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

Double Outlet Right Ventricle, With Transposition

Author: M Silvana Horenstein, MD, Consulting Staff, Department of Pediatrics, University of Texas Medical School Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc
Coauthor(s): Michael L Epstein, MD, Director, Division of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Michigan; Professor, Wayne State University School of Medicine
Contributor Information and Disclosures

Updated: Oct 2, 2008

Introduction

Background

Double outlet right ventricle (DORV) is a type of ventriculoarterial connection in which both the aorta (AO) and pulmonary artery (PA) arise entirely or predominantly from the right ventricle (RV). The only outlet from the left ventricle (LV) is a ventricular septal defect (VSD).

DORV is usually associated with concordant atrioventricular (AV) connections (ie, the right atrium drains into the RV and the left atrium drains into the LV). Fibrous discontinuity is present between the mitral and semilunar valves, which is referred to as subpulmonic and subaortic conus.

DORV is virtually always associated with a VSD and, occasionally, with an atrial septal defect. Patients with DORV may also present with varying degrees of left ventricular hypoplasia and mitral valve anomalies such as stenosis or atresia. Straddling of the AV valves across the VSD may be present. The aortic valve may be stenosed, and the aortic arch may show coarctation or even interruption. Anomalies of the coronary arteries (CAs), such as those that occur in patients with dextro-transposition of the great arteries may be present. These include the left circumflex arising from the right main, a single right CA, a single left CA, and inverted origin of the CA.

The AV node and His-Purkinje fibers may be displaced in DORV because of the anatomic characteristics of these hearts.

In DORV, the great arteries may take different relationships as follows:

  • In 64% of cases of DORV, the great arteries lie side by side with the AO to the right of the PA and both semilunar valves lying in the same transverse and coronal plane (physiologically similar to tetralogy of Fallot [TOF]).
  • In 26% of cases of DORV, the AO is anterior and to the right of the PA, physiologically resembling transposition of the great arteries (ie, dextro-transposition of the great arteries), with a VSD.
  • In 7% of cases of DORV, the AO is anterior and to the left of the PA (left-transposition of the great arteries).
  • Only 3% of cases of DORV have a normal great artery relationship with the AO arising posterior and to the right of the PA.

Pathophysiology

The pathophysiology of DORV varies, irrespective of the great arterial relationship (ie, side-by-side, dextro-transposition of the great arteries, left-transposition of the great arteries, normally related). Clinical manifestations may range from that of a large VSD to that of transposition of the great arteries and may mostly depend on the position of the VSD in relation to the great vessels (whether it is subpulmonary or subaortic) and the presence or absence of pulmonary valve stenosis (PS). Both of these factors contribute substantially to the hemodynamics of this congenital heart defect.

In cases of a subaortic VSD, which occurs in 60-70% of patients, the VSD is closer to the aortic valve, thus oxygenated blood from the LV is directed to the AO and desaturated blood from the right atrium (RA) is directed primarily to the PA (see Media file 1). PS occurs commonly and directs some desaturated blood into the AO. Because of the large VSD, the RV and the LV as well as the AO handle equal systolic pressures. When PS is present, this poses a restriction to flow to the pulmonary circuit, and thus, systolic pressure in the pulmonary arteries is lower. This physiology resembles that of TOF with cyanosis and no congestive heart failure (CHF).

In cases of a subaortic VSD with no PS, systolic pressure in both great vessels as well as in both ventricles is equal; thus, blood follows the path of least resistance (ie, usually towards the lungs) and the clinical picture is that of a large VSD. The degree of blood oxygenation in the systemic as well as the pulmonary circuits is determined by degree of mixing in the systemic (ie, right) ventricle, which, in turn, depends on the degree of resistance upstream of the pulmonary valve.

All patients with elevated pulmonary blood flow (PBF) at systemic or near systemic pressures are at increased risk of developing early pulmonary obstructive vascular disease regardless of their arterial oxygen saturation (ie, presence or absence of cyanosis).

With a subpulmonary VSD (Taussig-Bing anomaly), which occurs in 10% of patients, oxygenated blood from the LV is directed to the PA and desaturated blood from the RA is directed to the AO. This physiology resembles transposition of the great arteries with a VSD; thus, the patient presents with cyanosis and CHF.

In cases of a doubly committed VSD, the left ventricular outflow is not committed preferentially to either semilunar valve. In the presence of PS, the physiology resembles that of TOF, and in the absence of PS, it is that of a large VSD.

In remote VSD, the VSD is far from both semilunar valves. It is most commonly an AV canal-type VSD. Again, the physiology is that of TOF in cases involving PS and is that of a large VSD when flow through the pulmonary valve is not restricted (ie, absence of PS).

Frequency

United States

Congenital heart disease (CHD) occurs in fewer than 1% of all newborns, and DORV is present in 0.5-1.5% of all patients with CHD. The estimated frequency of DORV is 1 case per 10,000 live births.

Mortality/Morbidity

Mortality and morbidity depend not only on the overall clinical condition of the patient but also on the type and severity of associated anomalies.

  • Irrespective of the great vessel relationship, the mortality rate is less than 5% for simple subaortic VSD and is somewhat higher for a doubly committed VSD.
  • In cases of subpulmonary VSD (Taussig-Bing anomaly), morbidity and mortality depend on whether the patient has already developed pulmonary vascular obstructive disease and also on the type of surgery that is required. In cases of DORV with dextro-transposition of the great arteries, creation of an intraventricular tunnel between the VSD and the AO carries a mortality risk of 10-15%. In subpulmonary VSD with PS (ie, TOF-type physiology), an intraventricular tunnel between the VSD and the AO in addition to relief of PS by a patch graft also carries a mortality risk of 10-15%. In cases of remote VSD, the preferred surgical repair is creation of an interventricular tunnel between the VSD and the AO. However, it carries a mortality rate as high as 30-40%.
  • When the above surgical procedures cannot be performed (ie, hypoplastic LV, inadequate anatomy for an intracardiac conduit between the LV and the AO, hypoplastic AO, hypoplastic mitral valve), a Fontan-type operation is the choice; the mortality rate has decreased to approximately 5%.

Sex

No sex predilection is reported.

Age

Newborns usually present with this entity; however, in some circumstances (eg, subaortic VSD with mild-to-moderate PS), the diagnosis may not be made until later in infancy.

Clinical

History

History of fetal bradycardia heart block during the first trimester of pregnancy has been associated with double outlet right ventricle (DORV), as opposed to autoimmune causes of fetal heart block, which occur after the second and third trimesters. Fetal heart block can be diagnosed ultrasonographically depending on the subtype of DORV (eg, with or without transposition of the great arteries); clinical history differs. In patients with DORV and transposition of the great arteries, the clinical presentation depends on the location of the ventricular septal defect (VSD) and the presence of pulmonary valve stenosis (PS), the degree of PS, or both.

  • If the VSD is subpulmonic, the physiology resembles that of transposition of the great arteries with VSD. Patients with this anatomy usually present in the newborn period or within the first few weeks of life with cyanosis and signs of pulmonary overcirculation.
  • If the VSD is subaortic, the patient may be only mildly cyanotic and may present primarily with pulmonary overcirculation at 3-6 weeks of life when pulmonary vascular resistance drops. If PS is present, which is often the case in DORV with subaortic VSD, the degree of PS greatly affects clinical presentation.
    • If PS is mild or moderate, the patient may present with mild cyanosis and little or no pulmonary overcirculation.
    • If PS is severe, clinical presentation resembles that of tetralogy of Fallot (TOF). Cyanosis from diminished pulmonary blood flow (PBF) is likely to be the major clinical feature.
  • In patients with DORV and transposition of the great arteries (both uncommon lesions), the VSD may be doubly committed or remote from the great arteries.
    • If the VSD is doubly committed, the conus septum is deficient and the VSD usually lies above the crista supraventricularis, closely related to both semilunar valves. Clinical presentation is often that of DORV with a subpulmonic VSD, although the patient may have slightly higher systemic oxygen saturation.
    • In DORV with transposition of the great arteries and remote VSD, many variables determine clinical presentation. If the VSD is remote from both semilunar valves, it is often part of an AV canal-type defect, in which case many other anomalies are likely.
    • Alternatively, multiple muscular VSDs may be remote from the semilunar valves. Clinical presentation depends on factors such as the location of the VSDs, the presence or absence of PS (right ventricular outflow tract obstruction), and the direction of streaming of blood flow through VSDs.

Physical

Physical findings vary, depending on the location of the VSD and the presence or absence of PS.

  • With a subaortic VSD and no PS, cyanosis is mild or absent.
    • PBF is increased, thereby producing congestive heart failure (CHF).
    • The precordium is hyperactive with a loud second heart sound, which may appear to be single.
    • Harsh regurgitant systolic murmur is heard as pulmonary vascular resistance decreases.
    • Clinically, these patients resemble those with a large VSD.
  • In DORV with subaortic VSD and PS, physical findings depend on the degree of PS.
    • If PS is mild, little cyanosis and only mild CHF may be present.
    • These patients present with a murmur from PS (systolic ejection murmur), from the VSD (regurgitant murmur), or both.
    • If PS is moderate or severe, cyanosis is prominent because of decreased PBF (resembling TOF).
    • If uncorrected, cyanosis leads to late findings such as polycythemia and digital clubbing.
  • In those patients with subpulmonic VSD (PS is rare in these patients), PBF increases as vascular resistance falls.
    • These patients present similarly to those with transposition of the great arteries and VSD.
    • Cyanosis is prominent early, and pulmonary overcirculation develops.
    • Failure to thrive is likely to develop if treatment is not instituted.
    • The second heart sound is loud and possibly single, and a regurgitant systolic murmur develops.
    • If increased pulmonary vascular resistance occurs, signs of CHF diminish and the murmur decreases.
    • An ejection click may appear along with a diastolic murmur of pulmonary valve insufficiency (late findings).
  • Patients with doubly committed VSD also present similarly to those with transposition of the great arteries and VSD.
    • Cyanosis may be mild.
    • Signs of CHF, including tachypnea, tachycardia, and hepatomegaly, lead to failure to thrive.

Causes

DORV is thought to be the result of a malformation in the outlet portion of the embryonic ventricular loop at 3-4 weeks' gestation. Although mostly sporadic, familial cases have been reported.

  • Fluorescence in situ hybridization (FISH) analysis has shown deletions in the 22q11.2 region in certain individuals with TOF, DORV, transposition of the great arteries, and VSD associated with other congenital heart disease (CHD).1,2,3 As a matter of fact, DORV may be part of complex CHD in patients with DiGeorge syndrome, velocardiofacial syndrome, and conotruncal anomaly–face syndrome.
  • DORV has also been associated with trisomies 13 and 18 and tetrasomy 8p.
  • DORV has also been reported in patients with mutations in human cardiac transcription factor NKX2.5.
  • DORV and truncus arteriosus occur with a higher incidence in the offspring of mothers with diabetes mellitus than in the general population. Teratogenic mechanisms involved are obscure; however, in pregnant diabetic rats, antioxidant supplementation with vitamin E reduced the severity of malformations in their offspring.4
  • DORV has been reported to occur in mouse embryos homozygous for the JMJ mutation, which affects the nuclear protein jmj coded by chamber-specific genes.
  • Studies using animal models described a transcription factor that plays a critical role in directing cardiac asymmetric morphogenesis, known as Pitx2. Specifically, ectopic Pitx2c expression in the developing myocardium was found to correlate with the development of DORV. Whereas loss of function of the Pitx2 caused atrial isomerism, double inlet left ventricle, transposition of the great arteries, persistent truncus arteriosus, and abnormal aortic arch remodeling.
  • Most recently, hearts with persistent truncus arteriosus, DORV, and transposition of the great arteries, have been postulated to have rotation of the myocardial wall of the outflow tract that is arrested or fails to initiate.
  • In synthesis, the pathogenesis of DORV is currently believed to include impairment of neural crest–derivative migration and impairment of normal cardiac situs and looping.5

More on Double Outlet Right Ventricle, With Transposition

Overview: Double Outlet Right Ventricle, With Transposition
Differential Diagnoses & Workup: Double Outlet Right Ventricle, With Transposition
Treatment & Medication: Double Outlet Right Ventricle, With Transposition
Follow-up: Double Outlet Right Ventricle, With Transposition
Multimedia: Double Outlet Right Ventricle, With Transposition
References
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References

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Further Reading

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Keywords

double outlet right ventricle with transpositions of the great arteries, DORV with TGA, Taussig-Bing deformity, ventricular septal defect, VSD, left ventricular hypoplasia, coronary artery anomalies, dextro-transposition of the great arteries, D-TGA, left-transposition of the great arteries, L-TGA, tetralogy of Fallot, TOF, pulmonary valve stenosis, congenital heart disease, CHD, right ventricular outflow tract obstruction pulmonary vascular obstructive disease, failure to thrive, pulmonary overcirculation, hepatomegaly, DiGeorge syndrome, velocardiofacial syndrome, conotruncal anomaly–face syndrome, truncus arteriosus, diabetes mellitus

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Contributor Information and Disclosures

Author

M Silvana Horenstein, MD, Consulting Staff, Department of Pediatrics, University of Texas Medical School Houston; Medical Doctor Consultant, Legacy Department, Best Doctors, Inc
M Silvana Horenstein, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael L Epstein, MD, Director, Division of Pediatric Cardiology, Department of Pediatrics, Children's Hospital of Michigan; Professor, Wayne State University School of Medicine
Michael L Epstein, MD 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, 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
Disclosure: Nothing to disclose.

Managing Editor

Julian M Stewart, MD, PhD, Associate Chairman of Pediatrics, Director, Center for Hypotension, Westchester Medical Center; Professor of Pediatrics and Physiology, New York Medical College
Julian M Stewart, MD, PhD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

CME Editor

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

Chief Editor

Steven R Neish, MD, SM, Director of Pediatric Cardiology Fellowship Program, Associate Professor, Department of Pediatrics, Baylor College of Medicine
Steven R Neish, MD, SM is a member of the following medical societies: American Academy of Pediatrics, American College of Cardiology, and American Heart Association
Disclosure: Nothing to disclose.

 
 
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