CASE REPORTS

Circ J 2006; 70: 631 – 633

Tricuspid Pouch can Cause Systemic
Embolization in Adulthood
Akira Takaki, MD; Hiroshi Ogawa, MD; Takatoshi Wakeyama, MD; Takahiro Iwami, MD;
Masayuki Kimura, MD; Hitoshi Uchinoumi, MD; Shintarou Akashi, MD;
Susumu Matsuda, MD; Yousuke Miyazaki, MD; Masunori Matsuzaki, MD*;
Haruhiko Okada, MD**; Masahiko Nishida, MD**; Masanori Murakami, MD**
A 63-year-old-man with significant left hemiplegia was admitted to hospital. He had experienced a transient
cerebral ischemic attack 10 years ago. Computed tomography revealed hypodensity along the right lateral ventricle, which corresponded to the left paralysis. Echocardiography and left ventricular angiography revealed an
aneurysm of the membranous septum (AMS) without a ventricular septal defect (VSD). Therefore, the embolism
was thought to be of cardiac origin, but surgery revealed that it was not caused by AMS. The aneurysm was
created when the septal leaflet of tricupid valve formed a giant capsule during the process of natural closure of
the VSD. It was a large pouch, 2.0 cm in diameter, adjacent to the septal leaflet. Anomalies of the tricuspid valve,
including pouches, can resemble AMS. (Circ J 2006; 70: 631 – 633)
Key Words: Aneurysm; Cerebral infarction; Embolism; Membranous septum; Tricuspid pouch
he ricuspid pouch is a pouch-like structure that
bulges into the right ventricle near the interventricular membranous septum. It is commonly
reported at postmortem examination of infants, but is rarely
seen in adults. Hamby et al reported aneurysm of the pars
membranacea for the first time in 1970.1 The septal leaflet
of the tricuspid valve formed an irregular large capsule
during the process of natural closure of a ventricular septal
defect (VSD). Aneurysm of the interventricular membranous septum (AMS) is similar to anomalies of the tricuspid
valve, including pouches, and misinterpretations appear in
the literature. Complications such as rupture, endocarditis
or thrombosis are unusual for either a tricuspid pouch or
AMS.2 We report a patient with a large tricuspid pouch that
we thought was AMS until cardiac surgery.

T

Case Report
A 63-year-old man was admitted to hospital because of
left hemiplegia. Motor function of the left side was diminished, possibly as a sequel of a prior neurological accident
(transient cerebral ischemic attack) 10 years ago and a
more recent stroke. Brain computed tomography revealed a
low-density area within the right lateral ventricle, which
corresponded to the left paralysis.
Clinical examination revealed blood pressure of
120/70 mmHg, heart rate of 80 beats/min and respiratory
rate of 15 breaths/min. Chest X-ray was normal and electrocardiogram (ECG) showed sinus rhythm and left ventricu(Received November 18, 2005; revised manuscript received February
6, 2006; accepted February 9, 2006)
Division of Cardiology, Tokuyama Central Hospital, Shunan, *Division of Cardiovascular Medicine, Department of Medical Bioregulation, Yamaguchi University School of Medicine, Ube and **Division of
Cardiovascular Surgery, Tokuyama Central Hospital, Shunan, Japan
Mailing address: Akira Takaki, MD, Division of Cardiology,
Tokuyama Central Hospital, 1-1 Kouda-chou, Shunan 745-8522,
Japan. E-mail: atakaki@msf.biglobe.ne.jp

Circulation Journal Vol.70, May 2006

Fig 1. (A,B) Preoperative transthoracic and transesopageal echocardiograms in the 4-chamber view showing the tricuspid pouch at
inflow of the right ventricle. LA, left atrium; LV, left ventricle; RV,
right ventricule.

TAKAKI A et al.

632

A

B
Fig 2. Left ventricular angiography in left anterior oblique view shows
a pouch-like structure bulging into the right ventricle during sytole.

lar hypertrophic pattern. Transthoracic and transesophageal
echocardiography (TEE) revealed an aneurysm protruding
into the right ventricle (Fig 1A,B) with eddying of blood on
TEE, but we did not recognize the thrombus in the pouch
or its mobility. The findings of left ventricular angiography
(LVG) in the left anterior oblique projection were similar
to those for AMS (Fig 2). It protruded during inflow of the
right ventricle and its surface was regular and cauliflowerlike. There was no left-to-right shunt flow, no dilatation of
the right ventricle and trivial tricuspid regurgitation. We
could not confirm if the cerebral thrombosis had a cardiac
origin or not, but brain magnetic resonance imaging suggested that the cerebral infarction had been caused by
embolism because of the site and the sudden onset of
hemiparesis. Therefore, we considered that the protruding
aneurysm was the most likely culprit for blood stasis and
thrombus formation and that cardiac operation was necessary to prevent stroke attack in the future.
At operation, besides a perimembranous outlet type of
VSD, a pouch of 2.0 cm in diameter was found adjacent to
the septal leaflet of the tricuspid valve (Figs 3A,B). There
was not a residual membranous septum and the surface of
right ventricle that was adhered to the septal leaflet was
irregular and discolored. The tendon of the tricuspid valve
was slightly extended. The VSD was closed with a patch.
Based on these findings, we speculated that the tricuspid
pouch was formed by the effect of a jet stream through the
VSD.
After surgery, anticoagulant therapy was instituted for
3 months and to date the patient is healthy and has not had
other neurological events.

Discussion
A pouch-like structure that bulges into the right ventricle
on LVG is almost always considered to be AMS, which is a
rare congenital lesion that is almost always associated with
congenital anomalies such as VSD and endocardial cushion
defect.3,4 Many investigators have reported the occurrence
of AMS,2,5–7 but its mechanism of development is a matter
of argument. Baron et al2 reported that AMS is formed by

Fig 3. (A) Right atrium is opened to reveal a spherical aneurysmal
pouch 2 cm in diameter and formed by the adherence of the septal
leaflets. (B) Incision of the tricuspid leaflet exposes the true ventricular
septal defect.

projection of left ventricular pressure during spontaneous
closure of a VSD, which occurs in a significant percentage
of patients, usually during infancy. Except for muscular defects, the mechanism of closure is not clearly understood. It
may occur as a result of deposition of fibrin over the
margins of the defect or by attachment to the septum of the
septal leaflet of the tricuspid valve.1,6 In the presence of a
VSD, left-to-right shunt flow jet toward the tricuspid valve
may occur after adhesion of the septal leaflet of the tricuspid valve to the margin of the VSD. But this is not AMS,
rather it is a tricuspid pouch. Idriss et al3 reported that
tricuspid pouch was occurred in 12.2% of cases of VSD.
Tricuspid pouch sometimes causes subpulmonary obstruction in association with transposition of the great arteries,
but rarely does so without transposition.8 Generally, the
development of a tricuspid pouch is secondary to ineffective treatment of endocarditis. However, in the present
patient, the surface of the tricuspid valve was smooth and
there was no inflammatory change. The pouch was created
by a jet lesion of the VSD. Tricuspid pouch can be confused
with AMS and both are diagnosed by 2-dimensional echocardiography and LVG, although it is difficult to distinguish them before operation, as in the present case.
The clinical course of most cases of tricuspid pouch is
Circulation Journal Vol.70, May 2006

Tricuspid Pouch and Systemic Embolization

silent and complications, such as rupture, endocarditis or
thrombosis, are unusual. In the present case, the pouch was
not associated with interventricular communication and
repeated cerebrovascular embolism occurred. The risk of
thrombo-embolic complications for AMS and tricuspid
pouch is almost same. In cases with a small or negligible
VSD, conditions are favorable for blood stasis and thrombus formation. Thrombo-embolic complications with
tricuspid pouch are very rare, but may be underestimated,
as in the past with aneurysm of the interatrial septum,
which was considered to be a potential cause of thromboembolism. Previous investigators have reported complications of AMS, such as cerebral infarction,9–12 and all of
these previous cases underwent surgery because there was
possibility of thrombus in the future. A report of tricuspid
pouch is rare because the final diagnosis of tricuspid pouch
is made during cardiac surgery.
Rhythm disturbances have been reported in associated
with AMS,13 but none of the reported cases of AMS with
thrombo-embolism had cardiac arrhythmias,12 nor was there
evidence of atrial fibrillation or ventricular premature contraction on Holter ECG in the present case.
We could not confirm thrombus in the aneurysm, but
after the patient had had a transient ischemic attack approximately 10 years ago, he was administered aspirin and
nevertheless he had another severe stroke. Surgical investigation for a tricuspid pouch is essential when cerebral
embolism occurs despite anticoagulant therapy.
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