PICTORIAL ESSAY
Ventricular Septal Defects
Embryology and Imaging Findings
Carlos Andres Rojas, MD,* Camilo Jaimes, MD,w and Suhny Abbara, MDz
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Abstract: Ventricular septal defects are the most common congenital
abnormality diagnosed in children and the second most common
congenital heart condition diagnosed in adults. Depending on their
location in the interventricular septum, ventricular septal defects
are described as perimembranous, muscular, subarterial, and in-
flow. Awareness of the embryologic basis of these defects helps
understand the anatomy and recognize their typical appearance on
imaging. Diagnostic imaging plays a role in the characterization of
the defect, identification of associated anomalies, and evaluation
of hemodynamic repercussion, all of which contribute to guide
treatment.
Key Words: ventricular septal defects, interventricular septum,
congenital heart disease
(J Thorac Imaging 2013;28:W28–W34)
VENTRICULAR SEPTAL DEFECTS (VSDs):
BACKGROUND
VSDs are abnormal openings in the septum that allow
shunting of blood between the ventricles.1 VSDs are the most
common congenital abnormality diagnosed in children, with
a reported incidence of 53 per 10,000 live births.2 VSDs
occur in 50% of children with congenital heart disease and
are an isolated finding in 20% of them.1,2 In adults, VSDs
are the second most common congenital heart condition
(after bicuspid aortic valve), with an estimated prevalence of
0.3 per 1000.3
Echocardiography is the main imaging modality for
the diagnosis and follow-up of VSDs.1 Magnetic resonance
imaging (MRI) and computed tomography (CT) are not
routinely used in cases of VSDs. However, they are fre-
quently used to characterize complicated cardiovascular mal-
formations, many of which can have associated VSDs.4,5
Furthermore, with the recent surge in the use of MRI and
CT in cardiothoracic imaging, the detection of these defects
as incidental findings has increased substantially.5,6
From the *Department of Radiology, University of South Florida,
Tampa, FL; wDepartment of Radiology, The Children’s Hospital of
Philadelphia, Philadelphia, PA; and zDepartment of Radiology,
Division of Cardiovascular Imaging, Massachusetts General Hos-
pital, Harvard Medical School, Boston, MA.
The authors declare no conflicts of interest.
Reprints: Carlos Andres Rojas, MD, Department of Radiology,
University of South Florida, 12901 Bruce B. Downs Blvd. P.O.
Box 17, Tampa, FL 33612 (e-mail: caranrojas@gmail.com).
Supplemental Digital Content is available for this article. Direct URL
citations appear in the printed text and are provided in the HTML
and PDF versions of this article on the journal’s Website,
www.thoracicimaging.com.
Copyright r 2013 by Lippincott Williams & Wilkins
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DEVELOPMENT OF THE INTERVENTRICULAR
SEPTUM (IVS)
The IVS is the anatomic structure that divides the
right (RV) and left (LV) ventricles. The formation of
the IVS starts around the fifth week of embryonic devel-
opment and involves the sequential fusion of 3 independent
septa: muscular, outlet, and inlet septa (Fig. 1).7–9 A dis-
ruption in this process leads to the development of VSDs
(Fig. 2).
PATHOPHYSIOLOGY OF VSDs
During prenatal life, the vascular resistance in the
systemic and pulmonary circulations is similar; thus, mini-
mal flow occurs through VSDs regardless of their size.10 In
the early neonatal period, pulmonary vascular resistance
drops substantially, creating a pressure gradient. This
pressure gradient is the main determinant of the degree and
direction of the shunt across the VSD. The size of the defect
also influences the amount of blood that crosses the VSD.11
Smaller defects, also called restrictive defects, provide in-
trinsic resistance to flow and limit the amount of shunted
blood, maintaining a gradient between the 2 ventricles. In
contrast, large defects allow for unrestricted flow through
the defect and equalization of interventricular chamber
pressures.11
In the early stages of disease, blood crosses from the
LV into the RV. The increase in blood flow in the pulmo-
nary circulation leads to pulmonary hypertension and to an
increase in the preload in the left atrium and ventricle.12
At first, the vascular resistance in the pulmonary vessels
is only mildly elevated. However, chronic shunting across
the defect leads to structural and functional changes in
the pulmonary vessels, which ultimately result in an in-
crease in the pulmonary vascular resistance and worsening
of pulmonary hypertension.12 If the pressure in the
pulmonary circulation exceeds that in the systemic circu-
lation, the direction of the shunt is reversed (right-to-left
shunting). This condition, known as the Eisenmenger
complex, is a late stage in the course of disease, has a worse
prognosis, and leads to cyanosis, as venous blood crosses
the septal defect and reaches the systemic circulation.13,14
CONVENTIONAL RADIOGRAPHY
Conventional radiographs demonstrate findings sec-
ondary to the increase in pulmonary blood flow. Cardio-
megaly and prominent pulmonary vascularity are the most
common features (Fig. 3). However, these findings are
nonspecific and can be seen with other causes of left-
to-right shunts, such as an atrial septal defect (ASD) or
a patent ductus arteriosus. Additional imaging features
such as an enlarged left atrium and a normal-sized or small
aorta are characteristic of VSDs and can help narrow the
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FIGURE 1. Diagrammatic representation of normal development of the IVS. The IVS is formed from 3 separate septa: muscular, outlet,
and inlet septa. Early in embryologic development, the muscular septum (MS) grows upward from the floor of the ventricles toward the
already fused endocardial cushions (EC). The gap between the edge of the muscular IVS and EC is called the interventricular foramen
(IVF). Meanwhile, 2 spiral ridges of tissue, the conotruncal ridges or truncoconal swellings, appear on the sides of the truncus arteriosus
(TA). The conotruncal ridges grow toward each other and fuse, forming a spiral-shaped septum termed the aortopulmonary septum
(APS). The APS divides the TA into the pulmonary trunk and aorta. The conotruncal ridges also grow downward into the ventricles,
meeting with the already fused endocardial cushions and the muscular portion of the IVS. By the seventh to eighth week of gestation, the
membranous septum is formed when the APS, endocardial cushions, and muscular septum completely fuse, closing off the IVS.

FIGURE 2. Diagrammatic representation of normal common developmental anomalies of the IVS. Defects in the fusion of the muscular
septum (MS) and the endocardial cushions (EC) result in membranous VSDs. Openings in the trabecular portion of the IVS lead to muscular
VSDs. Incomplete fusion of the aortopulmonary septum (APS) with the EC-MS septum results in supracristal VSDs (SC-VSD).

FIGURE 3. Radiographic findings of VSDs. A, Frontal radiograph of the chest of a 1-year-old boy with a membranous VSD demonstrates an
enlarged cardiothymic silhouette with increase in pulmonary vascularity. The VSD was surgically closed at this time. B, Frontal radiograph
of the chest of the same boy 3 years later shows improved cardiomegaly and normal pulmonary vascularity. Sternal wires are seen as well.

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Rojas et al
FIGURE 4. Quantification of the shunt using MRI. A, Short-axis BSSFP MRI of the heart of an 8-year-old girl shows a small restrictive
perimembranous VSD (arrow) with a small jet into the right ventricular outflow tract from left-to-right shunting. B, Magnitude and (C)
velocity images obtained above the semilunar valves were used to quantify the flow in the main pulmonary artery (PA) and the aorta
(Ao) using a flow analysis software. The Qp:Qs shunt was estimated to be 1.5.
differential considerations, given that ASDs typically present
with a normal-sized left atrium, and a patent ductus arteriosus
is commonly associated with an enlarged aorta.15 In VSDs,
the degree of cardiomegaly is always proportional to the in-
crease in pulmonary vascularity. Disproportionate findings
should raise the concern for complex congenital heart disease
(with additional malformations) or a different diagnosis.
CARDIAC CT AND MRI
Advanced cardiac imaging with CT and MRI con-
tinues to evolve and its use continues to increase. Currently,
CT serves to assess morphology and detect associated
anomalies when echocardiography is limited. Imaging of
VSDs by CT requires an appropriate imaging protocol to
obtain ideal intracardiac opacification. At our institution,
contrast material is administered using a biphasic protocol
consisting of an initial contrast bolus at a rate of 4 to 7 mL/s,
followed by 40 to 50 mL of saline to flush out the contrast
from the right heart.16 This method provides an ideal opa-
FIGURE 5. Schematic diagram depicting the various types of
VSDs. Perimembranous VSD (yellow), subarterial VSD (red),
muscular VSD (blue), inlet VSD (green). IVC indicates inferior
vena cava; SVC, superior vena cava.
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J Thorac Imaging  Volume 28, Number 2, March 2013
cification of the left heart for the detection of left-to-right
shunts. Right-to-left shunts result in low attenuation jets
entering the opacified LV.
Images can be acquired with prospective triggering or
with retrospective gating. Prospectively triggered acquisition
yields images during a specific point in time, significantly
reducing radiation exposure. However, ventricular function
cannot be assessed. Retrospectively gated acquisition uses
helical scanning, exposing the patient to radiation during
the entire cardiac cycle.16,17 This method is preferred for
morphologic assessment, as it allows visualization of the
VSD during the entire cardiac cycle and also allows calcu-
lation of the biventricular volumes and function. It is
important to note that ventricular stroke volumes calculated
using the Simpson method do not allow quantification of
shunting in the setting of VSDs because of maintained
stroke volumes in both ventricles.18
MRI aids in the morphologic and functional evaluation
of VSDs. Multiple sequences including black blood images,
balanced steady-state free precession (BSSFP) images, velo-
city-encoded phase-contrast images, magnetic resonance an-
giography images, and three dimensional (3D) whole-heart
BSSFP images are usually acquired.19 The appearance of
VSDs varies depending on their location and hemodynamic
characteristics. Although large defects may be readily apparent
on morphologic or BSSFP imaging, a subtle jet of dephasing
across the IVS may be the only evidence of a small VSD.
BSSFP images in the short-axis plane covering the
ventricles can be used to determine biventricular volumes
and function using the Simpson method. As mentioned
above, this method is inaccurate to calculate the degree of
shunting in the presence of VSDs because of the maintained
stroke volumes in both ventricles.18 An alternative way to
estimate the degree of shunting is to use phase-contrast
MRI. Velocity-encoded phase-contrast images acquired of
regions above the level of the semilunar valves can be used
to calculate the volume of blood exiting the pulmonary
artery and aorta.18 This data can be used to calculate the flow
in the pulmonary (Qp) and systemic (Qs) circulations.19 The
rate of shunting (Qp:Qs) and the shunt fraction ([QpQs]/
Qp) can be calculated on the basis of these estimates
(Fig. 4).20 In general, shunts that result in a pulmonary blood
flow that is 1.5 times greater than the systemic blood flow
(Qp:Qs ratio>1.5) are considered significant.
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FIGURE 6. Interventricular septal aneurysms in 2 different patients. A, Short-axis view from a cardiac CT in a 40-year-old man demon-
strates the presence of an interventricular septal aneurysm (black arrows). No associated VSD was noted. B, A 5-chamber view of a
cardiac CT in a 67-year-old man with a history of perimembranous VSD. Note a ventricular septal aneurysm (white arrow) with high
attenuation jets entering the RV (black arrows) consistent with a partially closed membranous VSD. RVOT indicates right ventricular
outflow tract.
The estimates obtained using MRI are comparable to These defects can be associated with misalignment of the
those obtained with catheter-based approaches (invasive oxi- aortopulmonary septum, as in the setting of Tetralogy of
metry), although a small nonsignificant overestimation in the Fallot (anterior misalignment) or interrupted aortic arch
Qp:Qs ratio and shunt fraction has been described with (posterior misalignment). Approximately a third of isolated
MRI.20,21 A caveat to phase-contrast imaging are patients perimembranous VSDs close spontaneously, usually by ap-
with chronic shunting that has resulted in equalization of left position of the septal leaflet of the tricuspid valve or prolapse
and right ventricular pressures, which reduces, stops, or even of an aortic cusp (right or noncoronary) into the defect.24
reverses the shunt flow. Furthermore, phase-contrast imaging These mechanisms of spontaneous defect closure can result in
perpendicular to the shunt jet can also assess the volume and the formation of an aneurysm in the IVS with or without
peak gradient across the defect.22 residual shunting (Fig. 6).
On transthoracic echocardiography, perimembranous
VSDs are better visualized on parasternal short-axis views
TYPES OF VSDs AND IMAGING APPEARANCES at the level of the aortic valve. Typically, a flow jet arising
Congenital VSDs can be classified according to their at the 11 o’clock position can be readily identified.
location in the IVS as perimembranous, muscular, sub- The characteristic features of perimembranous VSDs
arterial, or inflow (Fig. 5).23 are well demonstrated in this 2D echocardiographic cine
Approximately 75% to 80% of VSDs occur in the clip from an asymptomatic 8-year-old boy. The parasternal
membranous septum. These defects are located below the short-axis view with color flow mapping at the level of the
crista supraventricularis and anterior to the septal leaflet of aortic valve shows the characteristic location of the defect
the tricuspid valve. Membranous VSDs are also known as and the typical jet at the 11 o’clock position. (Supplemental
infracristal, subaortic, perimembranous, or paramembranous. Digital Content 1, Video, http://links.lww.com/JTI/A19).

FIGURE 7. A 5-chamber view from a cardiac CT demonstrates

the presence of high attenuation contrast (arrows) on the ven-
tricular side of the septal leaflet of the tricuspid valve that could
be confused with a small membranous VSD. The transthoracic
echocardiogram of the same patient excluded the presence of a
defect in this location. Ao indicates aorta; LA, left atrium.
FIGURE 8. Muscular VSD in a 36-year-old man. A short-axis
BSSFP image incidentally demonstrates the presence of a small
anterior muscular VSD (white arrow). No significant right
ventricular enlargement is noted.

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FIGURE 9. Muscular VSD in a 46-year-old woman. A, The 4-chamber view from a cardiac CT demonstrates the presence of a small
defect in the apical muscular septum consistent with a muscular VSD (white arrow). B, The short-axis view clearly demonstrates contrast
coursing through the muscular VSD (white arrow) and spilling into the unopacified RV. No right chamber enlargement is noted.
LA indicates left atrium.

The videoclip of a 2D echocardiogram on a subcostal
frontal view shows that the VSD is located in the ante-
rosuperior portion of the IVS between the tricuspid and
aortic valves. The septal leaflet of the tricuspid valve is seen
in close proximity to the defect (Supplemental Digital
Content 2, Video, http://links.lww.com/JTI/A20). The video-
clip from the subcostal left anterior-oblique view with
color Doppler demonstrates left-to-right shunting through
the VSD and aneurysmal tricuspid valve tissue partially
occluding the defect. There is no obstruction of the left
ventricular outflow tract. A PFO with left-to-right shunting
is also evident (Supplemental Digital Content 3, Video,
http://links.lww.com/JTI/A21).
On electrocardiogram-gated multidetector computed
tomography images with contrast and a saline chaser, peri-
membranous VSDs are seen as a high attenuation jet crossing
through the septal defect and entering the washed-out
infracristal RV. A potential pitfall on CT imaging is the in-
complete washout of contrast on the ventricular side of the
tricuspid septal leaflet accompanied by a thin membranous
septum, which can simulate a membranous VSD (Fig. 7).
Large defects can result in right ventricular enlargement be-
cause of long-standing increased volume in the low-pressure
chamber. Morphologically, perimembranous VSDs are bound
by both membranous and muscular tissue. Diagnostic imag-
ing can also identify associated conditions, such as a subaortic
ridge, aortic valve prolapse, and aortic regurgitation.24
A Gerbode-type defect is a communication between
the LV and right atrium (RA) through the membranous
IVS.23 Gerbode-type defects can be further classified as
infravalvular or supravalvular in relation to the tricuspid
valve annulus. Supravalvular Gerbode defects involve the
atrioventricular portion of the membranous septum and
result in a direct communication between the LV and RA.
Infravalvular Gerbode defects include a defect in the in-
terventricular portion of the membranous septum and
fenestrations of the tricuspid septal leaflet, resulting in
LV-to-RA shunting. Imaging features that can aid in the
identification of Gerbode defects include atypical direction
of the flow jet, from the LV to the RA, and persistent
shunting during diastole.
Acquired causes of Gerbode defects include surgery,
endocarditis, trauma, and ischemia.25 Echocardiographic
images in this 6-year-old boy with persistent shunting after
surgical repair of an atrioventricular canal demonstrate the
characteristic imaging features in a postsurgical setting. 2D

FIGURE 10. Muscular VSD in a 37-year-old woman. A, Four-chamber and (B) short-axis BSSFP images in a patient with a dual-chamber
RV demonstrate a large apical muscular VSD (white arrows). The dense trabeculations of the RV (black arrowheads) serve as a barrier to
the functional RV; therefore, no chamber enlargement is noted despite the large VSD.

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VSDs located in the trabecular portion of the IVS are

FIGURE 11. Subarterial VSD in a 29-year-old man. The short-axis
view from a cardiac CT demonstrates the presence of a sub-
arterial VSD (black arrow). The small muscular ridge below the
defect represents the crista supraventricularis (white arrow).
RVOT indicates right ventricular outflow tract.
echocardiographic images with color flow mapping on a
4-chamber apical view show a flow jet extending from the LV
into the RA, consistent with a Gerbode-type VSD. The RA
appears slightly enlarged. Color Doppler images also dem-
onstrate smaller jets across the left and right AV valves, which
represent mild residual insufficiency. The RV and LV appear
normal in size (Supplemental Digital Content 4, Video, http://
links.lww.com/JTI/A22).
called muscular VSDs (Fig. 8). Approximately 5% to 20%
of all VSDs occur in this region. These defects are entirely
surrounded by muscle and vary in their number and size.26
The presence of multiple defects is known as the “swiss
cheese septum.” Two thirds of muscular VSDs are located
in the apical region. This type of VSD exhibits a marked
tendency to regress spontaneously (68% to 75% close be-
fore 2 y of age); thus, they are more commonly seen in
children.24 As with other types of VSDs, a high attenuation
jet crossing through the defect can be seen on electro-
cardiogram-gated multidetector computed tomography
images following administration of contrast and a saline
chaser (Fig. 9). Associated dilation of the RV can occa-
sionally be seen, especially with large defects (Fig. 10).
Small defects usually close during ventricular systole lim-
iting flow during this phase of the cardiac cycle. Potential
pitfalls include deep crypts, Thebesian sinuses, and coarse
trabeculations. The absence of high attenuation contrast
material entering the RV can help differentiate these entities
from true muscular VSDs.
VSDs located below the semilunar valve and above the
crista supraventricularis are known as subarterial, outlet,
supracristal, subpulmonary, infundibular, doubly commit-
ted, or conoseptal VSDs (Fig. 11).26 Overall, subarterial
VSDs account for 5% to 7% of isolated VSDs; however, a
substantially higher prevalence has been reported in Asian
populations.27 Defects in this location are frequently asso-
ciated with aortic valve prolapse or regurgitation, which
results from the loss of support of the right cusp of the
aortic valve.27 These defects can be bound by the fibrous
annulus of the semilunar valves and/or muscular tissue. On
transthoracic echocardiography, the shunt is best seen on a
parasternal short-axis view at the level of the aortic valve at
the 1 o’clock position. The shunt is well depicted on MRI

FIGURE 12. Subarterial VSD in a 31-year-old man with a history of subaortic membrane. A, Three-chamber and (B) short-axis BSSFP
images demonstrate a small defect (white arrows) in the supracristal region. Note that the defect is above the crista supraventricularis
(black arrow) in (B). C, A fat-saturated 3D SSFP image on the same patient in the short-axis plane demonstrates the small defect (white
arrow) above the crista supraventricularis (black arrow). D, A phase-contrast image at the level of the aortic annulus demonstrates a
systolic jet in the 1 o’clock position (white arrow) consistent with the subarterial VSD.

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Rojas et al
FIGURE 13. Corrected Tetralogy of Fallot in a 27-year-old man.
Volume-rendered image depicts patch closure of membranous
VSD (white arrows) and a bioprosthetic valve in the pulmonic
position. Incidentally noted is prominence of the pulmonary ar-
tery and right ventricular chamber. LVOT indicates left ventricular
outflow tract; PA, pulmonary artery; RVOT, right ventricular
outflow tract.
and CT images as well, at the level of the aortic valve
(Fig. 12). As with other VSDs, right ventricular chamber
enlargement can be seen, especially in large defects.
Inflow VSDs occur almost exclusively in association
with endocardial cushion defects. Thus, inflow VSDs are
uncommon in the general population but have a remark-
ably high prevalence in genetic conditions such as trisomy
18 and trisomy 21.28 These defects are bound by the tricuspid
valve annulus and extend to the muscular septum and variably
to the membranous septum. These defects can be associated
with ASDs (primum type) and atrioventricular valve clefts.
TREATMENT
Many factors influence treatment decision in patients
with VSDs, such as the presence of symptoms, coexisting
anomalies, age of the patient, right ventricular enlargement,
and size, number, and location of the defects. By fully
characterizing the anatomy, diagnostic imaging provides
valuable information to guide therapy.
The main alternatives in the treatment of VSDs are
open surgery with patch repair (Fig. 13) and endovascular
closure with devices. Currently, endovascular closure
is performed for perimembranous or muscular VSDs in
patients at high risk for standard surgical closure.
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