Shunting Lesions

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5 Shunting Lesions

Brandy Hattendorf

Cardiac shunting lesions include atrial septal defects, ventricular septal defects, and patent ductus arteriosus as the most common lesions seen in congenital heart disease. These lesions may be seen in isolation or in association with other congenital heart disease.

Atrial Septal Defects

Atrial deptal defects represent defects in septation of the atria. They are common, representing as much as 10% of cases of congenital heart disease. Anatomic types of defects include (Fig. 5-1):

• Patent foramen ovale (PFO).
• Ostium secundum atrial septal defect (ASD).
• Ostium primum ASD.
• Sinus venosus ASD.
• Coronary sinus (CS) ASD.
image

Figure 5-1 Diagram of the atrial septum showing several types of atrial septal defects.

(Adapted from Fyler DC [ed], Nadas’ Pediatric Cardiology. Philadadelphia: Hanley & Belfus, 1992.)

Patent Foramen Ovale

• An interatrial communication between the superior limb of the septum secundum on the right side and the septum primum on the left atrial side (Fig. 5-2).

• The flap of the foramen ovale (FO) can often be seen (Fig. 5-3).
• Functionally closes after birth but may be present in as many as 25% of normal hearts during pathologic evaluation.
image

Figure 5-2 Diagram of atrial septal components, showing foramen ovale (FO; arrow), septum primum (Sept 1°), left atrium (LA), left ventricle (LV), fossa ovalis, superior limbic bands (SLB) and inferior limbic bands (ILB), atrioventricular septum (AVS), right atrium (RA), and right ventricle (RV).

(From Keane JF, Lock, JE, Fyler DC [eds], Nadas’ Pediatric Cardiology, 2nd ed. Philadelphia: Elsevier/Saunders, 2006.)

image image

Figure 5-3 Subcostal image of a patent foramen ovale (PFO). A, A flap of tissue is seen partially occluding the communication. B, Subcostal image a PFO with color Doppler. Left-to-right shunting is seen. The size of the defect is overestimated by the width of the color jet compared with the two-dimensional size of the defect in part A.

Key Points

• Persists in a normal newborn to 6 months of age.
• Is not a congenital ASD.

Ostium Secundum Atrial Septal Defect

• Defect in the septum primum.
• Most common type of ASD.

• 70% of ASDs are secundum defects (Fig. 5-4).

image

Figure 5-4 Subcostal image of a secundum atrial septal defect (ASD). A, In this two-dimensional image, the true size of the atrial septal defect is seen. Septal rims are noted superior and inferior to the defect. Right atrial enlargement is also seen. B, With color on the same image, a red color jet is seen representing left-to-right flow across the defect.

Key Points

• Many secundum atrial septal defects may be closed percutaneously in the cardiac catheterization laboratory via device.
• Closure via device depends on the septal rims and size of the defect.
• A secundum atrial septal defect is best imaged from the subcostal plane.

Ostium Primum Atrial Septal Defect

• Located in the most anterior and inferior aspects of the atrial septum.
• Deficient atrioventricular (AV) septation.

Key Points

• Associated with trisomy 21.
• Usually seen in association with AV septal defects with a cleft in the anterior leaflet of the mitral valve, although primum defects can occur in isolation.
• Both AV valves (AVVs) appear at the same level.

• The tricuspid valve (TV) will not be apically displaced.

• Best imaged in apical view.

• Allows for assessment of the atrial septum in relationship to the crux of the heart.

Sinus Venosus Atrial Septal Defects: Two Types

• Superior sinus venosus defects: located in the most superior and posterior region of the atrial septum in close proximity to the right-sided pulmonary veins (PVs) and the entrance of the superior vena cava (SVC) into the right atrium (RA) (Fig. 5-5).
• Inferior sinus venosus defects: located posterior and inferior to the fossa ovalis and adjacent to the inferior vena cava.
image

Figure 5-5 Subcostal image of a sinus venosus defect located in the most superior and posterior region of the atrial septum. This defect is associated with partial anomalous pulmonary venous return.

Key Points

• Both types are associated with partial anomalous pulmonary venous return.

• Commonly the right upper PVs (Fig. 5-5).

Coronary Sinus Atrial Septal Defect

• Least common.
• The left SVC empties into the left atrium.

Key Point

• Associated with a persistent left SVC and unroofed CS.

The Echocardiography (Echo) Exam: Step-by-Step Approach

Step 1: Evaluate the Location of the Atrial Septal Defect

• Most ASDs are best imaged from a subcostal view.
• Parasternal short axis view may also be used.
• The apical view is not used for measurements or assessment of most ASDs.

• The atrial septum is thin, particularly in the region of the fossa ovalis.
• From an apical view, the septum is parallel to the ultrasound beam, resulting in dropout.

• Evaluate surrounding structures including PVs, the SVC, inferior vena cava, and CS.
• Pulmonary venous anomalies are associated with sinus venosus defects.

• Agitated saline solution is the preferred contrast used in pediatrics.
• Contrast echocardiography is performed by rapid injection of agitated saline solution into a peripheral vein.

• Upper extremity veins are preferred.
• Filling of the left atrium with contrast echoes confirms the presence of an interatrial communication.

Key Points

• Ostium primum defects are best imaged from an apical four-chamber (4C) view.
• Dropout can occur in the region of the fossa ovalis, giving the impression that an ASD exists in a normal heart or making an existing defect appear larger when imaged from an apical view.
• Evaluate AVV regurgitation, especially in the presence of a primum ASD or a cleft in the anterior leaflet of the mitral valve.
• Injection into the left arm in a patient with a persistent left superior vena caval draining to a CS may cause confusion by resulting in contrast seen in the left atrium.

Step 2: Evaluate the Atrial Septal Defect Dimensions and Position

• A PFO is a defect in the septum primum less than 3 mm in size without associated right atrial or right ventricular dilation and typically with a flap of tissue partially occluding the communication.
• ASD size is quantified as:

• Small: 3 to 5 mm in size.
• Moderate: 5 to 8 mm in size.
• Large: 8 mm or larger.

Key Points

• ASDs may enlarge over time as the right ventricle (RV) becomes more compliant.
• ASDs may also become smaller over time and close spontaneously.

• Spontaneous closure is more common in the first few years of life.

• Evaluate for additional defects and fenestrated defects.
• In ostium secundum ASDs, septal rims and total septal length should be measured to assess for possible transcatheter device closure.
• Contrast echocardiography (echo) can be used to detect interatrial communications if the atrial septum is not well visualized.

Step 3: Evaluate the Direction of the Shunt

• Can be determined primarily by color Doppler.
• Shunting can be phasic, varying during systole and diastole.

Key Points

• Most shunting is left to right.
• Spectral Doppler may be helpful if the ultrasound beam can be aligned in a parallel fashion. However, velocity of flow is not usually helpful in that a pressure gradient between left and right atria greater than 2 to 3 mm Hg is rare.

Step 4: Determine the Size of the Shunt

• The degree of shunting is determined by ventricular compliance.
• The left-to-right shunt across an ASD is often minimal during infancy as the RV is initially less compliant.

Key Points

• Left-to-right shunt increases with age.

• Shunting is usually low velocity and biphasic.

Step 5: Evaluate the Effects of Shunting

• In hemodynamically significant shunts, volume overload may result in:

• Right atrial enlargement.
• Right ventricular enlargement.
• Main and branch pulmonary artery (PA) enlargement.
• Left atrial enlargement.

• The interventricular septum (IVS) may appear flat during diastole.
• Right ventricular dilation with paradoxical septal motion may be present.

Post-Device Atrial Septum Defect Closure Evaluation: Special Considerations

• Evaluate the location of the device monitoring for device migration.
• Evaluate for impingement or distortion of surrounding structures.

• Aortic erosion is a rare but serious complication after device closure of an ASD.

Key Points

• Determine whether a residual shunt is present.
• “Speckling” may be seen representing blood swirling within the device without the presence of a shunt across the septum.
• Residual shunts may close spontaneously with endothelialization of the device over time after device closure.

Postoperative Evaluation: Special Considerations

• Primary closure: pericardial patch or artificial material such as GORE-TEX may be used to close the defect.
• An intra-atrial baffle may be present for sinus venosus or CS defects.
• Evaluate the atrial septum for any residual shunting as well.
• If a baffle is present, evaluate the baffle for leaks and stenosis.

Key Point

• The patch or baffle should appear well placed without dehiscence or impingement of surrounding structures.

Ventricular Septal Defects

A ventricular septal defect is a communication within the interventricular septum that seperates the left ventricle (LV) and RV, allowing for shunting for blood between the ventricles. VSDs represent 20% of congenital heart disease. VSDs can be classified as follows (Fig. 5-6):

• Membranous (Gerbode defect).
• Perimembranous.

• Also called infracristal.

• Muscular.
• Supracristal.

• Also called subpulmonic, doubly committed subarterial defect, and/or outlet ventricular septal defects (VSDs).

• Inlet.

• Also called AV canal (AVC) type defects.

image

Figure 5-6 Diagram of types of VSDs as viewed from the right ventricle.

(Adapted from Fyler DC [ed], Nadas’ Pediatric Cardiology. Philadadelphia: Hanley & Belfus, 1992.)

Key Points

• Most common isolated congenital cardiac defect.
• VSDs are frequently associated with more complex cardiac malformations such as:

• Conotruncal malformations including

• Double-outlet RV.
• Truncus arteriosus.
• Tetralogy of Fallot (TOF).
• Interrupted aortic arch.

• Complete AVC defects.
• Coarctation of the aorta (Ao).
• Single ventricles.

• VSDs may overlap two or more classifications depending on the size and shape of the defect.

Membranous

• The membranous septum is a very small area located between the anterior and septal leaflets of the TV.
• The defect is above the TV, which overlaps a small segment of the RA.

Key Points

• Results in a LV-to-RA shunt.

• Also called a Gerbode defect.

Perimembranous

• A defect in the IVS adjacent to the membranous portion of the IVS and septal leaflet of the TV.
• Most common type of VSD.

• Malalignment defects are more commonly associated with more complex congenital heart disease such as tetralogy of Fallot.
• AV conduction tissue is related to the posterior, inferior aspect of the defect.

Key Points

• 80% of all VSDs are perimembranous.

• There may be malalignment of the ventricles and great arteries.

• May be associated with right ventricular outflow tract obstruction (RVOTO).
• AV conduction tissue is related to the posterior inferior aspect of the defect.
• Best imaged in:

• Parasternal long axis view (Fig. 5-7).
• Parasternal short axis (with base-to-apex scanning) view.
• Apical 4C view (see Fig. 5-11).

image

Figure 5-7 Parasternal short axis view of a perimembranous VSD.

Muscular

• Second most common type of VSD.
• Can be located anywhere in the muscular septum, including:

• Anterior, posterior, mid, and apical.

• Multiple muscular VSDs with a net moderate to large shunt may be referred to as “Swiss cheese” defects.
• Atrioventricular conduction tissue is located superior and anterior to the defect.

Key Points

• Multiple muscular VSDs are commonly seen.
• Best imaged in:

• Parasternal long axis view (Fig. 5-8).
• Subcostal and parasternal short axis (anterior/posterior assessment) view.
• Apical view for base-to-apex assessment.

image

Figure 5-8 Parasternal long axis view of a small midmuscular VSD with left-to-right shunting.

Supracristal (Subpulmonary)

• Located inferior and anterior to the pulmonary valve (pulmV).
• Defects do not close spontaneously.
• Least common defect, representing 6% of VSDs.
• There is a higher incidence in the Asian population, with supracristal VSDs representing up to 30% of the VSDs in this population.

Key Points

• Associated with aortic valve right cusp prolapse with or without aortic regurgitation (AR).
• Best imaged in:

• Parasternal long axis view (for imaging aortic valve cusp prolapse) (see Fig. 5-12).
• Parasternal short axis view: at approximately the 1 o’clock position with the jet aimed toward the PA (Fig. 5-9).
• Subcostal long axis and short axis views.

image

Figure 5-9 Parasternal short axis view of a supracristal VSD. Left, The defect is seen at the 1 o’clock position. Right, The jet is seen by color Doppler aimed toward the pulmonary artery (PA). Aortic insufficiency, although not seen in this patient, is associated with a supracristal VSD.

Inlet

• Located posterior and superior in the inlet septum beneath the septal leaflet of the TV.
• May involve malalignment of the IVS with the atrial septum.

Key Points

• Associated with endocardial cushion defects (also called AVC defects) including AVV defects and primum ASDs.
• Best imaged in:

• 4C view: apical and subcostal views.
• Subcostal: long axis and short axis views.

The Echo Exam: Step-by-Step Approach

Step 1: Evaluate the Ventricular Septal Defect Location

• Scan the entire septum from the base of the heart to the apex of the heart.
• The IVS is a three-dimensional (3D) structure contained in many planes. To fully interrogate the septum, the plane of sound must be angulated both anteriorly and posteriorly in all “standard” views.

Key Points

• Evaluation of the septum requires multiple imaging planes with a segmental approach as the septum lies in many planes.
• Use both two-dimensional (2D) and color Doppler mapping to identify ventricular shunting lesions.

• Defects may be difficult to visualize by color in newborns or infants with increased pulmonary vascular resistance.

• Very small defects such as a tiny apical muscular VSD may only be seen by color Doppler.

• Such small defects can be obliterated by the cardiac muscle during systole.

• Multiple VSDs are common.

Step 2: Evaluate Ventricular Septal Defect Size

• VSDs are classified as:

• Small: less than one third the size of the aortic diameter (Fig. 5-10).
• Moderate: one third to two thirds the size of the aortic diameter.
• Large: greater than two thirds the size of the aortic diameter.

• Measurements should be obtained on 2D images. Measurements obtained on images with color Doppler overestimate size.
• VSDs do not enlarge in size.
• VSDs may become smaller and/or close spontaneously.
image

Figure 5-10 Parasternal short axis view of a perimembranous VSD. Left, This defect is small, measuring less than one third the aortic diameter. Right, The defect is located at the 11 o’clock position on the aorta and does not extend past the 12 o’clock position. There is left-to-right shunting seen with color Doppler.

Key Points

• 35% of small perimembranous and up to 80% of small muscular defects close spontaneously.
• Spontenous closure is most likely in the first few years of life.
• Redundant or aneurysmal TV tissue may result in reduction of the effective orifice perimembranous defects and may even result in spontaneous closure (Fig. 5-11).
• Spontaneous closure is unlikely in nonrestrictive defects.
• Supracristal (subpulmonic), inlet, and malalignment VSDs do not close spontaneously.
image

Figure 5-11 Apical four-chamber (4C) view demonstrating a perimembranous VSD partially occluded by tricuspid valve (TV) aneurysmal tissue. When the VSD is interrogated using color Doppler, the left-to-right shunt is quite small with a significant reduction of the effective orifice perimembranous defect by aneurysmal tissue.

Step 3: Evaluate the Direction of the Shunt

• Shunting primarily occurs in systole.
• The shunt is left to right in smaller lesions with normal pulmonary resistance.
• Both color Doppler and spectral Doppler evaluation are useful when evaluating shunt direction.

Step 4: Determine the Size of the Shunt

• In the absence of increased right ventricular pressure, the severity of left-to-right shunting is proportional to the size of the defect.

• In an unrestricted defect, equalization of ventricular pressure will occur over time, reflecting the development of pulmonary hypertension.

• The greater the size of the lesion and the lower the pulmonary resistance, the larger the left-to-right shunt.

Key Points

• Align the defect so that the VSD jet is parallel to the cursor to obtain a peak velocity via pulsed or continuous wave (CW) Doppler.
• Right ventricular pressure can be estimated from the modified Bernoulli equation using the peak velocity across a VSD based on blood pressure as an estimate of systemic pressure.
• 4 × (peak velocity across the VSD)2 = pressure difference between the LV and RV.
• Blood pressure—4 × (peak velocity across the VSD)2 = estimated right ventricular pressure.
• With equal ventricular pressure, the size of the shunt is determined by arterial and systemic vascular resistance.
• Use angulation of the plane of sound or alternative imaging rather than using theta (θ) to change your angle of interrogation. Using theta (θ) will provide an inaccurate measurement by altering the Bernoulli equation.

Step 5: Evaluate the Effects of Shunting

• Volume overload is reflected by:

• Left atrial dilation.
• Left ventricular enlargement and hypertrophy.

• Pulmonary hypertension may be present reflecting changes from chronic volume overload.

• Estimate PA pressure (in the absence of pulmV disease) using a tricuspid regurgitation (TR) jet.

• Use care to avoid contamination of the TR jet from the VSD jet.

• Indications of possible pulmonary hypertension include:

• Low-velocity shunting across the VSD.
• Right-to-left shunting across the VSD.
• Ventricular septal flattening.
• Right ventricular hypertrophy.

• Hypertrophied right ventricular muscle bundles (infundibular stenosis) can occur as an isolated finding or with the development of a double-chamber RV.

• Occurs in 3% to 7% of patients.
• Look for distortion of the aortic valve with a supracristal VSD (Fig. 5-12).

• Malalignment VSDs may be associated with anterior or posterior deviation of the septum with subvalvar outflow obstruction.
• TOF: anterior deviation of the conal septum results in RVOTO.
• Interrupted aortic arch: posterior deviation of the Zconal septum results in LVOTO.

image

Figure 5-12 Parasternal long axis view of a supracristal VSD. There is distortion of the aortic valve leaflets with prolapse of the right aortic cusp. The aortic cusp is seen filling and nearly obliterating the supracristal defect. Aortic regurgitation may also be present.

Key Points

• Evaluate for volume overload.
• VSD left-to-right shunt may result in an increased spectral Doppler velocity across the pulmonary valve in the absence of pulmonary valve disease (flow-related relative pulmonic stenosis).
• Subaortic membranes and fibrous ridges may form in association with a VSD, resulting in left ventricular tract obstruction (LVOTO).
• Depending on the size and angulation of the jet, shunting across a VSD may cause a hypertrophied right ventricular muscle bundle in the inferior infundibular septal region resulting in RVOTO.
• AR is seen in association with supracristal VSDs due to aortic cusp prolapse from a poorly supported right coronary cusp (RCC).

Postoperative Assessment: Special Considerations

• If the VSD was closed using a patch, this area may appear echo bright.
• The patched portion of the septum will be dyskinetic.
• Postoperatively, residual shunts may occur at the borders of the patch.
• Occasionally closing a large VSD may “unmask” smaller defects not previously detected.
• Monitor for LVOTO, particularly in malalignment VSDs.
• Evaluate for TR and/or valvular dysfunction.

Patent Ductus Arteriosus

• A patent ductus arteriosus is a persistent patency of a fetal connection between the descending aorta just distal to the origin of the left subclavian artery and PA (Fig. 5-13).
• The ductus is most commonly left sided regardless of the presence of a left or right aortic arch.
• Occasionally in the presence of a right aortic arch, the duct may be right sided.

• Joins the right aortic arch just distal to the right subclavian artery and the right PA.

• Rarely bilateral ducti are present.
image

Figure 5-13 Anatomic drawing of a large persistent patent ductus arteriosus.

(Adapted from Fyler DC [ed], Nadas’ Pediatric Cardiology. Philaladelphia: Hanley & Belfus, 1992.)

Key Point

• Delayed closure may be seen in:

• Premature infants.
• Children born at high altitudes.
• Children with maternal rubella exposure during early pregnancy.

The Echo Exam: Step-by-Step Approach

Step 1: Determine the Presence of a Patent Ductus Arteriosus

• Image using a high left parasternal short axis view (three-finger or three-prong view) (Fig. 5-14).
• The transducer can then be rotated clockwise to see insertion of the ductus into the descending aorta (Fig. 5-15).
image

Figure 5-14 High left parasternal short axis view demonstrating the three-finger or three-prong view demonstrating the ductus arteriosus (DA) and left and right branch PAs.

image

Figure 5-15 Parasternal short axis view with color in the DA. Note the ampulla of the DA is seen originating from the aorta (Ao) with flow from the aorta entering the PA (left-to-right flow).

Key Points

• A patent ductus arteriosus (PDA) in the presence of systemic to suprasystemic pulmonary pressures can be very difficult to identify by color Doppler.

• May only be seen by 2D imaging.

• Assess for the presence of pulmonary hypertension.

• The tricuspid regurgitant jet can be used to estimate pulmonary arterial systolic pressure.
• Secondary evidence of increased right ventricular and pulmonary pressures such as a flattened interventricular septal motion suggests the presence of pulmonary hypertension.

Step 2: Evaluate the Size of the Patent Ductus Arteriosus

• Quantitative methods may be used, but no single parameter should be used in isolation. These include:

• The ratio of the smallest duct diameter to the ostium of the left PA calculated using the following equation:Ductal diameter (mm)/diameter of the ostium of the left PA (mm)

• Small: <0.5.
• Moderate: >0.5 to 1.
• Large: >1.

• Percentage of retrograde diastolic flow to antegrade aortic flow in the descending aorta (estimated percentage by CW Doppler).

• Small: <30%.
• Moderate: 30% to 50%.
• Large: >50%.

Step 3: Evaluate the Direction of the Shunt

• Align the PDA flow such that the cursor is parallel to the flow to achieve a complete Doppler signal.

Key Points

• In a patient with a PDA and normal pulmonary resistance, there will be left-to-right shunting (Fig. 5-16).
• In the setting of pulmonary hypertension and/or complex CHD, the ductus may be bidirectional or right to left.
image

Figure 5-16 Doppler performed in the DA demonstrates continuous left-to-right shunting with a peak velocity of 4.5 m/s.

Step 4: Determine Whether the Shunt Is Hemodynamically Significant

• Left ventricular enlargement indicates a hemodynamically significant shunt.
• Measure peak velocity by pulsed wave at the pulmonary end of ductus:

• >1.5 m/s suggests that the ductus is not hemodynamically significant.
• <1.5 m/s suggest that the ductus is hemodynamically significant.

• The presence of turbulence in systole and diastole in the main PA suggests a hemodynamically significant shunt.

Step 5: Evaluate for Other Cardiac Disease

• A coarctation of the aorta may be masked in the presence of a ductus arteriosus (DA).
• Coarctation of the aorta is suggested by:

• Narrowing in the isthmus region of the descending aorta.
• The presence of a posterior shelf in the juxtaductal region of the aorta.
• An increased distance from the left carotid and left subclavian arteries.

• Obtain a suprasternal notch “candy cane” view of the aortic arch with alignment of the cursor parallel to the entire descending aorta.

Key Points

• CW Doppler should always be performed in the descending aorta.

• If the Doppler cursor is not aligned parallel to the entire descending aorta, a ductal dependent coarctation of the aorta may be missed.

• Many cyanotic congenital heart lesions depend on the presence of a DA to maintain circulation before surgical repair (Fig. 5-17).
image

Figure 5-17 Doppler performed in the ductus arteriosus of an infant with a ductal-dependent cardiac lesion. There is bidirectional shunting with primarily right-to-left flow (below the baseline) seen in systole.

Surgical Ligation and Device/Coil Closure: Special Considerations

• Ligation of the LPA is a known complication after surgical ligation.

Key Points

• Both branch pulmonary arteries should be assessed by 2D, color Doppler, and spectral Doppler.
• No residual shunting should be present after ductal closure.
• Assess the aortic arch to ensure that a coarctation of the aorta is not present after ligation.

Suggested Reading

1 Allen HD, Driscoll DJ, Shaddy RE, Feltes TF, editors Moss and Adams’ Heart Disease in Infants, Children and Adolescents: Including the Fetus and Young Adult. 7th ed. Philadelphia: Lippincott Williams & Wilkins; 2007: 632-645, 667-701.

These chapters review the basic anatomy and physiology of atrial and VSDs and PDA. Clinical presentation and pictures of anatomic specimens are included.

2 Keane JF, Fyler DC, Lock JE. Nadas’ Pediatric Cardiology, 2nd ed. Philadelphia: Saunders; 2006. 527-548, 603-626

A concise description and review of ventricular and atrial septal defects and PDA. Images include diagrams and angiograms.

3 Lai W, Mertens L, Cohen M, Geva T, editors Echocardiography in Pediatric and Congenital Heart Disease: From Fetus to Adult. Hoboken, NJ: Wiley-Blackwell; 2009:158-187, 283-296

Includes a description of the anatomic lesions and additional imaging techniques.

4 Praagh VS, Carrera ME, Sanders SP, et al. Sinus venosus defects: unroofing the right pulmonary veins—anatomic and echocardiographic findings and surgical treatment. Am Heart J. 1994;128:365-379.

Key paper describing the anatomic findings of a sinus venosus defect seen by echo.

5 Hubail Z, Lemler M, Ramaciotti C, et al. Diagnosing a patent foramen ovale in children: is transesophageal echocardiography necessary. Stroke. 2011;42:98-101.

Describes the key findings for diagnosis of an ASD by transthoracic echo and provides evidence that transthoracic imaging rather than transesophageal echo in children is very effective and less invasive due to better acoustic windows in children.

6 Butera G, Romagnoli E, Carminati M, et al. Treatment of isolated secundum atrial septal defects: impact of age and defect morphology in 1,013 consecutive patients. Am Heart J. 2008;156:706-712.

Demonstrates percutaneous closure via device of ASDs is possible on most patients and associated with a low complication rate.

7 Radzik D, Davignon A, van Doesburg N, et al. Predictive factors for spontaneous closure of atrial septal defects diagnosed in the first 3 months of life. J Am Coll Cardiol. 1994;23:851-853.

101 infants were followed, demonstrating that interatrial defects measuring less than 3 mm in size do not need to be followed and often close spontaneously (hence the definition of a patent foramen ovale). Defects larger than 8 mm do not close spontaneously and are considered large.

8 Berger F, Ewert P, Biornstad P, et al. Transcatheter closure as standard treatment for most interatrial defects: experience in 200 patients treated with Amplatzer Septal Occluder. Cardiol Young. 1999;9:468-473.

Device closure has replaced surgical closure as treatment for most ASDs. This paper validates this practice.

9 Chiu SN, Wang JK, Lin MT, et al. Aortic valve prolapse associated with outlet-type ventricular septal defect. Ann Thorac Surg. 2005;79:1366-1371.

Description of the association of an outlet defect with aortic RCC prolapse as well as the association of perimembranous VSDs with infundibular hypertrophy and a subaortic ridge.

10 Canale JM, Sahn DF, Allen HD, et al. Factors affecting real-time, cross-sectional echocardiographic imaging of perimembranous ventricular septal defects. Circulation. 1981;63:689-697.

This paper effectively describes the multiple imaging planes needed to identify and fully image a VSD. Patients had VSDs proven by angiography. It also correlates the size of the VSD to the diameter of the aorta and correlates this ratio with quantification of interventricular shunting (Qp/Qs) (pulmonary/systemic volume flow rate) data from the cardiac catheterization.

11 Mehta AV, Chidambaram B. Ventricular septal defect in the first year of life. Am J Cardiol. 1992;70:364-366.

Description of the isolated VSDs found in 124 infants who were followed over time. Spontaneous closure was seen in both perimembranous and muscular VSDs with a higher incidence of spontaneous closure in muscular VSDs.

12 Glen S, Burns J, Bloomfield P. Prevalence and development of additional cardiac abnormalities in 1448 patients with congenital ventricular septal defects. Heart. 2004;90:1321-1325.

13 Ramaciotti C, Vetter JM, Bornemeier RA, et al. Prevalence, relation to spontaneous closure and association of muscular ventricular septal defects with other cardiac defects. Am J Cardiol. 1995;75:61-65.

14 Turner SW, Hunter S, Wyllie JP. The natural history of ventricular septal defects. Arch Dis Child. 1999;81:413-416.

A group of 1448 patients with VSDs were followed. This article demonstrates the increased association of VSDs with cardiac abnormalities as well as the development of abnormalities over time, including infundibular pulmonary stenosis and AR. This article recommends that patients with VSDs be followed by a cardiologist until at least 30 years of age.

15 Sutherland GR, Godman M, Smallhorn F, et al. Ventricular septal defects: two dimensional echocardiographic and morphological correlations. Br Heart J. 1982;47:316-328.

Validates the use of echo in identifying VSDs.

16 Minette MS, Sahn DF. Ventricular septal defect. Circulation. 2006;114:2190-2197.

This article is a review of VSDs, including the basic anatomy, physiology, treatment, and long-term prognosis, and including findings in adult patients.

17 Su BH, Watanabe T, Mitsumasa S, et al. Echocardiographic assessment of patent ductus arteriosus shunt flow pattern in premature infants. Arch Dis Child. 1997;77:F36-F40.

This article outlines methods of echocardiographic assessment of PDA in premature infants to predict hemodynamically significant shunts.

18 Sehgal A, McNamara PJ. Does echocardiography facilitate determination of hemodynamic significance attributable to the ductus arteriosus? Eur J Pediatr. 2009;168:907-914.

Methods for ductal assessment including echocardiographic markers of hemodynamically shunting.

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