eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Cardiology

Truncus Arteriosus

Author: Doff B McElhinney, MD, Assistant Professor of Pediatrics, Harvard Medical School; Associate in Cardiology, Department of Cardiology, Children's Hospital of Boston
Coauthor(s): Gil Wernovsky, MD, FACC, FAAP, Children's Hospital of Philadelphia; Professor, Department of Pediatrics, University of Pennsylvania
Contributor Information and Disclosures

Updated: Nov 5, 2007

Introduction

Background

Truncus arteriosus (TA) is an uncommon congenital cardiovascular anomaly that is characterized by a single arterial trunk arising from the normally formed ventricles by means of a single semilunar valve (ie, truncal valve). In addition, the pulmonary arteries originate from the common arterial trunk distal to the coronary arteries and proximal to the first brachiocephalic branch of the aortic arch. The common trunk typically straddles a defect in the outlet portion of the interventricular septum (ie, conal septum); however, in rare cases, it may originate almost completely from the right or left ventricle. In patients with a patent and normal caliber aortic arch, the ductus arteriosus is either absent or diminutive.

Embryology

The anomaly is thought to result from incomplete or failed septation of the embryonic truncus arteriosus, hence the persistence of the Latin term truncus arteriosus and its variants. Aortopulmonary and interventricular defects are believed to represent an abnormality of conotruncal septation. Because the common trunk originates from both the left and right ventricles, and pulmonary arteries arise directly from the common trunk, a ductus arteriosus is not required to support the fetal circulation.

Accordingly, an inverse relationship between the caliber of the ductus arteriosus (derived from the sixth branchial arch) and that of the distal portion of the aortic arch (derived from the fourth branchial arch) is typically present. Although the hemodynamic consequences of a common arterial outflow may predispose to the development of the fourth or the sixth arch (but not both), anomalous development of the arch system is likely a fundamental aspect of the morphogenetic anomalies that produce truncus arteriosus.

Anatomy

Pulmonary arteries may arise from the common trunk in one of several patterns, which are often used to classify subtypes of truncus arteriosus. Several classification schemes have been proposed, none of which is ideal.

The earliest classification, developed by Collett and Edwards in 1949, includes truncus arteriosus types I-IV, as follows (see Media file 1):1

  • Truncus arteriosus type I is characterized by origin of a single pulmonary trunk from the left lateral aspect of the common trunk, with branching of the left and right pulmonary arteries from the pulmonary trunk.
  • Truncus arteriosus type II is characterized by separate but proximate origins of the left and right pulmonary arterial branches from the posterolateral aspect of the common arterial trunk.
  • In truncus arteriosus type III, the branch pulmonary arteries originate independently from the common arterial trunk or aortic arch, most often from the left and right lateral aspects of the trunk. This occasionally occurs with origin of one pulmonary artery from the underside of the aortic arch, usually from a ductus arteriosus.
  • Type IV truncus arteriosus, originally proposed by Collett and Edwards as a form of the lesion with neither pulmonary arterial branch arising from the common trunk, is now recognized to be a form of pulmonary atresia with ventricular septal defect rather than truncus arteriosus (not depicted in Media file 1).

Collett and Edwards describe variations of each of these types.

In 1965, Van Praaghs proposed the other commonly cited classification scheme that also includes 4 primary types, as follows (combined with Collett and Edwards types in Media file 1):2

  • Type A1 is identical to the type I of Collett and Edwards.
  • Type A2 includes Collett and Edwards type II and most cases of type III, namely those with separate origin of the branch pulmonary arteries from the left and right lateral aspects of the common trunk.
  • Type A3 includes cases with origin of one branch pulmonary artery (usually the right) from the common trunk, with pulmonary blood supply to the other lung provided either by a pulmonary artery arising from the aortic arch (a subtype of Collett and Edwards type III) or by systemic to pulmonary arterial collaterals.
  • Type A4 is defined not by the pattern of origin of branch pulmonary arteries, but rather by the coexistence of an interrupted aortic arch. In the vast majority of cases of type A4, which fall into the type I of Collett and Edwards, the pulmonary arteries arise as a single pulmonary trunk that then branches. In any of these patterns, intrinsic stenosis, hypoplasia, or both may be present in one or both branch pulmonary arteries, which may have an effect on management and outcome.

Associated cardiovascular anomalies

Various abnormalities may be associated with truncus arteriosus, some of which may have an impact on management and outcome.

Structural abnormalities of the truncal valve, including dysplastic and supernumerary leaflets, are frequently observed, and significant regurgitation (moderate or severe) through the truncal valve may be present in 20% or more patients.

Similarly, proximal coronary arteries are abnormal in many patients, with a single coronary artery and an intramural course as the most important variations.

The other major anomaly associated with truncus arteriosus in a substantial portion of cases is interruption of the aortic arch, which almost always occurs between the left common carotid and subclavian arteries.

Other relatively common but minor associations include right aortic arch, left superior caval vein, aberrant subclavian artery, and atrial septal defect. In addition to these defects found in the usual spectrum of truncus arteriosus, several other major but rare associated anomalies are reported, including complete atrioventricular septal defect, double aortic arch, and various forms of functionally univentricular heart.

Sepsis is probably the most important noncardiac problem in the differential diagnosis of neonates with truncus arteriosus, as well as other forms of complex congenital heart disease. Young infants with truncus arteriosus frequently present in shock because of high output heart failure with significant pulmonary overcirculation. This scenario may resemble the presentation of neonatal sepsis, especially when the ratio of pulmonary-to-systemic blood flow is sufficiently high that the patient is not cyanotic.

Pathophysiology

Pathophysiology of truncus arteriosus is typified by cyanosis and systemic ventricular volume overload. Outflow from both ventricles is directed into the common arterial trunk. Pulmonary blood flow is derived from this combined ventricular output, and its magnitude depends on the ratio of resistances to flow in the pulmonary and systemic vascular beds. Because of the mixing (although not complete) of left and right ventricular output that occurs primarily during systole and at the level of the common arterial trunk, subnormal systemic arterial oxygen saturation is common. Similarly, because the systemic and pulmonary circulations are essentially in parallel, pulmonary blood flow typically is at least 3-fold higher than systemic blood flow, with pulmonary overcirculation and increased myocardial work that results in increased resting oxygen demand and decreased metabolic reserve.

Frequency

United States

Truncus arteriosus represents 1-2% of congenital heart defects in liveborn infants. Based on an estimated incidence of congenital heart disease of 6-8 per 1,000 liveborn children, truncus arteriosus occurs in approximately 5-15 of 100,000 live births. Among aborted fetuses and stillborn infants with cardiovascular anomalies, truncus arteriosus represents almost 5% of defects.

International

No significant difference in the incidence of truncus arteriosus is noted among those born in the United States compared with other countries.

Mortality/Morbidity

  • The natural history of truncus arteriosus without surgical intervention is not well characterized. In a number of earlier series, the median age at death without surgery ranged from 2 weeks to 3 months, with almost 100% mortality by age 1 year. Cases of patients surviving into adulthood with unrepaired truncus arteriosus are reported, but they are extremely uncommon. Cause of death in unrepaired patients is usually cardiac arrest or multiple organ failure in the face of systemic perfusion that is inadequate to meet the body's metabolic demands; progressive metabolic acidosis and myocardial dysfunction results.
  • Currently, for patients undergoing complete repair in the neonatal or early infant periods, early postoperative mortality is generally less than 10%. This represents a substantial improvement from earlier eras; as recently as 20 years ago, the early mortality rate after complete repair was higher than 25% in most series. Among patients surviving the initial postoperative period, the survival rate at a 10- to 20-year follow-up is higher than 80%, with most deaths resulting from sequelae of late repair (pulmonary vascular obstructive disease), reinterventions, or residual/recurrent physiologic abnormalities.
  • Although rarely used today, surgical palliation by banding of the pulmonary artery to protect the pulmonary vascular bed was a frequently used strategy until the 1970s and early 1980s. This practice resulted in only minor improvement in the natural history of the disease, with substantial early and intermediate mortality rates.

Race

  • Based on limited data, no racial predilection is apparent.

Sex

  • Although many series report a slight male predominance, no significant predilection based on sex is apparent.

Age

  • Truncus arteriosus is a congenital anomaly that is present from early in embryonic gestation. Currently, truncus arteriosus is diagnosed using prenatal ultrasonography in a small percentage of patients. Among patients diagnosed after birth, the median age at presentation is generally a few days, which is significantly earlier than was the case 20 or more years ago. Occasionally, patients are not diagnosed until later in infancy, childhood, or even adulthood, although such cases are exceedingly rare in the United States and Europe.

Clinical

History

  • Historical presentation of patients with truncus arteriosus who are not diagnosed before the onset of symptoms typically consists of the following:
    • Poor feeding
    • Diaphoresis
    • Tachypnea
    • Cyanosis
  • Symptoms vary and may be more or less pronounced, depending on specific anatomic features and age at presentation. For example, patients with significant truncal valve regurgitation tend to present earlier with more profound symptoms of congestive heart failure.

Physical

  • Patients with truncus arteriosus often present with cyanosis and are typically found to have decreased systemic arterial oxygen saturation.
    • Cyanosis may not be evident, especially in very young neonates in whom pulmonary vascular resistance remains elevated.
    • Even in slightly older neonates and young infants, pulmonary overcirculation and streaming of left and right ventricular outflow into the aorta and pulmonary arteries, respectively, may occasionally result in systemic oxyhemoglobin saturation well above 90%.
  • Symptoms and signs of congestive heart failure are probably more common findings than cyanosis in patients presenting early in life.
    • Symptoms of failure typically manifest as pulmonary vascular resistance falls and pulmonary overcirculation increases.
    • With progressively increasing pulmonary blood flow and, consequently, myocardial work, the initial symptoms of congestive heart failure (eg, poor feeding, diaphoresis, mild lethargy) become more evident as failure to thrive ensues.
  • Patients occasionally present in extremis, with the usual high output failure exacerbated by significant regurgitation of the truncal valve. Patients with associated interruption of the aortic arch may exhibit a shocklike picture of cardiovascular collapse during ductal closure, although the arterial duct frequently remains patent in patients with truncus and interrupted arch, even without pharmacologic therapy.

Causes

  • As with most forms of congenital heart disease, the causes of truncus arteriosus are unknown. In experimental animal models, truncus arteriosus has been linked to abnormal development of cells from the neural crest that normally inhabit the outflow region of the developing heart. This is thought to be an important etiologic factor in at least some cases of human truncus arteriosus also.
  • As with various other congenital cardiac anomalies of the conotruncal region, a substantial number of patients with truncus arteriosus (approximately 30-40%) have microdeletions within chromosome band 22q11.2, which contains a number of characterized genes. This particular type of chromosomal deletion is thought to affect migration or development of cardiac neural crest cells and may contribute to the pathogenesis of truncus arteriosus in certain cases.
    • Patients with truncus arteriosus and anomalies of the branch pulmonary arteries, such as stenosis or separate origin from the undersurface of the aortic arch, may have a higher incidence of association with band 22q11 deletion. Other specific features of truncus arteriosus that may be related to chromosomal deletion have yet to be characterized.
    • The specific gene product or products responsible for cardiovascular anomalies in individuals with a 22q11 deletion has not been identified definitively in humans, although one of the genes in the 22q11.2 band, TBX1, has been shown to be involved pharyngeal arch and conotruncal development. Extensive research regarding truncus arteriosus and band 22q11 association is being conducted.
  • For the most part, other factors that may cause truncus arteriosus in humans have not been clearly identified.
    • Other sporadic chromosomal and genetic abnormalities have been reported in humans with truncus arteriosus, including duplication of chromosome arm 8q and mutation of the NKX2.6 gene.
    • Several other genes have been associated with truncus arteriosus in transgenic mouse models, including Tbx20, ALK2, Cited2, and Semaphorin 3c, but so far these genes have not been implicated in human truncus arteriosus.
    • One report found that children of mothers with significant diabetes mellitus during pregnancy had an increased incidence of truncus arteriosus; however, this is not widely recognized as a significant risk factor.3
    • Although certain teratogens (eg, retinoic acid, bis-diamine) have been found to predispose to truncus arteriosus in animal models, no evidence suggests that these or others contribute importantly to this anomaly in humans.
  • DiGeorge syndrome or velocardiofacial syndrome, often included together as variations of CATCH-22 syndrome, are present in approximately 30-35% of patients with truncus arteriosus; most of these patients have deletions in band 22q11.
  • The most common noncardiac anomalies in patients with truncus arteriosus are those typically found in association with CATCH-22 syndrome, such as velopharyngeal insufficiency, cleft palate, and thymic and parathyroid dysfunction.
  • Other noncardiac anomalies found sporadically in patients with truncus arteriosus include renal abnormalities, vertebral and rib anomalies, and anomalies of the alimentary tract.

More on Truncus Arteriosus

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Treatment & Medication: Truncus Arteriosus
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Multimedia: Truncus Arteriosus
References
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References

  1. Collett RW, Edwards JE. Persistent truncus arteriosus: a classification according to anatomic types. Surg Clin North Am. 1949;29:1245-70.

  2. Van Praagh R, Van Praagh S. The anatomy of common aorticopulmonary trunk (truncus arteriosus communis) and its embryologic implications. A study of 57 necropsy cases. Am J Cardiol. Sep 1965;16(3):406-25. [Medline].

  3. Chaoui R, Bollmann R, Zienert A, et al. [Prenatal diagnosis of truncus arteriosus communis (type I) in diabetic pregnancy]. Zentralbl Gynakol. 1992;114(4):198-200. [Medline].

  4. Alexiou C, Keeton BR, Salmon AP, Monro JL. Repair of truncus arteriosus in early infancy with antibiotic sterilized aortic homografts. Ann Thorac Surg. May 2001;71(5 Suppl):S371-4. [Medline].

  5. Anderson RH, Thiene G. Categorization and description of hearts with a common arterial trunk. Eur J Cardiothorac Surg. 1989;3(6):481-7. [Medline].

  6. Bamforth SD, Braganca J, Eloranta JJ, et al. Cardiac malformations, adrenal agenesis, neural crest defects and exencephaly in mice lacking Cited2, a new Tfap2 co-activator. Nat Genet. Dec 2001;29(4):469-74. [Medline].

  7. Barbero-Marcial M, Tanamati C. Alternative nonvalved techniques for repair of truncus arteriosus: Long-term results. Semin Thorac Cardiovasc Surg Pediatr Card Surg Annu. 1999;2():121-130. [Medline].

  8. Bartelings MM, Gittenberger-de Groot AC. Morphogenetic considerations on congenital malformations of the outflow tract. Part 1: Common arterial trunk and tetralogy of Fallot. Int J Cardiol. Aug 1991;32(2):213-30. [Medline].

  9. Becker AE, Becker MJ, Edwards JE. Pathology of the semilunar valve in persistent truncus arteriosus. J Thorac Cardiovasc Surg. Jul 1971;62(1):16-26. [Medline].

  10. Bove EL, Lupinetti FM, Pridjian AK, et al. Results of a policy of primary repair of truncus arteriosus in the neonate. J Thorac Cardiovasc Surg. Jun 1993;105(6):1057-65; discussion 1065-6. [Medline].

  11. Brizard CP, Cochrane A, Austin C, et al. Management strategy and long-term outcome for truncus arteriosus. Eur J Cardiothorac Surg. Apr 1997;11(4):687-95; discussion 695-6. [Medline].

  12. Brown JW, Ruzmetov M, Okada Y, et al. Truncus arteriosus repair: outcomes, risk factors, reoperation and management. Eur J Cardiothorac Surg. Aug 2001;20(2):221-7. [Medline].

  13. Chen JM, Glickstein JS, Davies RR, et al. The effect of repair technique on postoperative right-sided obstruction in patients with truncus arteriosus. J Thorac Cardiovasc Surg. Mar 2005;129(3):559-68. [Medline].

  14. Crupi G, Macartney FJ, Anderson RH. Persistent truncus arteriosus. A study of 66 autopsy cases with special reference to definition and morphogenesis. Am J Cardiol. Oct 1977;40(4):569-78. [Medline].

  15. Danton MH, Barron DJ, Stumper O, et al. Repair of truncus arteriosus: a considered approach to right ventricular outflow tract reconstruction. Eur J Cardiothorac Surg. Jul 2001;20(1):95-103. discussion 103-4. [Medline].

  16. de la Cruz MV, Cayre R, Angelini P, et al. Coronary arteries in truncus arteriosus. Am J Cardiol. Dec 15 1990;66(20):1482-6. [Medline].

  17. Di Donato RM, Fyfe DA, Puga FJ, et al. Fifteen-year experience with surgical repair of truncus arteriosus. J Thorac Cardiovasc Surg. Mar 1985;89(3):414-22. [Medline].

  18. Digilio MC, Angioni A, Giannotti A, et al. Truncus arteriosus and duplication 8q. Am J Med Genet A. Aug 15 2003;121(1):79-81. [Medline].

  19. Ebert PA, Turley K, Stanger P, et al. Surgical treatment of truncus arteriosus in the first 6 months of life. Ann Surg. Oct 1984;200(4):451-6. [Medline].

  20. Elkins RC, Steinberg JB, Razook JD, et al. Correction of truncus arteriosus with truncal valvar stenosis or insufficiency using two homografts. Ann Thorac Surg. Nov 1990;50(5):728-33. [Medline].

  21. Feiner L, Webber AL, Brown CB, et al. Targeted disruption of semaphorin 3C leads to persistent truncus arteriosus and aortic arch interruption. Development. Aug 2001;128(16):3061-70. [Medline].

  22. Fyfe DA, Driscoll DJ, Di Donato RM, et al. Truncus arteriosus with single pulmonary artery: influence of pulmonary vascular obstructive disease on early and late operative results. J Am Coll Cardiol. May 1985;5(5):1168-72. [Medline].

  23. Gerlis LM, Ho SY, Smith A, et al. The site of origin of nonconfluent pulmonary arteries from a common arterial trunk or from the ascending aorta: its morphological significance. Am J Cardiovasc Pathol. 1990;3(2):115-20. [Medline].

  24. Hanley FL, Heinemann MK, Jonas RA, et al. Repair of truncus arteriosus in the neonate. J Thorac Cardiovasc Surg. Jun 1993;105(6):1047-56. [Medline].

  25. Heathcote K, Braybrook C, Abushaban L, et al. Common arterial trunk associated with a homeodomain mutation of NKX2.6. Hum Mol Genet. Mar 1 2005;14(5):585-93. [Medline].

  26. Heinemann MK, Hanley FL, Fenton KN, et al. Fate of small homograft conduits after early repair of truncus arteriosus. Ann Thorac Surg. Jun 1993;55(6):1409-11; discussion 1411-2. [Medline].

  27. Imamura M, Drummond-Webb JJ, Sarris GE, et al. Improving early and intermediate results of truncus arteriosus repair: a new technique of truncal valve repair. Ann Thorac Surg. Apr 1999;67(4):1142-6. [Medline].

  28. Jahangiri M, Zurakowski D, Mayer JE, et al. Repair of the truncal valve and associated interrupted arch in neonates withtruncus arteriosus. J Thorac Cardiovasc Surg. Mar 2000;119(3):508-14. [Medline].

  29. Kaartinen V, Dudas M, Nagy A, et al. Cardiac outflow tract defects in mice lacking ALK2 in neural crest cells. Development. Jul 2004;131(14):3481-90. [Medline].

  30. Kirklin JW, Barratt-Boyes BG. Truncus arteriosus. In: Cardiac Surgery. New York, NY: John Wiley & Sons; 1992:1131-51.

  31. Lacour-Gayet F, Serraf A, Komiya T, et al. Truncus arteriosus repair: influence of techniques of right ventricular outflow tract reconstruction. J Thorac Cardiovasc Surg. Apr 1996;111(4):849-56. [Medline].

  32. Litovsky SH, Ostfeld I, Bjornstad PG, et al. Truncus arteriosus with anomalous pulmonary venous connection. Am J Cardiol. Mar 1 1999;83(5):801-4, A10. [Medline].

  33. Mavroudis C, Backer CL. Surgical management of severe truncal insufficiency: experience with truncal valve remodeling techniques. Ann Thorac Surg. Aug 2001;72(2):396-400. [Medline].

  34. McElhinney DB, Driscoll DA, Emanuel BS, Goldmuntz E. Chromosome 22q11 deletion in patients with truncus arteriosus. Pediatr Cardiol. Nov-Dec 2003;24(6):569-73. [Medline].

  35. McElhinney DB, Hedrick HL, Bush DM, et al. Necrotizing enterocolitis in neonates with congenital heart disease: risk factors and outcomes. Pediatrics. Nov 2000;106(5):1080-7. [Medline].

  36. McElhinney DB, Rajasinghe HA, Mora BN, et al. Reinterventions after repair of common arterial trunk in neonates and young infants. J Am Coll Cardiol. Apr 2000;35(5):1317-22. [Medline].

  37. McElhinney DB, Reddy VM, Rajasinghe HA, et al. Trends in the management of truncal valve insufficiency. Ann Thorac Surg. Feb 1998;65(2):517-24. [Medline].

  38. Mohammadi S, Belli E, Martinovic I, et al. Surgery for right ventricle to pulmonary artery conduit obstruction: risk factors for further reoperation. Eur J Cardiothorac Surg. Aug 2005;28(2):217-22. [Medline].

  39. Momma K, Ando M, Matsuoka R. Truncus arteriosus communis associated with chromosome 22q11 deletion. J Am Coll Cardiol. Oct 1997;30(4):1067-71. [Medline].

  40. Niwa K, Perloff JK, Kaplan S, et al. Eisenmenger syndrome in adults: ventricular septal defect, truncus arteriosus, univentricular heart. J Am Coll Cardiol. Jul 1999;34(1):223-32. [Medline].

  41. Rajasinghe HA, McElhinney DB, Reddy VM, et al. Long-term follow-up of truncus arteriosus repaired in infancy: a twenty- year experience. J Thorac Cardiovasc Surg. May 1997;113(5):869-78; discussion 878-9. [Medline].

  42. Reddy VM, Rajasinghe HA, McElhinney DB, et al. Performance of right ventricle to pulmonary artery conduits after repair of truncus arteriosus: a comparison of Dacron-housed porcine valves and cryopreserved allografts. Semin Thorac Cardiovasc Surg. Jul 1995;7(3):133-8. [Medline].

  43. Schreiber C, Eicken A, Balling G, et al. Single centre experience on primary correction of common arterial trunk: overall survival and freedom from reoperation after more than 15 years. Eur J Cardiothorac Surg. Jul 2000;18(1):68-73. [Medline].

  44. Silverman NH. Truncus arteriosus. In: Pediatric Echocardiography. Baltimore, Md: Williams & Wilkins; 1993:229-43.

  45. Stewart DE, Kirby ML, Sulik KK. Hemodynamic changes in chick embryos precede heart defects after cardiac neural crest ablation. Circ Res. Nov 1986;59(5):545-50. [Medline].

  46. Suzuki A, Ho SY, Anderson RH, et al. Coronary arterial and sinusal anatomy in hearts with a common arterial trunk. Ann Thorac Surg. Dec 1989;48(6):792-7. [Medline].

  47. Takeuchi JK, Mileikovskaia M, Koshiba-Takeuchi K, et al. Tbx20 dose-dependently regulates transcription factor networks required for mouse heart and motoneuron development. Development. May 2005;132(10):2463-74. [Medline].

  48. Thompson LD, McElhinney DB, Reddy M, et al. Neonatal repair of truncus arteriosus: continuing improvement in outcomes. Ann Thorac Surg. Aug 2001;72(2):391-5. [Medline].

  49. Tlaskal T, Hucin B, Kostelka M, et al. Successful reoperation for severe left bronchus compression after repair of persistent truncus arteriosus with interrupted aortic arch. Eur J Cardiothorac Surg. Mar 1998;13(3):306-9. [Medline].

  50. Tometzki AJ, Suda K, Kohl T, et al. Accuracy of prenatal echocardiographic diagnosis and prognosis of fetuses with conotruncal anomalies. J Am Coll Cardiol. May 1999;33(6):1696-701. [Medline].

  51. Tworetzky W, McElhinney DB, Brook MM, et al. Echocardiographic diagnosis alone for the complete repair of major congenital heart defects. J Am Coll Cardiol. Jan 1999;33(1):228-33. [Medline].

  52. Van Mierop LHS, Patterson DF, Schnarr WR. Pathogenesis of persistent truncus arteriosus in light of observations made in a dog embryo with the anomaly. Am J Cardiol. 1978;41(4):755-62. [Medline].

  53. Van Praagh R. Truncus arteriosus: what is it really and how should it be classified?. Eur J Cardiothorac Surg. 1987;1(2):65-70. [Medline].

  54. Volpe P, Paladini D, Marasini M, et al. Common arterial trunk in the fetus: characteristics, associations, and outcome in a multicentre series of 23 cases. Heart. Dec 2003;89(12):1437-41. [Medline].

  55. Williams JM, de Leeuw M, Black MD, et al. Factors associated with outcomes of persistent truncus arteriosus. J Am Coll Cardiol. Aug 1999;34(2):545-53. [Medline].

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Further Reading

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Keywords

truncus arteriosus, TA, common arterial trunk, truncus arteriosus communis, persistent truncus arteriosus, heart defect, interruption of the aortic arch, left superior caval vein, aberrant subclavian artery, atrial septal defect, atrioventricular septal defect, double aortic arch, functionally univentricular heart, sepsis, congenital heart disease, neonatal sepsis, cardiac arrest, valve regurgitation, failure to thrive, DiGeorge syndrome, CATCH-22 syndrome, velopharyngeal insufficiency, cleft palate, thymic dysfunction, parathyroid dysfunction

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Contributor Information and Disclosures

Author

Doff B McElhinney, MD, Assistant Professor of Pediatrics, Harvard Medical School; Associate in Cardiology, Department of Cardiology, Children's Hospital of Boston
Doff B McElhinney, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Cardiology
Disclosure: Nothing to disclose.

Coauthor(s)

Gil Wernovsky, MD, FACC, FAAP, Children's Hospital of Philadelphia; Professor, Department of Pediatrics, University of Pennsylvania
Gil Wernovsky, MD, FACC, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Juan Carlos Alejos, MD, Associate Clinical Professor, Department of Pediatrics, Division of Cardiology, University of California at Los Angeles
Juan Carlos Alejos, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association, American Medical Association, and International Society for Heart and Lung Transplantation
Disclosure: Actelion Honoraria Speaking and teaching

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Ameeta Martin, MD, Clinical Associate Professor, Department of Pediatric Cardiology, University of Nebraska College of Medicine
Ameeta Martin, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

CME Editor

Gilbert Herzberg, MD, Assistant Professor, Department of Pediatrics, Section of Pediatric Cardiology, New York Medical College
Gilbert Herzberg, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Chief Editor

Stuart Berger, MD, Professor of Pediatrics, Division of Cardiology, Medical College of Wisconsin; Chief of Pediatric Cardiology, Medical Director of Pediatric Heart Transplant Program, Medical Director of The Heart Center, Children's Hospital of Wisconsin
Stuart Berger, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American College of Chest Physicians, American Heart Association, and Society for Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

 
 
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