Download Prognostic Significance of Left Ventricular Aneurysms With Normal

Prognostic Significance of Left
Ventricular Aneurysms With Normal
Global Function Caused by Myocarditis*
Andrea Frustaci, MD, FCCP; Cristina Chimenti, MD; and Maurizio Pieroni, MD
Objectives: To evaluate the prognosis of left ventricular (LV) aneurysms with normal global
function caused by myocarditis.
Background: LV aneurysms may result from idiopathic or viral myocarditis. The prognosis of
inflammatory LV aneurysms when associated with a normal cardiac function is unknown.
Methods: Among 353 patients with a histologic diagnosis of myocarditis, 12 (3.3%) had single or
multiple localized LV aneurysms (length, 10.6 ⴞ 3.1 mm; width, 7.4 ⴞ 4.2 mm) with normal
cardiac function. Presenting symptoms were ventricular tachycardia (VT) in nine patients and
unexplained chest pain in three. All patients underwent laboratory tests and noninvasive and
invasive cardiac examinations, including biventricular endomyocardial biopsy.
Results: In all patients, LV endomyocardial biopsy specimen showed a lymphocytic myocarditis
with focal intense myocytolysis or damage of intramural vessels, whereas right ventricular biopsy
was diagnostic for myocarditis only in three. Serologic study suggested a viral infection in 3
patients and an immunologic disorder in 2, although it was negative in 7. Treatment included
antiarrhythmics in 9 patients with VT, ␤-blockers in 1 with chest pain, and immunosuppression
(prednisone and azathioprine for 5 months) in 4 with active myocarditis (2 with chest pain and 2
with VT). At intermediate-term follow-up (mean, 53 months; range, 12 to 120 months), LV
function was persistently normal in all patients, with an LV aneurysm occlusion being observed
in two patients. All patients were asymptomatic, with no VT recurrence or major clinical events.
None required implantable electrical devices or a surgical intervention.
Conclusions: LV aneurysms with normal global function caused by myocarditis are an uncommon
benign entity in which major therapeutic regimens are usually unnecessary.
(CHEST 2000; 118:1696 –1702)
Key words: angina; cardiac aneurysm; myocarditis; prognosis; ventricular tachycardia
Abbreviations: 2D-ECHO ⫽ two-dimensional color-Doppler echocardiography; LV ⫽ left ventricle; RV ⫽ right ventricle; VT ⫽ ventricular tachycardia
ventricular (LV) aneurysms are usually the
L eftconsequence
of coronary artery disease, but
1
they may also occur in congenital,2 traumatic,3,4
connective tissue,5,6 primary myocardial,7–10 or infective heart diseases. Chagas’ disease11 and infective
endocarditis most often cause LV aneurysms of
infective origin. Regional wall motion abnormalities
have been occasionally observed during myocarditis.12 Goudevenous et al13 reported a case of LV
aneurysm during infection with coxsackievirus B4
but without histologic evidence of myocarditis. More
recently, we documented14 a lymphocytic myocarditis in two patients with LV aneurysm and normal
* From the Cardiology Institute, Catholic University, Rome, Italy.
Manuscript received December 30, 1999; revision accepted June
26, 2000.
Correspondence to: Andrea Frustaci, MD, FCCP, Istituto di
Cardiologia, Università Cattolica del Sacro Cuore, Largo Gemelli
8, 00168 Rome, Italy; e-mail: [email protected]
global function, with more prominent inflammatory
changes being observed in the biopsy specimens
taken from the area closest to the aneurysms. Thereafter, several case reports of LV aneurysms related to
idiopathic or viral myocarditis have appeared in the
literature.15,16 However, the prognostic significance
of this entity, particularly when associated with a
normal global LV function, is poorly understood as
follow-up on a consistent number of patients is
lacking.
We report an intermediate-term follow-up on 12
patients with LV aneurysms, normal LV global function, and histologic evidence of a lymphocytic myocarditis.
Materials and Methods
Three hundred fifty-three patients in our institution between
January 1988 and November 1998 had a histologic diagnosis of
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Clinical Investigations
lymphocytic myocarditis as a result of an extensive cardiac study
including two-dimensional color-Doppler echocardiography (2DECHO), cardiac catheterization, angiography, and endomyocardial biopsy; 151 of them (42.7%; 104 men, 47 women; mean age,
47.5 ⫾ 13.2 years) had a preserved LV function (LV ejection
fraction ⱖ 0.50). Among the last group, 12 patients (3.3% and
7.9%, respectively; 4 men, 8 women; mean age, 38.1 ⫾ 17.9
years) had localized single or multiple LV aneurysms revealed
unexpectedly by LV angiography. LV aneurysm was defined as an
akinetic or dyskinetic well-defined wall bulge persisting during
both systole and diastole.17
Characteristics of Patient Population
Nine of these 12 patients were admitted to the hospital
because of sustained or nonsustained ventricular tachycardia
(VT) with right bundle branch block configuration (Fig 1),
whereas the remaining three patients (numbers 4, 5, and 6) had
atypical chest pain (Table 1). Five patients had a history of a
flulike syndrome, and none of them had previous cardiac ischemic events and risk factors for coronary artery disease (hypertension, hypercholesterolemia, smoking, family history). Physical
examination findings were within normal limits in all patients. In
particular, no precordial murmurs, abnormal heart sounds, or
basal rales were heard. Chest radiograph was normal in all cases.
Clinical Investigations
All patients underwent routine laboratory tests (hematologic,
biochemical, and urinalysis), serologic tests for cardiotropic viruses (echovirus, coxsackievirus B, cytomegalovirus, adenovirus,
influenza virus, and parainfluenza virus), and immunologic stud-
ies (antinuclear, anti-DNA, anticardiolipin, antisarcolemmal, and
antimyolemmal antibodies; antineutrophil cytoplasmic antibodies; circulating immune complex; and C3c and C4).
Cardiac studies included both noninvasive (resting ECG,
Holter monitoring, exercise stress testing, 2D-ECHO) and invasive examinations (cardiac catheterization, biplane left and right
ventriculography, coronary angiography, biventricular endomyocardial biopsy, and an electrophysiologic study in the four
patients with sustained VT).
In the three patients with chest pain, coronary angiography was
performed with an intracoronary ergonovine test18 to rule out a
potential coronary spasm.
Endomyocardial biopsies (three to four per ventricular chamber) were performed by a Bipal (Cordis; Miami, FL) bioptome,
approached by a 7F (501– 613A and B) long sheet in the
septal-apical region of the right ventricle (RV) and in different
segments of the LV. LV specimens were marked as close to (A)
or far from (B, C, or D) LV aneurysms. The areas selected for a
biopsy were identified on a radiographic view using flashing of
contrast medium. Tissue specimens were fixed in 10% buffered
formalin and embedded in paraffin wax; 5-␮m-thick sections
were cut and stained with hematoxylin-eosin, Miller’s elastic Van
Gieson, and Masson’s trichrome.
The four patients with sustained VT underwent an electrophysiologic study including a ventricular stimulation protocol
with up to three extra stimuli at two cycle lengths from at least
two RV sites. The study was performed with the patients
receiving the same antiarrhythmic drug (propafenone in patients
1 and 2 and amiodarone 800 mg in patients 3 through 9) that
resolved the arrhythmia. Antiarrhythmic treatment strategy implied the administration of the drug already used if sustained VT
was not inducible, and if a sustained VT was induced, metoprolol
(100 mg/d) was introduced, and the patient was tested again a
week later. Implantation of a cardioverter defibrillator was
planned in case an inducible or spontaneous VT was still present.
RV and LV mapping during sinus rhythm and during induction of
VT was performed in inducible patients. Areas of local activation
that were coincident with the onset of the abnormal QRS
complexes were considered to be the origin of the arrhythmia.
Follow-up
All patients were followed up at 4-week to 6-month intervals.
At each visit, they were questioned regarding the efficacy and
toxicity of drugs and underwent physical examination, ECG,
2D-ECHO, and Holter monitoring. At 1, 3, and 5 months, the
patients underwent cardiac catheterization with left ventriculography and an LV endomyocardial biopsy if an active lymphocytic
myocarditis was present, and an immunosuppressive treatment
was then instituted. MRI was performed between January 1997
and November 1998 in all patients to ascertain persistence of LV
aneurysms and obtain information on LV dimension and function
by a reliable noninvasive procedure.
Statistical Analysis
All values are expressed as mean ⫾ SD.
Results
Clinical Study
Figure 1. Twelve-lead ECG of patient 1 at admission (top) and
after IV bolus of propafenone (bottom) showing sustained VT
with right bundle branch block configuration and a normal
tracing, respectively.
All patients were in sinus rhythm with the exception of patient 9, who was in atrial fibrillation. Holter
monitoring revealed frequent ventricular ectopic
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Table 1—Intermediate-term Follow-up on 12 Patients With LV Aneurysms and Normal Global Function Caused by
Myocarditis*
Age,
Presenting
Patient
yr
Sex Symptoms
Aneurysm
Localization
RAO View
LV Function,
EF%
Serology
(Diagnostic
Antibody Titer)
Histology
Treatment at Hospital
Discharge, mg/d
Follow-up,
mo
65%
60%
Negative
Negative
aM
M
Propafenone (600) ⫹ I
Propafenone (600)
120/A/AnO
108/A
M
sVT
Apical
Anterolateral;
posterobasal
Apical
55%
Influenza B
M
18/A/AnO
51
26
42
49
14
47
F
M
F
F
F
F
Chest pain Posterobasal
Chest pain Anterolateral
Chest pain Apical
nsVT
Posterobasal
nsVT
Posterobasal
sVT
Double
posterobasal
51%
58%
62%
53%
62%
57%
Influenza A
Negative
Anticardiolipin
Coxsackie B3–B5
Negative
Negative
10
53
F
nsVT
60%
Antinuclear
M
Amiodarone
(400) ⫹ Metoprolol
(100)
I
I
Metoprolol (100)
Sotalol (240)
Sotalol (240)
Amiodarone
(400) ⫹ Metoprolol
(100) ⫹ I
Sotalol (240)
11
12
55
16
F
F
nsVT
nsVT
63%
52%
Negative
Negative
M
M
Sotalol (240)
Metoprolol (100)
1
2
16
24
M
M
sVT
sVT
3
65
4
5
6
7
8
9
Apical;
posterobasal
Posterobasal
Several along
all segments
aM
aM
M
M
M
aM ⫹ V
22/A
110/A
65/A
72/A
68/A
13/A
12/A
12/A
16/A
*RAO view ⫽ LV angiography in right anterior oblique view; EF ⫽ ejection fraction; sVT ⫽ sustained VT; nsVT ⫽ nonsustained VT;
M ⫽ myocarditis; a ⫽ active; V ⫽ vasculitis; I ⫽ immunosuppressive therapy (prednisone 1 mg/kg/d ⫹ azathioprine 50 mg/bid);
A ⫽ asymptomatic; AnO ⫽ aneurysm occlusion.
beats with some couples and triplets, phases of
bigeminy or trigeminy, and runs of nonsustained VT
in nine patients (1, 2, 3, and 7 through 12) and failed
to show transient ST-T segment ischemic changes in
all patients.
Ergometric test performed with the Bruce protocol on specific antiarrhythmic regimen (Table 1)
failed to show signs and symptoms of myocardial
ischemia in all patients. No repetitive ventricular
ectopic beats appeared during the test.
2D-ECHO showed normal atrial and ventricular
dimension (LV end-diastolic diameter, 48⫾ 2.6 mm;
left atrium, 0.30 ⫾ 3.4 mm), normal thickness of
cardiac walls, and global LV contractility (LV ejection fraction, 58.1 ⫾ 4.6%) without segmental wall
motion or valvular abnormalities. None of the patients
had echocardiographic evidence of LV aneurysm.
Cardiac catheterization showed normal pulmonary
and LV end-diastolic pressure. Biplane LV angiography revealed normal LV contractility with the
unpredictable presence of single or multiple small
aneurysms (Figs 2, top, 4, middle, and 5) with
different localization (Table 1). Aneurysm size was
10.6 ⫾ 3.1 mm in length and 7.4 ⫾ 4.2 mm in width
measured with a cardiac angiography measurement
system (quantitative coronary angiography MEDIS,
Rotterdam, Netherlands). The RV angiography was
normal in all cases. Coronary angiography showed
normal epicardial coronary arteries. The intracoro-
nary ergonovine test failed to show diffuse or segmental coronary artery spasm, symptoms, or significant ECG changes.
At electrophysiologic study, programmed ventricular stimulation induced rapid monomorphic (right
bundle branch block configuration) sustained VT in
patients 3 and 9, without hemodynamic deterioration. Ventricular mapping showed the arrhythmia originating within the apical and posterobasal aneurysm in
patients 3 and 9, respectively. Patients 1 and 2 treated
with propafenone were no longer inducible.
Histology
Diffuse inflammatory lymphomononuclear infiltrates associated with focal necrosis of adjacent
myocytes were observed in all patients meeting the
Dallas criteria for myocarditis.19 In four patients (1,
4, 5, and 9), the inflammatory changes were not
associated with fibrosis (active myocarditis; Figs 4,
bottom, and 5, top). The other eight patients also had
interstitial and focal replacement fibrosis. RV endomyocardial biopsy specimen showed histologic
changes diagnostic for myocarditis in only three
patients (3, 9, and 10), although LV specimens from
all patients suggested that entity. Moreover, in the
specimens obtained in the region closest to the
aneurysm, the myocarditis process was more prom-
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Clinical Investigations
Treatment and Follow-up
Figure 2. End-systolic left ventriculographic frame from patient
1 showing a small apical aneurysm (top) that appears to be
occluded at a 5-month control (bottom).
inent and severe, being associated with intense myocytolysis (Fig 5, top). There were no signs of ischemic damage. Abnormalities of the intramyocardial
vessels were documented in patient 9, consisting of
lymphocytic infiltration with focal wall fragmentation of
an arteriole (Fig 3, bottom), and in patient 12, in whom
a small artery occluded by an organized thrombus was
surrounded by a discrete area of myocardial fibrosis
(Fig 4, bottom). The endocardium was normal in all
patients.
Serology
Serologic tests for cardiotropic viruses were positive in three patients (3, 4, and 7) at dilutions ⱖ 1/64
(Table 1). Viral particles in the myocardium were not
searched for. Immunologic studies were positive in
patient 6, showing abnormal titer (IgG ⬎ 26 U/mL)
of anticardiolipin antibodies, and in patient 10, showing a positivity of antinuclear antibodies.
At repeated electrophysiologic study, induction of
sustained VT was prevented in patients 3 and 9 with
the addition of metoprolol. These patients were
discharged from the hospital on a regimen of amiodarone (400 mg/d, tapered to 200 mg after 2 weeks)
and metoprolol (100 mg daily) therapy. The other
two noninducible patients were discharged with the
drug that prevented the induction of VT (propafenone, 600 mg/d). Patients with nonsustained VT
were treated with sotalol (80 mg tid). Among the
three patients with chest pain, patient 6 was treated
with metoprolol (100 mg daily) and sedatives, and
patients 4 and 5, who had histologic evidence of
active myocarditis, received an immunosuppressive
treatment with steroids (prednisone 1.5 mg/kg daily
tapered to 0.33 mg/kg daily from the fifth week to
the fifth month) and azathioprine (2 mg/kg/d for 5
months). Patients 1 and 9, with active myocarditis,
vasculitis (patient 9), and VT, were also treated with
the same immunosuppressive therapy in addition to
antiarrhythmics.
The patients were clinically followed, and ECG,
chest radiograph, and 2D-ECHO were performed at
4-week intervals.
The mean follow-up was 53 months (range, 12 to
120 months). During the follow-up, no death, cardiac arrest, aneurysm rupture, or thromboembolic
phenomena were recorded. Among patients with
VT, none required surgical treatment or had the
need for an implantable electrical device. No patient
showed significant pharmacologic side effects, and
no LV dilatation or impairment of LV function was
observed. In patients 1 and 3, LV angiography performed at 5 months showed the occlusion of the LV
aneurysm (Fig 2, bottom). In the arrhythmic patients,
the antiarrhythmic treatment was gradually reduced,
and in patients 1, 3, and 9, it was withdrawn. In these
patients, sequential Holter recordings failed to show
the presence of repetitive ventricular ectopic beats.
In patients 1, 4, 5, and 9, with an active myocarditis at the first biopsy, the control biopsy performed
after 4 weeks of immunosuppressive therapy showed
a healing of the inflammatory process, which progressed to a healed phase (Fig 5, bottom) at follow-up (3 and 5 months) cardiac biopsy. Cardiac
MRI documented normal LV dimension and function in all patients, occluded apical and posterobasal
LV aneurysm in patients 1 and 3, respectively, and
the persistence of the three cardiac layers (endocardium, myocardium, and epicardium) in the aneurysm wall with no evidence of pericardial reaction in
all cases. Particularly in these patients, we observed
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Figure 4. top: 12-lead ECG of patient 9 showing sustained VT
with right bundle branch block configuration. middle: endsystolic left ventriculographic frame from patient 9 showing a
double posterobasal aneurysm. bottom: LV endomyocardial biopsy specimen taken from the area nearby the aneurysm represented in Figure 3, middle. An active lymphocytic myocarditis
with cell necrosis and inflammatory infiltration (arrows) of an
arteriole (A) is shown (hematoxylin-eosin, original ⫻ 250).
the disappearance of the ventricular arrhythmias
after the withdrawal of the immunosuppressive and
antiarrhythmic drugs.
Discussion
Figure 3. LV endomyocardial biopsy specimen from the area
surrounding the aneurysm of Figure 2 at presentation (top;
hematoxylin-eosin) and after 5 months of follow-up (bottom;
Masson trichrome). An active lymphocytic myocarditis with
localized intense myocytolysis is followed by replacement fibrosis
(original ⫻ 160).
Small, localized LV aneurysms associated with a
normal global function occurred in 3.3% of our 353
patients with myocardial inflammation and in 7.9%
of those with preserved global contractile function.
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Clinical Investigations
arrhythmias (sustained VT in four patients, nonsustained VT in five patients) or unexplained chest pain
(three patients).
Aneurysm Detection
In our study, aneurysms were not visualized by
2D-ECHO performed by an expert operator, and
they were an unexpected angiographic finding. This
may be because of their small dimensions and the
limited ability of 2D-ECHO to explore all the cardiac borders. Recently, cardiac three-dimensional
echocardiogram and MRI have proved to be more
sensitive than 2D-ECHO in detecting ischemic LV
aneurysms.20 This fact should be taken into consideration when a nonischemic cardiac aneurysm is
suspected because of unexplained chest pain or
malignant ventricular arrhythmias occurring in
young people.
Inflammatory Origin
Figure 5. Top: biplane left ventriculography in right anterior
view (upper) and left anterior view (lower) from patient 12
showing several aneurysms distributed along all (arrows) LV
segments. Bottom: LV endomyocardial biopsy specimen from
patient 12 showing a small coronary artery (A; 250 ␮m wide in
diameter) occluded by an organized thrombus (T) and surrounded by a discrete area of myocardial fibrosis (F).
Serologic studies suggested a viral infection in three
patients and an immunologic disorder in two patients
(presence of anticardiolipin antibodies and antinuclear antibodies), whereas they were negative in the
remaining seven patients with LV aneurysms. Presenting symptoms consisted of severe ventricular
In our study, the inflammatory origin of cardiac
aneurysms has been supported by the morphologic
characteristics of the aneurysms (small size, fairly
localized, sometimes multiple), the usually young age
of patients, the absence of risk factors for ischemic
heart disease, the normal coronary arteriogram, and
the histologic findings indicating a severe lymphocytic myocarditis. A pathologist blinded to the clinical data applying the Dallas criteria on bi-ventricular
endomyocardial biopsy specimens provided the histologic diagnosis. Interestingly, RV biopsy specimen
showed histologic changes diagnostic for a myocarditis process in only 3 of our 12 patients, whereas LV
specimens from all patients suggested that entity. In
addition, among LV biopsy specimens, those taken
from the areas closest to the aneurysm showed the
most severe inflammatory changes. This observation
suggests that a myocarditis may predominantly affect
a single cardiac chamber and inside that, a specific
myocardial segment. The reason for such an occurrence is actually obscure, although an inflammatory
involvement of arterial vessels supplying localized
areas of myocardium is likely to occur. In our study,
abnormalities of intramyocardial vessels associated
with a myocarditis were documented in two patients
(9 and 12) from biopsy samples taken from areas
close to the LV aneurysms. The outstanding observation resulting from our study is that the definition
of “idiopathic LV aneurysm” may not be reliably
supported by an RV endomyocardial biopsy alone
but requires a LV or biventricular biopsy. Indeed, a
previous study,21 comparing RV biopsy specimens
(up to eight per patient) with the histologic examination of 14 autopsied or explanted hearts, recognized a low sensitivity to RV biopsy for the diagnosis
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of myocarditis. Better results have been obtained by
us using a biventricular bioptic approach.22
Prognostic Significance
The intermediate-term (mean follow-up, 53
months) observation of our patients failed to document major adverse events. In fact, no deaths,
systemic thromboembolic phenomena, aneurysm
ruptures, or cardiac arrests were registered. Ventricular arrhythmias were controlled by antiarrhythmic
drugs, and no need for an implantable cardioverter
defibrillator emerged during the study. Furthermore, at a control ventriculography, LV aneurysms
were no longer documented because of thrombus
occlusion in 2 (patients 1 and 3) of our 12 patients
early in the follow-up, having been documented in
the first 5 months of observation. As far as patients
with LV aneurysms and chest pain are concerned,
they showed some benefits from the administration
of ␤-blocking agents and sedatives, and mostly from
the reassurance that there was no coronary artery
disease and no present risk for a heart attack.
Patients treated with steroids and immunosuppressive drugs because of an active myocarditis (in one
patient associated with vasculitis) had a positive
histologic evolution to a healed myocarditis. However, spontaneous resolution of the inflammatory
process cannot be excluded, as it has been reported
in up to 53% of cases.23
Clinical Implications
In conclusion, LV aneurysms with normal global
function caused by myocarditis seem to represent an
uncommon benign entity with a good prognosis even
at intermediate-term follow-up. Major therapeutic
regimens such as aneurysmectomy or implantable
electrical devices are usually unnecessary.
References
1 Abrams DL, Ederlist A, Luria MH, et al. Ventricular aneurysm: a reappraisal based on a study of 65 consecutive
autopsied cases. Circulation 1963; 27:164 –168
2 Chesler E, Mitha AS, Edwards JE. Congenital aneurysms
adjacent to the anuli of the aortic and/or mitral valves. Chest
1982; 82:334 –337
3 Grieco JG, Montoya A, Sullivan HJ, et al. Ventricular aneurysm due to blunt chest injury. Ann Thorac Cardiovasc Surg
1989; 47:322–329
4 Kissane RN. Traumatic heart disease: nonpenetrating injuries. Circulation 1952; 6:421– 435
5 Frustaci A, Gentiloni N, Caldarulo M. Acute myocarditis and
left ventricular aneurysm as presentations of systemic lupus
erythematosus. Chest 1996; 109:282–284
6 Jain A, Starek PJ, Delany DL. Ventricular tachycardia and
ventricular aneurysm due to unrecognized sarcoidosis. Clin
Cardiol 1990; 13:738 –740
7 Hirakawa Y, Koyanagi S, Matsumoto T, et al. Familial dilated
cardiomyopathy complicated by left ventricular aneurysm.
Jpn Heart J 1990; 31:245–249
8 Nishikawa H, Ono N, Unno M, et al. Two cases of biventricular dysplasia associated with ventricular tachycardia
and familial occurrence of sudden death. J Cardiol 1991;
21:735–747
9 Partanen J, Kupari M, Heikkila J, et al. Left ventricular
aneurysm associated with apical hypertrophic cardiomyopathy. Clin Cardiol 1991; 14:936 –939
10 Mestroni L, Morgera T, Miani D, et al. Idiopathic left
ventricular aneurysm: a clinical and pathological study of a
new entity in the spectrum of cardiomyopathies. Postgrad
Med J 1994; 70(suppl):S13–S20
11 Oliveira JSM, Oliveira JAM, Frederique V, et al. Apical
aneurysms of Chagas’ heart disease. Br Heart J 1981; 46:432–
437
12 Pinamonti B, Alberti E, Cigalotto A, et al. Echocardiographic
findings in myocarditis. Am J Cardiol 1988; 62:285–291
13 Goudevenous J, Parry G, Gold RG. Coxsackie B4 viral
myocarditis causing ventricular aneurysm. Int J Cardiol 1990;
27:122–124
14 Frustaci A, Maseri A. Localized left ventricular aneurysm
with normal global function caused by myocarditis. Am J
Cardiol 1992; 70:1221–1224
15 Li YH, Lai LP, Liau CS, et al. Acute myocardial infarction
and left ventricular aneurysm in a patient with normal
coronary arteries. Cardiology 1993; 83:280 –284
16 Fisher DZ, Di Salvo TG, Dec GW, et al. Transient left
ventricular aneurysm in a patient with hypertrophic cardiomyopathy and myocarditis. Clin Cardiol 1993; 16:253–256
17 Visser CA, Kon G, David GK, et al. Echocardiographiccineangiographic correlation in detecting left ventricular aneurysm: a prospective study of 422 patients. Am J Cardiol
1982; 50:337–340
18 Hackett D, Larkin S, Chierchia S, et al. Induction of coronary
artery spasm by a direct local action of ergonovine. Circulation 1987; 75:577–582
19 Aretz H, Billingham ME, Edwards WD, et al. Myocarditis: a
histopathologic definition and classification. Am J Cardiovasc
Pathol 1986; 1:3–14
20 Buck T, Hunold P, Wentz KU, et al. Tomographic threedimensional echocardiographic determination of chamber
size and systolic function in patients with left ventricular
aneurysm. Circulation 1997; 96:4286 – 4297
21 Chow LH, Radio SJ, Sears TD, et al. Insensitivity of right
ventricular endomyocardial biopsy in the diagnosis of myocarditis. J Am Coll Cardiol 1989; 14:915–920
22 Frustaci A, Bellocci F, Olsen EGJ. Results of biventricular
endomyocardial biopsy in survivors of cardiac arrest with
apparently normal hearts. Am J Cardiol 1994; 74:890 – 895
23 Mason JW, O’Connel JB, Herskowitz A, et al. A clinical trial
of immunosuppressive therapy for myocarditis. N Engl J Med
1995; 333:269 –275
1702
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Clinical Investigations