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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5761_Библиотеки_им_академика_М_И_Перельмана
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177
Diagnosis
The patient was diagnosed with a perimembranous VSD,
which was partially closed by the septal leafl et of the tricuspid valve and the aneurysm formation of the interventricular
septum. Only a small defect remained poorly visualized, but
a small mobile mass was present on the right ventricular side
of this defect, highly suggestive of vegetation.
Comment
Work-up for infective endocarditis was recommended for the
patient.
Lesson
1. Even when the VSD is partially closed, the risk of infective endocarditis persists.
2. Vegetation is found on the right ventricular side of the
VSD [ 84 , 85 ].
c
ab
Fig. 56.6 A small turbulent fl ow can be seen on TEE (long-axis view)
( arrow ) ( a ). The defect can be visualized by two-dimensional echocar-
diography ( b ). There is a small mobile mass on the right ventricular
side of this defect ( curved arrow ), which is highly suggestive of vegeta-
tion. The mass is 3 mm in size ( c ). LA left atrium, LV left ventricle,
AO aorta, RV right ventricle
Case 56 Ventricular Septal Defect with Infective Endocarditis
179
H. Sadeghian, Z. Savand-Roomi, Echocardiographic Atlas of Adult Congenital Heart Disease,
DOI 10.1007/978-3-319-12934-1_57, © Springer International Publishing Switzerland 2015
A 29-year-old man referred for the evaluation of a holosystolic
murmur. He had no symptoms.
Ventricular Septal Defect
with Subvalvular Membranous
Aortic Stenosis
Case 57
c
a
b
Fig. 57.1 The parasternal long-axis view shows a membrane ( arrow )
below the aortic valve ( a ) and mild aortic regurgitation ( arrow head )
( a ). There is also a turbulent systolic fl ow across the interventricular
septum toward the right ventricle, in favor of a perimembranous ventricular septal defect (VSD) ( curved arrow ) ( b ). The VSD is located
between this membrane and the aortic valve. No systolic turbulency
caused by this membrane is seen ( b ). The peak systolic gradient across
this VSD is 122 mmHg ( c ). LA left atrium, LV left ventricle, RV right
ventricle, AO aorta
Electronic supplementary material The online version of this
chapter (doi:
10.1007/978-3-319-12934-1_57 ) contains supplementary
material, which is available to authorized users.
180
Fig. 57.2 This perimembranous VSD is also visualized by the para-
sternal short-axis view (turbulent systolic fl ow toward the right ventricle) ( arrow ). RVOT right ventricular outfl ow tract
Fig. 57.3 The left ventricular outfl ow tract gradient is about 13 mmHg
a
b
Fig. 57.4 Transesophageal echocardiography (TEE) (long-axis view)
shows the membrane ( arrow ) and mild aortic regurgitation ( a ) (dias-
tole). A small turbulent fl ow across the interventricular septum is also
visualized in this view ( arrow ) ( b ) (systole). LA left atrium, LV left
ventricle, RV right ventricle, AO aortic valve
Case 57 Ventricular Septal Defect with Subvalvular Membranous Aortic Stenosis
181
Diagnosis
The patient was diagnosed with a perimembranous VSD
with a subvalvular membrane without a signifi cant gradient.
Also, there was a mass on this membrane, suggestive of
infective endocarditis.
Comment
The mobile mass was suggestive of vegetation. Accordingly,
work-up for infective endocarditis was recommended.
Lesson
1. The membrane produced a low gradient in the left ventricular outfl ow tract and mild aortic regurgitation. The
VSD was small (about 3 mm). The patient was asymptomatic and had a Qp/Qs of about 1.28 and a pulmonary
arterial systolic pressure of about 30 mmHg. Therefore,
the only reason for surgery is to prevent endocarditis.
2. One of the associated anomalies with the VSD is the subvalvular membrane. When confronting a VSD with a
membrane, it is crucial to determine the exact site and
location of the VSD and the membrane. It should be clarifi ed whether the VSD is between the membrane and the
aortic valve or vice versa. If the membrane produces a
gradient, the left ventricular systolic pressure below that
membrane is high. A VSD located between the membrane and the aortic valve is less likely to produce pulmonary arterial hypertension compared to a VSD that is
below the membrane [ 86 , 87 ]. It has been suggested that
this membrane may be a result of VSD and some degrees
of interventricular septal malalignment [ 7 , 88 ].
ab
Fig. 57.5 TEE (long-axis view) reveals that the membrane measures
3 mm in size, and its distance from the aortic valve is 11 mm ( a ). There
is a mobile mass, about 2 mm in size, on that membrane, which is
suggestive of vegetation ( b ). LA left atrium, LV left ventricle, RV right
ventricle, AO aorta
Case 57 Ventricular Septal Defect with Subvalvular Membranous Aortic Stenosis
183
H. Sadeghian, Z. Savand-Roomi, Echocardiographic Atlas of Adult Congenital Heart Disease,
DOI 10.1007/978-3-319-12934-1_58, © Springer International Publishing Switzerland 2015
A young woman presented with a history of long-standing
easy fatigability and recent exacerbation of dyspnea on exertion. Physical examination revealed a harsh systolic murmur
(grade IV/VI) at the left sternal border and clubbing.
Echocardiography showed a normal left ventricular size
with moderate systolic dysfunction and a left ventricular
ejection fraction of about 35 % with paradoxical septal
motion. There was also severe right ventricular dilation with
severe systolic dysfunction. The fractional area change of the
right ventricle was approximately 13 %.
Ventricular Septal Defect
with Eisenmenger’s Syndrome
Case 58
a
b
Fig. 58.1 The short-axis view reveals a large perimembranous ven-
tricular septal defect (VSD) and a bidirectional non-turbulent fl ow
across it ( arrow ) ( a , b ), in systole ( red ) and diastole ( blue ). LA left
atrium, RA right atrium, AOV aortic valve
a
b
Fig. 58.2 A large VSD ( arrow ), which extends below the tricuspid
valve, is evident in the modifi ed right ventricular infl ow view with a
bidirectional shunt fl ow across it, red in systole ( a ) and blue in diastole
( b ). LV left ventricle, RV right ventricle
Electronic supplementary material The online version of this
chapter (doi:
10.1007/978-3-319-12934-1_58 ) contains supplementary
material, which is available to authorized users.
184
Diagnosis
The patient was diagnosed with a VSD and Eisenmenger’s
syndrome.
Comment
The estimated pulmonary arterial resistance in this
patient was 16 units. After 10 min of O 2 administration,
no change was detected in the mean pulmonary arterial
pressure and right ventricular outflow tract velocity time
integral. Owing to the significantly high pulmonary vascular resistance and no change with O 2 , medical treatment with sildenafil and bosentan was commenced for
the patient [ 89 ].
Lesson
For patients with a VSD, a pulmonary vascular resistance
greater than seven units is elevated and needs more evaluation before intervention. A pulmonary vascular resistance
greater than 12 units is inoperable [ 2 , 75 , 90 ]. Some authors
believe that with Qp/Qs more than 1.5/1 and pulmonary vascular resistance/systemic vascular resistance less than twothirds or pulmonary/systemic arterial pressure less than
two-thirds (baseline or with vasodilators), VSD closure
should be considered [ 7 ]. In cases of VSD and high pulmonary vascular resistance, surgery with fenestrated patch has
been performed [ 91 ]. Use of fenestrated atrial septal occluder
has been reported for large VSD and pulmonary hypertension [ 92 ].
In Eisenmenger’s syndrome, there is pulmonary hyper-
tension, and the shunt is bidirectional or right to left.
Fig. 58.3 The patient has moderate pulmonary insuffi ciency with a
mean pulmonary arterial pressure of about 53 mmHg. The right ventricular outfl ow tract is 22 mm in diameter. The velocity time integral of
the right ventricular outfl ow tract is 11.7 cm, and the heart rate is 73
beats per minute. Estimated pulmonary valve resistance = mean pulmonary arterial pressure pulmonic/Q pulmonic. Q pulmonic = stroke volume × heart rate = right ventricular outfl ow tract velocity time integral
× right ventricular outfl ow tract area × heart rate. Right ventricular outfl ow tract area = 3.14 × (right ventricular outfl ow tract D/2)2
Case 58 Ventricular Septal Defect with Eisenmenger’s Syndrome
185
H. Sadeghian, Z. Savand-Roomi, Echocardiographic Atlas of Adult Congenital Heart Disease,
DOI 10.1007/978-3-319-12934-1_59, © Springer International Publishing Switzerland 2015
A 32-year-old woman referred to our center because of dys-
pnea on exertion (functional class III). Physical examination
revealed a faint systolic murmur, and the electrocardiogram
showed a tall R in the right precordial leads. Chest X-ray
demonstrated cardiomegaly, prominent pulmonary knob,
and mild pulmonary congestion. She had given birth to two
children and had experienced mild symptoms during the
pregnancies.
Ventricular Septal Defect,
Patent Ductus Arteriosus,
and Eisenmenger’s Syndrome
Case 59
a
b
Fig. 59.1 The parasternal long-axis view shows a perimembranous
ventricular septal defect (VSD) ( arrow ), right ventricular hypertrophy
( curved arrow ), and dilated coronary sinus ( double arrow ) ( a ) as well
as a bidirectional fl ow across the VSD ( blue and red in systole) ( b ), in
favor of pulmonary arterial hypertension. LA left atrium, LV left ven-
tricle, RV right ventricle, AO aorta
Electronic supplementary material The online version of this
chapter (doi:
10.1007/978-3-319-12934-1_59 ) contains supplementary
material, which is available to authorized users.
186
a
b
c
Fig. 59.3 The peak pulmonary arterial systolic pressure can be
estimated by adding the right atrial pressure to the tricuspid regurgitation gradient. In addition, the pulmonary arterial diastolic pressure can
be estimated by adding the right atrial pressure to the pulmonary
insuffi ciency gradient at late diastole. The mean arterial pulmonary
arterial pressure is estimated to be equal to the pulmonary insuffi ciency
gradient at early diastole. The continuous wave study of the tricuspid
valve in the apical four-chamber view shows that the peak arterial systolic pressure is 118 + 10 = 128 mmHg ( a ). This is the continuous wave
study of the pulmonary valve in the parasternal short-axis view ( b , c ),
mean arterial pressure is 75 mmHg ( b ) and the diastolic arterial pres-
sure is 44 + 10 = 54 mmHg ( c )
Fig. 59.2 A fl at septum in systole ( arrow ), which is in
favor of pulmonary arterial hypertension, is evident in
this short-axis view. LV left ventricle, RV right ventricle
Case 59 Ventricular Septal Defect, Patent Ductus Arteriosus, and Eisenmenger’s Syndrome
187
Diagnosis
VSD and PDA with Eisenmenger’s syndrome
Comment
The patient had high peak pulmonary arterial systolic pressure, mean pulmonary arterial pressure, and pulmonary arterial diastolic pressure as well as high pulmonary vascular
resistance. Consequently, medical treatment with sildenafi l
and bosentan and follow-up echocardiography were
recommended.
Fig. 59.4 The patent ductus arteriosus (PDA) fl ow ( arrow ) in short-
axis view is still left to right ( red ) but nonturbulent. PA pulmonary
artery, AO aorta, DAO descending aorta. The estimated Qp/Qs was 1.3,
pulmonary vascular resistance was 12 units, and systemic valve resistance was 20 units. Also, no signifi cant change could be seen in the
pulmonary arterial resistance and mean pulmonary arterial pressure
with O
2
(10 units and 75 mmHg, respectively) [ 24 ]. Although the coronary sinus was dilated, contrast injection was not performed to rule out
a left persistent superior vena cava because of the bidirectional shunt.
Nevertheless, it should be considered that the dilated coronary sinus
may have been due to moderate right ventricular systolic dysfunction
and high right atrial pressure in this case
Case 59 Ventricular Septal Defect, Patent Ductus Arteriosus, and Eisenmenger’s Syndrome
189
H. Sadeghian, Z. Savand-Roomi, Echocardiographic Atlas of Adult Congenital Heart Disease,
DOI 10.1007/978-3-319-12934-1_60, © Springer International Publishing Switzerland 2015
A 33-year-old man was referred to our center due to sustained ventricular tachycardia (VT).
Ventricular Septal Defect
Completely Closed
Case 60
a
c
b
Fig. 60.1 The parasternal long-axis view shows left ventricular hypertro-
phy ( a ). The proximal part of the interventricular septum is thin in the
apical four-chamber view ( arrow ) ( b ), and there is no fl ow across it
( arrow ) ( c ). It seems that there is a perimembranous ventricular septal
defect (VSD), which is completely closed by the aneurysm formation of
the interventricular septum and the septal leafl et of the tricuspid valve ( b ).
LA left atrium, LV left ventricle, RV right ventricle
Electronic supplementary material The online version of this
chapter (doi:
10.1007/978-3-319-12934-1_60 ) contains supplementary
material, which is available to authorized users.
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