**5.2.4 Cardiac catheterization & cineangiography**

Many of the issues that require definition by catheterization in the past can be resolved by good quality echo-Doppler studies and catheterization is not routinely required. When questions cannot be satisfactorily answered, cardiac catheterization may be useful.

Step-up in oxygen saturation is observed in the right ventricle. The saturations in the leftside of the heart are usually normal. The right ventricular and pulmonary arterial pressures are normal in small VSDs and are elevated in moderate to large defects; the magnitude of elevation is proportional to the size of the VSD. Calculated Qp:Qs gives an estimate of degree of left-to-right shunting. A Qp:Qs greater than 2:1 is generally considered an indication for intervention. Pulmonary vascular resistance may be calculated:

PVR = (Mean PA presence - Mean LA pressure)/Pulmonary blood flow index

Where, PVR is pulmonary vascular resistance, PA and LA are pulmonary artery and left atrium respectively.

The calculated resistance is usually 1 to 2 units and a resistance in excess of 3.0 units is considered elevated. Marked elevation of the resistance (>8.0 units) contraindicates surgical repair. When the resistance is elevated, oxygen and other vasodilating agents (Nitric oxide[NO]) should be administered to demonstrate the reversibility.

Selective left ventricular angiography in a left axial oblique view is usually required to demonstrate size and location of the VSD.

#### **Natural history of VSDs**

Knowledge of the natural history of these defects is interesting and such understanding is important in the management of children with these defects.

#### **5.2.4.1 Spontaneous closure**

Approximately 40% of VSDs spontaneously and completely close. Additional 25% to 30% of defects may become small enough not to require surgical intervention. Muscular VSDs tend to close more frequently than membraneous defects. While small defects tend to close more frequently than large defects (60% vs. 20%), even defects large enough to produce congestive heart failure or require pulmonary artery banding in infancy go on to close spontaneously. The majority of the defects close by age 2 years, most close by age 5 to 7 years, but the process of spontaneous closure continues through adolescence and adulthood. Most commonly the defect closes by apposition of leaflets of the tricuspid valve against it or by aneurysmal formation of the membranous ventricular septum.

#### **5.2.4.2 Pulmonary vascular obstructive disease**

Pulmonary vascular obstructive disease may develop in 10% of VSDs. This is probably related to the exposure of the pulmonary vascular bed to high pressure and high flow. Prompt diagnosis and closure of the defect at least prior to 18 months of age is likely to reduce the incidence of development of pulmonary vascular disease.

#### **5.2.4.3 Development of infundibular stenosis.**

Development of infundibular stenosis, the so called Gasul's transformation of the VSD may occur in 8% of the defects. There may be specific markers such as right aortic arch and increased angle of the right ventricular outflow tract that may predispose a VSD to undergo Gasul's transformation. While development of infundibular stenosis eventually requires the

Congenital Heart Defects – A Review 23

closed by hybrid procedures via sternotomy and a purse-string suture in the right ventricle under transesophageal echo guidance (Amin et al 2008). No device is yet approved for closure of perimembranous VSD, presumably because of concern for development of heart

Ductus arteriosus, one of the fetal circulatory pathways, diverts the desaturated blood from the pulmonary artery into the descending aorta and placenta for oxygenation (Rao 1991a). After the infant is born, the ductus arteriosus constricts and closes spontaneously, presumably secondary to increased PO2. But in some children, such spontaneous closure does not occur. This is more frequent in prematurely born infants. Patent ductus arteriosus (PDA) may be an isolated lesion and may be present in association with other defects. Isolated PDA constitutes 6 to 11% of all CHDs. In this section, isolated PDA beyond neonatal (and premature) period will be discussed. PDA is a muscular structure connecting the main pulmonary artery (at its junction with the left pulmonary artery) with the descending aorta at the level of left subclavian artery. The configuration of PDA varies considerably but most often it has a conical or funnel shape. The aortic end is wide and gradually narrows (ampulla) towards the pulmonary end. The narrowest segment is most often at the pulmonary end. Other types which are short and tubular and those with multiple constrictions and bizarre configuration can also be seen. Because of usually higher pressure and resistance in the systemic circuit than in the pulmonary circuit, leftto-right shunt takes place across the PDA. The degree of left-to-right shunting depends upon the minimal diameter of the ductus and ratio of pulmonary to systemic vascular

Clinical presentation depends upon the size of the ductus. If the PDA is small, there are no symptoms and it is usually detected because of a murmur detected on a routine examination. Moderate to large ducti with large shunt may either present with symptoms of easy fatigability, symptoms associated congestive heart failure or respiratory symptoms

Left ventricular impulse is normal in small ducti and may be hyperdynamic with large shunts. A thrill may be felt at the left upper sternal border and in the suprasternal notch. The first heart sound is usually normal and the second heart sound may be buried within the murmur. In the majority of cases, a continuous murmur (Figure 11, top) is heard best at the left upper sternal border. The murmur begins in systole and continues through the second heart sound into the diastole. The systolic component of the murmur crescendos up to the second heart sound while the diastolic part descrescendos to a varying distance (time) into the diastole. The continuous murmur must be distinguished from the to-and-fro murmur; the latter is a combination of an ejection systolic murmur and an early diastolic descrescendo murmur (for example aortic stenosis and insufficiency) (Figure 11, bottom)

suggestive of lung collapse (very large ductus in small babies).

block (Rao 2008).

resistance.

**5.3.1 Symptoms** 

**5.3.2 Physical findings** 

(Rao 1991b).

**5.3 Patent ductus arteriosus** 

patient to have surgery, it indeed protects the pulmonary vascular bed and prevents development of pulmonary vascular obstruction disease.

#### **5.2.4.4 Aortic insufficiency**

Aortic insufficiency develops in approximately 5% of patients. This may either be related to prolapse of an aortic valve cusp into the VSD or lack of support to the aortic root. This complication appears to occur more commonly with supracristal VSDs than with other types. Surgical correction is indicated if moderate to severe aortic insufficiency is present.

#### **5.2.5 Management**

The management strategies depend, to a large degree, on the size of the VSD. In small VSDs, reassurance of the parents, subacute bacterial endocarditis prophylaxis and periodic clinical follow-up are all that are necessary.

In moderate-sized defects, treatment of heart failure, if present, should be undertaken. Failure to thrive and markedly enlarged left ventricle are probably indications for surgical closure. In very large defects the heart failure should be treated aggressively. If the congestive heart failure is difficult to control with the usual anti-congestive measures or if failure to thrive is present, surgical closure should be undertaken.

In large defects with near systemic pressures in the right ventricle and pulmonary artery, surgical closure should be performed prior to 18 to 24 months of age even if heart failure control and adequate weight gain are present. Total surgical correction is currently recommended. The previously used approach of initial pulmonary artery banding in small and young babies followed by surgical closure of the VSD later is no longer recommended. However, in muscular, Swiss-cheese variety of defects, initial pulmonary artery banding may be appropriate.

When the pulmonary vascular resistance is elevated, its response to oxygen and other vasodilator agents (NO), pulmonary arterial wedge angiography and sometimes, even lung biopsy may be necessary to determine the suitability for surgical closure. Patients with calculated pulmonary vascular resistance less than 8 wood units with a Qp:Qs >1.5 are generally considered suitable candidates for surgery. If the resistance drops to levels below 8 units after administering oxygen or other vasodilator agents, the patient becomes a candidate for surgery.

Large VSDs with severe elevation of pulmonary resistance (irreversible pulmonary vascular obstructive disease) are not candidates for surgery. Symptomatic treatment and erythropheresis for symptoms of polycthemia should be undertaken. These patients may eventually become candidates for lung transplantation.

When surgery is indicated, open heart surgical technique is the treatment of choice. Several investigators have attempted transcatheter occlusion of VSD in a manner similar to ASD closure. Such methods may be feasible in muscular defects (Thanopoulos et al 1999) and membranous defects with sufficient septum in the subaortic region so that the device can be implanted without interfering with aortic valve function. Specially designed Amplatzer perimembranous VSD occluders were used to close the perimembranous VSDs in clinical trials (Fu et al 2006, Holzer et al 2006), but with significant incidence of heart block (Rao 2008). At the present, FDA has only approved Amplatzer muscular VSD occluder for transcatheter closure of muscular VSDs. Some large muscular VSDs in small babies may be

patient to have surgery, it indeed protects the pulmonary vascular bed and prevents

Aortic insufficiency develops in approximately 5% of patients. This may either be related to prolapse of an aortic valve cusp into the VSD or lack of support to the aortic root. This complication appears to occur more commonly with supracristal VSDs than with other types. Surgical correction is indicated if moderate to severe aortic insufficiency is present.

The management strategies depend, to a large degree, on the size of the VSD. In small VSDs, reassurance of the parents, subacute bacterial endocarditis prophylaxis and periodic clinical

In moderate-sized defects, treatment of heart failure, if present, should be undertaken. Failure to thrive and markedly enlarged left ventricle are probably indications for surgical closure. In very large defects the heart failure should be treated aggressively. If the congestive heart failure is difficult to control with the usual anti-congestive measures or if

In large defects with near systemic pressures in the right ventricle and pulmonary artery, surgical closure should be performed prior to 18 to 24 months of age even if heart failure control and adequate weight gain are present. Total surgical correction is currently recommended. The previously used approach of initial pulmonary artery banding in small and young babies followed by surgical closure of the VSD later is no longer recommended. However, in muscular, Swiss-cheese variety of defects, initial pulmonary artery banding

When the pulmonary vascular resistance is elevated, its response to oxygen and other vasodilator agents (NO), pulmonary arterial wedge angiography and sometimes, even lung biopsy may be necessary to determine the suitability for surgical closure. Patients with calculated pulmonary vascular resistance less than 8 wood units with a Qp:Qs >1.5 are generally considered suitable candidates for surgery. If the resistance drops to levels below 8 units after administering oxygen or other vasodilator agents, the patient becomes a

Large VSDs with severe elevation of pulmonary resistance (irreversible pulmonary vascular obstructive disease) are not candidates for surgery. Symptomatic treatment and erythropheresis for symptoms of polycthemia should be undertaken. These patients may

When surgery is indicated, open heart surgical technique is the treatment of choice. Several investigators have attempted transcatheter occlusion of VSD in a manner similar to ASD closure. Such methods may be feasible in muscular defects (Thanopoulos et al 1999) and membranous defects with sufficient septum in the subaortic region so that the device can be implanted without interfering with aortic valve function. Specially designed Amplatzer perimembranous VSD occluders were used to close the perimembranous VSDs in clinical trials (Fu et al 2006, Holzer et al 2006), but with significant incidence of heart block (Rao 2008). At the present, FDA has only approved Amplatzer muscular VSD occluder for transcatheter closure of muscular VSDs. Some large muscular VSDs in small babies may be

development of pulmonary vascular obstruction disease.

failure to thrive is present, surgical closure should be undertaken.

eventually become candidates for lung transplantation.

**5.2.4.4 Aortic insufficiency** 

**5.2.5 Management** 

may be appropriate.

candidate for surgery.

follow-up are all that are necessary.

closed by hybrid procedures via sternotomy and a purse-string suture in the right ventricle under transesophageal echo guidance (Amin et al 2008). No device is yet approved for closure of perimembranous VSD, presumably because of concern for development of heart block (Rao 2008).

#### **5.3 Patent ductus arteriosus**

Ductus arteriosus, one of the fetal circulatory pathways, diverts the desaturated blood from the pulmonary artery into the descending aorta and placenta for oxygenation (Rao 1991a). After the infant is born, the ductus arteriosus constricts and closes spontaneously, presumably secondary to increased PO2. But in some children, such spontaneous closure does not occur. This is more frequent in prematurely born infants. Patent ductus arteriosus (PDA) may be an isolated lesion and may be present in association with other defects. Isolated PDA constitutes 6 to 11% of all CHDs. In this section, isolated PDA beyond neonatal (and premature) period will be discussed. PDA is a muscular structure connecting the main pulmonary artery (at its junction with the left pulmonary artery) with the descending aorta at the level of left subclavian artery. The configuration of PDA varies considerably but most often it has a conical or funnel shape. The aortic end is wide and gradually narrows (ampulla) towards the pulmonary end. The narrowest segment is most often at the pulmonary end. Other types which are short and tubular and those with multiple constrictions and bizarre configuration can also be seen. Because of usually higher pressure and resistance in the systemic circuit than in the pulmonary circuit, leftto-right shunt takes place across the PDA. The degree of left-to-right shunting depends upon the minimal diameter of the ductus and ratio of pulmonary to systemic vascular resistance.

#### **5.3.1 Symptoms**

Clinical presentation depends upon the size of the ductus. If the PDA is small, there are no symptoms and it is usually detected because of a murmur detected on a routine examination. Moderate to large ducti with large shunt may either present with symptoms of easy fatigability, symptoms associated congestive heart failure or respiratory symptoms suggestive of lung collapse (very large ductus in small babies).

#### **5.3.2 Physical findings**

Left ventricular impulse is normal in small ducti and may be hyperdynamic with large shunts. A thrill may be felt at the left upper sternal border and in the suprasternal notch. The first heart sound is usually normal and the second heart sound may be buried within the murmur. In the majority of cases, a continuous murmur (Figure 11, top) is heard best at the left upper sternal border. The murmur begins in systole and continues through the second heart sound into the diastole. The systolic component of the murmur crescendos up to the second heart sound while the diastolic part descrescendos to a varying distance (time) into the diastole. The continuous murmur must be distinguished from the to-and-fro murmur; the latter is a combination of an ejection systolic murmur and an early diastolic descrescendo murmur (for example aortic stenosis and insufficiency) (Figure 11, bottom) (Rao 1991b).

Congenital Heart Defects – A Review 25

The echo may reveal varying degrees of left atrial and left ventricular enlargement, again depending upon the size of the ductus. The left ventricular contraction indices are normal unless severe myocardial dysfunction set in. Doppler echocardiography shows characteristic diastolic flow pattern in the pulmonary artery, indicative of PDA. Characteristic color flow

Fig. 12. Color Doppler flow mapping of the main pulmonary artery (PA) in a parasternal short axis view demonstrating the flow of the patent ductus arteriosus (PDA). Ao, Aorta;

These invasive studies are not necessary in the usual cases of PDA, although these

Oxygen saturation data show a step up in oxygen saturation at the pulmonary artery level. The left heart saturations are usually normal. Calculated Qp:Qs, though usually indicates degree of shunting, it may not be accurate because of the difficulty in obtaining reliable mixed pulmonary arterial saturations. The right ventricular and pulmonary arterial pressures are normal in patients with small PDA but may be elevated if the PDA is moderate or large. Wide pulse pressure is observed in the aorta. Selective aortic arch

It is generally believed that the presence of an isolated ductus is an indication for closure, mainly to prevent bacterial endocarditis. This can be performed at anytime, especially if associated with heart failure or pulmonary compromise. If the patient is asymptomatic,

Until recently, surgical closure was the treatment of choice. While the risk of surgical closure is low, morbidity associated with it, namely anesthesia, endotrachial intubation and thoracotomy is universal. Because of this reason, less invasive, transcatheter closure

**5.3.4 Cardiac catheterization and selective cine angiography** 

injection demonstrates the size, shape and location of the ductus.

waiting until 6 to 12 months of age is generally recommended.

procedures are integral parts of transcatheter closure.

**5.3.3.3 Echocardiogram** 

mapping distribution is also present (Figure 12).

LA, Left atrium; RV, Right ventricel

**5.3.5 Management** 

Fig. 11. Graphic representation of continuous and to-and-fro murmurs. The continuous murmur (top) begins in systole shortly after the first heart sound (S1), crescendos up to the second heart sound (S2) and decrescendos to a varying distance (time) into the diastole. In contradistinction to this murmur, the to-and-fro murmur (bottom) consists of an ejection systolic murmur with a separate early diastolic decrescendo murmur; note that there is a definite gap between the end of the ejection murmur and S2.

The continuous murmur of PDA may be of grade I-V/VI in intensity. There is some beat-tobeat variation in the intensity of the murmur and for this reason it is described as machinery murmur. Multiple ejection clicks are usually heard within the murmur and this is rather characteristic of the PDA. The majority of the time, the murmur does not change with the position of the body, although the diastolic component of the murmur is heard better in a supine than in an upright position. However, in patients with very small PDA, the continuous murmur of the PDA either completely disappears or becomes only systolic in timing when the patient sits up and returns to continuous quality when the patient assumes supine position. The postulated cause of this is "kinking" of the ductus in the upright position (Thapar et al 1978). When the ductus is moderate to large in size, a mid-diastolic murmur may be heard at the apex because of increased flow across the mitral valve, such a mid-diastolic murmur suggests a Qp:Qs greater than 2:1. Arterial pulses are bounding in all but patients with very small ductus.

#### **5.3.3 Noninvasive evaluation**

#### **5.3.3.1 Chest x-ray**

Chest film may show a normal-sized heart with normal pulmonary vascular markings with small ductus while cardiomegaly, increased pulmonary blood flow and left atrial enlargement may be seen with moderate to large ductus. Collapse with secondary inflammatory process may be observed in the lung fields of small children with large ducti.

#### **5.3.3.2 Electrocardiogram**

The ECG may be normal or may show left atrial and left ventricular enlargement, depending upon the size of the ductus.

#### **5.3.3.3 Echocardiogram**

24 Congenital Heart Disease – Selected Aspects

Fig. 11. Graphic representation of continuous and to-and-fro murmurs. The continuous murmur (top) begins in systole shortly after the first heart sound (S1), crescendos up to the second heart sound (S2) and decrescendos to a varying distance (time) into the diastole. In contradistinction to this murmur, the to-and-fro murmur (bottom) consists of an ejection systolic murmur with a separate early diastolic decrescendo murmur; note that there is a

The continuous murmur of PDA may be of grade I-V/VI in intensity. There is some beat-tobeat variation in the intensity of the murmur and for this reason it is described as machinery murmur. Multiple ejection clicks are usually heard within the murmur and this is rather characteristic of the PDA. The majority of the time, the murmur does not change with the position of the body, although the diastolic component of the murmur is heard better in a supine than in an upright position. However, in patients with very small PDA, the continuous murmur of the PDA either completely disappears or becomes only systolic in timing when the patient sits up and returns to continuous quality when the patient assumes supine position. The postulated cause of this is "kinking" of the ductus in the upright position (Thapar et al 1978). When the ductus is moderate to large in size, a mid-diastolic murmur may be heard at the apex because of increased flow across the mitral valve, such a mid-diastolic murmur suggests a Qp:Qs greater than 2:1. Arterial pulses are bounding in all

Chest film may show a normal-sized heart with normal pulmonary vascular markings with small ductus while cardiomegaly, increased pulmonary blood flow and left atrial enlargement may be seen with moderate to large ductus. Collapse with secondary inflammatory process may be observed in the lung fields of small children with large ducti.

The ECG may be normal or may show left atrial and left ventricular enlargement,

definite gap between the end of the ejection murmur and S2.

but patients with very small ductus.

**5.3.3 Noninvasive evaluation** 

**5.3.3.2 Electrocardiogram** 

depending upon the size of the ductus.

**5.3.3.1 Chest x-ray** 

The echo may reveal varying degrees of left atrial and left ventricular enlargement, again depending upon the size of the ductus. The left ventricular contraction indices are normal unless severe myocardial dysfunction set in. Doppler echocardiography shows characteristic diastolic flow pattern in the pulmonary artery, indicative of PDA. Characteristic color flow mapping distribution is also present (Figure 12).

Fig. 12. Color Doppler flow mapping of the main pulmonary artery (PA) in a parasternal short axis view demonstrating the flow of the patent ductus arteriosus (PDA). Ao, Aorta; LA, Left atrium; RV, Right ventricel

#### **5.3.4 Cardiac catheterization and selective cine angiography**

These invasive studies are not necessary in the usual cases of PDA, although these procedures are integral parts of transcatheter closure.

Oxygen saturation data show a step up in oxygen saturation at the pulmonary artery level. The left heart saturations are usually normal. Calculated Qp:Qs, though usually indicates degree of shunting, it may not be accurate because of the difficulty in obtaining reliable mixed pulmonary arterial saturations. The right ventricular and pulmonary arterial pressures are normal in patients with small PDA but may be elevated if the PDA is moderate or large. Wide pulse pressure is observed in the aorta. Selective aortic arch injection demonstrates the size, shape and location of the ductus.

### **5.3.5 Management**

It is generally believed that the presence of an isolated ductus is an indication for closure, mainly to prevent bacterial endocarditis. This can be performed at anytime, especially if associated with heart failure or pulmonary compromise. If the patient is asymptomatic, waiting until 6 to 12 months of age is generally recommended.

Until recently, surgical closure was the treatment of choice. While the risk of surgical closure is low, morbidity associated with it, namely anesthesia, endotrachial intubation and thoracotomy is universal. Because of this reason, less invasive, transcatheter closure

Congenital Heart Defects – A Review 27

With wide spread use of color-Doppler echocardiography, a group of patients with color-Doppler evidence for small PDA, but without clinical features of PDA (no continuous murmur on auscultation), the so called "silent ductus" has emerged. There is no unanimity

Subacute bacterial endocarditis prophylaxis is recommended for all ducti prior to closure. There may not be any need for this prophylaxis three months following surgical or transcatheter closure, provided there is no residual shunt. Considerations with regard to elevated pulmonary vascular resistance with PDA are similar to those discussed under VSD

In cyanotic congenital heart defects systemic venous blood bypasses the pulmonary circulation and gets shunted across into the left side of the heart. Thus, there is systemic arterial desaturation. By definition, cyanotic congenital heart disease does not include cyanosis due to intrapulmonary right-to-left shunting and pulmonary venous desaturation secondary to congestive heart failure. There are usually multiple defects of the heart causing right-to-left shunt. Obstruction to pulmonary blood flow (for example tetralogy of Fallot), complete admixture of pulmonary and systemic venous returns (for example, total anomalous pulmonary venous return and double-inlet left ventricle) and parallel rather than in-series circulation (transposition of the great arteries) are the causes of right-to-left shunts and cyanosis. The most important of the cyanotic CHDs are what are called "5 Ts"

of opinion with regard to management of these patients.

**6. Right-to-left shunts (cyanotic heart defects)** 

1. Tetralogy of Fallot

3. Tricuspid atresia

5. Truncus arteriosus

Table 2. Common Cyanotic Congenital Heart Defects (5 Ts)

tricuspid atresia will be reviewed in this chapter.

2. Transposition of the great arteries

4. Total anomalous pulmonary venous connection

Three of these defects, namely tetralogy of Fallot, transposition of the great arteries and

Tetralogy of Fallot (TOF) is the most common cause of cyanosis beyond one year of age and constitutes 10% of all congenital heart defects. Fallot defined it as a constellation of four abnormalities to include a VSD, PS, right ventricular hypertrophy and dextroposition of the aorta. The ventricular defect is always large and non-restrictive and is located in the membranous septum in the subaortic region. Pulmonary stenosis is variable in severity and nature of obstruction. The right ventricular outflow obstruction may be mild resulting in initial left-to-right shunt at ventricular level or it may be severe causing severe cyanosis

section.

and are listed in table 2.

**6.1 Tetralogy of Fallot** 

techniques have been developed. These transcatheter methods are increasingly being used in closing PDAs. Gianturco coil occlusion of the PDA can be performed with small caliber catheters (#4F) and is the currently preferred method of occlusion for small to medium sized ducti.

Fig. 13. Selected cine frames demonstrating a small to medium-sized patent ductus arteriosus (D) in a right anterior oblique view (A) which was occluded with a Gianturco coil (B). Dense opacification of the main pulmonary artery (MPA) prior to occlusion and no opacification following occlusion (B) are shown. DAo, descending aorta.

For large-sized PDA, surgical, video-thoracoscopic and transcatheter device closure are the available options, but most cardiologist prefer transcatheter occlusion (Rao and Sideris 1996). Amplatzer duct occluder is preferred for moderate to large PDA.

Fig. 14. Selected cine frames demonstrating a medium to large-sized patent ductus arteriosus (PDA) in a lateral view (A) which was occluded with an Amplatzer Duct Occluder (Amplatzer). Dense opacification PDA and the main pulmonary artery prior to occlusion and no opacification following occlusion (B) are shown. DAo, Descending aorta.

techniques have been developed. These transcatheter methods are increasingly being used in closing PDAs. Gianturco coil occlusion of the PDA can be performed with small caliber catheters (#4F) and is the currently preferred method of occlusion for small to medium sized

Fig. 13. Selected cine frames demonstrating a small to medium-sized patent ductus

Fig. 14. Selected cine frames demonstrating a medium to large-sized patent ductus arteriosus (PDA) in a lateral view (A) which was occluded with an Amplatzer Duct Occluder (Amplatzer). Dense opacification PDA and the main pulmonary artery prior to occlusion and no opacification following occlusion (B) are shown. DAo, Descending aorta.

opacification following occlusion (B) are shown. DAo, descending aorta.

1996). Amplatzer duct occluder is preferred for moderate to large PDA.

arteriosus (D) in a right anterior oblique view (A) which was occluded with a Gianturco coil (B). Dense opacification of the main pulmonary artery (MPA) prior to occlusion and no

For large-sized PDA, surgical, video-thoracoscopic and transcatheter device closure are the available options, but most cardiologist prefer transcatheter occlusion (Rao and Sideris

ducti.

With wide spread use of color-Doppler echocardiography, a group of patients with color-Doppler evidence for small PDA, but without clinical features of PDA (no continuous murmur on auscultation), the so called "silent ductus" has emerged. There is no unanimity of opinion with regard to management of these patients.

Subacute bacterial endocarditis prophylaxis is recommended for all ducti prior to closure. There may not be any need for this prophylaxis three months following surgical or transcatheter closure, provided there is no residual shunt. Considerations with regard to elevated pulmonary vascular resistance with PDA are similar to those discussed under VSD section.
