BAB III

Tinjauan pustaka
Anatomi

Sinus aorta

The aortic valve guards the base of the aorta and prevents backflow of blood during
diastole. Opposite each aortic valve cusp is an aortic sinus, which contains baroreceptors important
in reflex regulation of blood pressure.8.

In a normal heart, the left and right sinus each contain their respective coronary artery ostia,
whereas the posterior sinus is a noncoronary sinus. Sinuses function to permit aortic valve opening
during systole without the occlusion of coronary artery ostia. Sinus diameter varies by gender. The
upper limit of normal for men is 4.0 cm and 3.6 cm for women, with slight variations when adjusted
for body surface area. The anatomic positioning of each sinus within the heart is a major
determinant of clinical outcome in the case of sinus of Valsalva aneurysm formation and/or
rupture. The right sinus lies adjacent to the interventricular septum and the right ventricular parietal
bands. The left sinus is proximal to the anterior left ventricular free wall as well as the anterior
mitral leaflet. The noncoronary (posterior) sinus rests above the interventricular septum, a portion
of the anterior mitral leaflet, and forms a complex with the transverse sinus.9

Gambar 1 . Ventrikel Kiri Jantung10

Definisi dan etiologi

Aneurysma sinus valsalva

A sinus of Valsalva aneurysm (SOVA) is an enlargement of the aortic root area between
the aortic valve annulus and the sinotubular ridge.3,9,11 The cause of their appearance is an
incomplete fusion of the distal bulbar septum that divides the pulmonary artery and the aorta and
attaches to the annulus fibrosus of the aortic valve. There is also thinning of the aortic media
observed in affected sinus which can progressively dilate over time, especially in cases of arterial
hypertension.11 On histopathologic examination, SoV aneurysms demonstrate a characteristic
separation between the aortic valve annulus and media that gradually enlarges when exposed to
systemic pressure.12

SOVAs can be either acquired or congenital. Although there is debate regarding whether
congenital or acquired subtypes are more frequent, SOVA is a consequence of weakness of the
elastic lamina at the junction of the aortic media and the annulus fibrosis. In congenital SOVA, the
pathology is frequently associated with Marfans syndrome, Ehlers-Danlos syndrome, or other
connective tissue disorders.9

Acquired SOVAs are similarly associated with connective tissue pathologies. Infectious
etiologies are well established mechanisms for elastic tissue weakening. Syphilis, bacterial
endocarditis, and tuberculosis have each been linked to SOVA formation. Chronic changes of
atherosclerosis and cystic medial necrosis can weaken the intimal layer of vasculature and lead to
SOVA. Chest trauma, vasculitic diseases, and iatrogenic injury during aortic valve replacement
have all been reported as causes of acquired SOVA.9

The specific etiology of a given sinus of Valsalva aneurysm may be difficult to determine,
and the interrelationship between the various pathologic processes may affect the long-term
outcome. Bacterial endocarditis of the aortic valve may cause aortic medial necrosis secondary to
infection and lead to aneurysm formation. Progression of the disease process may result in a dilated
annulus and deformed aortic valve cusps that are increasingly predisposed to recurrent
endocarditis. On the other hand, a congenital lack of continuity between the aortic media and
annulus fibrosis may initiate aneurysm formation, leading to local turbulence, laminar flow
separation, or dilatation of the annulus and deformity of the valve cusps. Again, each process may
increase the predisposition to bacterial endocarditis.12
 Ruptur aneurisma sinus valsalva (RSVA)

Aneurysm rupture happens usually in adulthood. It

may follow strenuous effort, infection or trauma. In the oldest
patient from our group (51-year-old male) the first symptoms
appeared during infection. Another predisposing factor for
rupture is arterial hypertension. In our group, arterial
hypertension was observed in 3 patients. RSVA can appear
as acquired malformation, as was observed in one young
woman after surgical correction of TOF, and was considered
as iatrogenic. Other causes of acquired RSVA can be aortic
valve replacement, infective endarteritis, tuberculosis,
syphilis or mechanical injury such as a car accident.11

Congenital ruptured sinus of Valsalva aneurysm is a

rare lesion. It is produced by mural deficiencies or
outpouchings of an aortic sinus that perforate into a cardiac
chamber resulting in an aorto-cardiac fistula. The fistula
develops either as a windsock deformity or simple fistulous connection.13
Gambar 2. Fistula
deformitaswindsock14 The natural history of the lesion depends on the size
of the shunt, presence of associated defects, or endocarditis,
all of which accelerate development of symptoms and timing of presentation. Increased pulmonary
blood flow produces left ventricular volume overload, right ventricular hypertension, and
ultimately, congestive heart failure. Presence of the lesion is usually an indication for repair.
However, there are documented cases of RSVAs with small, asymptomatic shunts, no associated
lesions, and normal right sided size/pressures that have been left unrepaired for up to 15 years
(unpublished data, Toronto General Hospital, cardiovascular surgery database).13

Epidemiologi

Sinus Valsalva aneurysms are rare, accounting for only 0.14% of all open-heart surgical
procedures. Because they are often clinically silent for many years, autopsy studies may give a
more accurate estimation of prevalence, quoting approximately 0.09% of the general population.
SV aneurysms are more common in Asian populations and, in addition, have a marked male
preponderance (four times more common in men). The reasons for these racial and sex differences,
and the extent of the genetic determination of this lesion, are unclear. A symptomatic SV aneurysm
is particularly uncommon in childhood. In these circumstances extra care should be taken to
prevent a hereditary connective tissue disorder, such as Ehlers-Danlos or Marfan syndrome, from
being overlooked.15 A family history is generally lacking, although Johnson et al. described a case
of two brothers with SVA that perforated into the right atrium.3

They are associated with other heart defects, VSD in 30-60% of cases, aortic valve
abnormalities such as aortic insufficiency in 20-30%
of cases, bicuspid valve (10%), aortic stenosis (6.5%).
They may also be associated with pulmonary stenosis
(9.7%), coarctation of the aorta (6.5%), persistence of
the conductus arteriosus (3.2%), tricuspid
insufficiency (3.2%) and interatrial defect.16

The incidence of associated VSD is also

higher in eastern countries. The supracristal VSD
(type I) is the predominant type seen in Asian
countries, whereas perimembranous VSD (type II) is
often seen in western countries . Congenital
aneurysms consist of a localized burrowing of part of
the aortic sinus into the neighboring myocardium, one
of the cardiac chambers, or the free pericardium. Such
aneurysms of the sinuses of Valsalva tend to be
Gambar 3. Location of Valsalva sinus aneurysm
single, although, rare reports of congenital ruptures: 5 between right coronary sinus and right
ventricle (RV), 3 between non-coronary sinus and
involvement of more than one sinus have been right atrium (RA) and 1 between right coronary sinus
and right atrium. All ruptures draining into the right
described.3 ventricle were associated with ventricular septa1
defect.14
Chu et al. reported that the incidence of
ruptured SVA is five times higher in Asian countries (0.46-3.5% in Eastern and 0.14-0.23% in
Western areas). Of the group, 65-80% are males (male/female ratio 4:1). Diagnosis can occur at
any age (average: 39 years old, range: 2-74 years).1,2,3,8,11,14 SVA affect the right sinus in 65-
86% of cases, noncoronary sinus in 10-30% and the left sinus in 2-5%.16

The frequency of ruptured SVA varies according to the location: 60% in the right sinus,
42% in the noncoronary sinus and only 10% in the left sinus.Rupture of a SVA occurs principally
at the RV (60%) or at the RA (29%), the LA (6%), LV (4%) or at the pericardium (1%).
Extracardiac ruptures are rare, usually fatal, and occur towards the pericardium or the pleural space
and are more common when the SVA is of acquired origin.16

Patofisiologi

The clinical course of a ruptured sinus of Valsalva direction of the perforation.

Dimensions is perhaps a more appropriate characterization than size, as these ruptured aneurysms
tend to be tubular in form. The pressure-flow relationships will therefore follow Poiseuilles law
unless interfered with by intracardiac compression or kinking of the diverticulum. In a typical
rupture draining into the right heart, there is sudden increase in pulmonary flow and drop in
diastolic aortic pressure. Cardiac failure ensues if considerable volume overloading results from
left-to-right shunting, and the lowered diastolic pressure compromises effective coronary
circulation. The outcome has been described as poor in cases with dramatic onset of progressive
heart failure, unless relieved by surgical intervention.17

Clinical manifestation

Unruptured SVA are usually not associated with clinical symptoms but may be
complicated by endocarditis, intraventricular conduction disturbances, right ventricular outflow
tract obstruction, systemic embolization, and even coronary artery compression with myocardial
infarction has been reported. The risk of scrious and potentially lethal complications of unruptured
SVA such as myocardial infarction, hemodynamic decompensation, and sudden death suggests
that aggressive surgical correction for even asymptomatic SVA is optimal.18

In rare instances, an unruptured sinus of Valsalva aneurysm may lead to cardiac

arrhythmias, myocardial ischemia, or aortic valve incompetance. Generally, however, the lesion
remains clinically silent until rupture. An unusual event, rupture into the pericardial sac, results in
almost immediate death. More typically, a fistulous tract forms between the aortic sinus and the
right side of the heart. The magnitude of the hemodynamic derangement resulting from this left-
to-right shunt determines the clinical course of the patient. Congestive heart failure is the most
common clinical presentation. Experimental evidence and clinical experience show that the
characteristic dilatation and "wind-sock" deformity of the aortic sinus aneurysms with fistula
severely predisposes the patient to bacterial endocarditis-the second most common clinical
presentation.19

Classically, acute shortness of breath and substernal chest pain are coincident with rupture
of the aortic sinus aneurysm. These patients may then enter a relatively symptom free, often
prolonged latent period before fatal heart failure results. Other patients follow a more insidious
course of cardiac decompensation without an acute episode associated with aneurysm rupture.
Most surgically untreated patients die of cardiac failure or bacterial endocarditis within a year after
onset of symptoms. A third group of patients have no cardiac symptomatology despite aneurysmal
rupture and fistula formation. These patients may initially present with malignant bacterial
endocarditis. Alternatively, they may be seen for evaluation of other cardiac abnormalities or an
undiagnosed heart murmur.19

On physical examination, patients with a ruptured sinus of Valsalva aneurysm with fistula
generally have a loud, continuous "machinery-type" murmur which is loudest in the fourth left
intercostal space and reaches its peak with the second heart sound. Peripheral pulses often have a
collapsing quality. Signs of congestive heart failure will be present in patients with decompensated
cardiac function. The remainder of the examination may be within normal limits.19

Since the sinuses of Valsalva occupy an intra-cardiac position, roentogenographic findings

tend to be non-specific. With modest dilatation of an aortic sinus, the chest roentgenogram may be
entirely normal. Larger aneurysms can be visualized indirectly since they displace cardiac
structures laying in juxtaposition to them. Depending on the sinus involved, left atrial enlargement,
right atrial enlargement, right ventricular hypertrophy or right ventricular outflow tract prominance
can be simulated. Sequelae of the left-to-right shunt, left ventricular hypertrophy and pulmonary
vasculature add to the roentgenographic picture. Fluoroscopy commonly shows active aortic
pulsations, the so-called "hilar dance". Luetic aneurysms may contain calcium.19
 The electrocardiogram generally shows left ventricular hypertrophy and, often, right
ventricular hypertrophy. Interventricular conduction defects of the right bundle branch variety and
complete heart block are also commonly encountered. Although not specific in themselves, these
conduction disturbances occur more frequently in conjunction with aortic sinus abnormalities than
with other lesions which have similar physical findings and may, therefore, suggest the diagnosis.
Aortic sinus fistulae can be present, albeit the electrocardiogram normal.19

Pemeriksaan penunjang

The electrocardiogram usually shows voltage criteria for left ventricular hypertrophy and
ST-T wave abnormalities. Chest X-ray may reveal a bulge to the right of the caval shadow in the
postero-anterior view and appear as an excessive anterior-superior bulge in the left anterior oblique
view.3

Prior to the advent of noninvasive imaging modalities, SVA were diagnosed by cardiac
catheterization. In 1967, De Bakey et al. published a series of 35 cases of fistulized SVA diagnosed
by aortography. Cardiac catheterization demonstrates a finger-like projection of the ruptured
aneurysm into the receiving chamber (wind-sock image), and dye may be visualized in the
receiving chamber. The presence of aortic insufficiency may be evaluated by contrast aortography.
Right heart catheterization allows determination of pulmonary pressure and resistance and permits
quantitative shunt assessment.3

In 1974, Rothbaum et al. reported echocardiographic findings of ruptured SVA and, since
then, the usefulness of two-dimensional and Doppler echocardiography in the assessment of such
aneurysms has been well documented.3 Although recently, the diagnosis of SVA has been made
by magnetic resonance imaging, intravascular ultrasound, and three-dimensional reconstruction
from echocardiography, these patients are rare and consist of case reports only. TTE and TEE has
reduced the need for coronary contrast angiography and has become the principal diagnostic tool
over the duration of the last decade.18

However, TTE images are often suboptimal, resulting in imprecise delineation of the
anatomy and anatomic relations of the aneurysm and associated lesions, which do not provide the
surgeon with a complete definition of the SVA and its associated anomalies. In contrast, TEE
provides high-quality, high-resolution tomographic images of the SVA and aortic root. Multiplane
TEE provides further detail including the spatial arrangement of normal and abnormal cardiac
structures in the aortic root and sinuses which may not be fully appreciated by single or biplane
TEE studies. Ruptured SVA can be distinguished from VSD associated with septal aneurysm
echocardiographically by the timing of the turbulent flow. However, occasionally the systolic
stream from a ruptured SVA mad a coexistent VSD might comingle and make differentiation
difficult. Unruptured SVA and an closely adjacent VSD might be misdiagnosed as a ruptured SVA.
On the basis of our experience, multiplane TEE is useful in precisely defining the anatomic
relations between them. The different shapes of SVA are most likely a functional characteristic of
the imaging plane rather than the actual shape of the lesion.18

Color Doppler flow mapping was helpful in defining the site of rupture when the SVA
bridges two anatomic locations or the rupture hole can not be clearly defined by two-dimensional
echocardiographic imaging.18

Chiang et al. underscore the importance of multiple echocardiographic and Doppler

modalities in the detection and characterization of sinus of Valsalva aneurysms. Because of the
occurrence of a variety of anatomic derangements attributable to aneurysm compression of
adjacent structures and because of a high frequency of associated congenital anomalies, we believe
transesophageal echocardiography is indicated in cases in which routine transthoracic
echocardiography cannot completely characterize the anatomy and pathophysiology of sinus of
Valsalva aneurysms. More precise anatomic localization is possible, including detailed assessment
of coronary artery ostia, the aortic root and valve, and associated conditions such as ventricular
septal defect. Complications such as infective endocarditis, aneurysm thrombosis, intracardiac
obstruction, and aneurysm rupture can also be delineated.20

Diagnosis banding

Generally, the murmur of an aortic sinus fistula differs from that of a patent ductus by
having its peak intensity one of two interspaces lower and being closer to the midline, more
superficial and less well transmitted posteriorly. Using these criteria, however, a number of
patients have undergone thoracotomy for a patent ductus arteriosum, only to have a normal
ligamentum arteriosum and a ruptured aortic sinus with fistula. A pulmonary arteriovenous fistula
may also be associated with a continuous murmur, but this murmur should vary with respiration
and may be associated with cyanosis and hereditary telangiectasias. Final differentiation will again
be dependent upon cardiac catheterization with angiocardiogaphy.19

Clinical differentiation between a sinus of Valsalva aneurysm with fistula and a coronary
arteriovenous fistula may well be impossible. Both have continuous murmurs which are similar in
character and location and both may be associated with a wide pulse pressure. Since coronary
arteriovenous fistual are congenital lesions present from early childhood, the sudden appearance
of a continuous murmur at the lower left sternal border would be more indicative of a ruptured
aortic sinus aneurysm. An acute episode of chest pain with dyspnea in conjunction with the
appearance of a continuous murmur would further point toward an abnormality of the sinus of
Valsalva. Onset after a bout of bacterial endocarditis or with a history of syphilis would also more
likely be a ruptued sinus of Valsalva aneurysm with fistula. Definitive diagnosis, however, cannot
be made without cardiac catheterization.19

A prolapsed aortic valve secondary to a high congenital ventricular septal defect may be
quite difficult to differentiate from a sinus of Valsalva aneurysm with fistula formation. (This
condition is similar to a congenital combination of ventricular septal defect with sinus of Valsalva
aneurysm found relatively frequently in Japan and well described elsewhere.) On auscultation, the
murmur may sound like that of a ventricular septal defect, thus being harsher than the murmur
associated with the previously described entities. Angiography will show aortic insufficiency, but
a definitive differentiation from a sinus of Valsalva aneurysm with fistula may not be possible as
there can be aneurysmal bulging of the aortic valve so that it may appear to be an aortic sinus
aneurysm. In fact, Burchell and Edwards describe autopsy findings in a case of rupture of the right
aortic sinus into the right ventricle on a patient diagnosed and even reported in the literature as
having a ventricular septal defect with aortic insufficiency.19

Diagnosis kerja
The physical findings on examination which lead to the diagnosis were a continuous
murmur and palpable thrill over the mid-left sternal border which were present in all patients with
ruptured SVA. All patients except one were in sinus rhythm. Left ventricular hypertrophy with or
without strain was the most common electrocardiographic abnormality.18
 A detailed echocardiographic study (two-dimensional, Doppler, and color flow imaging)
is accurate in the diagnosis of ASOV, in the identification of its site of origin and rupture, and in
the evaluation of the associated defects; in the vast majority of cases, it can totally supplant the
need for angiography.21

Tatalaksana
The mainstay of treatment for ruptured SVA is surgical intervention, since prognosis of
patients without urgent surgical repair is very poor. Early aggressive treatment is recommended
for ruptured SVA in order to prevent endocarditis or enlargement of the lesion, which might
necessitate more extensive repair. Because of recent advances in diagnostic technique, the number
of patients undergoing surgery has been increasing, including patients with unruptured
aneurysms.3

The first surgical repair of SVA was described independently by Morrow et al. and Bigelow
and Barnes in the mid-1950s using hypothermia and infl ow occlusion. The conventional surgical
repair under cardiopulmonary bypass was first attempted by Lillehei et al. and since then has been
commonly used. Depending on the size and location of the aneurysm, the site of rupture, and
associated cardiac anomalies, primary suture closure, patch closure, or aortic root replacement
have been used in the operative repair of the aneurysm.3

In early studies, the repair was approached through the cardiac chamber into which rupture
occurred. In the current surgical era, dual chamber exposure has been favored by most surgical
centers. A combined approach, in which both the involved chamber and aortic root are opened,
allows meticulous closure of the rupture, better evaluation of coexistent anomalies, avoidance of
distortion of the aortic valve cusps, and reduction in the incidence of late aortic insuffi ciency. In
addition, aortotomy allows selective perfusion of the coronary ostea in larger patients. Several
investigators have suggested that direct closure with sutures may be associated with a higher
incidence of aneurysm recurrence. Many centers have been using patch closure for all SVA repairs,
regardless of size, to avoid tension on the annulus, especially in complex cases.3

Surgical repair is highly successful with low operative risk. The life expectancy of patients
who have successful repair of a ruptured aneurysm approximates that of the healthy population
(10 year survival rates of 9095%), although survival rates may be worse in predominantly western
patient populations. In one of the largest series involving 129 patients, the perioperative mortality
was 3.9% and was associated with presence of preexisting sepsis and endocarditis. In cases with
severe infection, complex procedures such as aortic root replacement or Ross procedure may be
necessary. Late complications were due to prosthetic valve malfunction, prosthetic valve
endocarditis, aneurysm recurrence, and anticoagulation-related bleeding. The risk for recurrent
fistula or VSD is minimal in the current surgical era.3

In several of the case studies, surgery was performed to correct a hemodynamic

abnormality caused by aneurysm compression of adjacent structures. The second reason to operate
before rupture is to avoid untimely rupture and hemodynamic instability. We would therefore favor
repair oflarge aneurysms, those that cannot definitively be distinguished from dissection, and those
that have shown interval enlargement on serial examinations. Comprehensive assessment
preoperatively may facilitate elective repair in unruptured aneurysms, in which the goals should
include annuloplasty or valvuloplasty and preservation of the native aortic valve when possible.
Intraoperative transesophageal echocardiography may be useful in assessment of the adequacy of
repair.20

Komplikasi
Depending on the anatomic location of the aneurysmal bulge, a number of complications
may ensue. These aneurysms frequently rupture although death may or may not occur
immediately. The perforation may occur in the right atrium, right ventricle, left atrium, left
ventricle, pericardial sac, mediastinum, pulmonary artery, superior vena cava, and left pleural
cavity. A rare case in which the pericardial sac was obliterated and the aneurysm eroded through
the chest wall to rupture externally has been recorded. The most frequent clinical picture of
aneurysm of one or more of Valsalvas sinuses is that of aortic insufficiency or regurgitation, due
to dilatation of the aortic ring. Bulging of the aneurysm into the right ventricle may produce a
clinical picture of stenosis or insufficiency of the tricuspid valve and/or pulmonary stenosis.
Encroachment of an aneurysm of the right anterior sinus on the A-V node or bundle of His in the
interventricular septum often leads to heart block or other A-V conduction defects. Rare cases of
myocardial infarction caused by the compression of a coronary artery by an extrinsic aneurysm of
the sinus of Valsalva have been reported. Death is usually the result of one or more of the
mentioned complications and congestive heart failure.22

There have been reports of unruptured aneurysms with intraluminal thrombus.aneurysm

was the source of cerebral embolism and that subsequent organisation of the clot prevented further
embolisation.23 Aortic regurgitation commonly results from prolapse of the affected sinus cusp.
Prolapse can occur secondary to involvement of the annulus, loss of infundibular support with a
conal VSD, or a Venturi affect on the involved cusp.24

Prognosis
Once rupture has occurred, mean survival is 1 to 2 years. Death is usually due to congestive
heart failure, but infective endocarditis has been the cause of death in approximately 8% of cases.
The prognosis after the surgical repair of SVAs is satisfactory.5
 BAB III

Pembahasan
a
 BAB IV
Kesimpulan
a
 Daftar pustaka
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