ECG findings in comparison to cardiovascular MR imaging in viral myocarditis.

Abstract

OBJECTIVES: We sought (1) to assess prevalence and type of ECG abnormalities in patients with biopsy proven myocarditis and signs of myocardial damage indicated by LGE, and (2) to evaluate whether ECG abnormalities are related to the pattern of myocardial damage. BACKGROUND: Prevalence and type of ECG abnormalities in patients presenting biopsy proven myocarditis, as well as any relation between ECG abnormalities and the in vivo pattern of myocardial damage are unknown. METHODS: Eighty-four consecutive patients fulfilled the following criteria: (1) newly diagnosed biopsy proven viral myocarditis, and (2) non-ischemic LGE, and (3) standard 12-lead-ECG upon admission. RESULTS: Sixty-five patients with biopsy proven myocarditis had abnormal ECGs upon admission (77%). In this group, ST-abnormalities were detected most frequently (69%), followed by bundle-branch-block in 26%, and Q-waves in 8%. Atrial fibrillation was present in 6%, and AV-Block in two patients. In patients with septal LGE ST-abnormalities were more frequently located in anterolateral leads compared to patients with lateral LGE, in whom ST-abnormalities were most frequently observed in inferolateral leads. Bundle-branch-block occurred more often in patients with septal LGE (11/17). Four of five patients with Q-waves had severe and almost transmural LGE in the lateral wall. CONCLUSION: ECG abnormalities can be found in most patients with biopsy proven viral myocarditis at initial presentation. However, similar to suspected acute myocardial infarction, a normal ECG does not rule out myocarditis. ECG findings are related to the amount and area of damage as indicated by LGE, which confirms the important clinical role of ECG.

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ECG findings in comparison to cardiovascular MR imaging in viral myocarditis
Claudia C. Deluigia, Peter Onga, Stephan Hilla, Anja Wagnerb, Eva Kisperta, Karin Klingelc,
Reinhard Kandolfc, Udo Sechtema, Heiko Mahrholdta,⁎
aDivision of Cardiology, Robert-Bosch-Hospital, Stuttgart, Germany
bDepartment of Cardiology, Hahnemann University Hospital, Drexel University College of Medicine, Philadelphia, USA
cDepartment of Molecular Pathology, University of Tuebingen, Germany
a b s t r a c ta r t i c l ei n f o
Article history:
Received 12 April 2011
Received in revised form 12 July 2011
Accepted 27 July 2011
Available online xxxx
Keywords:
Electrocardiography
Cardiovascular MR imaging
Myocarditis
Biopsy
Objectives: We sought (1) to assess prevalence and type of ECG abnormalities in patients with biopsy proven
myocarditis and signs of myocardial damage indicated by LGE, and (2) to evaluate whether ECG abnormalities
are related to the pattern of myocardial damage.
Background: Prevalence and type of ECG abnormalities in patients presenting biopsy proven myocarditis, as
well as any relation between ECG abnormalities and the in vivo pattern of myocardial damage are unknown.
Methods: Eighty-four consecutive patients fulfilled the following criteria: (1) newly diagnosed biopsy proven
viral myocarditis, and (2) non-ischemic LGE, and (3) standard 12-lead-ECG upon admission.
Results: Sixty-five patients with biopsy proven myocarditis had abnormal ECGs upon admission (77%). In this
group, ST-abnormalities were detected most frequently (69%), followed by bundle-branch-block in 26%, and
Q-waves in 8%. Atrial fibrillation was present in 6%, and AV-Block in two patients. In patients with septal LGE
ST-abnormalities were more frequently located in anterolateral leads compared to patients with lateral LGE,
in whom ST-abnormalities were most frequently observed in inferolateral leads. Bundle-branch-block
occurred more often in patients with septal LGE (11/17). Four of five patients with Q-waves had severe and
almost transmural LGE in the lateral wall.
Conclusion: ECG abnormalities can be found in most patients with biopsy proven viral myocarditis at initial
presentation. However, similar to suspected acute myocardial infarction, a normal ECG does not rule out
myocarditis. ECG findings are related to the amount and area of damage as indicated by LGE, which confirms
the important clinical role of ECG.
© 2011 Elsevier Ireland Ltd. All rights reserved.
1. Introduction
Viral myocarditisis a commoncardiac diseasethat may progressto
chronic dilated cardiomyopathy, and is a major cause of sudden death.
For the clinical work-up of patients suspected to have myocarditis a
12-lead ECG is one of the most widely employed techniques.
However, most data on ECG abnormalities in myocarditis are either
based on post mortem comparison of ECG and necropsy findings [1],
are limited to small patient populations [2,3], or were never verified
against any gold standard for the diagnosis of myocarditis such as
endomyocardial biopsy. Thus, the prevalence and type of ECG
abnormalities in living patients presenting with new onset of biopsy
proven myocarditis, as well as any relation between ECG abnormal-
ities and the in vivo pattern of myocardial damage are unknown.
Recently, cardiovascular MR imaging has emerged as a new non-
invasive modality for the diagnosis of myocarditis. This technique is
capable of identifying myocardial regions with maximum inflamma-
tory involvement in vivo [4,5], providing information on myocardial
damage that previously could only be obtained in the dissecting room
[6–8].
Consequently, our aim was (1) to assess the prevalenceand type of
ECG abnormalities in patients with biopsy proven myocarditis and
signs of myocardial damage indicated by CMR, and (2) to evaluate
whether ECG abnormalities are related to the pattern of myocardial
damage demonstrated by LGE.
2. Methods
2.1. Patient population
We initially identified 215 consecutive patients clinically suspected to have acute
myocarditis based on a variable combination of chest-discomfort, dyspnea, altered
electrocardiogram, in conjunction with a history compatible with inflammatory disease
suchas cough,diarrhea, fever, ormalaise.Patients wereexcludedifthey had concomitant
International Journal of Cardiology xxx (2011) xxx–xxx
Abbreviations: CMR, cardiovascular MR imaging; ECG, electrocardiography; EMB,
endomyocardial biopsy; GRE, gradient echo CMR; HHV6, human herpes virus 6; IQR,
interquartile range; LGE, late gadolinium enhancement; PVB19, parvovirus B19; SD,
standard deviation.
⁎ Corresponding author at: Robert-Bosch Medical Center, Auerbachstrasse 110,
70376 Stuttgart, Germany. Tel.: +49 711 8101 3456; fax: +49 711 8101 3795.
E-mail address: Heiko.Mahrholdt@rbk.de (H. Mahrholdt).
IJCA-13794; No of Pages 7
0167-5273/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijcard.2011.07.090
Contents lists available at ScienceDirect
International Journal of Cardiology
journal homepage: www.elsevier.com/locate/ijcard
Please cite this article as: Deluigi CC, et al, ECG findings in comparison to cardiovascular MR imaging in viral myocarditis, Int J Cardiol
(2011), doi:10.1016/j.ijcard.2011.07.090

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coronary artery disease (stenosisN50%) (n=21); coronary spasm defined by catheter-
ization (n=13), or had refused to undergo catheterization (n=6). Eighty-four of the
remaining175patientsfulfilledthefollowingcriteria:(1)biopsyprovenviralmyocarditis,
and (2) late gadolinium enhancement typical for non-ischemic heart disease [9], either
focused in the septal or lateral regions of the left ventricle, and (3) standard 12-lead ECG
upon admission. All patients gave written informed consent and were included in our
study. Some of the patients (43/84) were also included in a previous study [8].
2.2. ECG recording and analysis
Standard 12-lead ECGs were recorded at 25 mm/s speed and 10 mm/mV upon
admission. The ECG recordings were reviewed by two independent investigators
blinded to clinical and CMR data. In cases of discrepancy, a third investigator made the
final decision.
ECGs were evaluated for atrial fibrillation, AV-Block, bundle-branch-block, Q-
waves and ST-abnormalities. Q-waves were defined according to the Minnesota Code
[10]. The presence of RS in V1, R in V1>40 ms, and QR or low voltage (Rb5 mm) were
considered as Q wave equivalent. ST-abnormalities were defined as significant ST-
segment elevation and/or significant ST-segment depression and/or T-wave inversion
[11]. ST elevation or depression, respectively, exceeding 1 mm measured 60 ms after
the J point was considered significant.
2.3. CMR protocol
ECG gated CMR imaging was performed in breath-hold using a 1.5 T Magnetom
Sonata (Siemens-Medical-Systems, Germany) within the first 48 h after initial
presentation. Both cine and LGE short axis CMR images were prescribed every
10 mm (slice thickness 6 mm) from base to apex. In-plane resolution was typically
1.2×1.8 mm. Cine CMR was performed using a steady-state-free precession-sequence.
LGE images were acquired on average 5–10 min after contrast administration using a
segmented IR-GRE technique [12] constantly adjusting inversion time as previously
described [5]. The contrast dose (Omniscan™ [gadodiamide], Amersham-Health,
Germany) was 0.15 mmol/kg. In addition, fat-saturated and T2-weighted images
were obtained to allow differentiation between subepicardial LGE, epicardial fat and
pericardial effusion.
2.4. CMR analysis
Contrast images were evaluated separately by two blinded observers as described
elsewhere [5] using an image intensity level ≥2 SD above the mean of remote
myocardium to define LGE.
Regional parameters were assessed dividing each short-axis into twelve circum-
ferential segments. For each segment the extent of LGE was analyzed using the NIH-
Image analysis software package (National Institute of Health, Maryland), and the
results were expressed as a percentage of the area of the outer, middle, and inner third
of each segment.
As we only included patients with LGE either focused in the septal or lateral regions
of the left ventricle, all patients could be assigned to two groups with the main focus of
LGE in the septum or the lateral wall for comparison to ECG results, respectively.
2.5. Myocardial biopsy protocol and histopathological analysis
At least five endomyocardial biopsies were taken from the region showing LGE and
myocarditis was defined as myocardial inflammation on histology/immunohistology
and presence of viral genome on polymerase chain reaction as described previously [8].
EMBs were stained with Masson's trichrome as well as Giemsa stain and examined by
light microscopy. For immunohistology, tissue sections were treated with an avidin-
biotin immunoperoxidase method (Vectastain Elite ABC Kit, Vector, Burlingame, CA),
applying the following monoclonal antibodies: CD3 (T cells; Novocastra Laboratories,
Newcastle, UK), CD68 (macrophages; DAKO, Hamburg, Germany), and HLA-DR (DAKO,
Hamburg, Germany) as described [13,14]. The detection of N14 infiltrating leukocy-
tes/mm2(CD3+ T lymphocytes and/or CD68+ macrophages) in the presence of
myocyte damage and/or fibrosis in addition to enhanced HLA class II expression in
professional antigen-presenting immune cells and endothelium was used for the
diagnosis of myocarditis [8,15].
2.6. Detection of viral genomes
DNA and RNA were extracted with the use of proteinase-K digestion followed by
extraction with phenol/chloroform. Nested polymerase chain reaction/reverse tran-
scriptase–polymerase chain reaction was performed for the detection of enteroviruses
(including coxsackieviruses of group B, various coxsackieviruses of group A and
echoviruses), parvovirus B19 (PVB 19), adenoviruses, human cytomegalovirus,
Epstein–Barr virus, and human herpes virus type 6 (HHV 6). As a control for successful
extraction of DNA and RNA, oligonucleotide sequences were chosen from the
glyceraldehyde-3-phosphate-dehydrogenase gene. Specificity of all viral amplification
products was confirmed by automatic DNA sequencing [5,8].
2.7. Statistical analysis
Data for continuous variables are expressed as mean value and range, whereas data
for categorical variables are expressed as the number, and the percentage of patients.
Comparisons between groups were done using a two-tailed unpaired Student's t-test
for normally distributed, and Mann–Whitney U test for non-normally distributed
continuous variables. For categorical variables we used the Chi-square test, and Fisher's
exact test, where appropriate. The difference between two groups was defined to be
statistically significant if the two-tailed p-value was b0.05.
3. Results
3.1. Patient characteristics
The main reasons to seek medical attention were chest pain
(n=35) or new onset of heart failure (n=31). Seventeen patients
presented due to malaise and/or palpitations, and one patient
presented for work-up of syncope and AV block. Troponin I was
elevated in 49 patients at initial presentation (median 34 μg/l, IQR 9–
88.5 μg/l). The median time between onset of symptoms and the
initial presentation was 8 days (IQR 1–19 days).
Patients with chest pain were most frequently diagnosed with
parvovirus B19 myocarditis (27/35; 77%), followed by herpes virus
type 6 myocarditis (6/35; 17%), and combined PVB19/HHV6 myocar-
ditis (2/35; 6%). Patients presenting with new onset of heart failure
were less frequently diagnosed with PVB19 (15/31; 48%), but more
frequently with combined PVB19/HHV6 myocarditis (9/31; 29%).
HHV6 was found in six of the 31 heart failure patients (17%).
A pericardial effusion was detected by CMR in 43 of the 84 patients
(51%). Additional clinical characteristics can be viewed in Table 1.
3.2. Prevalence and type of ECG abnormalities
Sixty-five of the 84 patients with biopsy proven myocarditis and
signs of myocardial damage by LGE had an abnormal ECG upon
admission (77%), whereas 19 patients presented with a normal ECG to
the emergency room (23%).
In the group of patients with abnormal ECG, ST-abnormalities
were detected most frequently (45/65; 69%, Fig. 1), followed by
Table 1
Patient characteristics.
Lateral LGE Septal LGEp-value
Number of patients
Age (mean)
M/F
Type of virus
PVB 19
HHV 6
HHV+PVB
Main symptom
Chest pain
Heart failure
Other
ECG finding
Normal ECG
A-fib
AV-Block
BBB
ST-elevation
ST-depression
T-inversion
ST-abnormality
Q-wave
LGE (%LV)
PE
44
49
33/11
40
55
29/11
ns
ns
ns
38 (86%)
3 (7%)
3 (7%)
16 (40%)
14 (35%)
10 (25%)
b0.001
0.002
0.032
29 (66%)
5 (11%)
10 (23%)
6 (15%)
26 (65%)
8 (20%)
b0.001
b0.001
ns
12 (27%)
0 (0%)
1 (2%)
6 (14%)
15 (34%)
8 (18%)
21 (47%)
25 (57%)
4 (9%)
5.5 [1–18]
20 (45%)
7 (17%)
4 (10%)
1 (2%)
11 (28%)
5 (13%)
7 (18%)
19 (48%)
20 (50%)
1 (2%)
9.0 [1–22]
23 (57%)
ns
0.05
ns
ns
0.023
ns
ns
ns
ns
0.002
ns
“Age”, mean; M, male; F, female; LGE, late gadolinium enhancement; PVB19, parvovirus
B19; HHV6, human herpes virus 6; A-fib, atrial fibrillation; BBB, bundle branch block;
ST-abnormality, ST-elevation and/or ST-depression and/or T-wave inversion; “LGE
(%LV)”, mean [range]; PE, pericardial effusion.
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Please cite this article as: Deluigi CC, et al, ECG findings in comparison to cardiovascular MR imaging in viral myocarditis, Int J Cardiol
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bundle-branch-block in 17 (26%, Fig. 2), and Q-waves in five of the 65
patients (8%, Fig. 3). Atrial fibrillation was present in four patients
(6%), and AV block (II and III) in one patient each.
ST-abnormalities were most frequently detected either in the
(antero)lateral leads (I,II AVL,V3–V5) or the inferolateral leads (II,III,
AVF,V4–V6) (Fig. 4a). The most frequent ST-abnormality was T-wave
inversion (n=40), followed by ST-segment elevation (n=20), and ST-
segment depression (n=15) (Fig. 4b–d). ST-abnormalities were
associated with a clinical presentation due to severe chest pain, and
were present in 22/35 chest pain patients (63%, p=0.07). Twenty-seven
of those 35 chest pain patients had PVB19 myocarditis by biopsy (77%,
p=0.021). In patients admitted due to heart failure and/or persisting
malaise, ST-abnormalities were only present in 13/31 patients (32%).
Fifteen of the 17 patients presenting with bundle-branch-block
had left bundle-branch-block, whereas only two patients had right
bundle-branch-block. Patients with bundle-branch-block were most
frequentlydiagnosed withcombinedPVB19/HHV6myocarditis(8/17;
47%) followed by PVB19 (6/17; 35%), and HHV6 (3/17, 18%).
Fig. 1. Contrast CMR images (left) and 12 lead ECGs (right) obtained in a 38 year old male patient (upper row) and a 35 year old male patient (bottom row) presenting to our
emergency room with acute onset of infarct like symptoms. Endomyocardial biopsy revealed acute PVB19 myocarditis in both cases. Arrows indicate typical lateral LGE.
Fig. 2. Contrast CMR images (left) and 12 lead ECGs (right) obtained in a 36 year old male patient (upper row) and a 70 year old male patient (bottom row), both admitted due to
new onset of congestive heart failure. Endomyocardial biopsy revealed HHV6 virus myocarditis in the younger and combined HHV6/PVB19 myocarditis in the older patient. Arrows
indicate typical septal LGE. Note the left bundle branch block visible in most leads.
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Interestingly, all five patients with Q-waves were diagnosed with
PVB19 myocarditis by histopathology. Additional information see
Table 1.
When comparing the group with abnormal ECG (n=65) to the
group with normal ECG (n=19), no significant differences in the
clinical presentation could be detected.
3.3. Relation between ECG abnormalities and the pattern of myocardial
damage
In the group of patients with abnormal ECG upon presentation, the
mean amount of myocardial damage indicated by LGE was 6.8% of the
left ventricle, whereas the mean amount of damage in the group of
patients with normal ECG was only 3.8% of the left ventricle
(p=0.002).
According to our study design, we only included patients with LGE
either focused in the septal or lateral regions of the left ventricle to
allow comparison of ECG findings to the area of myocardial damage.
Lateral damage was present in 44 patients, often focused in the
inferolateral epicardial area (Fig. 1). Septal damage was present in 40
patients, mainly located in the midwall area of the interventricular
septum (Fig. 2). The mean amounts of myocardial damage assessed by
LGE for both patterns can be viewed in Table 1.
Despitethetwocompletelydifferentpatternsofmyocardialdamage,
therewasnosignificantdifferenceintheprevalenceofST-abnormalities
between the group of patients with LGE in the lateral, and the septal
partsoftheleftventricle(Table1).However,inpatientswithseptalLGE,
ST-abnormalities were more frequently located in the (antero)lateral
leads (I,II,AVL,V3–V5) compared to the patients with lateral LGE, in
whom ST-abnormalities were most frequently observed in the
inferolateral leads (II,III,AVF,V4–V6) (Fig. 4a).
On a per patient basis, patients with lateral LGE had ST-segment
elevations significantly more often than patients with septal LGE, but
there was no difference in the presence of ST-segment depression or
T-wave inversion between the groups (Table 1). However, when
focusing on abnormal ECG leads instead of patients, ST depression and
T-wave inversion were more frequently found in combination with
septal LGE (Fig. 4b–d).
Fig. 3. Contrast CMR images (left rows) and 12 lead ECG (right row) obtained in a 16 year old male patient admitted due to severe chest pain. Arrows indicate severest, almost
transmural LGE originating from subepicardial in large proportions of the lateral wall causing Q-waves in leads II, III and AVF as well as precordial leads V5–V6 (bottom rows).
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Fig. 4. Prevalence of ST-abnormalities in our 84 patients (=100%, Y-axis) displayed per ECG lead in normal (left row) as well as Cabrera format (right row). Note that
ST-abnormalities were most frequently detected either in the lateral leads (I,II AVL,V3–V5), or the inferolateral leads (II,III,AVF,V4–V6) (panel a). Septal LGE was found more
frequently in combination with ST-segment depression and T-wave inversion than in combination with ST-segment elevation (panels b–d).
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Bundle-branch-block also occurred more frequently in patients
with septal LGE (11/17), but this difference did not reach statistical
significance in the current study (Table 1).
All patients with Q-waves had lateral LGE except one (Table 1). In
thosefour patients Q-waveswere found in inferolateral leads (II,III,AVF,
V5–V6) in addition to ST-abnormalities. In this group LGE was severe,
almost transmural in large proportions of the lateral wall (Fig. 3).
4. Discussion
This study is unique in that the prevalence and type of ECG
abnormalities were evaluated in living patients with biopsy proven
myocarditis and signs of myocardial damage as visualized by LGE. We
found that 77% of patients with biopsy proven viral myocarditis had
an abnormal ECG upon admission, whereas 23% presented with
completely normal ECG. This is of clinical importance, since ECG is one
of the key routine techniques for the clinical work-up of patients
suspected to have myocarditis.
Furthermore, we found that ECG abnormalities in biopsy proven
myocarditis are related to the amount and pattern of myocardial
damage demonstrated by LGE, which may help to understand the
underlying pathophysiology of ECG abnormalities in myocarditis.
4.1. Prevalence and type of ECG abnormalities
In our patient population ST-abnormalities were the most common
findingsintheadmissionECG.Interestingly,mostofthepatientswithST-
abnormalities presented with chest pain that usually was severe and/or
recurring, forcing them to seek medical attention early after onset. Most
of those patients were found to have PVB19 myocarditis (n=27).
This finding is consistent with other reports demonstrating that
PVB19 myocarditis may cause chest pain and even clinically mimic
acute myocardial infarction [8,17–19]. Why should PVB19 myocardi-
tis frequently cause severe chest pain and ST-abnormalities of acute
onset? One possible explanation is based on the fact that PVB19
infects endothelial cells of myocardial vessels, causing endothelial
dysfunction and coronary vasospasm, as well as inducing migration of
inflammatory cells into the myocardial interstitium with subsequent
myocyte damage [20,21]. Thus, this combination of ischemia and
inflammation may explain the chest pain as well as ST-abnormalities
and even infarct like ECGs.
Bundle-branch-block was the second most frequent ECG abnormal-
ity(17/84),whereasAV-Blockwasfoundintwopatientsonly.Thismay
beexplainedbythefactthatAV-Blockinmyocarditisismostlytransient
for some hours or a few days, but bundle-branch-block persists after
occurrence [22]. Thus, since the onset of myocarditis may be insidious,
nonspecific, and difficult to recognize, AV-Block may have disappeared
already in many patients upon admission.
Atrial fibrillation was found in four patients presenting in overt
heart failure and may be explained by atrial dilatation and overload
due to impaired ventricular function.
Although patients with biopsy proven myocarditis usually do not
have normal ECGs (77%), it is not safe to assume that a normal ECG
upon admission rules out myocarditis.
4.2. Relation between ECG abnormalities and the pattern of
myocardial damage
Patients with abnormal ECG had significantly more myocardial
damage as indicated by LGE than patients with normal ECG (6.8% vs.
3.8%, p=0.002), underscoring a general relation between ECG
abnormalities and myocardial damage, as known from ischemic
heart disease [23].
Inaddition,wefoundthatinpatientswithseptalLGEST-abnormalities
where more frequently located in the (antero)lateral leads (I,II,AVL,V4–
V5) compared to the patients with lateral LGE (Fig. 4a), in whom ST-
abnormalities where more frequently observed in the inferolateral leads
(II,III,AVF,V4–V6). Furthermore, when focusing on abnormal ECG leads
instead ofpatients,septalLGEwasfoundmorefrequentlyincombination
with ST-segment depression and T-wave inversion than in combination
with ST-segment elevation [8,16–19] (Fig. 4b–d).
These findings may be explained by the pattern of myocardial
damage [8] as visualized by LGE in our patients (Fig. 5). When
myocardial damage is located mainly in the left inferolateral wall, one
would obviously expect direct or indirect signs of myocardial injury,
such as ST-segment elevations, depressions, or T-wave inversion, to
occur in the inferolateral leads (II,III,AVF,V4–V6) [24], which is in line
with our data (Figs. 4 and 5).
Conversely, if the focus of myocardial damage is located in the
intramuralareaoftheanteriorseptum,onewouldexpectdirectsignsof
myocardial damage, such as ST-segment elevations, to occur in leads
V1–V3 [24], which is also in line with our results (Figs. 4 and 5). These
ST-segment elevations are most likely caused by currents of injury
flowingtowardstheinjuredareafromnormalremotemyocardium,due
to a lower myocardial membrane resting potential in the area of injury
caused by cell membrane damage. In addition, this mechanism could
explain ST-segment depression and/or T-wave inversion in leads I,II,
AVL,V4–V6(Figs.4and5),whichmayrepresentregionswithintactcells
and normal myocardial membrane resting potential, from which
currents of injury are flowing towards the injured areas [25].
Interestingly, patients with LGE confined to the interventricular
septum were twice as likely to show bundle-branch-block than those
without LGE involving the septum (Fig. 2, Table 1). This may be
explained by the fact that the left as well as the right bundle-branch of
the cardiac conduction system are located in the interventricular
septum. Thus, any inflammation, necrosis or scarring neighboring
those structures is much more likely to cause conduction abnormal-
ities, compared to damage located in the lateral wall. Furthermore,
patients with septal LGE had significantly more myocardial damage
than patients with lateral LGE (9.0% vs. 5.5%LV, see Table 1). However,
the mechanism why some forms of myocarditis cause damage to the
septal area more frequently and more extensively than others cannot
be explained on the basis of current knowledge [8].
In the present study, Q-waves were mostly found in cases with
severe, almost transmural LGE in large proportions of the lateral wall.
This is consistent with data from ischemic heart disease, indicating that
the presence of Q-waves is related to myocardial damage with
transmural or nearly transmural extent [23]. Since transmural damage
is not a frequent findingin myocarditis [5–8] Q-waves are not expected
to be frequently found in myocarditis. However, our findings indicate
thatmyocarditisisnotnecessarilyrestrictedtotheepicardialportionsof
the posterolateral wall, and that transmural involvement may occur.
It is important to keep in mind, however, that ECG findings in this
patient population are not perfect predictors of the region of
myocardial damage. Some scatter may be caused by the fact that in
both groups (septal and lateral myocarditis by CMR) the extent of LGE
crossed the cut-off line between septal and lateral into neighboring
segments throughout the ventricle in some patients (Fig. 5, white
asterisks). In addition it is likely that small areas of myocardial
damage caused by myocarditis, which are below the resolution of
current CMR techniques, may also affect ECG findings. This may also
explain why 23% of patients with biopsy proven myocarditis and signs
of myocardial damage visualized by CMR still had normal ECG upon
admission. Nevertheless, this finding is in line with reports from
ischemic heart disease, demonstrating that ECG is not diagnostic in
45% and even normal in 20% of patients presenting with acute
myocardial infarction [26,27].
5. Conclusion
ECGabnormalitiescanbefoundinmostpatientswithbiopsyproven
viral myocarditis at initial presentation (77%). However, similar to the
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clinicalsituationofsuspectedacutemyocardialinfarction,anormalECG
does not rule out viral myocarditis. ECG findings are related to the
amount and area of damage as indicated by CMR, which confirms the
important clinical role of the ECG for the diagnosis of viral myocarditis.
Acknowledgment
The authors of this manuscript have certified that they comply
with the principles of ethical publishing in the International Journal of
Cardiology [28].
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septallateral
septal lateral
ST- elevation / T-wave inversion:
most often in II, III, AVF, V4-V6
ST-depression
most often in II, III, AVF
ST- elevation:
most often in V1-V3
ST- depression / T- inversion:
most often in I, II, AVL, V4-V6
Most often bundle branch block
lateral
lateral
septal
septal
Lateral LGE
Septal LGE
*
*
*
*
*
Fig. 5. Spatial distribution of the mean values for segmental extent of contrast enhancement represented as gray-scale maps averaged for the entire ventricle in all patients (left
column) for both groups (septal and lateral LGE). Note how typical ECG findings (text, right column) are related to the area of maximum myocardial damage as indicated by CMR
(cartoon, mid column).
7
C.C. Deluigi et al. / International Journal of Cardiology xxx (2011) xxx–xxx
Please cite this article as: Deluigi CC, et al, ECG findings in comparison to cardiovascular MR imaging in viral myocarditis, Int J Cardiol
(2011), doi:10.1016/j.ijcard.2011.07.090