Download Pseudoaneurysm of the Left Ventricle following Mitral Valve

Pseudoaneurysm of the Left Ventricle
following Mitral Valve Replacement*
Richard D.Spellberg, M.D.and Ronald J . O'ReiUy, M.D.
Two patients with prosthetic m i l d vshres demonstrated
clinkal deterioration and were found by kft ventriculogrcrphy to have pseud~~lleurysmuof the inferior left
venlricohr wall. Both patients had lysis of pericardial
adhesiom at the time of valve replacement mrgery and
8ho had moderate aortic regurgitation. It Is posSrme that
myocardial muma secondary to dissection of adhesion8
or from overzealow mcker recovery of mtie regnrgibnt
flow was d c i e n t to nsPH in mbscquent myoaudial
dehiseence. Both patients bad loud apical systolic murmur& The inferior location of the aneurysms prevented
mmct diagnosis before left vemMcdography lud been
performed. The importance of left ventriedography in
evahmm petiprasthetk systolic murmws is emph.sized.
We have not found previously reported errscs of pseudoaneurysm formation foUowing heart surgery in which no
kft venldcuhr incision had been mde.
P
seudoaneurysms of the left ventricle have been reported following penetrating and nonpenetrating
chest wall trauma,l myocardial infarction2 and rarely as
a complication of cardiotomy i n c i s i ~ n . ~We
- ~ have
encountered this unusual operative complicatiou in two
patients following mitral valve replacement, both of
whom presented with clinical deterioration and prominent pansystolic apical murmur. Precatheterization
diagnosis in both of these patients was mitral prosthetic
regurgitation.
We have not found previously reported cases of left
ventricular pseudoaneurysm formation following cardiac
surgery in patients in whom no left ventricular incision
had been made.
*From the Cardiovascular and Radiology Departments, St.
Mary's Long Beach Hospital, Lon Beach, California.
Reprant requssts: Dr. Spellberg, 5 f Chrk
~ Auenue, Lde-
wood, Califomio 90712
CASE
REPORTS
A 42-year-old woman related a history of acute rheumatic
fever at age 18. In 1964. cardiac catheterization mc$ed
pressures consistent with moderately severe mitral stenosis
and insufficiency and mild aortic indiciency. Left ventriculography was not performed. In June 1964, mitral valve
replacement was performed through a right subcostal indsion. The pericardial space was found to be obliterated by
pericardial adhesions and blunt dissection was necessary to
free the heart from the pericardial sac. Under cardiopulmonary bypess, a left atriotomy was performed and the apex of
the left ventricle was vented with a Foley catheter. A
noncal& mitral valve was easily removed and replaced by a
No. 3 Starr-Edwards prosthesis. Reexploration was necessitated by postoperative bleeding 24 hours following the initial
operation. At that time, an extrapleural hematoma was evacuated and bleeding controlled. No mention was made of
bleeding sites on or about the myocadum. In 1986, a loud
systolic apical murmur was described for the k t time. In
1968 following recurrent chest discomfort, selective coronary
arteriograms were performed and were normal. A left ventriculogram revealed only minimal mitral prosthetic regurgitation. Recurrent chest discomfort, arrhythmia, and dyspnea
necessitated readmission in 1970. Chest x-ray examination at
that time revealed no change in heart size or d g u r a t i o n
compared to previous studies. P h o d o g r a p h y documented the apical systolic murmur with an aortic closure
( AC ) to mitral opening click ( OC ) interval of 0.16 second
(Fig 1). Cardiac catheterization revealed moderate prosthetic obstruction at rest with a mean diastolic m i d valve
gradient of 8.5 mm Hg, with slight elevation of mean left
atrial pressure ( M W P = 13 mm Hg) and elevation of the
left ventricuh end diastolic pressure ( LVED = 19 mm Hg ).
Exercise increased the diastolic gradient to 23 mm Hg and
the MLAP to 32 mm Hg. Left ventriculography revealed DO
change in the mild mitral regtqitation (Fig 2) since the
study of 1968. However, a pseudoaneurysm arising from the
inferior wall of the left ventricle was discovered. Retrospective review of the 1968 ventrimlogram revealed the narrow
neck of the pseudoaneurym but inadequate filling of the sac
for diagnostic purposes. Surgery in December 1970 revealed
a 2 x 3 cm pseudoawuymd sac of the inferior left
ventricular wall. The sac consisted of thickened epicardium
which was slightly adherent to the diaphragm. The sac
expanded with systole and communicated with the ventrimlar lumen through a 1 mm opening well below the posterior
FIGURE1 (Case 1). Phonocardiogram and apex cardiogram.
Paper speed 100 mrn per second. Time hues 0.02 second.
The AC (aortic closure) to
mitral opening click ( OC ) measures 0.16 second. ACG=apex
cardiogram: MC=mitral closure:
SM=systolic murmur. The small
arrows incidentally indicate a
summation -prosthetic third and
fourth heart sound. Note also
diminution in the intensity of
MC.
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SPELLBERG AND O'REILLY
FIGURE2 (Case 1 ). Left ventriculogram-right anterior
oblique projection. Note the oval shaped pseudoaneurysm of
the inferior left ventricular wall. The aneurysmal sac comrnr~nicateswith the left ventricular cavitv. bv. a narrow neck.
atrial-ventricular groove. he prosthetic valve was explored
and found to be mrmal. Her ~'Jstoperative course was
uncomplicated. The systolic murmur was no longer audible;
the AC-OC interval remained unchanged. She is clinically
improved,
A 57-year-old woman with rheumatic heart disease was
evaluated in 1970 for recurrent left heart failure. A closed
mitral commissuratomy had been performed in 1958 with
slight symptomatic relief. Catheter studies in 1970 revealed
severe mitral stenosis (mitral valve area = 0.9 cmz), and
mild aortic insufficiency. A left ventriculogram c o n h e d
mild rnitral regurgitation but was otherwise unremarkable.
Surgery was performed in March 1970 through a right
subcostal incision. Pericardial adhesions were noted and were
subsequently lysed by sharp and blunt dissection before
beginning cardiopulmonary bypass, performing left atriotomy, and venting the left ventricle at the apex. A noncalcific deformed mitral valve was removed without difEculty
and was replaced with a No. 2 Starr-Edwards valve. The
FIGURE 4 (Case 2 ) . Left ventriculogram-right anterior
oblique projection. A large pseudoaneurysm of the posterior
left ventricular wall is shown. The communication between
the left ventricular cavity and the wsterior aneuwsmal sac is
not identified in this patient. The cine frame selecied was late
in the sequence accounting for the relatively small amount of
contrast media in the left ventricular cavity. An incidental
finding is the presence of two small pseudoaneurysms of the
left ventricular apex.
postoperative course was complicated by elevated central
venous pressure, recurrent arrhythmia, and low urinary output. A loud pansystotic apical murmur was described on the
k t postoperative day. Phonocardiography confirmed the
murmur with a normal AC-OC interval (Fig 3). The plain
chest films revealed no significant change in cardiac size or
configuration compared to the preoperative study. Fluoroscopy demonstrated no abnormal prosthetic motion or abnormal cardiac pulsation. Electrocardiogram revealed loss of
R wave voltage in the right precordial leads compared to a
e
-~ r e o- ~ e r a t i vrecord.
Left ventriculography was performed on the second postoperative day. Resting LVED pressure was 15 mm Hg.
Minimal mitral regurgitation was present. A large pseudoaneurysm was noted arising from the inferior wall of the
heart (Fig 4 ) with two small aneurysms at the left ventricular apex. Repeat surgery revealed a soft dome-shaped
FIGURE3 (Case 2). Phonocardiogram and apex cardiogram.
Paper speed 100 mm per second. Time lines 0.02 seconds.
AC to OC interval equals 0.12
seconds. Abbreviations as in
Figure 2. The OC occurs a t the
"0"point of the ACC.
CHEST, VOL. 62, NO. 1, JULY, 1972
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PSEUDOANEURYSM OF LEFT VENTRICLE
aneurysmal mass 5 cm in diameter arising from the posterior
left ventricular wall. The aneurysm filled in systole from a
defect in the endocardium which was 2 cm in diameter and
located just below the posterior atrial ventricular groove. The
aneurysm was excised and the communication closed. Failure
of adequate contractility of the posterior left ventricular wall
and recurrent ventricular fibrillation prevented successful
recovery from cardiopulmonary bypass. Necropsy revealed
successful repair of the aneurysm. Multiple small hematornas
were described over the epicardial surface. Diffuse atherosclerotic coronary narrowing involved the three major vessels.
There was no gross or microscopic evidence of acute myocardial infarction. Patchy areas of myocardial fibrosis were
described on microscopic examination.
Pseudoaneurysms can develop in the ventricular wall
at the site of previous laceration, rupture or incision.
Unlike true aneurysms whose wall is composed of myocardium or its fibrous tissue replacement, pseudoaneurysms are retained by pericardium or extracardiac
tissue. They communicate with the ventricular lumen
through a small channel representing the site of previous
myocardial dehiscence. The formation of these extracardiac "pulsating hematomas"6 may prevent more extensive bleeding into the pericardium with resultant
tamponade or death or both.
At the time of valve replacement surgery, both of our
patients were found to have extensive pericardial adhesions. In patient 1, these were presumably due to previous rheumatic pancarditis and in patient 2 from previous surgery. In addition, both patients had moderate
aortic regurgitation. We hypothesize that myocardial
trauma secondary to dissection of myopericardial adhesions, or excessive suction (utilized to return aortic regurgitant flow from the left ventricle) was sufficient to
result in eventual myocardial rupture and false aneurysm
formation. The apical aneurysms in case 2 at the site of
the ventricular vent suggests inherent weakness in the
patient's myocardium and indeed postmortem examination revealed patchy myocardial fibrosis with coronary
vessel disease.
In the majority of previously reported cases of false
aneurysms of the left ventricle following cardiotomy
incision, the diagnosis was apparent from the abnormal
cardiac silhouette and fluoroscopic evidence of paradox~.~
ical motion secondary to the aneurysm l ~ c a t i o n . Both
patients in the current report had inferior wall lesions
which could not be demonstrated by noncontrast radiography. T o further confuse the clinical picture the loud
systolic apical murmurs suggested mitral regurgitation.
It should be noted that periprosthetic systolic murmurs
are somewhat unreliable in estimating the severity or
indeed even the presence of mitral prosthetic regurgita-
t i ~ n . ~ -Indeed,
O
left atrial hypertension in the presence
of mitral prosthetic regurgitation narrows the AC to OC
interval and may be somewhat of a more reliable index
than murmur alone in assessing the severity of mitral
prosthetic insufficiency. This interval has been previously found in "normal" patients to vary between 0.07 to
0.15 seconds.lO-l2Careful attention to this phonocardiographic finding might have excluded a clinical diagnosis
of prosthetic mitral insufficiency in our patients. However, in view of the subsequent outcome, the importance
of left ventriculography in the assessment of mitral
prosthetic murmurs, particularly in patients demonstrating clinical deterioration is emphasized.
ACKNOWLEDGMENTS: We gratefully acknowledge the
assistance of Dr. Aurelius Domanchich who performed the
phonocardiograrns and Mr. Thomas King, RT and Mr. Paul
Artrnan who prepared the illustrations.
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120:252-254, 1970
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13:309-323, 1971
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the left ventricle: diagnosis by direct cardioangiography.
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Dis Chest 44: 11-19, 1963
CHEST, VOL. 62, NO. 1, JULY, 1972
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