Multiple Left Ventricular Aneurysms in Silent Coronary Artery

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2006
17
244-248
Multiple Left Ventricular Aneurysms in
Silent Coronary Artery Disease
A Case Report
1
2
1
Chung-Lieh Hung , Jiun-Yi Li , Charles Jia-Yin Hou ,
Hung-I Yeh1, Yu-San Chou1, and Cheng-Ho Tsai1
1
Section of Cardiology, Mackay Memorial Hospital,
Main Branch Hospital, Taipei, Taiwan
2
Section of Cardiovascular Surgery, Mackay Memorial Hospital,
Main Branch Hospital, Taipei, Taiwan
Abstract
Myocardial infarction leading to left ventricular aneurysm was found in less than 5% of patients.
Usually, aneurysm is located at anterior wall, and is rare in other segment. Heart failure could be the
major clinical manifestation in a patient with aneurysm, and surgical approach may provide clinical benefit. Here, we report a case with coexistent multiple left ventricular aneurysms without previous chest
pain presenting with progressive dyspnea at rest. Reduction myoplasty was successfully performed
with bypass graft of coronary arteries leading to subsequent functional improvement. ( J Intern Med
Taiwan 2006; 17: 244-248 )
Key Words
Left ventricular aneurysm, Heart failure, Reduction myoplasty
Case Report
with recent aggravation. Orthopnea developed one
week ago, and paroxysmal nocturnal dyspnea with
A 61 year-old, male who visited our emergency
resting dyspnea was also noted at the same time. At
depart denied any systemic diseases before. He de-
emergency department, chest radiology revealed
nied chest discomfort and angina sensation during ex-
right side pleural effusion with pulmonary conges-
ercise. Progressive dyspnea on exertion since about
tion. Electrocardiography revealed pathological Q
2 months ago with decreased urine output was noted
wave over leads II, III, AVF and V5, V6. Cardiac en-
Correspondence and requests for reprints : Dr. Chung-Lieh Hung
Address : Department of Cardiovascular Medicine; Mackay Memorial Hospital, Taipei, Taiwan. 8F-1, No. 17, 93rd Lane, Chung-Shan North
Road, 2nd Section, Taipei, 104 Taiwan.
Multiple Left Ventricular Aneurysm
245
zymes were within normal limits, and other blood
was 30%, and a moderate mitral regurgitation was ob-
chemistry data was unremarkable. Diuretics were
served. The myocardial thinning and dyskinetic mo-
prescribed and he was admitted for further evalua-
tion at left ventricular apical, apical-inferior and
tion.
basal-inferior segments were noted (Figure 1). A mild
Echocardiography revealed enlargement of four
degree pulmonary hypertension with right ventricu-
cardiac chambers. Left ventricular ejection fraction
lar systolic pressure of 42mmHg was measured using tricuspid regurgitation Doppler flow velocity calculation by Bernoulli equation. Cardiac catheterization was performed later, which showed a 70% steno-
Fig.1.Echocardiography revealed multiple pouches with
wall thinning character during systolic phase from
apical four chambers view (panel a, white arrow),
and from two chamber view (panel b, white arrow).
Apical aneurysm was observed in panel a, and
panel b revealed baso-inferior aneurysm (lower
arrow) and another infero-apical aneurysm (upper
arrow).
Fig.2.Left ventriculography during catheterization
demonstrated multiple aneurysms formation distributed at left ventricular antero-lateral (white arrow, right-upper location), apical-inferior (white arrow, right-lower location) and baso-inferior segments (white arrow, left-lower location).
Fig.3.MRI images cutting from left ventricular basal area
(upper panel) to apical area (lower panel) in a
short-axis plane. Panel a to c revealed baso-inferior aneurysms formation (lower solid white arrow)
with delayed enhancement, indicating infarction
zone with pouch-out configure. Panel d to f revealed antero-lateral (upper dotted white arrow)
and apical-inferior (lower solid white arrow)
aneurysms with the same characteristics.
Fig.4.Scarred, fibrotic tissue indicated true aneurismal
area. Upper dark arrow corresponds to antero-lateral aneurysm, and lower dark arrow corresponds
to apical-inferior one. (A: viable, non-aneurysmal
area located at the apex of left ventricle)
246
C. L. Hung, J. Y. Li, C. J. Y. Hou, H. I. Yeh, Y. S. Chou, and C. H. Tsa
1
sis in middle left anterior descending artery (LAD)
ally mixed with viable myocardium . With the pas-
and a 90% stenosis at proximal circumflex artery
sage of time, the wall of aneurysm becomes more
(LcX). Right coronary artery (RCA) revealed a total
densely fibrotic and interferes with ventricular per-
occlusion at proximal to middle portion. Collateral
formance through paradoxical expansion and inef-
vessels supplying RCA from left side coronary ar-
fective left ventricular contraction during each sys-
teries were also demonstrated. Left ventriculography
tole . Most aneurysms are located anterolaterally, or
revealed multiple aneurysm-like dyskinetic wall mo-
near the LV apex and are often associated with total
tions at antero-lateral, apical and basal-inferior seg-
occlusion of LAD with poor collateral supply. Only
ments (Figure 2). Magnetic resonance imaging (M-
5-10% of aneurysms located posteriorly, and even are
RI) was then performed for further surgical planning
more rare in inferior wall . The ventricular aneurysms
and assessment (1.5T MRI scanner, ECG-triggering
needs for aneurysmectomy have declinded dramati-
Dark-blood sequence-Double IR, Bright blood se-
cally during the past 5 years due to the new era of ear-
quence-Cine image). And a pouch-like thinning my-
ly reperfusion therapy in acute myocardial infarc-
ocardial wall with delayed enhancement was noted at
tion . True LV aneurysms rarely rupture early or late
mid anterior, anterolateral and apical wall of the left
after its development, and late rupture almost never
ventricle (Figure 3). Other delayed and mild thinning
occur3. Review of previous literature1-4, in addition to
myocardial wall at basal infero-septal, inferior wall,
rare location, the multiple, and rarely developed lo-
mid inferior wall of LV and antero-inferior wall of
cation coexisted in one case, which had never been
RV were also noted. Multiple true aneurysms forma-
reported before.
tion with scarred and infarcted character was diagnosed for this patient.
2
3
3
The exact diagnosis of LV aneurysms is best
made non-invasively by two-dimension echocardio-
LV aneurysmectomy (anterolateral aneurysm)
graphy (2DE) study. 2DE is also helpful in distin-
and coronary artery bypass graft was successfully
guishing between a true and false aneurysm based on
performed. Whitish, thinning scar tissue distributed
the demonstration of a narrow neck in relation to ca-
at the multiple aneurysms area mentioned above was
vity size . Left ventriculography may also provide ano-
observed (Figure 4), which had histopathological
ther potential tool, however, it is an invasive method
prove of a fibrous tissue mixed with some viable my-
in detecting an abnormal bulge or dyskinetic wall mo-
ocardium after resection. This patient was discharged
tion in the LV contour during systole. Other clues in-
three weeks later and remained uneventful with a
clude the presence of a persistent ST segment eleva-
functional class two heart failure in the two months
tion on resting electrocardiography and a characte-
outpatient clinic follow-up.
ristic bulge and calcified LV silhouette on chest
Discussion
4
5
roentgenogram. These findings, however, are of low
specific and with limited sensitivity. We hypothesized
True left ventricular (LV) aneurysm formation
that multiple LV aneurysms just like this case might
develops in less than 5% of all patients with ST ele-
have reciprocal effect which made no definite ST seg-
vation myocardial infarction and somewhat more fre-
ments changes on electrocardiography, and this issue
quently in transmural infarct, especially in anterior
had never been discussed before. Recently, MRI has
1
wall . It occurs when intraventricular tension stretch-
emerged as a preferred non-invasive technique for
es the non-contracting infarcted myocardium, thin
pre-operative assessment of LV shape, the degree of
layer of necrotic muscle, and even totally fibrous tis-
aneurysm thinning, and its resectability2. The present
sue. The thinning myocardial wall may be occasion-
reported case demonstrated obviously infarcted and
Multiple Left Ventricular Aneurysm
scar formation with delayed enhancement in multiple aneurysmal area on MRI (Figure 3), which were
compatible with surgical findings (Figure 4).
The clinical features of LV aneurysm include
symptoms of heart failure (with or without angina) in
50% of patients, severe angina alone was observed in
one-third of the patients, and symptomatic ventricular arrhythmias in approximately 15%6. The associated ventricular arrhythmia may even be refractory
6,7
and life threatening . There was no associated arrhythmia in the present case, and no angina by history taking, which made an initial correct diagnosis
difficult. Mural thrombi usually can be found in
almost half patients with chronic LV aneurysm, and
can be detected by 2DE or by angiography8. Systemic
embolic events in patients with thrombi and LV
aneurysm were extremely uncommon at 1 month af8
ter an acute myocardial infarction .
Improvement of complicated true LV aneurysm
can be carried out by aneurysmectomy, if there were
no complicated condition, such as heart failure, angi2
na, embolization, or life-threatening arrhythmias .
Coronary revascularization is frequently performed
along with aneurysmectomy in patients with multivessels disease accompaning heart failure.
Improvement of left ventricular function has been reported in survivors after resection of LV aneurysm9
by removing the abnormal mechanical burden leading to a poor global LV systolic function. The nonischemic myocardium remote to the resected ischemic area also had an improvement on diastolic relaxation through a cardiovascular neuroregulatory
9
mechanisms . Standard surgical modalities in patients
10
with multiple aneurysms have never been discussed .
It has been reported that symptoms of angina with
heart failure would benefit more from surgical treatment as in the present reported case, the refractory
heart failure also improved after surgery.
References
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247
early myocardial infarction: A critical review of the evolution
and usefulness of modern techniques. Mod Pathol 1999; 12: 63545.
2.Mickleborough LL, Merchant N, Provost Y et al. Ventricular reconstruction for ischemic cardiomyopathy. Ann Thorac Surg
2003; 75: S6-12.
3.Lundblad R, Abdelnoor M, Svennevig JL. Repair of left ventricular aneurysm: Surgical risk and long-term survival. Ann
Thorac Surg 2003; 76: 719-25.
4.Buck T, Hunold P, Wentz KU et al. Tomographic three-dimensional echocardiographic determination of chamber size and
systolic function in patients with left ventricular aneurysm:
Comparison to magnetic resonance imaging, cineventriculography, and two-dimensional echocardiography. Circulation
1997; 96: 4286-97.
5.Candell-Riera J, Santana-Boado C, Armadans-Gil L, et al.
Comparison of patients with anterior wall healed myocardial infarction with and without exercise-induced ST-segment elevation. Am J Cardiol 1998; 81: 12-6.
6.Zipes DP, Libby P, Bonow RO, et al. Braunwald's heart disease:
A textbook of cardiovascular medicine. 7th ed. Philadelphia:
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7.Cannom DS, Prystowsky EN. Management of ventricular arrhythmias: Detection, drugs, and devices. JAMA 1999; 281:
172-179.
8.Zipes DP, Libby P, Bonow RO, et al. Braunwald's heart disease:
A textbook of cardiovascular medicine. 7th ed. Philadelphia:
Elsevier Saunders, 2005: 243-5.
9.Athanasuleas CL, Stanley AW, Buckberg GD et al. Surgical anterior ventricular endocardial restoration (SAVER) for dilated
ischemic cardiomyopathy. Semin Thorac Cardiovasc Surg 2001;
13: 448-58.
10.Ohara K. Current surgical strategy for post-infarction left ventricular aneurysm-From linear aneurysmectomy to Dor's operation. Ann Thorac Cardiovasc Surg 2000; 6: 289-94.
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C. L. Hung, J. Y. Li, C. J. Y. Hou, H. I. Yeh, Y. S. Chou, and C. H. Tsa
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