Download Idiopathic left ventricular aneurysm and sudden cardiac

Europace (2006) 8, 607–612
doi:10.1093/europace/eul074
SHORT SERIES REPORT
Idiopathic left ventricular aneurysm and sudden
cardiac death in young adults
Matthias Paul1*, Michael Schäfers2, Matthias Grude1, Florian Reinke1, Kai Uwe Juergens3,
Roman Fischbach3, Otmar Schober2, Günter Breithardt1, and Thomas Wichter1
1
Department of Cardiology and Angiology, University Hospital of Münster, Albert-Schweitzer-Str. 33, D-48149 Münster,
Germany; 2 Department of Nuclear Medicine, University Hospital of Münster, Germany; and 3 Department of Clinical
Radiology, University Hospital of Münster, Germany
Received 12 December 2005; accepted after revision 18 April 2006
KEYWORDS
Aims We report three young patients presenting with life-threatening ventricular tachycardia (VT) or
ventricular fibrillation (VF) and/or survived sudden cardiac arrest, who were admitted to our institution
for further diagnostic evaluation.
Methods and results In all patients, idiopathic left ventricular (LV) aneurysms were identified after a
detailed non-invasive and invasive evaluation. Sustained VT/VF was inducible during programmed ventricular stimulation in two of the three patients. Left ventricular aneurysms were depicted and characterized by various imaging modalities (echocardiography, magnetic resonance imaging, LV angiography).
To elucidate the pathogenesis further, both myocardial viability and regional sympathetic innervation
were assessed by radionuclide imaging techniques. Defects of innervation and metabolism were documented in the area of the aneurysm but distal to the aneurysm there were no signs of downstream
denervation.
Conclusion Life-threatening arrhythmias may be the first manifestation of an idiopathic LV aneurysm,
which can be reliably diagnosed with modern imaging techniques. Radionuclide imaging may yield
additional information as to the involvement of the autonomic nervous system potentially associated
with arrhythmogenesis. Management strategies in patients with an idiopathic LV aneurysm range from
antiarrhythmic drug treatment, implantation of an automatic cardioverter–defibrillator to surgical
aneurysmectomy.
Introduction
Left ventricular (LV) aneurysms most frequently develop
after myocardial infarction. Other underlying diseases
include, for instance, sarcoidosis, Chagas disease, or myocarditis. Idiopathic LV aneurysms without identifiable underlying cause are rare. However, they may be associated with
life-threatening ventricular tachyarrhythmias1 and cardiac
arrest,2 even as a first manifestation of the disease.
Therefore, they represent an uncommon but important
cause of sudden death in a young population. Idiopathic LV
aneurysms are anatomically distinguished from congenital
diverticula, which are denoted to have only a narrow communication with the ventricle3 and which are partly associated with the Cantrell syndrome.4 So far, little is known
about the pathogenesis of idiopathic LV aneurysms. The
present report summarizes the findings of three young
* Corresponding author. Tel: þ49 251 83 47581; fax: þ49 251 83 47864.
E-mail address: [email protected]
patients with idiopathic LV aneurysms associated with ventricular tachyarrhythmias and reviews the data from the literature. New and interesting pathoanatomical and clinical
findings with potential implications for further investigations in larger patient cohorts are presented and
discussed.
Patient characteristics
Case 1
A 27-year-old female architect presented in 2001 with palpitations and short episodes of paroxysmal tachycardia associated with dizziness first starting in 1993. During such an
attack, ventricular tachycardia (VT) with right bundle
branch block morphology (cycle length 333 ms) was documented by 12-lead ECG and terminated by intravenous
ajmaline. Initially, the patient refused further diagnostic
evaluation and treatment. Treatment with beta-blockers
(metoprolol) at a low dose (25 mg daily) was initiated but
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Left ventricle;
Aneurysm;
Sudden death;
Cardiomyopathy;
Sympathetic nervous system
608
Case 2
A 24-year-old female student and competitive track and
field athlete was referred and admitted to our hospital
after an episode of aborted sudden cardiac arrest. While
climbing a staircase, she collapsed with cardiac arrest
without a prodrome. The emergency physician recorded
Figure 1 Magnetic resonance imaging of an LV aneurysm. Diastolic
(A) and systolic (B) imaging of the LV in a vertical long-axis view with
detection of an aneurysm of the inferior LV wall. Delayed enhancement images of the LV (15 min after application of 2 mL/kg gadolinium) (C) in a mid-ventricular short-axis view showed increased
signal intensity inferior and inferior-septal.
Figure 2 Left ventricular aneurysm during cardiac catheterization. The aneurysm (indicated by arrows) is depicted in the lateral
LV wall in a right anterior oblique projection (RAO 308).
ventricular fibrillation restored sinus rhythm and systemic
circulation by defibrillation (3 200 J). In the preceding
4 years, the patient had experienced episodes of palpitations
and symptomatic tachycardias (no ECG documentation).
Antiarrhythmic drug treatment with sotalol (240 mg/day)
was initiated but discontinued 2 months later because of
symptomatic bradycardia. The patient remained asymptomatic until the episode of resuscitated cardiac arrest.
The medical history was unremarkable for infectious or
inherited diseases, allergies, as well as of surgical procedures. Physical examination, bicycle exercise test, and
laboratory tests showed normal findings. Twelve-lead
surface ECG revealed no signs of a long or short QT syndrome, arrhythmogenic right ventricular cardiomyopathy,
or Brugada syndrome. Provocation with intravenous ajmaline exhibited no signs of Brugada syndrome. The patient
had no cardiovascular risk factors: There was no history of
unexplained syncope and no family history of premature
sudden death or ventricular tachyarrhythmias.
Transthoracic echocardiography revealed a circumscript
area with dyskinesia and thinning of the lateral LV wall. No
other abnormalities of RV or LV structure, wall motion, or
valvular function were detected.
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was only sporadically taken by the patient due to side
effects of hypotension and fatigue.
The family history was unremarkable with respect to
cardiac arrest, unexplained syncope, ventricular tachyarrhythmias, or cardiomyopathy. The patient reported moderate physical activity with workout in a gym once weekly.
Physical examination, 12-lead surface ECG, bicycle exercise
test, laboratory tests, and intravenous ajmaline provocation
to unmask a potential Brugada syndrome showed normal
findings.
Transthoracic echocardiography revealed an aneurysm
of the infero-lateral LV wall. No other structural, wall
motion, or valvular abnormalities were detected.
Magnetic resonance imaging (MRI) (Philips Gyroscan
Intera, 1.5 T) clearly depicted the aneurysm as an area of
circumscript wall thinning showing regional dyskinesia
(balanced FFE; short-axis and LV two-chamber views). A
region of hyperintensity (‘delayed enhancement’) indicating
myocardial fibrosis or scar was identified at the location of
the aneurysm in images (inversion recovery T1-weighted
3D turbo-field-echo pulse sequence) acquired 15 min after
intravenous administration of gadolinium–DTPA (0.2 mmol/
kg) (Figure 1).
Cardiac catheterization with LV angiography also demonstrated the aneurysm with dyskinesia and prolonged dye
persistence in the infero-lateral LV (Figure 2). No abnormalities of valves, right ventricle (RV), coronary arteries, or
haemodynamics were observed.
Right ventricle endomyocardial biopsy samples from the
outflow tract, mid-septal, and apical area of the RV revealed
no signs of myocarditis, sarcoidosis, arrhythmogenic right
ventricular cardiomyopathy, or storage disease.
Programmed ventricular stimulation in the RV outflow
tract (370/210/170 ms basic drive cycle and two extrastimuli) reproducibly induced haemodynamically nontolerated polymorphic ventricular tachyarrhythmias that
were terminated by external defibrillation (Figure 3).
Radionuclide imaging was performed to characterize
further the LV aneurysm. 18F-FDG-PET (2-[fluorine-18]fluoro-2deoxy-D -glucose single photon emission tomography)5
demonstrated a transmural defect of myocardial glucose
uptake matching with the aneurysm as detected by MRI and
LV angiography. 123I-MIBG-SPECT scintigraphy was performed
to assess the presynaptic cardiac noradrenaline reuptake
(innervation) according to a protocol published earlier.6 The
test showed a regional defect in tracer uptake concordant
with the location and extent of the LV aneurysm as demonstrated by the other imaging techniques (Figure 4).
Because of the documented spontaneous VT, the inducible
fast polymorphic VT, and the presence of a structural LV
abnormality, the implantation of an automatic cardioverter–
defibrillator (ICD) was strongly recommended but refused by
the patient. During a follow-up of 37 months, the patient
experienced one further episode of self-limiting tachycardia
(no ECG registration) 24 days after discharge.
M. Paul et al.
Idiopathic LV aneurysm and SCD
609
Figure 4 Case 1. 123I-MIBG-SPECT and 18F-FDG-PET images in a
patient with an LV aneurysm. 18F-FDG-PET depicts a transmural
defect of myocardial glucose metabolism in the infero-apical area
matching with the location and extent of the LV aneurysm.
123
I-MIBG-SPECT demonstrates a reduction in tracer uptake in this
region, indicating regional sympathetic denervation. HLA, horizontal long-axis; VLA, vertical long-axis; SA, short-axis.
Magnetic resonance imaging depicted a circumscript
lateral LV aneurysm with local myocardial thinning and corresponding dyskinesia. Increased signal intensity was
observed in the contrast-enhanced delayed images (late
enhancement).
Cardiac catheterization with LV angiography confirmed
the aneurysm of the LV postero-lateral wall with prolonged
dye persistence. During right heart catheterization, a fast
sustained polymorphic VT was mechanically induced and
successfully converted into sinus rhythm with a single
200 J defibrillation shock. No other pathological findings
were documented. The RV was normal in size, shape, and
function. Coronary arteries as well as right and left ventricular and atrial chamber pressures and resting cardiac
output were normal.
Endomyocardial biopsies taken from the RV apex, outflow
tract, and mid-septal region showed no signs of myocarditis,
sarcoid disease, arrhythmogenic right ventricular cardiomyopathy, or storage disease. Biopsies obtained from the
site of the LV aneurysm disclosed fibrotic and scar tissue
(Figure 5) with compensatory hypertrophy of cardiomyocytes located on the borders. No signs of inflammation or
fibrofatty replacement were observed.
Programmed ventricular stimulation reproducibly induced
a fast polymorphic VT (cycle length 150–190 ms) with one
extrastimulus during sinus rhythm (coupling interval
280 ms). The arrhythmia terminated spontaneously after
18 s or was terminated by a 200 J defibrillation shock.
18
F-FDG-PET measuring myocardial glucose uptake
detected a transmural defect located in the mid-lateral LV,
matching with the location and extent of the aneurysm as
depicted in MRI and LV angiography.
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Figure 3 Case 1. Programmed ventricular stimulation. A polymorphic ventricular tachycardia is induced in the right ventricular outflow tract
at a basic drive cycle of 370 ms and two extrastimuli (coupling interval 210/170 ms).
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M. Paul et al.
and empiric treatment with amiodarone was advised. During
a follow-up of more than 39 months, no episodes of syncope
or other serious cardiac events occurred. The patient complains of sporadic palpitations, which were documented on
Holter-ECG as ventricular couplets (no non-sustained or sustained VT). The medication with amiodarone was discontinued due to side effects and changed to an oral beta-blocker
(bisoprolol).
Figure 5 Case 2. Histopathology of endomyocardial biopsies from
the site of idiopathic LV aneurysm. Myocardial fibrosis (scarring)
without signs of inflammation or active myocytolysis is demonstrated 200-fold magnification with Haematoxylin–Eosin staining
(A) and 400-fold magnification with van-Gieson staining (B).
123
Case 3
A 31-year-old male student was operated for a right-sided
chromophobic grade II renal carcinoma in June 2001. Postoperatively, ventricular premature beats with left bundle
branch block morphology were documented on a routine
12-lead surface ECG. A Holter-recording revealed multiple
asymptomatic ventricular couplets and triplets that triggered further cardiovascular workup. The family history
was unremarkable with regard to premature death, unexplained syncope, or ventricular tachyarrhythmias. He had
no history of palpitations or arrhythmic events and no cardiovascular risk factors or allergies. Physical examination,
12-lead surface ECG, bicycle exercise test, and laboratory
tests showed normal findings.
LV angiography confirmed an infero-basal aneurysm with
polycyclic-bordered prolonged dye persistence, which had
also been detected on transthoracic echocardiography and
MRI. No other abnormalities were observed during right ventricular angiography, coronary angiography, and haemodynamic assessment, respectively.
Programmed ventricular stimulation reproducibly induced
polymorphic, fast (cycle length 160–230 ms) non-sustained
VT with three extrastimuli.
18
F-FDG-PET demonstrated a transmural defect of myocardial glucose metabolism in the area of the LV aneurysm.
123
I-MIBG-SPECT showed a concordant defect of presynaptic
innervation confined to the aneurysmatic region but without
‘distal denervation’.
As no spontaneous or inducible sustained ventricular
tachyarrhythmias were present, the implantation of an ICD
on the basis of primary or secondary prevention of sudden
cardiac death was not recommended. However, prophylactic
Three young patients with idiopathic LV aneurysms and lifethreatening ventricular tachyarrhythmias underwent
detailed evaluation by imaging techniques (echo, MRI).
Additional radionuclide tests showed a transmural defect
of myocardial glucose metabolism with concordant defects
in MIBG uptake limited to the aneurysmal segment but
without distal denervation.
Pathogenesis of LV aneurysm
LV aneurysms are usually classified as congenital or acquired,
i.e. arising from a cardiac or non-cardiac disorder (Figure 6).
Acquired LV aneurysms mainly result from myocardial
infarction7 or coronary artery malformations (i.e. fistula).8
However, they may also be present in arrhythmogenic right
ventricular cardiomyopathy,9 hypertrophic cardiomyopathy,10 or myocarditis11 (Figure 6). Non-cardiac or systemic
diseases include sarcoidosis,12 Chagas’ disease,13 lupus
erythematosus,14 Behçet’s disease,15 tuberculosis,16 or
HIV.17 As a rare complication, LV aneurysms were also
observed in glycogen storage diseases18 and in the hyperimmunoglobulin E syndrome.19 Furthermore, blunt chest
trauma may lead to the development of an LV aneurysm.20
Congenital LV aneurysms, comprising the perinatal period,
have been detected as early as the second trimester of
gestation21 and were associated with severe co-morbidity
(hydrops fetalis,22 ventricular arrhythmias,23 heart
failure3) and intra-uterine fetal death.
To investigate further the underlying pathophysiology of
arrhythmogenic LV aneurysms in the reported three cases,
we assessed myocardial morpholology, function, metabolism, and sympathetic innervation by means of MRI, echo,
angiography, and radionuclide imaging. Consistent defects
of myocardial glucose metabolism and presynaptic adrenergic sympathetic innervation were displayed in the area of
the LV aneurysm. However, the area of denervation did not
exceed that of the LV aneurysm, as is usually the case in
post-myocardial infarction scarring (distal denervation).24
LV aneurysm and malignant tachyarrhythmias
In the present report as well as in previous studies,3,25 the
tissue of the LV aneurysm was found to be inhomogeneous
with viable, normal myocytes, fibrotic tissue, and/or hypertrophic myocytes. As in non-transmural myocardial infarction, this may well represent an arrhythmogenic substrate
due to local conduction delay and dispersion of excitability
and refractoriness which may even be augmented by catecholamines during physical exercise and/or mental
stress.26,27 These factors may increase the propensity to
potentially lethal arrhythmias in idiopathic LV aneurysms.
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I-MIBG-SPECT detected defects of early (15 min post
injection) and late (4 h post injection) 123I-MIBG-uptake in
the aneurysmal segment. Again, as in Case 1, sympathetic
dysinnervation was confined to the area of aneurysm and
did not exceed it.
Because of aborted cardiac arrest, inducible polymorphic
VT, and documented structural heart disease, the implantation of an ICD was recommended and performed without
complications. The patient was discharged on concomitant
treatment with metoprolol (95 mg/day) to prevent frequent
relapses of VT and inappropriate ICD shocks. During
follow-up of 40 months with regular interrogations of the
ICD at 3-month intervals, no episodes of ventricular tachyarrhythmias occurred.
Discussion
Idiopathic LV aneurysm and SCD
611
Figure 6 Pathogenesis of LV aneurysms. Systematic overview and differential diagnosis.
Sympathetic denervation in LV aneurysm
This report describes for the first time a match between
myocardial adrenergic innervation and metabolism in
patients with idiopathic LV aneurysms. Regional sympathetic
innervation itself can be influenced by factors such as
ischaemia or local tissue destruction (e.g. infection, systemic metabolic disorders). It is generally accepted that a
local sympathetic nerve destruction results in a distal denervation of non-affected myocardium because the sympathetic nerves travel epicardially from the base to the apex
of the heart, parallel to the coronary arteries. Therefore,
a ‘downstream sympathetic denervation’ was described
after myocardial ischaemia24 as well as following epicardial
application of phenol to proximal parts of the myocardium in
experimental animal studies.34 A subsequent imbalance of
denervated but viable myocardium results in dispersion of
refractoriness and increased sensitivity toward catecholamines (‘supersensitivity’), thus providing a substrate for
the high propensity of malignant ventricular tachyarrhythmias. However, such a ‘downstream sympathetic denervation’ was not present in the investigated patients, because
the defect in 123I-MIBG-SPECT consistently matched the
tissue defect displayed by the 18F-FDG PET scintigraphy
and MRI. It is therefore hypothesized that these aneurysms
may have occurred early in the evolution of the heart
where nerve travel still has the chance to circumvent the
structural defect or where re-innervation has already
occurred.
The young age of the patients studied with no history of
angina, no clinical event indicative of myocardial infarction,
and normal coronary arteries and flow strongly argues
against myocardial infarction as the underlying cause for
the development of the described LV aneurysms, which
cannot, however, be completely excluded.
It remains unclear why a congenital origin of the LV aneurysms should lead to ventricular tachyarrhythmias as late as
in adolescence. However, this is in line with previous
reports of non-acquired LV aneurysms,25,31,33,35,36 and has
also been observed in other arrhythmogenic diseases with
a congenital or genetic background (e.g. arrhythmogenic
right ventricular cardiomyopathy, idiopathic VT, Brugada
syndrome, hypertrophic cardiomyopathy, and others).
Study limitations
Although this report included only a small number of
patients with a rare cardiac disease, the patients are well
characterized and underwent detailed diagnostic evaluation
to assess the morphological, functional, and pathophysiological characteristic features of this rare disorder.
Conclusions
Patients with an idiopathic LV aneurysm are at potential risk
for life-threatening ventricular tachyarrhythmias and
sudden death, which may sometimes occur as the first
clinical presentation.
Transthoracic echocardiography, MRI, and cardiac catheterization can reliably detect the location, extent, and
morphology of the aneurysm. Modern contrast-enhanced MR
imaging provides additional information on myocardial tissue
characteristics, perfusion, and viability. Radionuclide
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Treatment options and treatment dilemma
Patients with LV aneurysms may present with a variety of
symptoms, encompassing ventricular tachyarrhythmias and
sudden cardiac death, angina pectoris,28 congestive heart
failure,3 or recurrent arterial emboli.29,30 Treatment and
prognosis of idiopathic LV aneurysms are dependent on
their size, location, and degree of valvular involvement,
functional class of congestive heart failure, and the presence of ventricular tachyarrhythmias. Therapeutic options
therefore range from antiarrhythmic drug treatment31 to
VT ablation,32 implantation of an ICD,25 or (less frequently)
aneurysmectomy.33
However, prospective
long-term
follow-up studies comparing the different management
strategies are not available.
612
imaging with analysis of viability (18F-FDG-PET) and sympathetic innervation (123I-MIBG-SPECT) can help to elucidate
further the pathogenesis of idiopathic LV aneurysms.
Management strategies should be individualized and are
mainly directed toward prevention of sudden death and
recurrent life-threatening arrhythmias by antiarrhythmic
drug therapy,31 VT ablation,32 ICD implantation, or (less frequently) aneurysmectomy.33 In addition, treatment of heart
failure may be required in selected cases.
Acknowledgement
This work was supported in part by grants from the Deutsche
Forschungsgemeinschaft (DFG), Bonn, Germany, Sonderforschungsbereich 556 (Projects C4 and C1). The authors thank Mrs Petra
Gerdes (RN), Mrs Silke Schroer, and Mrs Christine Bätza (technicians)
for their excellent technical assistance. There are no competing
interests concerning this manuscript. This study was conducted
with the approval of the Ethics Committee of the Chamber of
Physicians Westfalen-Lippe and the Medical Faculty of the
Westfalian Wilhelms-University Muenster, Germany, after informed
consent was obtained from the patients.
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