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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3676_Библиотеки_им_академика_М_И_Перельмана
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5 Cardiac CTA of Congenital Coronary and Other Anomalies
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5.13 Case 5.13
5.13.1 History
A 54-year-old female presented with history of
progressive shortness of breath.
5.13.2 Findings
There is an ostium secundum type atrial septal
defect (ASD) (Fig. 5.13a). There is right chamber
enlargement and cardiomegaly. There is left-toright shunt with equalization of the contrast density
between the right and left chambers. There is dilatation of the pulmonary arterial trunk (Fig. 5.13b).
a
5.13.3 Diagnosis
The diagnosis is secundum ASD.
5.13.4 Discussion
The ASD was successfully repaired percutaneously with a closure device (Fig. 5.13a).
There are four basic types of ASDs: The most
common is the ostium secundum defect and is
the least serious. The defect occurs in the area
of the fossa ovalis as a result of excessive fenestration or resorption of the septum primum,
underdevelopment of the septum secundum,
or a combination of both. A variant of ostium
de f
Fig. 5.13 (a) Axial. Ostium secundum atrial septal defect
(ASD) (arrow). (b) Axial thick maximum intensity projection: ASD closure with a 35-mm Helix Septal Occluder
(arrow). (c) Axial. Dilated pulmonary arteries (double
arrows). (d) Axial. In a different patient, previous surgical
repair of an ostium primum ASD with placement of a
Dacron patch (long arrow). Also, status post repair of a
cleft in the anterior leaflet of the mitral valve (short
arrow). (e) Axial. Sinus venosus ASD (arrow) in a different patient. (f) Sagittal. In a different patient, coronary
sinus defect (long arrow) with anomalous vein (short
arrow) communicating with the left atrium. Right ventricle (RV) and left atrium (LA)
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secundum defect is the association with an
aneurysm of the atrial septum.
The second type of ASD is the ostium primum
defect (Fig. 5.13c). This type of ASD results
from failure of closure of the endocardial cushion
and is associated with a cleft in the anterior leaflet of the mitral valve.
The third type of ASD is a sinus venosus
defect (Fig. 5.13d). This is located in the posterior aspect of the septum near the superior vena
cava and is associated with right partial anomalous pulmonary venous return.
The fourth and least common type is a coronary sinus septal defect (Fig. 5.13d). This results
from an unroofed coronary sinus or coronary
sinus septal defect. A segment of the roof of the
coronary sinus is absent, with blood shunted
from the left atrium into the coronary sinus and
subsequently into the right atrium. It may also be
associated with a persistent left superior vena
cava.
5.13.5 Pearls and Pitfalls
ASDs may not be readily apparent on the CTA and
require careful inspection of the images. Secondary
clues alerting to the presence of a shunt are equalization of the contrast density between the right
and left chambers, right chamber enlargement, and
dilatation of the pulmonary arteries.
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5.14 Case 5.14
5.14.1 History
5.14.3 Diagnosis
The diagnosis is muscular septum restrictive ven-
tricular septal defect (VSD).
A 64-year-old male presented with a history of
CAD and recent abnormal stress test result.
5.14.4 Discussion
5.14.2 Findings
There is a small defect in the muscular septum
that communicates with the right and left ventricles. There is mild dilatation of the main pulmonary arteries (Fig. 5.14a–c).
abc
The small VSD was previously undiagnosed and
found incidentally on the cardiac CT. VSDs rep-
resent approximately one fifth of all congenital
cardiac anomalies. It is usually diagnosed during
childhood. A VSD refers to a defect in the inter-
ventricular septum that is composed of muscular
d
Fig. 5.14 (a, b) Axial coronal maximum intensity pro-
jection (MIP). Restrictive muscular septum ventricular
septal defect (VSD) (arrow). (c) Axial MIP. Mildly dilated
pulmonary arteries (double arrows). (d) Septal rupture
from an MI (arrows) (Courtesy of Dr. Robert Quaife,
University of Colorado, Denver.)
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and membranous segments. Defects are most
commonly classified according to occurring in or
adjacent to one or more septal components. The
most common defect occurs in the region of the
membranous septum and is referred to as a para-
membranous or perimembranous defect because
it is larger than the membranous septum itself
and has a muscular defect in the segment of its
perimeter.
The second type is entirely within the muscular rim, as in this case. These muscular defects
can be defined as inlet, trabecular, central, apical, marginal or Swiss cheese, or outlet and may
vary greatly in size, shape, and number. The
third type of VSD occurs when the outlet septum
is deficient and commonly is referred to as a
supracrystal, subpulmonic, outlet, infundibular,
or conoseptal.
The hemodynamic significance of a VSD
depends primarily on its size and the status of the
pulmonary vascular bed rather than the location
of the defect. When a small communication is
present (usually <0.5 cm2), the VSD is referred to
as restrictive, and the right ventricular pressure is
normal. A small VSD with high resistance to
flow permits only a small left-to-right shunt.
Larger VSDs, particularly of the nonrestrictive
type (usually >1.0 cm2), are hemodynamically
significant and may cause dyspnea, congestive
heart failure, arrhythmias, or sudden death or
progress to Eisenmenger’s syndrome.
An acquired VSD (Fig. 5.14d) may result
from myocardial rupture from an acute myocardial infarct, blunt and penetrating trauma, primary cardiac infection, primary and secondary
tumors, infiltrative diseases of the heart, and
aortic dissection. These have extremely high
mortality.
5.14.5 Pearls and Pitfalls
Larger and hemodynamically significant VSDs
are usually diagnosed in infancy. Clinically
silent VSDs that are incidentally found in adults
are visualized as small communicating defects.
These can be suspected on the axial images in a
localized segment of LV non-compaction.
Coronal sagittal and oblique views may be
needed to confirm the communication. Other
findings include equalization of the contrast
density in the right and left ventricles, cardiac
chamber enlargement, and enlargement of the
pulmonary arteries.
ab
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5.15 Case 5.15
5.15.1 History
A 77-year-old male with a previous CABG was
evaluated for an abnormal nuclear perfusion
stress test result.
5.15.2 Findings
The IV contrast was injected into the left arm.
There is a dilated vascular structure adjacent to
the left atrium, lipomatous hypertrophy of the
atrial septum, and heavily diseased anomalous
origin of the left circumflex coronary artery from
the right coronary sinus (Fig. 5.15a). There is a
dilated coronary sinus (Fig. 5.15b).
5.15.3 Diagnosis
The diagnosis is persistent left superior vena cava.
5.15.4 Discussion
Persistent left superior vena cava is also called
double superior vena cava. It is caused by the
failure of regression of the left anterior cardinal
vein and of the left horn of the venous sinus
between the 24th and 56th days of pregnancy. It
is the most common cause of a dilated coronary
sinus.
Persistent left superior vena cava occurs in
0.1–0.5% of the general population, with 8%
draining into the left atrium. Unroofed coronary
sinus ASD is seen in 75% of patients with an
LSVC that drains into the left atrium and is usually associated with other forms of congenital
heart disease and heterotaxy syndromes.
5.15.5 Pearls and Pitfalls
Left superior vena cava should be suspected in
the presence of a dilated coronary sinus.
Fig. 5.15 (a) Axial
maximum intensity
projection. Left superior
vena cava (double
arrows), anomalous left
circumflex artery (single
long arrow), lipomatous
hypertrophy of the atrial
septum (short arrow).
(b) Sagittal maximum
intensity projection. Left
superior vena cava
(single arrow). Dilated
coronary sinus (double
arrows)
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5.16 Case 5.16
5.16.1 History
A 43-year-old male presented to outpatient clinic
with atypical chest pain. Normal EKG.
5.16.2 Findings
There is a single large coronary trunk arising
from the right sinus of Valsalva (Fig. 5.16a–d).
5.16.3 Diagnosis
Congenital single coronary trunk.
a
5.16.4 Discussion
The case demonstrates a rare congenital coronary
anomaly, where a single arterial trunk is present,
perfusing the entire myocardium.
5.16.5 Pearls and Pitfalls
Since the patient has “all his eggs in one basket,”
it is important to minimize the risk of developing
coronary artery disease by careful risk stratification and preventive measures.
c
Fig. 5.16 (a) Oblique
MIP. Single right trunk
(arrow). (b) Volume
Rendered (VR)-anterior
view. (c) VR-posterior
view. Posterior
descending artery
coming off of the right
coronary artery.
(d) Coronary tree
b
d
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5.17 Case 5.17
5.17.1 History
A 31-year-old male presented to emergency
department with SOB with previous outside
diagnosis of dextrocardia.
5.17.2 Findings
The anatomic right and left ventricles are
switched in position with anatomical atrioventricular discordance. There is a small perimembranous ventricular septal defect (Fig. 5.17a–d).
a
5.17.3 Diagnosis
Congenital corrected transposition of great vessels (TGA) with a ventricular septal defect.
5.17.4 Discussion
Congenital corrected transposition is a rare congenital heart defect, where aortopulmonary septum fails to rotate 180° with atrioventricular
discordance, during embryogenesis. Effectively,
venous blood flows through the right atrium to the
left ventricle (via mitral valve) and eventually to
the lungs via pulmonary veins. Oxygenated blood
b
Fig. 5.17 (a) Coronal.
The right atrium
draining to the left
ventricle. The left atrium
draining to the right
ventricle, which supplies
the systemic circulation.
VSD noted (arrow).
(b) Axial. (c, d) Sagittal.
The right ventricle
pumping blood into the
aorta for the systemic
circulation. VSD noted
(arrow)
c
d
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is returned via pulmonary arteries back to the left
atrium and out to systemic circulation via the
right ventricle and the aorta. Unlike congenital
transposition of great arteries, which require a
shunt for survival, this condition manifests in
childhood or in early adulthood. Symptoms
mimic heart failure and are usually due to right
ventricular decompensation because the right
ventricle supports the systemic circulation.
Moreover, this condition is associated with AV
heart block and tachyarrhythmia. Symptomatology
will vary depending on other associated anomalies
like tricuspid valve abnormalities, pulmonic stenosis, and/or ventricular septal defects.
5.17.5 Pearls and Pitfalls
Finding complex coronary anomalies in adults is
becoming more common since there are thousands of patients that have had corrective surgery
during the first decade of life. Thorough knowledge of the expected congenital and post-surgical
findings is essential for an accurate diagnosis and
appropriate patient management.
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5.18 Case 5.18
5.18.1 History
A 65-year-old female status post mitral valve
replacement and tricuspid valve repair in the previous week. Patient developed persistent congestive heart failure with pleural effusions. An astute
cardiologist heard a roaring precordial murmur
on physical examination and requested CCTA to
rule out a post-surgical fistula complication.
5.18.2 Findings
Figure 5.18a demonstrates the cardiac surgery, a
pacemaker wire and a large pleural effusion.
a
b
Figure 5.18b demonstrates a patent ductus arteriosus (PDA). Figure 5.18c confirms PDA on
invasive angiography. Figure 5.18d demonstrates
successful placement of a closure device. The IV
contrast opacification was suboptimal due to the
patient’s hemodynamic status.
5.18.3 Diagnosis
Patent ductus arteriosus in an adult.
5.18.4 Discussion
A patent ductus arteriosus is a process, where the
ductus arteriosus fail to close after birth. The ductus
c d
Fig. 5.18 (a) Oblique coronal. Large pleural effusion
noted (star). Mechanical mitral valve and tricuspid valvular ring (labeled MV and TV Ring, respectively) (b) MIP
and VR. Patent Ductus Arteriosus (PDA) (c, d) Coronary
angiogram. Figure (c) showing PDA and figure (d) showing closed PDA, post intervention
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arteriosus creates a shunt from the pulmonary artery
to the aorta, effectively shunting fetal blood around
the lungs. After delivery, physiological circulation
pressure change constricts this blood vessel and the
ductus arteriosus eventually obliterates. If left
uncorrected, especially in adults, this condition can
lead to pulmonary vascular disease. In adults with a
patent ductus arteriosus, a percutaneous intervention is recommended.
This case is remarkable that even though
she had two previous cardiac surgeries, PDA
was never diagnosed, which aggravated her
postoperative course. Following the percutaneous closure of the PDA, the patient was
promptly diuresed with resolution of symptoms and was discharged after 3 days.
5.18.5 Pearls and Pitfalls
In complex clinical situations, it is advisable to
expand the field of view on the CT scan in order
to obtain a complete assessment of thoracic
structures.
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