eMedicine Specialties > Cardiology > Congenital Heart Disease in the Adult

Aortic Coarctation

Sandy N Shah, DO, MBA, Private Practice, Houston, Texas
Dawn M Calderon, DO, Co-Director of Center for Adults With Congenital Heart Disease, Clinical Associate Professor, Departments of Cardiology and Internal Medicine, Deborah Heart and Lung Center, Robert Wood Johnson School of Medicine

Updated: Oct 2, 2008

Introduction

Background

Coarctation of the aorta is a narrowing of the aorta most commonly found just distal to the origin of the left subclavian artery. Most patients with coarctation have juxtaductal coarctation. Older terms, such as preductal (infantile-type) or postductal (adult-type), are often misleading.

Pathophysiology

The vascular malformation responsible for coarctation is a defect in the vessel media, giving rise to a prominent posterior infolding (the "posterior shelf"), which may extend around the entire circumference of the aorta. The gross pathology of coarctation varies considerably. The lesion is often discrete but may be long, segmental, or tortuous in nature.

Histology

The coarctated aortic segment reveals an intimal and medial lesion consisting of thickened ridges that protrude posteriorly and laterally into the aortic lumen. The ductus (ie, patent embryonic remnant) or ligamentum arteriosus (closed and fibrosed) inserts at the same level anteromedially. Intimal proliferation and disruption of elastic tissue may occur distal to the coarctation. At this site, infective endarteritis, intimal dissections, or aneurysms may occur. Cystic medial necrosis occurs commonly in the aorta adjacent to the coarctation site and acts as a substrate for late aneurysm formation or aortic dissection in some patients.

Embryology

Coarctation is due to an abnormality in development of the embryologic left fourth and sixth aortic arches that can be explained by 2 theories, the ductus tissue theory and the hemodynamic theory.

In the ductus tissue theory, coarctation develops as the result of migration of ductus smooth muscle cells into the periductal aorta, with subsequent constriction and narrowing of the aortic lumen. Commonly, coarctation becomes clinically evident with closure of the ductus arteriosus. This theory does not explain all cases of coarctation. Clinically, coarctation may occur in the presence of a widely patent ductus arteriosus, and it may occur quite distant from the insertion of the ductus arteriosus, such as in the transverse arch or abdominal aorta.

In the hemodynamic theory, coarctation results from reduced volume of blood flow through the fetal aortic arch and isthmus. In a normal fetus, the aortic isthmus receives a relatively low volume of blood flow. Most of the flow to the descending aorta is derived from the right ventricle through the ductus arteriosus. The left ventricle supplies blood to the ascending aorta and brachiocephalic arteries, and a small portion goes to the aortic isthmus. The aortic isthmus diameter is 70-80% of the diameter of the neonatal ascending aorta.

Based on this theory, lesions that diminish the volume of left ventricular outflow in the fetus also decrease flow across the aortic isthmus and promote development of coarctation. This helps to explain the common lesions associated with coarctation, such as ventricular septal defect, bicuspid aortic valve, left ventricular outflow obstruction, and tubular hypoplasia of the transverse aortic arch. This theory does not explain isolated coarctation without associated intracardiac lesions.

Frequency

United States

This condition represents 5-10% of all congenital cardiac lesions. It represents 7% of critically ill infants with heart disease.

Mortality/Morbidity

• Patients who are not treated for coarctation of the aorta may reach the age of 35 years; fewer than 20% survive to age 50 years. If coarctation is repaired before the age of 14 years, the 20-year survival rate is 91%. If coarctation is repaired after the age of 14 years, the 20-year survival rate is 79%.
• After repair of the aortic coarctation, 97-98% of patients are New York Heart Association (NYHA) class I. Impaired diastolic left ventricular function and persistent hypertrophy due to increased pressure gradient at the coarctation site during exercise may result in myocardial hypertrophy despite successful hemodynamic results. Overall, left ventricular systolic function is normal or hyperdynamic in these patients.
• Pregnancy: Most women reach childbearing age. If maternal coarctation is not repaired, the risk to fetus and mother is increased. The maternal mortality rate is approximately 3-8%. Even women who have had their coarctation repaired have an increased risk of aortic dissection and rupture of a cerebral aneurysm in the third trimester and peripartum period due to hemodynamic and hormonal changes. All pregnant women with a history of coarctation, either native or repaired, should be considered high risk. Significant stenosis—native, residual, or recurrent—is a contraindication to pregnancy.

Race

Coarctation is 7 times more common in whites than Asian persons. It has a lower incidence among Native Americans than other population groups in Minnesota.

Sex

Male-to-female predominance is 1.3-2:1 in most series.

Age

Age at detection of coarctation of the aorta is dependent on severity of obstruction and coexistence of other lesions.

Clinical

History

The history of those with coarctation of the aorta includes the following.

• Early life: Depending on severity of obstruction and associated cardiac lesions, patients may present with congestive heart failure, severe acidosis, or poor perfusion to the lower body.
• Beyond infancy: Patients are usually asymptomatic. They may present with hypertension, headache, nosebleed, leg cramps, muscle weakness, cold feet, or neurologic changes.

Physical

The diagnosis of coarctation generally can be made on physical examination. Blood pressure differential and pulse delay are pathognomonic.

• Physical appearance
  • Patients may appear healthy. If coarctation compromises the origin of the left subclavian artery, the left arm is smaller than normal. Otherwise, general development is normal.
  • In XO Turner syndrome, a condition frequently associated with coarctation, a phenotypic female has the following features: short stature, webbed neck, absent or scanty axillary and pubic hair, broad chest and widely spaced hypoplastic or inverted nipples, low posterior hairline, small chin, prominent ears, cubitus valgus, short fourth metacarpals and metatarsals, distal palmar triaxial radii, narrow hyperconvex nails, and extensive pigmented cutaneous nevi.
• Arterial pulse: Abnormal differences in upper and lower extremity arterial pulses and blood pressures are clinical hallmarks of coarctation of the aorta. Pulses distal to the obstruction are diminished and delayed. This may be appreciated best by simultaneous arm and leg pulse palpation.
• Auscultation
  • A continuous and/or late systolic murmur is best heard posteriorly over the thoracic spine. Collateral arterial murmurs are crescendo-decrescendo in shape and delayed in onset and termination because of their origins in vessels some distance from the heart. The collateral murmurs are present bilaterally.
  • If the patient has associated bicuspid aortic valve, an aortic ejection sound, a short midsystolic murmur, and/or early diastolic murmur of aortic regurgitation may be audible.
• Associated cardiac defects
  • These are observed in approximately 50% of patients with coarctation.
  • The most commonly reported defects are left-sided obstructive or hypoplastic defects and ventricular septal defects. Bicuspid aortic valve is observed in 85% of patients. Also, aortic arch hypoplasia is commonly found in coarctation associated with intracardiac defects.
  • Right-sided cardiac obstructive lesions, such as pulmonary stenosis, pulmonary atresia, or tetralogy of Fallot, are observed rarely.
• Extracardiac vascular anomalies
  • These commonly occur in patients with coarctation. A right subclavian artery that arises aberrantly from the descending aorta distal to the coarctation occurs in 5% of patients. Rarely, both subclavian arteries originate distal to the coarctation.
  • Berry aneurysms of the circle of Willis occur in 3-5% of patients and may result in subarachnoid bleed.
  • After years of coarctation, large collateral arteries develop from the upper to lower body (ie, internal mammaries connecting to external iliac arteries and spinal and intercostal arteries connecting to the descending aorta).
  • Hemangiomas also have been reported with coarctation.
• Extracardiac nonvascular anomalies
  • Extracardiac nonvascular anomalies occur in 25% of patients with coarctation of the aorta. Coarctation of the aorta occurs in 35% of patients with Turner syndrome.
  • Abnormalities of the musculoskeletal system, genitourinary system, gastrointestinal system, or respiratory system may be observed in as many as 25% of children with coarctation. In addition, an increasing number of children have head and neck abnormalities observed by ultrasonography.

Causes

The exact etiology of coarctation of the aorta is not known.

• Genetics: Coarctation is 7 times more common in white persons than Asian persons. It has a lower incidence among Native Americans than other population groups in Minnesota.
• Environment: Environmental variation and seasonal variation have been suggested to influence the development of coarctation. A study has shown increased incidence of coarctation in late fall and winter births.
• Gridlock mutation: In 1995, Weinstein et al discovered a recessive mutation in zebrafish that causes a focal malformation resembling coarctation in humans.¹ The mutation, named gridlock, results in failure of vascular channel formation at the site where bilaterally paired dorsal aortas join together and continue posteriorly as a dorsal midline channel, the medial dorsal aorta.

Workup

Laboratory Studies

No specific laboratory tests are necessary for coarctation of the aorta.

Imaging Studies

• Radiograph
  • Radiograph findings vary with the clinical presentation of the patient. In coarctation diagnosed early in life, chest radiograph shows cardiac enlargement and pulmonary venous congestion. Associated cardiac defects may mask these findings.
  • In older children, chest radiograph findings are usually normal. The study typically shows a prominent aortic knob, and the stenotic region may be observed as an indentation of the proximal thoracic descending aorta in the shape of a number 3.
  • Rib notching is observed as irregularities and scalloping on the undersurface of the posterior ribs. This finding is unusual in children younger than 5 years and is observed more frequently in patients with significant gradient across coarctation of long standing.
• Barium esophagram: Barium esophagram shows the classic "E sign," representing compression from the dilated left subclavian artery and poststenotic dilatation of the descending aorta.
• Echocardiography
  • Diagnosis of coarctation of the aorta is made by 2-dimensional echocardiography, pulsed-wave Doppler, and color flow mapping. Classic findings are narrowing of the isthmus and posterior indentation or shelf. Blood flow velocities proximal and distal to obstruction, measured by Doppler tracings, can be used to estimate pressure gradient across the coarctation by a modified Bernoulli equation. Color flow mapping shows changes in color at the site of obstruction due to increases in blood velocity and turbulence.
  • In older patients, coarctation may be difficult to diagnose by surface echocardiography. For these patients, MRI, transesophageal echocardiography, or cardiac catheterization with angiogram may be necessary to make the diagnosis.
• Fetal echocardiography
  • Detection of coarctation in utero is a difficult task for the echocardiographer.
  • Some features suggest the presence of coarctation: enlargement of right ventricle compared to left ventricle, isthmus and transverse aortic diameters less than 3% for gestational age, hypoplasia of left-sided structures, and decrease or reversal of flow in the foramen ovale.
• Magnetic resonance imaging
  • MRI is a sensitive test for location and extent of coarctation as well as involvement of adjacent vessels and presence of collaterals. However, it is expensive, time consuming, and not universally available.
  • MRI is seldom used as a primary diagnostic tool. It is a useful tool for detecting and monitoring aneurysms and restenosis.
• Cardiac catheterization
  • If the peak gradient across the coarctation is less than 20 mm Hg, the coarctation is mild.
  • A gradient of greater than 20 mm Hg across the coarctation is suggestive of the need for intervention.

Other Tests

• Electrocardiogram
  • Newborns and older children with milder forms of coarctation may have a normal electrocardiogram (ECG) finding. If associated cardiac defects present, then ECG finding may be abnormal.
  • In older patients, long-standing coarctation of the aorta or a higher gradient across the coarctation stimulates left ventricular hypertrophy.

Treatment

Medical Care

• Severe coarctation of the aorta
  • Neonates with severe coarctation of the aorta should first have their condition stabilized.
  • First, support respiratory collapse with intubation. Second, infuse prostaglandin E₁ to open the ductus arteriosus. Third, correct acidosis. Finally, provide inotropic support to improve symptoms of congestive heart failure.
• Less severe coarctation of the aorta
  • Patients presenting with less severe coarctation of the aorta beyond the neonatal period usually have chronically increased afterload and show signs of congestive heart failure. These patients should be treated with digoxin and diuretics.
  • Attempts should be made to postpone intervention, such as surgery or balloon dilatation, until the patient is hemodynamically stable.

Surgical Care

• Indication for intervention: At present, 3 specific indications exist for intervention in patients with coarctation of the aorta.
  • Significant coarctation or recoarctation of the aorta with long-standing hypertension with or without symptoms
  • Hemodynamically significant aortic stenosis
  • Female patient contemplating pregnancy
• Types of surgery
  • In 1944, Blalock and Park performed the first experimental surgical repair of coarctation of the aorta in animals, which involved use of the left common carotid or subclavian artery to bypass the coarctation with end-to-end anastomosis.
  • Resection of the coarctation site and end-to-end anastomosis to repair coarctation was performed first on humans in 1944 by Crafoord, Nylin, Gross, and Hufagel. This is the preferred surgical method even today. In this technique, the aorta is cross-clamped above and below the obstruction, and the discrete narrowing is resected. The advantage of this procedure is that the obstructed site is completely resected. It also avoids the use of prosthetic material and maintains a functioning left subclavian artery. The disadvantages of this procedure involve the sacrifice of spinal and intercostal vessels resulting in paralysis. Also, a high rate of restenosis exists with use of continuous running suture or circumferential fibrosis. This problem is overcome by use of interrupted and absorbable sutures, which allows for improved growth of the anastomotic site.
  • Patch aortoplasty was first performed by Vossschulte in 1961 to repair coarctation of the aorta.² This technique involves cutting across the obstruction and augmenting the area with a patch of prosthetic material. The advantages of this procedure include the ability to repair a long segment of coarctation; sparing of the left subclavian, intercostal, and spinal arteries; and preserving native aortic tissue to allow for growth. The disadvantage of this procedure is that it uses prosthetic material, which may gradually result in aneurysm formation.
  • Left subclavian flap angioplasty, introduced in 1966 by Waldhausen and Nahrwold, involves ligating the left subclavian artery and dividing it distally.³ A longitudinal incision is made from the descending aorta to the coarctation superiorly into the origin of the left subclavian artery. The subclavian artery is turned down and used to enlarge the narrowing. To prevent subclavian steal phenomena, the vertebral artery is ligated. The advantages to this procedure include preservation of native vascular tissue and avoidance of circumferential sutures, which allows for better growth of the involved area. The disadvantage to this procedure is the sacrifice of a major artery to the left arm, resulting in poor growth of that extremity.
  • Bypass graft repair bridges the ascending and descending aorta. The major disadvantage of this procedure is that prosthetic material does not grow as the child grows, and it becomes calcified and narrow with time.

Endovascular Care

Catheter-based intervention is now the preferred therapy for recurrent coarctation when the anatomy permits and necessary skills are available. Its use in native or unoperated coarctation is less well established. Treatment may be with balloon angioplasty alone or with a stent. Outcomes are good in skilled hands, but residual or recurrent coarctation with resultant hypertension and repair site aneurysms can occur. Catheter-based treatment can cause death from aortic rupture and dissection, but mortality compares favorably with surgery if coarctation is recurrent, and perhaps for initial treatment.

Endovascular Versus Surgical Care

The immediate improvement in hypertension and morbidity were similar across all groups. Surgical therapy was associated with a low risk of restenosis and recurrence, whereas endovascular therapy had much higher incidence of restenosis and need for repeat interventions.⁴ Endovascular therapy is highly promising in elderly and frail patients with multiple comorbidities who pose a high surgical risk. Overall, long-term outcome of endovascular approaches need to be evaluated.

Consultations

See Surgical Care.

Activity

As with all aortopathies and aortic valve problems, significant and prolonged isometric activities are contraindicated. The risk of dissection, even in repaired coarctation, remains significant and may be increased with isometric activity.

Medication

No specific medications are used to treat coarctation of the aorta because it is a mechanical obstruction. In the neonate, management of concomitant congestive heart failure may include prostaglandin E₁ to maintain patency of the ductus arteriosus. Beyond the neonatal period, management of congestive heart failure may include digoxin and diuretics.

Prostaglandins

This agent promotes vasodilatation by direct effect on the vasculature and smooth muscle of the ductus arteriosus.

Alprostadil; Prostaglandin E1 (Prostin VR)

Used to maintain patency of ductus arteriosus when cyanotic lesion or interrupted aortic arch presents in newborn. Most effective in premature infants.

Dosing

Adult

Currently used as part of protocols; recommended dosages have yet to be established

Pediatric

For palliation: 0.05-0.1 mcg/kg/min continuous IV infusion; may be increased to 0.2 mcg/kg/min if necessary

Interactions

None reported

Contraindications

Documented hypersensitivity; respiratory distress syndrome; persistent fetal circulation

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Because of potential risk of apnea, neonates are usually intubated prophylactically; caution in neonates with bleeding tendencies; prolonged use occasionally necessary (eg, in patients with hypoplastic left heart syndrome who are transplant candidates) and may be associated with third spacing of fluid

Cardiac glycosides

These agents increase the contractility of cardiac muscle in a dose-dependent manner (ie, positive inotropic effect).

Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Dosing

Adult

Loading dose: 1 mg (0.5 mg then 0.25 mg q6h X 2) PO/IV
Maintenance dose: 0.125-0.375 mg/d PO/IV

Pediatric

Dosing is age and weight based; total digitalizing dose (TDD) is administered in mcg/kg/d
Loading dose: 1/2 TDD followed by 1/4 TDD q8h X 2
Maintenance dose <10 years: Divided dose bid
Maintenance dose >10 years: Administered qd

Interactions

Medications that may increase digoxin levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil; medications that may decrease serum digoxin levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Contraindications

Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis

Loop diuretics

These agents inhibit electrolyte reabsorption in the thick ascending limb of the loop of Henle, thus promoting diuresis.

Furosemide (Lasix)

Commonly used diuretic with moderate diuretic potency.

Dosing

Adult

Usual dose: 20-80 mg PO/IV q6-12h; not to exceed 600 mg/d
Continuous IV infusion: 0.05 mg/kg/h; titrate to effect

Pediatric

Dosages are age and weight based
Usual dose: 0.5-2 mg/kg/dose PO/IV q6-12h
Maximum dose: 6 mg/kg/dose PO; 2 mg/kg/dose IV

Interactions

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; increases auditory toxicity associated with aminoglycosides—hearing loss of varying degrees may occur; may increase anticoagulant activity of warfarin; may increase plasma lithium levels and toxicity

Contraindications

Documented hypersensitivity; hepatic coma; anuria; severe electrolyte depletion

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

Follow-up

Further Outpatient Care

• According to the Canadian Adult Congenital Heart Association, all patients with coarctation of the aorta need to be monitored by a cardiologist.
• Patients should have at least one MRI or angiogram following repair of the coarctation.
• Close surveillance and aggressive management are necessary for residual hypertension, heart failure or intracardiac disease, associated bicuspid aortic valve, recurrent coarctation of the aorta, or significant arm-leg blood pressure gradient at rest or with exercise.
• Ascending aortic dilation in the presence of a bicuspid aortic valve, new or unusual headache from berry aneurysm formation, late dissection proximal or distal to the repair site, and aneurysm formation at the site of coarctation repair are late sequelae of this disease.

Complications

• Postoperative complications
  • Hoarseness due to damage to the recurrent laryngeal nerve as it loops around the patent ductus arteriosus or ligamentum.
  • Ipsilateral diaphragmatic paralysis may result from injury to the phrenic nerve.
  • Chylothorax can occur due to damage to the thoracic duct that crosses behind the aortic arch and left subclavian artery.
  • Serious postoperative hemodynamic collapse may result from hemorrhage due to injury to the chest wall collaterals.
  • Rebound and paradoxical hypertension is observed frequently and may be related to the baroreceptor-mediated increase in sympathetic activity and reflex vasospasm in the vascular territory distal to the coarctation.
  • Postcoarctectomy syndrome is a unique problem early in the postoperative period. Increases in blood flow and pressure in the mesenteric arteries after repair of coarctation may result in abdominal distention and pain, vomiting, and decreased bowel sounds. This syndrome may be masked because of poorly controlled postoperative hypertension and early enteral feeding. By aggressively controlling postoperative hypertension and delaying enteral feeding for 2 days after surgery, incidence of postcoarctectomy syndrome may be reduced.
  • Paralysis of the lower body resulting from spinal cord injury is the most serious complication. Because of complex collateral formation, ischemia of the spinal cord is often difficult to predict and, therefore, may be unavoidable.
• Long-term complications
  • Systemic hypertension is the most common long term complication. This may be accentuated by exercise, creating a need to exclude residual or recurrent obstruction.

Prognosis

• Patients who are not treated for coarctation of the aorta may reach the age of 35 years; fewer than 20% survive to age 50 years. If coarctation is repaired before the age of 14 years, the 20-year survival rate is 91%. If coarctation is repaired after the age of 14 years, the 20-year survival rate is 79%.
• After repair of coarctation of the aorta, 97-98% of patients are NYHA class I. Impaired diastolic left ventricular function and persistent hypertrophy due to increased pressure gradient at the coarctation site during exercise may result in myocardial hypertrophy despite successful hemodynamic results. Overall, left ventricular systolic function is normal or hyperdynamic in these patients.
• Pregnancy
  • Most women reach childbearing age. If maternal coarctation is not repaired, risks to fetus and mother are increased. The maternal mortality rate is approximately 3-8%.
  • Despite repair, women have an increased risk of aortic dissection and rupture of cerebral aneurysm in the third trimester and peripartum period due to hemodynamic and hormonal changes.
  • All pregnant women with a history of coarctation, either native or repaired, should be considered high risk.
  • Significant stenosis—native, residual, or recurrent—is a contraindication to pregnancy.

Patient Education

• Most adults with coarctation have undergone repair; however, continued education regarding exercise, endocarditis and endarteritis prevention, and pregnancy issues is necessary.
• For the rare adult with uncorrected coarctation, extensive patient education is necessary on issues ranging from pathology and repair to lifestyle modification and follow-up care.
• The medical practitioner must understand that coarctation is a complex lifelong condition that may be repaired but is never truly corrected.

References

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Keywords

aorta coarctation, coarctation of aorta, cardiac lesion, juxtaductal coarctation, preductal coarctation, postductal coarctation, vascular malformation, coarctated aortic segment, infective endarteritis, cystic medial necrosis, coarctation of the aorta, narrowing of the aorta, ductus tissue theory, hemodynamic theory, ventricular septal defect, bicuspid aortic valve, left ventricular outflow obstruction, tubular hypoplasia of the transverse aortic arch, congenital cardiac lesions, XO Turner syndrome, aortic arch hypoplasia, extracardiac vascular anomalies

Contributor Information and Disclosures

Author

Sandy N Shah, DO, MBA, Private Practice, Houston, Texas
Sandy N Shah, DO, MBA is a member of the following medical societies: American College of Cardiology, American Heart Association, and American Osteopathic Association
Disclosure: Nothing to disclose.

Coauthor(s)

Dawn M Calderon, DO, Co-Director of Center for Adults With Congenital Heart Disease, Clinical Associate Professor, Departments of Cardiology and Internal Medicine, Deborah Heart and Lung Center, Robert Wood Johnson School of Medicine
Dawn M Calderon, DO is a member of the following medical societies: American College of Cardiology and American Osteopathic Association
Disclosure: Nothing to disclose.

Medical Editor

Alan D Forker, MD, Professor of Medicine, Program Director of Cardiovascular Fellowship, University of Missouri at Kansas City School of Medicine; Director, Outpatient Lipid Diabetes Research Center, MidAmerica Heart Institute of St Luke's Hospital
Alan D Forker, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, American Society of Hypertension, and Phi Beta Kappa
Disclosure: Research Grant Grant/research funds Hospital contracts to do research; I am a hospital employee with no personal profit; Speakers Bureau Honoraria Speaking and teaching

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Frank M Sheridan, MD, Cardiology, Providence Everett Medical Center
Frank M Sheridan, MD is a member of the following medical societies: American College of Cardiology, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

George A Stouffer III, MD, Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center
George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

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