contributing to the collateral circulation may become markedly enlarged and tortuous by early adulthood. After pharmacologic interventions that dilate the ductus arteriosus (prostaglandin E1 infusion) are administered, the pressure difference may be obliterated across the site of coarctation because the fetal flow pattern is reestablished.

The pathogenesis of juxtaductal coarctation already described accounts for the prevalence of associated intracardiac anomalies that foster reduced ascending aortic flow and augmented ductus arteriosus flow in utero, as well as the absence of associated intracardiac anomalies in which conditions of converse flow exist in utero.

The dependence of aortic obstruction on constriction of the ductus arteriosus postnatally accounts for the variable onset after birth of the clinical manifestations of coarctation, as well as the dramatic alleviation of the obstruction produced pharmacologically by dilatation of the ductus arteriosus.

Frequency

United States

Aortic coarctation accounts for 8% of congenital heart defects in children and about 6% of congenital heart diseases in adults.

International

The incidence of aortic coarctation internationally is similar to that in the United States.

Mortality/Morbidity

Abnormalities of the aortic valve are present in most patients. Bicuspid aortic valves are common but usually do not produce clinical signs unless the stenosis is significant. The association of a patent ductus arteriosus (PDA) with coarctation of the aorta is also common.

VSDs and atrial septal defects (ASDs) may be suspected when signs of a left-to-right shunt are present. Shunting is worsened by increased resistance to flow through the left side of the heart. Mitral-valve abnormalities are also occasionally seen, as is subvalvular aortic stenosis.

In rare cases, severe neurologic damage or even death may occur from associated cerebrovascular disease. Subarachnoid or intracerebral hemorrhage may result from rupture of congenital aneurysms in the circle of Willis, of other vessels with defective elastic and medial tissue, or of normal vessels; these accidents are secondary to hypertension. Abnormalities of the subclavian arteries may include involvement of the left subclavian artery in the area of coarctation, stenosis of the orifice of the left subclavian artery, and anomalous origin of the right subclavian artery.

If untreated, the great majority of older patients with coarctation of the aorta succumb to the disease between the ages of 20-40 years. Some live well into mid life without serious disability. The common serious complications are related to systemic hypertension, which may result in premature coronary artery disease, heart failure, hypertensive encephalopathy, or intracranial hemorrhage.

Heart failure may be worsened by associated anomalies. Infective endocarditis or endarteritis is a significant complication in adults. Aneurysms of the descending aorta or of the enlarged collateral vessels may develop. In infants with severe coarctation, heart failure and hypoperfusion may be life threatening and require immediate medical intervention.

Race

No particular racial predilection is described in aortic coarctation.

Sex

This left-sided obstructive lesion occurs most frequently in males, with a male-to-female ratio approaching 3:1.

Age

• Aortic coarctation associated with arch hypoplasia is referred to as infantile-type coarctation because it usually manifests itself in early infancy, owing to its severity.
• The adult type is isolated juxtaductal coarctation; if mild, it usually does not manifest itself until later in childhood.
• If the diagnosis is not made in early childhood, 25% of patients die by 20 years of age; almost 50% die by 30 years of age.

Anatomy

Normal anatomy

Coarctation of the aorta is a narrowing that usually occurs in the region of the ligamentum arteriosum. It may be discrete, or it may be associated with hypoplasia of the aortic arch and isthmus. The specific anatomy, severity, and degree of hypoplasia proximal to the coarctation are highly variable. Complex coarctation is coarctation in the presence of other important intracardiac anomalies (eg, VSD, left ventricular outflow tract obstruction [LVOTO], and mitral stenosis); it is usually detected in infancy.

Simple coarctation is coarctation in the absence of such lesions. It is the most common form detected de novo in adults. Associated abnormalities include bicuspid aortic valve, which is seen in in 50-85% of cases; intracranial aneurysms, most commonly of the circle of Willis; and acquired intercostal artery aneurysms.

According to one definition, significant coarctation is coarctation with a gradient of greater than 20 mm Hg across the coarctation site, as seen on angiography; proximal systemic hypertension may or may not be present. A second definition of significant coarctation requires the presence of proximal hypertension in the company of echocardiographic or angiographic evidence of aortic coarctation. Of note, if extensive collateral circulation is present, a pressure gradient may be minimal or absent, and acquired aortic atresia may be present.

The conventional anatomic and clinical divisions into preductal (infantile) and postductal (adult) coarctation are misleading because the anatomic localization is inaccurate and the age-dependency of the clinical presentation does not always hold true (ie, the adult type often is seen in the first weeks of life).

A spectrum of anatomic lesions cause obstruction of the aortic arch or proximal portion of the descending aorta. These lesions range from a localized coarctation or constriction of the lumen, most commonly located just distal to the origin of the left subclavian artery and closely related to the attachment of the ductus arteriosus with the aorta, to diffuse narrowing or interruption of a portion of the aortic arch.

In this article, aortic arch obstruction is classified into 3 types: (1) localized juxtaductal coarctation, (2) hypoplasia of the aortic isthmus, and (3) aortic arch interruption.

Pseudocoarctation is used synonymously with kinking or buckling of the aorta; it is a subclinical form of localized juxtaductal coarctation of the aorta.

Pathologic anatomy

About 98% of coarctations occur immediately beneath the origin of the left subclavian artery at the site of attachment of the ductus arteriosus (juxtaductal coarctation). Coarctation of the aorta may be a feature of Turner syndrome.

Aortic coarctation is associated with a bicuspid aortic valve in more than 70% of patients. Mitral valve abnormalities, such as a supravalvular mitral ring or parachute mitral valve, and subaortic stenosis may be associated lesions. When these left-sided obstructive lesions occur together, they are referred to as the Shone complex.

When coarctation occurs in infancy, it is often associated with other major cardiovascular anomalies, including hypoplastic left heart, severe mitral valve or aortic valve disease, transposition of the great arteries, and variations of double-outlet or single ventricle. Severe coarctation may also be associated with endocardial fibroelastosis.

The clinical manifestations depend on the effects of the associated malformations and on the coarctation itself.

Clinical Details

Clinical findings

In aortic coarctation, the clinical findings are highly variable and range from left ventricular failure in infancy to systemic hypertension in otherwise asymptomatic adult patients, depending on the site and severity of the coarctation and the presence of associated abnormalities.

The classic sign of coarctation of the aorta is a disparity in pulsations and blood pressures of the arms and legs. The femoral, popliteal, posterior tibial, and dorsalis pedis pulses are weak or absent (such pulses are found to be absent in up to 40% of patients); by contrast, bounding pulses are present in the arms and the carotid vessels.

The radial and femoral pulses should always be palpated simultaneously for the presence of a radial-femoral delay. Normally, the femoral pulse occurs slightly before the radial pulse. A radial-femoral delay occurs when blood flow to the descending aorta is dependent on collateral vessels, in which case the femoral pulse is felt after the radial pulse.

In healthy persons, the systolic blood pressure in the legs obtained by the cuff method is 10-20 mm Hg higher than that in the arms. In patients with coarctation of the aorta, the blood pressure in the legs is lower than that in the arms; frequently, blood pressure is difficult to obtain in the legs. This differential in blood pressures is common in patients with coarctation who are older than 1 year of age; about 90% of these patients have systolic hypertension in an upper extremity that is greater than that of the 95th percentile for age.

It is important to determine the blood pressure in each arm; a pressure higher in the right arm than the left suggests involvement of the left subclavian artery in the area of coarctation. Occasionally, the right subclavian artery may arise anomalously from below the area of coarctation, causing the pressure in the left arm to be higher than that in the right. With exercise, there is a more prominent rise of systemic blood pressure, and the upper-to-lower extremity pressure gradient increases.

The precordial impulse and heart sounds are usually normal; the presence of a systolic ejection click or thrill in the suprasternal notch suggests the presence of a bicuspid aortic valve (present in 70% of cases). A short systolic murmur is often heard along the left sternal border at the third and fourth intercostal spaces. The murmur is well transmitted to the left infrascapular area and, occasionally, to the neck. Often, the typical murmur of mild aortic stenosis is heard in the third right intercostal space.

Occasionally, more significant degrees of obstruction across the aortic valve are present. The presence of a low-pitched mid-diastolic murmur at the apex suggests the presence of mitral valve stenosis. Among older patients with well-developed collateral blood flow, systolic or continuous murmurs may be heard over the left and right sides of the chest laterally and posteriorly. In these patients, a palpable thrill may occasionally be appreciated in the intercostal spaces on the back.^{2, 3, 4, 5}

Age-related considerations

Coarctation of the aorta recognized after infancy is rarely associated with significant symptoms. Some children or adolescents complain about weakness or pain (or both) in the legs after exercise, but in many cases, even patients with severe coarctation are asymptomatic. Older children are frequently brought to the cardiologist's attention when they are found to be hypertensive on routine physical examination.

Neonates or infants with more severe coarctation, usually involving some degree of hypoplasia of the transverse arch, present with signs of lower-body hypoperfusion, acidosis, and severe heart failure. This presentation may be delayed days or weeks until after closure of the ductus arteriosus. If identified before ductal closure, patients may exhibit differential cyanosis, which is best demonstrated by simultaneous oximetry of the upper and lower extremities. On physical examination, the heart is found to be large; a systolic murmur is heard along the left sternal border, and there is a loud second heart sound.

Associated anomalies

The most common associated anomaly is a bicuspid aortic valve, which occurs in as many as 85% of patients with coarctation of the aorta.

Other associated anomalies include the following: VSD, stenosis or atresia of the left subclavian artery, PDA, Turner syndrome PDA, and mitral valve prolapse.

Preferred Examination

Blood pressure evaluation

The diagnosis of aortic coarctation may be made by a careful evaluation of the pulses in all major accessible peripheral arteries and by comparative blood pressure measurements in the arms and legs.

Electrocardiography

The electrocardiogram is usually normal in young children but reveals evidence of left ventricular hypertrophy in older patients. Neonates and young infants display right ventricular or biventricular hypertrophy.

Radiography

The findings on radiographic examination depend on the age of the patient and on the effects of hypertension and collateral circulation. Infants with severe coarctation have cardiac enlargement and pulmonary congestion. During childhood, the findings are not striking until after the first decade, when the heart tends to be mildly or moderately enlarged because of the prominence of the left ventricle.

The enlarged left subclavian artery commonly produces a prominent shadow in the left superior mediastinum. Notching of the inferior border of the ribs from pressure erosion by enlarged collateral vessels is common by late childhood. In most instances, an area of poststenotic dilatation of the descending aorta is present.⁶

Echocardiography

The segment of coarctation may usually be visualized by 2-dimensional echocardiography; associated anomalies of the mitral and aortic valve may also be demonstrated. The descending aorta is hypopulsatile.

Color Doppler imaging is useful for demonstrating the specific site of the obstruction. Pulsed and continuous-wave Doppler study may be used to determine the pressure gradient directly at the area of coarctation. However, in the presence of a patent ductus arteriosus, the severity of the narrowing may be underestimated.

Cardiac catheterization

Cardiac catheterization with selective left ventriculography and aortography is useful in evaluating selected patients who have additional anomalies; it is also useful as a means of visualizing collateral blood flow. In cases that are well defined by echocardiography, diagnostic catheterization is usually not required before surgery.

Limitations of Techniques

Radiographs are of limited usefulness in aortic coarctation. CT or MRI may be helpful.

DIFFERENTIALS

Section 3 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Other Problems To Be Considered

Turner syndrome
Shone complex
Bicuspid aortic valve
Hypertension

RADIOGRAPH

Section 4 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Findings

The diagnosis of coarctation of the aorta may be established from the posteroanterior (PA) chest image alone in up to 92% of patients. Widening of the left subclavian artery border is the most common finding, but the most useful radiographic sign is an abnormal contour of the aortic arch, which may appear as a double bulge above and below the usual site of the aortic knob.

This pattern has been described as a figure-3 sign. The upper arc of the 3 is the dilated arch proximal to the coarctation and/or a dilated left subclavian artery. The lower arc or bulge represents poststenotic dilatation of the aorta immediately below the coarctation. The indentation between the 2 bulges is the coarctation itself. When the esophagus is filled with barium, a reverse 3 or E sign is often seen; it is a mirror image of the areas of prestenotic and poststenotic dilatation.

The 3 sign is variable in that the upper arc may be small and the lower arc large, or vice versa. Superior mediastinal widening or sternal scalloping, caused by large internal mammary collateral arteries, is visible in some patients. A prominent left ventricular border often occurs with coarctation, particularly when a bicuspid aortic valve is associated with aortic stenosis.

Bilateral symmetrical rib notching, readily appreciated on the chest image, is diagnostic of aortic coarctation. It is the result of obstruction of blood flow at the narrowed aortic segment, in conjunction with collateral blood flow through the intercostal arteries. Rib notching is unusual in infancy but becomes more frequent with increased age; it is present in 75% of adults with coarctation. Rib notching occurs along the inferior margin of the third to the eighth ribs; it is caused by pulsation of dilated intercostal arteries.

The major pathways of collateral flow include the following: (1) subclavian artery to the internal mammary artery to the intercostal arteries, (2) subclavian artery to the costovertebral trunk to the intercostal arteries, and (3) transverse cervical and suprascapular arteries to the intercostal arteries.

Radiographic findings depend on the age of the patient and on the effects of hypertension and collateral circulation. In infants with severe coarctation, cardiac enlargement and pulmonary congestion are present.

During childhood, the findings are not striking until after the first decade, when the heart tends to be mildly or moderately enlarged because of the prominence of the left ventricle. The enlarged left subclavian artery commonly produces a prominent shadow in the left superior mediastinum. Notching of the inferior border of the ribs from pressure erosion by enlarged collateral vessels is common by late childhood. In most instances, an area of poststenotic dilatation of the descending aorta is present.^{7, 8}

Degree of Confidence

The diagnosis of coarctation of the aorta can be established from the PA chest image alone in up to 92% of patients.

CT SCAN

Section 5 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Findings

CT scanning does not play a significant role in the evaluation of aortic coarctation.

MRI

Section 6 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Findings

MRI vividly portrays the anatomy of the coarctation. It also demonstrates the bicuspid valve and the state of left ventricular function, as well as restenosis following angioplasty or surgical repair (see Image 2).^{9, 10}

Degree of Confidence

The degree of confidence is very high.

ULTRASOUND

Section 7 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Findings

The segment of coarctation may usually be visualized by means of 2-dimensional echocardiography. Associated anomalies of the mitral and aortic valve may also be demonstrated. The descending aorta is hypopulsatile. Color Doppler imaging is useful for demonstrating the specific site of the obstruction. Pulsed and continuous-wave Doppler imaging may be used to determine the pressure gradient directly at the area of coarctation.

Degree of Confidence

In the presence of a patent ductus arteriosus, the severity of the narrowing may be underestimated.

ANGIOGRAPHY

Section 8 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Findings

Cardiac catheterization with selective left ventriculography and aortography is useful in selected patients who have additional anomalies. It is also useful in visualizing collateral blood flow. In cases that are well defined by echocardiography, diagnostic catheterization is usually not required before surgery (see Image 1).¹¹

INTERVENTION

Section 9 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

In neonates with severe coarctation of the aorta, closure of the ductus often results in hypoperfusion, acidosis, and rapid deterioration. These patients should be given an infusion of prostaglandin E1 to reopen the ductus and to reestablish adequate lower-extremity blood flow. Once a diagnosis has been confirmed and the patient stabilized, surgical repair should be performed. For older infants who present with heart failure but who have good perfusion, anticongestive measures should be employed to improve clinical status before surgical intervention.

Older children with significant coarctation of the aorta should be treated relatively soon after diagnosis. Delay is unwarranted, especially after the second decade of life, when the operation may be less successful because of decreased left ventricular function and degenerative changes in the aortic wall. Nevertheless, if cardiac reserve is sufficient, satisfactory repair is possible well into midadult life. Associated valvular lesions increase the hazards of late surgery.

The procedure of choice for isolated juxtaductal coarctation of the aorta is controversial. This operation remains the procedure of choice, and several surgical techniques are used. The area of coarctation may be excised, and a primary reanastomosis may be performed. Often, the transverse aorta is splayed open and an extended end-to-end anastomosis is performed to increase the effective cross-sectional area of the repair. The subclavian flap procedure, which involves division of the left subclavian artery and its incorporation into the wall of the repaired coarctation, is used by some, often for younger patients. Others favor a patch aortoplasty, in which the area of coarctation is enlarged with a roof of prosthetic material.

After operation, a striking increase in the amplitude of pulsations occurs in the lower extremities. In the immediate postoperative course, rebound hypertension is common and requires medical management. This exaggerated hypertension gradually subsides; in most patients, antihypertensive medications may be discontinued. Residual murmurs are common. Such murmurs may be caused by associated cardiac anomalies, or they may be the result of a residual flow disturbance across the repaired area or of collateral blood flow. Rare additional operative problems include spinal cord injury resulting from aortic cross-clamping of poorly developed collaterals; chylothorax; diaphragm injury; and laryngeal nerve injury.

If a left subclavian flap is used, the radial pulse and blood pressure in the left arm are diminished or absent.

In some centers, balloon angioplasty has been used for the treatment of native coarctation or of a coarctation that has not been operated on. Early reports of results in these patients indicate good relief of the obstruction. However, there are several reports of the subsequent development of aortic aneurysms. Revised techniques have reduced the incidence of this complication, although the use of angioplasty for patients with native coarctation remains controversial.

Substantial controversy exists regarding the role of balloon angioplasty, with or without the use of stents, in the treatment of native coarctation, especially in younger patients. There is strong concern about the possiblity of residual pressure gradients, aneurysm formation, aortic dissection and rupture, and the occurrence of femoral arterial complications following angioplasty. Although angioplasty may effectively reduce obstruction in many patients, the late outcome is often unpredictable.

Repair of coarctation in the second decade of life or thereafter may be associated with a higher incidence of premature cardiovascular disease, even in the absence of residual cardiac abnormalities. There is a possibility of the early onset of adult hypertension, which has occurred even in patients whose coarctation was adequately resected.

Although restenosis in older patients after coarctectomy is rare, a significant number of infants who undergo operation before the age of 1 year require operative revision later in childhood. All patients should be followed carefully for the development of re-coarctation and aortic aneurysm. Should re-coarctation occur, balloon angioplasty is the procedure of choice. In these patients, scar tissue from prior surgery makes repeat operation more difficult, although it makes balloon angioplasty safer, because the incidence of aneurysm formation is lower. This technique usually provides excellent relief of obstruction. Intravascular stents have been used in some patients.

Coarctation of the aorta in association with severe mitral valve and aortic valve disease may require treatment within the setting of the hypoplastic left heart syndrome even if the left ventricular chamber is not severely hypoplastic. Such patients usually have a long segment of narrow transverse aortic arch with or without an isolated coarctation at the site of the ductus arteriosus. Coarctation of the aorta in association with transposition of the great arteries or a single ventricle may be repaired alone or in combination with other palliative measures.^{12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25}

Medical/Legal Pitfalls

• Aortic coarctation should be suspected in patients with hypertension, especially patients with upper body hypertension.
• Missing the diagnosis may have adverse legal consequences.

FURTHER READING

Section 10 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

VHA/DoD clinical practice guideline for the diagnosis and management of hypertension in the primary care setting. Department of Defense - Federal Government Agency [U.S.]
Department of Veterans Affairs - Federal Government Agency [U.S.]
Veterans Health Administration - Federal Government Agency [U.S.].  1999 May (revised 2004).  99 pages.  NGC:004198

Hypertension.
University of Texas Medical Branch Correctional Managed Care.  1997 Mar (revised 2003 Apr).  9 pages.  NGC:003304

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

Media file 1:  Aortic coarctation visualized by aortic angiography.
	View Full Size Image
Media type:  Image

Media file 2:  Aortic coarctation visualized by MR imaging.
	View Full Size Image
Media type:  MRI

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Further Reading
• Multimedia
• References

1. Brueck M, Janka R, Daniel WG. Coarctation of the aorta. Circulation. Feb 13 2001;103(6):E27. [Medline].
2. Rahiala E, Tikanoja T. Suspicion of aortic coarctation in an outpatient clinic: how should blood pressure measurements be performed?. Clin Physiol. Jan 2001;21(1):100-4. [Medline].
3. Santoro G, Caianiello G, Palladino MT, Iacono C, Russo MG, Calabrò R. Aortic coarctation with persistent fifth left aortic arch. Int J Cardiol. Aug 8 2008;[Medline].
4. Verheugt CL, Uiterwaal CS, Grobbee DE, Mulder BJ. Long-term prognosis of congenital heart defects: A systematic review. Int J Cardiol. Aug 5 2008;[Medline].
5. Kühn A, Baumgartner D, Baumgartner C, Hörer J, Schreiber C, Hess J, et al. Impaired elastic properties of the ascending aorta persist within the first 3 years after neonatal coarctation repair. Pediatr Cardiol. Aug 7 2008;[Medline].
6. Greenberg SB, Balsara RK, Faerber EN. Coarctation of the aorta: diagnostic imaging after corrective surgery. J Thorac Imaging. Winter 1995;10(1):36-42. [Medline].
7. Gross GW, Steiner RM. Radiographic manifestations of congenital heart disease in the adult patient. Radiol Clin North Am. Mar 1991;29(2):293-317. [Medline].
8. Neitzschman H, Ram SK, Ram PB. Radiology case of the month. An 11-year-old girl with a pulse discrepancy between the upper and lower extremities. Coarctation of aorta. Widening of the radioulnar joint. J La State Med Soc. Jun 2001;153(6):269-70. [Medline].
9. Greenberg SB, Marks LA, Eshaghpour EE. Evaluation of magnetic resonance imaging in coarctation of the aorta: the importance of multiple imaging planes. Pediatr Cardiol. Sep-Oct 1997;18(5):345-9. [Medline].
10. Latrabe V. [MRI of aortic coarctation: impact in daily practice]. J Radiol. May 2001;82(5):539. [Medline].
11. Bogaert J, Kuzo R, Dymarkowski S, et al. Follow-up of patients with previous treatment for coarctation of thethoracic aorta: comparison between contrast-enhanced MR angiography andfast spin-echo MR imaging. Eur Radiol. 2000;10(12):1847-54. [Medline].
12. Bhat MA, Neelakandhan KS, Unnikrishnan M, et al. Fate of hypertension after repair of coarctation of the aorta in adults. Br J Surg. Apr 2001;88(4):536-8. [Medline].
13. Bouchart F, Dubar A, Tabley A, et al. Coarctation of the aorta in adults: surgical results and long-termfollow-up. Ann Thorac Surg. Nov 2000;70(5):1483-8; discussion 1488-9. [Medline].
14. Gibbs JL. Treatment options for coarctation of the aorta. Heart. 2000;84(1):11-3. [Medline].
15. Harrison DA, McLaughlin PR, Lazzam C, et al. Endovascular stents in the management of coarctation of the aorta in the adolescent and adult: one year follow up. Heart. May 2001;85(5):561-6. [Medline].
16. Mann C, Goebel G, Eicken A, et al. Balloon dilation for aortic recoarctation: morphology at the site of dilation and long-term efficacy. Cardiol Young J. 2001;11(1):30-5. [Medline].
17. Pacileo G, Pisacane C, Russo MG, et al. Left ventricular remodeling and mechanics after successful repair of aortic coarctation. Am J Cardiol. Mar 15 2001;87(6):748-52. [Medline].
18. Perloff JK. Congenital heart disease in the adult: clinical approach. J Thorac Imaging. Fall 1994;9(4):260-8. [Medline].
19. Rao PS. Balloon angioplasty of native coarctation of the aorta. J Invasive Cardiol. Aug 2000;12(8):407-9. [Medline].
20. Saba SE, Nimri M, Shamaileh Q, et al. Balloon coarctation angioplasty: follow-up of 103 patients. J Invasive Cardiol. Aug 2000;12(8):402-6. [Medline].
21. Saliba Z, Aggoun Y, Iserin L, et al. [Baloon angioplasty with stent implantation in recoarctation of the aorta: an attractive alternative]. Arch Mal Coeur Vaiss. May 2001;94(5):427-32. [Medline].
22. Thanopoulos BD, Hadjinikolaou L, Konstadopoulou GN, et al. Stent treatment for coarctation of the aorta: intermediate term follow upand technical considerations. Heart. Jul 2000;84(1):65-70. [Medline].
23. Tabbutt S, Nicolson SC, Adamson PC, Zhang X, Hoffman ML, Wells W, et al. The safety, efficacy, and pharmacokinetics of esmolol for blood pressure control immediately after repair of coarctation of the aorta in infants and children: a multicenter, double-blind, randomized trial. J Thorac Cardiovasc Surg. Aug 2008;136(2):321-8. [Medline].
24. Stanley JC, Criado E, Eliason JL, Upchurch GR Jr, Berguer R, Rectenwald JE. Abdominal aortic coarctation: Surgical treatment of 53 patients with a thoracoabdominal bypass, patch aortoplasty, or interposition aortoaortic graft. J Vasc Surg. Aug 8 2008;[Medline].
25. Paddon AJ, Nicholson AA, Ettles DF, et al. Long-term follow-up of percutaneous balloon angioplasty in adult aortic coarctation. Cardiovasc Intervent Radiol. Sep-Oct 2000;23(5):364-7. [Medline].

Article Last Updated: Sep 16, 2008