Dr.Elamaran.E

Senior Resident Dept. of CTVS,JIPMER

o Congenital cardiac anomaly

o Atrioventricular concordance and Ventriculo arterial discordance.

o Aorta arises from the morphologic right ventricle and the pulmonary artery arises from the morphologic left ventricle.

Morphologic description of TGA –Baillie(1797)

Transposition of the aorta and pulmonary artery was coined - Farre (1814)

Surgery for TGA Atrial septectomy - Blalock and

Hanlon(1950) Balloon atrial septostomy - Rashkind

and Miller - (1966)

Partial physiological correction – Lillehei (1953)

Physiologic correction at the atrial level –Senning(1959) and Mustard(1963)

Arterial switch procedure –Jatene (1975)

Etiology for transposition of the great arteries is unknown and is presumed to be multifactorial.

Common association in infants of diabetic mothers.

Persistence of sub Aortic conus and absorption of sub pulmonary conus

Failure of the Truncus Arteriosus to septate normally

Transposition of the great arteries (TGA) is the most common cyanotic congenital heart lesion that presents in neonates.

 This lesion presents in 5-7% of all patients with congenital heart disease.

Male-to-female ratio is 2:1. Male predominance increases to 3.3 : 1 (ventricular septum is intact)

Right ventricle –Hypertrophied, Sub aortic conusLeft ventricle- Normal to thinned out, Pulmonary-Mitral continuityAorta- Anterior and right of PAAtria – Normal (RA>LA)Atrio-Ventricular valves – Same levelConduction tissue – Normal position and abnormal shape

Normal -2/3 and Abnormal -1/3

The pulmonary and systemic circulations function in parallel, rather than in series.

When patients with all varieties of TGA are considered

55% - 1 month 15% - 6 months 10% - 1 year

Transposition of the great arteries with intact ventricular septum – Hypoxia

Transposition of the great arteries with ventricular septal defect –cardiac failure

Transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction- Hypoxia

Aggressive medical and surgical management in the neonate has around 90% early and midterm survival

1. TGA with intact ventricular septum

2. TGA with VSD

3. TGA with VSD and LVOTO

4. TGA with VSD and pulmonary vascular obstructive disease.

Patent foramen ovale or Atrial septal defect- 75%

Ventricular septal defect- 25% -40% Patent ductus Arteriosus-functionally

closes by 1 month Left ventricular outflow obstruction-5% Mitral valve-cleft leaflet/accessory

chordal tissue Tricuspid valve – regurgitation/dysplasia

Symptoms and clinical presentation

Depend on degree of mixing between the two parallel circulatory circuits.

TGA with intact ventricular septum – Cyanosis within 24 hours

TGA with VSD– congestive heart failure (2 to 4 months)

TGA with VSD and LVOTO- similar to TOF

TGA with VSD and PVOD – develop Hypoxia after 6 months

An oval-or egg-shaped cardiac silhouette with a narrow superior mediastinum

Mild cardiac enlargement

Moderate pulmonary plethora

Simple TGA – Neonates- Arterial switch within 1 month

Simple TGA – after 30 days Pulmonary artery banding- Arterial

switch after 2 weeks Atrial switch

TGA with VSD- Arterial switch within few weeks

TGA with VSD and LVOTO – repair - 6 months

Establishing Ventriculo-arterial concordance

Anatomical correction

Coronary artery lesions

Neo Aortic valve regurgitation

RVOTO and LVOTO obstruction

Cardiac failure- Secondary to severe LV dysfunction(imperfect coronary artery transfer to Neoaorta)

RV dysfunction – Progressive pulmonary vascular disease (1%)

Coronary events

Physiological correction

Baffle obstruction and leak

Rhythm disturbances

Severe Tricuspid regurgitation

Right ventricle failure

Low output – early post op period

Systemic RV failure

Aortic translocation(TGA with VSD & LVOTO) – Nikaidoh

Damus-Kaye-Stansel(TGA with large VSD and RVOTO)

TGA with posterior Aorta- Arterial switch procedure without Lecompte maneuver

Thank You