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Atraumatie Right Ventricular Aneurysm
Report of Case
By WILLIAM B. WEGLICKI, M.D., JEROME RuSKIN, M.D.,
AND
HENRY D. MCINTOSH, M.D.
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substantiated. There was no evidence of a cardiac aneurysm in the chest x-ray at that time.
Because of the possibility of a collagen disease,
the patient was treated empirically with steroids
and discharged. He continued to be symptomatic. Infiltrates in the right lower lung field were
apparent in the chest x-ray obtained 4 months
later at another hospital. There was no significant cardiac enlargement. However, in another 6 months, the chest film demonstrated enlargement which was compatible with, but not
diagnostic of, pericardial effusion. Over the next
5 years the patient received intermittent steroid
therapy for vague, ill-defined symptoms. During
the year prior to the present admission, he developed paroxysmal supraventricular tachycardias and mild congestive failure and was treated
with digitalis and quinidine. He experienced progressive fatigue and dyspnea on slight exertion;
episodes of palpitations increased the dyspnea.
The development of atrial fibrillation prompted the readmission to the Duke University
Medical Center in June 1965. Pertinent physical
findings on admission included blood pressure of
110/70 mm Hg and an irregular pulse of 80/
min. The venous pulsations in the left anterior
triangle of the neck were prominent and of much
greater amplitude than the pulsations of the
right superficial veins; the veins of the right
arm were more distended than those of the left.
The lungs were clear to percussion and auscultation. The point of maximal cardiac impulse was
at the midelavicular line. A grade I/VI early
systolic ejection murmur was audible in the
second intercostal space along the left sternal
border. A faint ventricular diastolic gallop was
also present.
The chest x-ray demonstrated a bulging mass
in the region of the left hilum (fig. 1). Review
of all previous chest x-rays indicated that the
aneurysmal bulge developed between 1957 and
1961. Except for the preadmission electrocardiogram, which demonstrated atrial fibrillation, repeated tracings were normal except for occasional premature ventricular contractions and digitalis
effect. At fluoroscopic examination the mass
was seen to pulsate in a paradoxical manner in
the area of the right ventricle. During cinefluorography contrast media injected into the right atrium
THE DEVELOPMENT of an aneurysm
of the left ventricle is a relatively common sequela of myocardial infarction. 1-4 The
pathophysiological consequences of such aneurysms have been defined by hemodynamic
and cinefluorographic studies both before
and after successful resection.5-8 In contrast,
aneurysms of the right ventricle are rare and
coronary artery disease is not thought to be an
important etiological factor. The majority of
such aneurysms are secondary to trauma or
surgical procedures involving the right ventricle.9-18 Comparatively few successful surgical resections of aneurysms of the right ventricle have been reported.9' 13-15, 18
The present communication describes a patient with an aneurysm of the right ventricle
which, unlike that in most other reported
cases, developed without antecedent surgery
or trauma. Hemodynamic and cinefluorographic data were obtained at cardiac catheterization. Surgical resection of the aneurysm
was accomplished.
Report of Case
H. B., a 44 year old white man, had been admitted to the Duke University Medical Center 8
years prior to the present admission. At that
time he complained of fever, migratory polyarthralgias, fatigue, and loss of weight. Examination strongly suggested the presence of polyarteritis nodosa, but this diagnosis was never clearly
From the Cardiovascular Laboratory, Department
of Medicine, Duke University Medical Center, Durham, North Carolina.
This study was supported in part by Program
Project Grant HE-07563, and Grants H-4807 and
HTS-5369 from the U. S. Public Health Service, National Heart Institute of the National Institutes of
Health, and grants-in-aid from the John A. Hartford
Foundation, The Council for Tobacco Research,
U.S.A., and the North Carolina Heart Association.
Circulation, Volume XXXIV, July 1966
123
WEGLICKI ET AL.
124
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(fig. 2) opacified a large dilated right atrium; the
body of the right ventricle was not enlarged but
appeared to be tipped upward and displaced medially from the apex. The right ventricular outflow tract was distorted by a saccular aneurysmal
outpouching. The pulmonary arteries were normal. The aneurysmal sac pulsated paradoxically,
distending during systole and emptying incompletely during diastole. Selective coronary ar-
teriography revealed no gross pathologic
changes. Retrograde injection of contrast media
into the innominate vein through the femoral
vein catheter did not opacify the right subclavian and deep jugular veins. Intracardiac electrocardiographic findings were not compatible
with Ebstein's anomaly.
Open-heart surgery with total cardiopulmonary
bypass was performed and successful resection
of the thin-walled right ventricular aneurysm
was accomplished without difficulty.* The aneurysm was observed to pulsate paradoxically
during surgery, and supporting the aneurysm
by hand appeared to increase the tension of the
pulmonary artery. Pressure tracings of the right
ventricle and pulmonary artery were obtained
by direct needle puncture during surgery (table
1).
No histological evidence of abnormal myocardial tissue was observed by microscopic examination of the resected aneurysmal wall. No
mural thrombi were present.
The patient had an unremarkable postoperative course. Cardiac catheterization was performed 3 weeks postoperatively, and hemodynamic data were similar to the preoperative
values except for a slight decrease in cardiac output (table 1); cinefluorography showed the absence of the major portion of the aneurysm (fig.
3).
The etiology of this right ventricular aneurysm
was not clear; however, its evolution and pro-
Figure 1
*Surgery was performed by Dr. David Sabiston, Jr.,
Professor and Chairman of the Department of Surgery, Duke University Medical Center, Durham, North
Carolina.
Posteroanterior roentgenogram demonstrating left hilar
bulging due to right ventricular aneurysm.
Figure 2
Preoperative cinefluorogram showing right ventricular aneurysm.
Circulation, Volume XXXIV, July 1966
RIGHT VENTRICULAR ANEURYSM
125
Table 1
Blood Pressure before, during and after Operation
Site
Preoperative
Right atrium
Right ventricle
Pulmonary artery
Cardiac output
13/5 (9 )
18/4-10
2.7 L/min
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Figure 3
Postoperative right ventricular cinefluorogram revealing the absence of the right ventricular aneurysmal
sac.
gression over an 8-year period was well documented radiographically. The ventricular wall
weakness was thought to be secondary to previous infection. The normal coronary arteriograms and the absence of histological evidence of
muscle pathology in the aneurysmal wall militated against a diagnosis of coronary artery disease.
Review of all the myocardial sections taken at
the time of operation revealed no evidence of
polyarteritis nodosa or infection.
Discussion
The rarity of right ventricular aneurysms in
comparison to those of the left ventricle has
been well documented in the literature.1-3 9, 10
The reasons for this difference in incidence are
uncertain but the frequent occurrence of myocardial infarction in the left ventricular wall
and the hemodynamic differences between
the greater and lesser circulations are signifiCirculation, Volume XXXIV, July 1966
Blood pressure (mm Hg)
Operative
Postoperative
14/6 (10)
11/4
11/7
16/4-12
2.0 L/min
cant factors.1-4 Aneurysms due to congenital
malformations have been found in both ventricles,18-20 but they are rare in relation to
the number of acquired lesions that have been
diagnosed in vivo and at the autopsy table.
Accidental9' 16, 17 and operative8,10-15 trauma
comprise the overwhelming majority of etiological factors leading to the development of
right ventricular aneurysms.
The paradoxical movement of such aneurysms during ventricular systole is thought to
lead to reduced stroke volume. Predisposition
to rupture has been described, but it is not a
common occurrence. The aneurysms may also
serve as a nidus for thrombus formation. In
our laboratory we have studied a second patient with a right ventricular aneurysm who
did have pulmonary emboli which were
thought to arise from the aneurysmal defect;
however, no cinefluorographic evidence of
thrombi in the aneurysm was noted at the time
of cardiac catheterization. No further emboli
have occurred in this patient since the institution of anticoagulant therapy.
In the case presented, the first suspicion
of a myocardial lesion was prompted by an
unusual left hilar shadow on routine chest
x-rays. Unequivocal confirmation of thbe existence of a right ventricular aneurysm was obtained by cinefluorographic delineation of the
lesion (fig. 2). Coronary arteriography was
performed but did not demonstrate evidence
of coronary artery disease. The absence of a
positive history of previous trauma, surgery,
infarction, or other pathology precluded definitive etiological classification. The age of
the patient at the time the aneurysm developed seemed to militate against a congenital
origin. The appearance of the aneurysm after
an illness in which pneumonitis and loculated
WEGLICKI ET AL.
126
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pleural effusion were documented and perncarditis was suspected, strongly suggested that
the cause was an inflammatory process. The
presence of normal myocardial tissue and the
absence of coronary insufficiency were compatible with this thesis.
The decision to resect the aneurysm was
made because of the incapacitating symptoms
of recurrent supraventricular tachycardia, fatigue, and congestive failure. Successful resection of the aneurysm was accomplished,
and the patient had an uneventful postoperative course. He was restudied by cardiac
catheterization (table 1), and cinefluorography (fig. 3) demonstrated the absence of the
aneurysmal bulge. Unfortunately, the desired
improvement in the cardiac output was not
demonstrated, but the patient has improved
clinically during the 5 months since discharge.
References
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Vt-x
Circulation, Volume XXXIV, July 1966
Atraumatie Right Ventricular Aneurysm: Report of Case
WILLIAM B. WEGLICKI, JEROME RUSKIN and HENRY D. MCINTOSH
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Circulation. 1966;34:123-126
doi: 10.1161/01.CIR.34.1.123
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Copyright © 1966 American Heart Association, Inc. All rights reserved.
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