Medscape is available in 5 Language Editions – Choose your Edition here.


Truncus Arteriosus

  • Author: Doff B McElhinney, MD; Chief Editor: Howard S Weber, MD, FSCAI  more...
Updated: Jan 14, 2015


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.


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.


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[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.

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[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.

The Van Praagh scheme is combined with Collett and Edwards types in the image below.

Anatomic subtypes of truncus arteriosus (TA), acco Anatomic subtypes of truncus arteriosus (TA), according to the classification systems of both Collett and Edwards (I, II, III) and the Van Praaghs (A1, A2, A3, A4).

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 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.




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.

A population-based review of all cases of live births from 1999 to 2008 identified as having severe congenital heart disease from the Nationwide Inpatient Sample (NIS) database indicated a decrease of the conditions over the study period.[3] There was a significant decreased incidence of truncus arteriosus as well as tetralogy of Fallot, pulmonary atresia, and hypoplastic left heart syndrome; however, these trends varied with sociodemographic factors. The investigators suggested a possible reason for the decreasing prevalence trend was the increased numbers of terminated fetuses with prenatally diagnosed congenital heart disease.[3]


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

However, a Canadian longitudinal study (1983-2010) of all individual with congenital heart disease noted a more than 50% increase of severe and other congenital heart disease after the year 2000, with adults comprising two thirds of the cases by 2010.[4] The prevalence of congenital heart disease in the first year of life between 1998 and 2005 was 8.21 per 1000 live births; in 2010, the overall prevalence was 13.11 per 1000 in children and 6.12 per 1000 in adults. A temporal increase in prevalence of congenital heart disease and severe congenital heart disease was noted for children and adults.[4]


The natural history of truncus arteriosus without surgical intervention is not well characterized. In numerous 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.


Based on limited data, no racial predilection is apparent.


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


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.

Contributor Information and Disclosures

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, American College of Cardiology

Disclosure: Nothing to disclose.


Gil Wernovsky, MD, FACC, FAAP Professor, Department of Pediatrics, University of Pennsylvania, Children's Hospital of Philadelphia

Gil Wernovsky, MD, FACC, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

Chief Editor

Howard S Weber, MD, FSCAI Professor of Pediatrics, Section of Pediatric Cardiology, Pennsylvania State University College of Medicine; Director of Interventional Pediatric Cardiology, Penn State Hershey Children's Hospital

Howard S Weber, MD, FSCAI is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, Society for Cardiovascular Angiography and Interventions

Disclosure: Received income in an amount equal to or greater than $250 from: St. Jude Medical.

Additional Contributors

Juan Carlos Alejos, MD Clinical Professor, Department of Pediatrics, Division of Cardiology, University of California, Los Angeles, David Geffen School of Medicine

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, International Society for Heart and Lung Transplantation

Disclosure: Received honoraria from Actelion for speaking and teaching.

  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. 1965 Sep. 16(3):406-25. [Medline].

  3. Egbe A, Uppu S, Lee S, Ho D, Srivastava S. Changing prevalence of severe congenital heart disease: a population-based study. Pediatr Cardiol. 2014 Oct. 35(7):1232-8. [Medline].

  4. Marelli AJ, Ionescu-Ittu R, Mackie AS, Guo L, Dendukuri N, Kaouache M. Lifetime prevalence of congenital heart disease in the general population from 2000 to 2010. Circulation. 2014 Aug 26. 130(9):749-56. [Medline].

  5. Kodo K, Nishizawa T, Furutani M, Arai S, Yamamura E, Joo K, et al. GATA6 mutations cause human cardiac outflow tract defects by disrupting semaphorin-plexin signaling. Proc Natl Acad Sci U S A. 2009 Aug 18. 106(33):13933-8. [Medline]. [Full Text].

  6. Lisowski LA, Verheijen PM, Copel JA, Kleinman CS, Wassink S, Visser GH, et al. Congenital heart disease in pregnancies complicated by maternal diabetes mellitus. An international clinical collaboration, literature review, and meta-analysis. Herz. 2010 Jan. 35(1):19-26. [Medline].

  7. 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].

  8. Swanson TM, Selamet Tierney ES, Tworetzky W, Pigula F, McElhinney DB. Truncus arteriosus: diagnostic accuracy, outcomes, and impact of prenatal diagnosis. Pediatr Cardiol. 2009 Apr. 30(3):256-61. [Medline].

  9. Turan S, Turan OM, Desai A, Harman CR, Baschat AA. First-trimester fetal cardiac examination using spatiotemporal image correlation, tomographic ultrasound and color Doppler imaging for the diagnosis of complex congenital heart disease in high-risk patients. Ultrasound Obstet Gynecol. 2014 Nov. 44(5):562-7. [Medline].

  10. Rao PS. Diagnosis and management of cyanotic congenital heart disease: part I. Indian J Pediatr. 2009 Jan. 76(1):57-70. [Medline].

  11. [Guideline] Saxena A. Consensus on timing of intervention for common congenital heart disease. Indian Pediatr. 2008 Feb. 45(2):117-26. [Medline].

  12. Russell HM, Pasquali SK, Jacobs JP, Jacobs ML, O'Brien SM, Mavroudis C, et al. Outcomes of repair of common arterial trunk with truncal valve surgery: a review of the society of thoracic surgeons congenital heart surgery database. Ann Thorac Surg. 2012 Jan. 93(1):164-9; discussion 169. [Medline]. [Full Text].

  13. Lund AM, Vogel M, Marshall AC, Emani SM, Pigula FA, Tworetzky W, et al. Early reintervention on the pulmonary arteries and right ventricular outflow tract after neonatal or early infant repair of truncus arteriosus using homograft conduits. Am J Cardiol. 2011 Jul 1. 108(1):106-13. [Medline].

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

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

  16. 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. 2001 Dec. 29(4):469-74. [Medline].

  17. 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].

  18. 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. 1991 Aug. 32(2):213-30. [Medline].

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

  20. 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. 1993 Jun. 105(6):1057-65; discussion 1065-6. [Medline].

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

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

  23. 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. 2005 Mar. 129(3):559-68. [Medline].

  24. 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. 1977 Oct. 40(4):569-78. [Medline].

  25. 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. 2001 Jul. 20(1):95-103. discussion 103-4. [Medline].

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

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

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

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

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

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

  32. 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. 1985 May. 5(5):1168-72. [Medline].

  33. 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].

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

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

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

  37. 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. 1999 Apr. 67(4):1142-6. [Medline].

  38. 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. 2000 Mar. 119(3):508-14. [Medline].

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

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

  41. 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. 1996 Apr. 111(4):849-56. [Medline].

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

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

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

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

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

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

  48. 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. 2005 Aug. 28(2):217-22. [Medline].

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

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

  51. 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. 1997 May. 113(5):869-78; discussion 878-9. [Medline].

  52. 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. 1995 Jul. 7(3):133-8. [Medline].

  53. 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. 2000 Jul. 18(1):68-73. [Medline].

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

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

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

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

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

  59. 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. 1998 Mar. 13(3):306-9. [Medline].

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

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

  62. 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].

  63. 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].

  64. 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. 2003 Dec. 89(12):1437-41. [Medline].

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

Anatomic subtypes of truncus arteriosus (TA), according to the classification systems of both Collett and Edwards (I, II, III) and the Van Praaghs (A1, A2, A3, A4).
Pathologic specimen with truncus arteriosus (TA), viewed through the opened right ventricle and truncal valve. The common trunk (CT) can be seen giving off the ascending aorta (AA) as well as the left (LPA) and right (RPA) pulmonary arteries. The truncal valve straddles the ventricular septal defect (VSD). The tricuspid valve (TV) also is labeled. Photograph courtesy of Robert H. Anderson, MD.
Pathologic specimen with truncus arteriosus (TA) and interruption of the aortic arch between the left (L) common carotid (CCA) and subclavian (SCA) arteries, viewed from the anterior aspect. The common trunk (CT) is seen arising from the ventricular mass, including the right ventricular (RV) infundibulum. Pulmonary arteries arise as a single trunk from the leftward aspect of the common trunk, which then divides into left and right branches (not shown) and the arterial duct (DA), which continues into the descending aorta, from which the left subclavian artery arises. The ascending aorta (AA), which supplies only the right (R) and left common carotid arteries (the right subclavian artery, which arises anomalously as the last brachiocephalic branch, is not shown), continues from the rightward aspect of the common trunk and is much smaller than in patients without an interrupted arch. RA=right atrial appendage. Photograph courtesy of Robert H. Anderson, MD.
Echocardiographic images of truncus arteriosus (TA). The top image is from the subcostal coronal window (SC COR) and shows the common trunk (TR) arising from the left ventricle (LV), overriding the interventricular septum. The common trunk branches into the pulmonary trunk and the ascending aorta (AO). The left pulmonary artery (LPA) may be seen branching from the pulmonary trunk. RA=right atrium; RPA=right pulmonary artery. In the bottom image, which is from the suprasternal notch sagittal window, the truncal origin and course of the pulmonary trunk and left pulmonary artery can be appreciated. DAO=descending aorta; IV=innominate vein; LA=left atrium.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.