Surgical Approach to Coarctation of the Aorta and Interrupted Aortic Arch

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Coarctation is a term derived from the Latin coarctation, meaning a drawing or pressing together. More precisely, coarctation refers to a narrowing of the lumen of a vessel producing an obstruction to flow. A localized segment of narrowing is called a coarctation, whereas a diffuse segment of narrowing is known as tubular hypoplasia.

Coarctation was once described as infantile and adult; however, these descriptions were not accurate because both types can be observed in either age group. As our understanding of the pathophysiology of coarctation evolved, the terms preductal and postductal were often used to categorize coarctation in relation to the ductus arteriosus. Although this anatomic description remains true, the exact location usually does not change the presentation; this knowledge has led to the unified description of most neonatal coarctation as juxtaductal.

Meckel originally noted coarctation on autopsy in 1750, and Morgagni again noted it in 1760. Forty-four years after Paris provided the first accurate description of coarctation of the aorta in 1791, Legrand made the first diagnosis in a living patient in 1835. Bonnet was the first to categorize coarctation into infantile and adult forms, which were later revised to preductal and postductal forms.

Blalock and Park proposed the first surgical repair in 1944, describing a bypass from the left subclavian artery to the aorta to circumvent the area of narrowing. Crafoord and Nylin performed the first resection with end-to-end reanastomosis in 1945, whereas Gross used homografts to replace the narrowed segments of aorta. In 1966, Waldhausen and Nahrwold performed the first subclavian-flap aortoplasty. More recently, advanced interventional cardiology techniques have led to an interest in percutaneous transluminal aortoplasty for both native coarctation and recoarctation. [1]

Coarctation is defined as a narrowing of the lumen of the aorta that obstructs flow. Variations of coarctation depend on the length of the involved segment. Typically located at the insertion of the ductus or ligamentum arteriosum, a localized coarctation may occur at any point along the length of the aorta. Coarctation rarely occurs at multiple sites, a phenomenon sometimes observed in Turner syndrome. Diffuse long-segment coarctation, also known as tubular hypoplasia, is typically found at the aortic isthmus (ie, the segment between the left subclavian artery and the insertion of the ductus). With extreme coarctation, the entire transverse arch may be hypoplastic.

Souders first described pseudocoarctation in 1951. Often discovered on simple chest radiography, the aorta has an abnormal contour. Aortography shows a tortuous, kinked aorta with no gradient. Kinking or buckling of the aorta changes the healthy conformation of the aorta but does not obstruct flow. Once thought benign, aneurysmal dilation can occur distal to the affected area, leading to the specter of rupture of the aorta. Current therapy requires close follow-up care. Aggressively pursue surgical repair after the aorta begins to demonstrate progressive dilation.

Complete interruption of the aorta, or interrupted aortic arch (IAA), is a fairly rare condition. First described in 1778 by Steidele, IAA accounts for less than 1.5% of all instances of congenital heart disease. Complete interruption of the aorta is usually associated with other anomalies, including DiGeorge syndrome (29% incidence). [2] In 1955, Samson performed the first known surgical correction of IAA. Sirak performed the first repair in a neonate in 1968.

Defined as a complete absence of a segment of the aortic arch, the description of IAA is based on the absent segment. In 1959, Celoria and Patton developed the following classification of IAA [3] ; Schreiber et al provided the percentages in 1997 [2] :

Type A (13%): Interruption occurs between the left subclavian artery and the descending aorta.

Type B (84%): Interruption occurs between the left subclavian artery and the left common carotid artery.

Type C (3%): The absent segment occurs between the left common carotid artery and the innominate artery.

Subtypes A1, B1, and C1: All describe an anomalous origin of the right subclavian artery from the distal aorta.

Although the cause is unknown, IAA is associated with defects that decrease ascending aortic flow and increase ductal flow. As with coarctation, abnormal fetal blood-flow patterns are theorized to substantially contribute to the etiology of IAA.

Previously uniformly fatal, the development of prostaglandin E1 (PGE1) therapy to maintain ductal patency has greatly improved surgical results by allowing time to optimize the patient’s hemodynamic state before surgery. The prognosis of patients with IAA is poor if the condition is uncorrected. The mean age at death is 4-10 days, with 90% dying within the first year of life. After repair, the 10-year survival rate has improved from approximately 47% to 81% in non-complex cases and 54% in complex cases. [4]

Noncomplex cases included concomitant ventricular septal defect (VSD), aortopulmonary window, or left ventricular outflow tract obstruction. Complex cases included concomitant Taussig-Bing double-outlet right ventricle and truncus arteriosus. Risk factors for increased mortality included primary aortic anastomosis, presence of complex anomalies, and initial IAA repair before 1994.

Whether a staged repair or a single operation should be used to repair IAA remains controversial. Median sternotomy is still preferred if correction of associated anomalies is to occur concomitantly. Methods of surgical correction are similar to those of coarctation repair and include end-to-end anastomosis of the remaining segments with or without patch augmentation, end-to-side anastomosis of the arch vessel with either the proximal or distal segment, or use of an interposition graft to take the place of the missing segment. Long-term probability for reintervention remains high regardless of operative technique. [4, 5, 6]

Ohye et al describe operative techniques for IAA with special circumstances in the second edition of Mastery of Cardiothoracic Surgery. [7] These include IAA with aortic valve hypoplasia or atresia, IAA with truncus arteriosus, IAA with transposition of the great arteries, and IAA with single ventricle.

Most data demonstrate that mortality rates decrease and outcomes improve with increasing experience. In their series, Schreiber et al demonstrated that early mortality rates decreased from 42% in 1975-1985 to only 17% in 1985-1995, which was a result of improved surgical techniques and advances in the preoperative and postoperative treatment of neonates. [2] Immediate surgical intervention remains the only therapy. IAA is a difficult surgical problem, although the most recent results have been encouraging, with increased survival and decreased morbidity rates.

Observed in 1 in 3000 to 1 in 4000 autopsies, coarctation accounts for approximately 5-10% of cases of congenital heart disease. Isolated coarctation is more common in males than in females, whereas the incidence of complex lesions is equal in males and females. The birth prevalence of coarctation for patients in 1980-1994 was 0.32 case per 1000 live births. [8]

Although the cause of coarctation remains controversial, 2 major theories are supported by the current literature.

The muscular theory suggests that extension of tissue from the ductus arteriosus (a muscular artery) extends into the aorta (an elastic artery) during development. When the ductus contracts and fibroses at birth, it leads to a narrowing of the aortic lumen.

The second theory is related to abnormal fetal blood-flow patterns. During fetal development, the aortic isthmus is a watershed area, as the ascending aorta receives blood from the heart, sending it to the head, while the descending aorta receives ductal blood to send to the rest of the body. As a result, the initial diameter of the isthmus is small, and if the proper molecular cues are not present, it may not grow sufficiently. The incidence of coarctation is increased in disorders in which an obstruction of the left ventricular outflow tract reduces ascending aortic flow. In converse, the incidence is decreased in disorders in which decreased ductal flow is present, such as tetralogy of Fallot.

Although both theories provide ample evidence, a combination probably best encompasses the likely etiology. [9]

Common associated anomalies of coarctation of the aorta include bicuspid aortic valve, VSD, patent ductus arteriosus, and various mitral-valve disorders. Congenital aortic stenosis, aortic atresia, and hypoplastic left heart syndrome are less common. Coarctation of the aorta may be observed in transposition of the great vessels, particularly when the right ventricular outflow tract is obstructed. Data suggest that more than 70% of VSDs that occur with coarctation may close spontaneously. [10, 11] Coarctation is observed in as many as 50% of patients with the Taussig-Bing anomaly. [12, 13] A genetic or familial basis may be involved because 15-36% of children with Turner syndrome may have coarctation.

The pathophysiology of untreated coarctation revolves around the associated hypertension. A 3-pronged hypertensive response occurs in the presence of coarctation. Blood pressure is mechanically affected at all levels and at the level of the kidneys, and recent data suggest that hypertension evolves from an endothelial process as well.

The natural history of coarctation depends on the age of the individual at presentation and on the associated anomalies. Symptomatic infants have a high mortality rate, and those who survival to adulthood still have greatly decreased life expectancy, even with surgical correction. The data have changed somewhat over the years with the introduction of antibiotics and improved neonatal care; however, untreated coarctation still results in a grave prognosis.

In 1928, Abbott reviewed 200 cases with coarctation in patients older than 2 years and found that 34% died by the time they were aged 40 years, with an average age at death of 42 years. At that time, the 3 major causes of death were spontaneous rupture of the aorta, bacterial endocarditis, and cerebral hemorrhage.

Neonates usually present with left ventricular failure as a result of severe and acute afterload, which is further exacerbated by acidosis. This acidosis results from diminished peripheral flow secondary to the coarct itself, in addition to the failing left ventricle.

Twenty years later, in 1947, Reifenstein reviewed 104 cases and found little change, with an average age at death of 35 years. The 2 leading causes of death were unchanged. By 1970, the results had improved somewhat; however, the mortality rate was still 75% by the time a person with coarctation was aged 46 years. [14] In persons with untreated coarctation, the coronary arteries have intimal degeneration, medial thickening, and increased mineralization, all of which are secondary to the hypertension associated with untreated disease.

The clinical presentation of patients with coarctation depends on their age at presentation and on the presence and severity of any associated anomalies. The 2 clinically significant variants, preductal and postductal coarctation, can manifest in different ways.

Preductal coarctation is associated with an increased incidence of cardiac defects, and the patient may present with congestive heart failure (CHF) if a VSD is present. A preductal defect does not change normal fetal blood-flow patterns. As a result, no collaterals form in utero. If blood flows through the patent ductus arteriosus, pulses are often palpable in the lower extremities. Symptoms develop as the ductus closes, leading to a clinically significant obstruction.

Upon clinical examination, the infant is often irritable and disinterested in feeding. Tachycardia is often present. Few findings may be apparent on physical examination in a healthy-appearing infant. However, in the uncompensated patient, differential cyanosis may be observed between the upper body and the lower body. A systolic murmur may be present over the left precordium or between the scapulae on the patient’s back. An infant who is compensating (ie, one with a left-to-right shunt through a patent foramen ovale) should have a substantial systolic blood-pressure gradient between the arms and the legs.

Physical findings in a neonate who is decompensating and critically ill may differ substantially. The blood-pressure gradient is often absent secondary to diminished cardiac output. Hypotension, oliguria, and severe metabolic acidosis are concurrent with severe coarctation, as blood flow to the kidneys and all distal structures is drastically impaired. In severe obstruction or in IAA, diagnosis by physical examination can be obscured as long as the ductus remains patent because the pulmonary artery pulse is palpated in the femoral arteries.

Paraductal and postductal anomalies are often isolated defects, and the incidence of associated anomalies is low. Later in life, patients may present with headache, epistaxis, or visual disturbances. Exertional dyspnea and stroke are other presenting symptoms. [15]

Coarctation can be clinically diagnosed depending on the available evidence, as described above. To summarize, hypertension or a systolic blood-pressure gradient between the arms and legs may be observed. Checking the patient’s blood pressure in both arms is important because an anomalous origin of the right subclavian distal to the coarcted segment may be present. A systolic murmur over the left precordium or between the scapulae may be heard, and the femoral pulses may be absent or diminished with a delayed upstroke. In children older than 5 years, look for the signs of collateral circulation (ie, enlarged and palpable collateral vessels, audible bruits, and dilatation of the intercostals [rib notching]).

The presence of coarctation alone is usually indication for surgery. Timing of the operation and the method of repair are decisions to be made. Symptomatic infants often require urgent surgery. However, the patient’s condition must be stabilized with medical therapy before the coarctations is repaired. Neonates often present with profound acidosis and respiratory distress. An infusion of prostaglandin E1 (PGE1) may be administered within a month of birth and often opens a closed ductus.

The most relevant anatomy for understanding coarctation of the aorta is the aortic arch, the great vessels, and the insertion of the ductus. Because coarctation and interrupted aortic arch (IAA) can occur anywhere along the arch, being able to recognize the origins of the great vessels, especially on aortography, is important. The ductus arteriosus is a remnant of the sixth left aortic arch; it connects the pulmonary trunk with the aorta in utero and attaches to the lower concave surface of the aortic arch directly opposite the left common carotid and left subclavian arteries. The left recurrent laryngeal nerve hooks around the lower border of this structure and can easily be damaged if care is not taken to avoid it.

Generally considered a life-saving procedure, repair of coarctation has few absolute contraindications. Coexisting illnesses or anomalies in an infant (eg, necrotizing enterocolitis) make take initial precedence in treatment. Sepsis is likely the greatest relative contraindication to surgery. This condition is related to the overall inflammatory response and to edema formation observed with the septic immune response. Dissection into the periaortic space is made more difficult that is otherwise would be, and the crucial tension-free anastomoses are considerable more difficult to construct than they are in other situations.

Luijendijk P, Boekholdt SM, Blom NA, Groenink M, Backx AP, Bouma BJ, et al. Percutaneous treatment of native aortic coarctation in adults. Neth Heart J. 2011 Oct. 19(10):436-9. [Medline]. [Full Text].

Schreiber C, Mazzitelli D, Haehnel JC, et al. The interrupted aortic arch: an overview after 20 years of surgical treatment. Eur J Cardiothorac Surg. 1997 Sep. 12(3):466-9; discussion 469-70. [Medline].

Celoria GC, Patton RB. Congenital absence of the aortic arch. Am Heart J. 1959. 58:408.

Brown JW, Ruzmetov M, Okada Y, Vijay P, Rodefeld MD, Turrentine MW. Outcomes in patients with interrupted aortic arch and associated anomalies: a 20-year experience. Eur J Cardiothorac Surg. 2006 May. 29(5):666-73; discussion 673-4. [Medline].

Liu JY, Jones B, Cheung MM, Galati JC, Koleff J, Konstantinov IE, et al. Favourable Anatomy After End-to-Side Repair of Interrupted Aortic Arch. Heart Lung Circ. 2013 Aug 30. [Medline].

Miyamoto T, Yoshii T, Inui A, Ozaki S. Staged repair for aortic arch reconstruction and intracardiac repair following bilateral pulmonary artery banding in 3 critical patients. Interact Cardiovasc Thorac Surg. 2013 Jun. 16(6):892-4. [Medline]. [Full Text].

Shen I, Ungerleider RM; Ohye RG, Suzuki T, Devaney EJ, Bove EL. Coarctation of the Aorta, Interrupted Aortic Arch Complex. Kaiser LR, Kron IL, Spray TL. Mastery of Cardiothoracic Surgery. Second. Philadelphia, PA: Lippincott, Williams and Wilkins; 2007. chap 78-79.

Grech V. Diagnostic and surgical trends, and epidemiology of coarctation of the aorta in a population-based study. Int J Cardiol. 1999 Feb 28. 68(2):197-202. [Medline].

Van Son JA, Mohr FW, Hess H, et al. Early repair of coarctation of the aorta. Ann Thorac Cardiovasc Surg. 1999 Aug. 5(4):237-44. [Medline].

Moene RJ, Gittenberger-de Groot AC, Oppenheimer-Dekker A, Bartelings MM. Anatomic characteristics of ventricular septal defect associated with coarctation of the aorta. Am J Cardiol. 1987 Apr 15. 59(9):952-5. [Medline].

Park JK, Dell RB, Ellis K, Gersony WM. Surgical management of the infant with coarctation of the aorta and ventricular septal defect. J Am Coll Cardiol. 1992 Jul. 20(1):176-80. [Medline].

Parr GV, Waldhausen JA, Bharati S, et al. Coarctation in Taussig-Bing malformation of the heart. Surgical significance. J Thorac Cardiovasc Surg. 1983 Aug. 86(2):280-7. [Medline].

Sadow SH, Synhorst DP, Pappas G. Taussig-Bing anomaly and coarctation of the aorta in infancy: surgical options. Pediatr Cardiol. 1985. 6(2):83-9. [Medline].

Campbell M. Natural history of coarctation of the aorta. Br Heart J. 1970 Sep. 32(5):633-40. [Medline].

Shearer WT, Rutman JY, Weinberg WA, Goldring D. Coarctation of the aorta and cerebrovascular accident: a proposal for early corrective surgery. J Pediatr. 1970 Dec. 77(6):1004-9. [Medline].

Kpodonu J, Ramaiah VG, Diethrich EB. Intravascular ultrasound imaging as applied to the aorta: a new tool for the cardiovascular surgeon. Ann Thorac Surg. 2008 Oct. 86(4):1391-8. [Medline].

Rudolph AM, Heymann MA, Spitznas U. Hemodynamic considerations in the development of narrowing of the aorta. Am J Cardiol. 1972 Oct. 30(5):514-25. [Medline].

Jurcut R, Daraban AM, Lorber A, Deleanu D, Amzulescu MS, Zara C, et al. Coarctation of the aorta in adults: what is the best treatment? Case report and literature review. J Med Life. 2011 May 15. 4(2):189-95. [Medline]. [Full Text].

Korkmaz AA, Guden M, Onan B, Tarakci SI, Demir AS, Sagbas E, et al. New technique for single-staged repair of aortic coarctation and coexisting cardiac disorder. Tex Heart Inst J. 2011. 38(4):404-8. [Medline]. [Full Text].

Ungerleider RM, Ebert PA. Indications and techniques for midline approach to aortic coarctation in infants and children. Ann Thorac Surg. 1987 Nov. 44(5):517-22. [Medline].

Alsoufi B, Cai S, Coles JG, Williams WG, Van Arsdell GS, Caldarone CA. Outcomes of different surgical strategies in the treatment of neonates with aortic coarctation and associated ventricular septal defects. Ann Thorac Surg. 2007 Oct. 84(4):1331-6; discussion 1336-7. [Medline].

Kanter KR, Mahle WT, Kogon BE, Kirshbom PM. What is the optimal management of infants with coarctation and ventricular septal defect?. Ann Thorac Surg. 2007 Aug. 84(2):612-8; discussion 618. [Medline].

Aebert H, Laas J, Bednarski P, et al. High incidence of aneurysm formation following patch plasty repair of coarctation. Eur J Cardiothorac Surg. 1993. 7(4):200-4; discussion 205. [Medline].

Kawauchi M, Tada Y, Asano K, Sudo K. Angiographic demonstration of mesenteric arterial changes in postcoarctectomy syndrome. Surgery. 1985 Sep. 98(3):602-4. [Medline].

Cunningham JN Jr, Laschinger JC, Spencer FC. Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. IV. Clinical observations and results. J Thorac Cardiovasc Surg. 1987 Aug. 94(2):275-85. [Medline].

Seirafi PA, Warner KG, Geggel RL, et al. Repair of coarctation of the aorta during infancy minimizes the risk of late hypertension. Ann Thorac Surg. 1998 Oct. 66(4):1378-82. [Medline].

Backer CL, Mavroudis C, Zias EA, et al. Repair of coarctation with resection and extended end-to-end anastomosis. Ann Thorac Surg. 1998 Oct. 66(4):1365-70; discussion 1370-1. [Medline].

Allen BS, Halldorsson AO, Barth MJ, Ilbawi MN. Modification of the subclavian patch aortoplasty for repair of aortic coarctation in neonates and infants. Ann Thorac Surg. 2000 Mar. 69(3):877-80; discussion 881. [Medline].

Sciolaro C, Copeland J, Cork R, et al. Long-term follow-up comparing subclavian flap angioplasty to resection with modified oblique end-to-end anastomosis. J Thorac Cardiovasc Surg. 1991 Jan. 101(1):1-13. [Medline].

Fiore AC, Fischer LK, Schwartz T, et al. Comparison of angioplasty and surgery for neonatal aortic coarctation. Ann Thorac Surg. 2005 Nov. 80(5):1659-64; discussion 1664-5. [Medline].

Cowley CG, Orsmond GS, Feola P, et al. Long-term, randomized comparison of balloon angioplasty and surgery for native coarctation of the aorta in childhood. Circulation. 2005 Jun 28. 111(25):3453-6. [Medline].

Karl TR. Surgery is the best treatment for primary coarctation in the majority of cases. J Cardiovasc Med (Hagerstown). 2007 Jan. 8(1):50-6. [Medline].

Al-Ata J, Arfi AM, Hussain A, Kouatly A, Galal MO. Stent angioplasty: an effective alternative in selected infants with critical native aortic coarctation. Pediatr Cardiol. 2007 May-Jun. 28(3):183-92. [Medline].

Marshall AC, Perry SB, Keane JF, Lock JE. Early results and medium-term follow-up of stent implantation for mild residual or recurrent aortic coarctation. Am Heart J. 2000 Jun. 139(6):1054-60. [Medline].

Thanopoulos BD, Hadjinikolaou L, Konstadopoulou GN, et al. Stent treatment for coarctation of the aorta: intermediate term follow up and technical considerations. Heart. 2000 Jul. 84(1):65-70. [Medline].

Kutty S, Greenberg RK, Fletcher S, Svensson LG, Latson LA. Endovascular stent grafts for large thoracic aneurysms after coarctation repair. Ann Thorac Surg. 2008 Apr. 85(4):1332-8. [Medline].

Abbott ME. Coarctation of the aorta of the adult type. Am. Heart J. 1928. 3:574.

Aeba R, Katogi T, Ueda T, et al. Complications following reparative surgery for aortic coarctation or interrupted aortic arch. Surg Today. 1998. 28(9):889-94. [Medline].

Bogers AJ, Contant CM, Hokken RB, Cromme-Dijkhuis AH. Repair of aortic arch interruption by direct anastomosis. Eur J Cardiothorac Surg. 1997 Jan. 11(1):100-4. [Medline].

DeLeon MM, DeLeon SY, Quinones JA, et al. Management of arch hypoplasia after successful coarctation repair. Ann Thorac Surg. 1997 Apr. 63(4):975-80. [Medline].

Hirooka K, Fraser CD Jr. One-stage neonatal repair of complex aortic arch obstruction or interruption. Recent experience at Texas Children”s Hospital. Tex Heart Inst J. 1997. 24(4):317-21. [Medline]. [Full Text].

Jahangiri M, Shinebourne EA, Zurakowski D, et al. Subclavian flap angioplasty: does the arch look after itself?. J Thorac Cardiovasc Surg. 2000 Aug. 120(2):224-9. [Medline].

Jenkins NP, Ward C. Coarctation of the aorta: natural history and outcome after surgical treatment. QJM. 1999 Jul. 92(7):365-71. [Medline].

Jimenez M, Daret D, Choussat A, Bonnet J. Immunohistological and ultrastructural analysis of the intimal thickening in coarctation of human aorta. Cardiovasc Res. 1999 Mar. 41(3):737-45. [Medline].

Mainwaring RD, Lamberti JJ. Mid- to long-term results of the two-stage approach for type B interrupted aortic arch and ventricular septal defect. Ann Thorac Surg. 1997 Dec. 64(6):1782-5; discussion 1785-6. [Medline].

O’Connor AR, Moody AR, Ludman CN. Images in cardiology. Aortic coarctation diagnosed by magnetic resonance angiography. Heart. 1999 Jun. 81(6):671. [Medline].

Ovaert C, McCrindle BW, Nykanen D, et al. Balloon angioplasty of native coarctation: clinical outcomes and predictors of success. J Am Coll Cardiol. 2000 Mar 15. 35(4):988-96. [Medline].

Reifenstein GH, Levine SA, Gross RE. Coarctation of the aorta: a review of 104 autopsied cases of the “adult type” 2 years of age or older. Am Heart J. 1947. 33:146.

Rothman A. Coarctation of the aorta: an update. Curr Probl Pediatr. 1998 Feb. 28(2):33-60. [Medline].

Saba SE, Nimri M, Shamaileh Q, et al. Balloon coarctation angioplasty: follow-up of 103 patients. J Invasive Cardiol. 2000 Aug. 12(8):402-6. [Medline].

Sakopoulos AG, Hahn TL, Turrentine M, Brown JW. Recurrent aortic coarctation: is surgical repair still the gold standard?. J Thorac Cardiovasc Surg. 1998 Oct. 116(4):560-5. [Medline].

Thanopoulos BV, Eleftherakis N, Tzanos K, Skoularigis I, Triposkiadis F. Stent implantation for adult aortic coarctation. J Am Coll Cardiol. 2008 Nov 25. 52(22):1815-6. [Medline].

Tlaskal T, Hucin B, Hruda J, et al. Results of primary and two-stage repair of interrupted aortic arch. Eur J Cardiothorac Surg. 1998 Sep. 14(3):235-42. [Medline].

Vitullo DA, DeLeon SY, Graham LC, et al. Extended end-to-end repair and enlargement of the entire arch in complex coarctation. Ann Thorac Surg. 1999 Feb. 67(2):528-31. [Medline].

Wong CH, Watson B, Smith J. The use of left heart bypass in adult and recurrent coarctation repair. Eur J Cardiothorac Surg. 2001 Dec. 20(6):1199-201. [Medline].

Wood MK. Acyanotic cardiac lesions with normal pulmonary blood flow. Neonatal Netw. 1998 Apr. 17(3):5-11. [Medline].

Dale K Mueller, MD Co-Medical Director of Thoracic Center of Excellence, Chairman, Department of Cardiovascular Medicine and Surgery, OSF Saint Francis Medical Center; Cardiovascular and Thoracic Surgeon, HeartCare Midwest, Ltd, A Subsidiary of OSF Saint Francis Medical Center; Section Chief, Department of Surgery, University of Illinois at Peoria College of Medicine

Dale K Mueller, MD is a member of the following medical societies: American College of Chest Physicians, American College of Surgeons, American Medical Association, Chicago Medical Society, Illinois State Medical Society, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Rush Surgical Society

Disclosure: Received consulting fee from Provation Medical for writing.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mary C Mancini, MD, PhD, MMM Surgeon-in-Chief and Director of Cardiothoracic Surgery, Christus Highland

Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons

Disclosure: Nothing to disclose.

Jonah Odim, MD, PhD, MBA Section Chief of Clinical Transplantation, Transplantation Branch, Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH)

Jonah Odim, MD, PhD, MBA is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American Association for Physician Leadership, American College of Surgeons, American Heart Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, Association for Academic Surgery, Association for Surgical Education, International Society for Heart and Lung Transplantation, National Medical Association, New York Academy of Sciences, Royal College of Physicians and Surgeons of Canada, Society of Critical Care Medicine, Society of Thoracic Surgeons, Canadian Cardiovascular Society

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Daniel S Schwartz, MD, MBA, FACS Medical Director of Thoracic Oncology, St Catherine of Siena Medical Center, Catholic Health Services

Daniel S Schwartz, MD, MBA, FACS is a member of the following medical societies: American College of Chest Physicians, American College of Surgeons, Society of Thoracic Surgeons, Western Thoracic Surgical Association

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Theodore C Koutlas, MD Assistant Professor, Department of Surgery, Division of Cardiothoracic Surgery, Pitt County Memorial Hospital

Theodore C Koutlas, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Southern Thoracic Surgical Association

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Katie Love, MD Clinical Instructor, Department of Surgery, University of Louisville School of Medicine

Katie Love, MD is a member of the following medical societies: American College of Surgeons, Eastern Association for the Surgery of Trauma, and Society of Critical Care Medicine

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David M Maziarz, MD Thoracic Surgeon, St Francis Cardiovascular & Thoracic Associates

David M Maziarz is a member of the following medical societies: American College of Surgeons

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Clifton C Reade, MD Fellow, Department of Cardiothoracic Surgery, University of Pennsylvania School of Medicine

Clifton C Reade, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, Society of Thoracic Surgeons, and Southeastern Surgical Congress

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Surgical Approach to Coarctation of the Aorta and Interrupted Aortic Arch

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