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Canadian Journal of Cardiology 29 (2013) 1138.e3e1138.e5 www.onlinecjc.

ca

Case Report

Erysipelas and Acute Myocarditis: An Unusual Combination


Fernando Domnguez, MD,a Marta Cobo-Marcos, MD,a Gonzalo Guzzo, MD,a
Miguel A. Cavero, MD,a Jess G. Mirelis, MD,a,b Luis Alonso-Pulpon, MD, PhD,a and
Pablo Garcia-Pavia, MD, PhDa
a

Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain


b

Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain

ABSTRACT



RESUM
E

Myocarditis is a rare disease with variable clinical presentation and


diverse electrocardiographic and echocardiographic features. Viral
infection is the most common cause, but myocarditis can also be
caused by bacterial infection. The most frequently involved bacterial
agent is group A Streptococcus, which is also an etiologic agent of
erysipelas. We present the case of a man aged 46 years with left-leg
erysipelas who developed myocarditis. Cardiac magnetic resonance
played an essential role in diagnosis. This case is, to our knowledge,
the rst description of an association between erysipelas and
myocarditis.

La myocardite est une maladie rare ayant un tableau clinique


ristiques e
lectrocardiographiques et
variable, et diverses caracte
chocardiographiques. Linfection virale est la cause la plus fre
quente,
e
galement tre cause
e par linfection
mais la myocardite peut e
rienne. Lagent bacte
riologique le plus fre
quemment en cause
bacte
galement un agent
est le streptocoque du groupe A, qui est e
tiologique de le
rysiple. Nous pre
sentons le cas dun homme ge
 de
e
rysiple la jambe gauche chez qui une myocardite
46 ans ayant un e
sonance magne
tique cardiaque a joue
 un rle
est survenue. La re
diagnostique primordial. notre connaissance, ce cas montre pour la
rysiple et la myocardite.
premire fois un lien entre le

Case Presentation
A man aged 46 years with a history of tobacco abuse and
hypertension presented to emergency with 24-hour lower left
limb pain and circumscribed erythema. The lesion did not
disappear after pressure, there was no edema, and the patient
denied previous trauma or insect bite (Fig. 1). However, the
patient did have a painless hyperkeratotic lesion with a central
crack on his left sole. The patient denied chest pain, dyspnea,
palpitations, presyncope, syncope, and recent viral illness and
was not taking medication. Physical examination was normal
besides the skin lesion.
While in the emergency department, the patient suffered
vasovagal syncope with a pulse of 60 beats per minute and
blood pressure 74/45 mm Hg, preceded by diaphoresis,
dizziness, and blurred vision. After a few seconds, he recovered
consciousness and reported no chest pain, palpitations, or
other symptoms. An immediately postsyncope electrocardiogram (ECG) showed junctional rhythm at 60 beats per

minute, which persisted for 10 minutes. Thirty minutes later,


the ECG showed ST elevation in leads I and II and from V2
to V6.
Cardiac enzymes were elevated (Troponin I, 33 mg/L,
and creatine kinase, 514 U/L; normal values: < 0.06 mg/L
and < 195 U/L, respectively). An urgent coronary angiogram
showed normal epicardial arteries, and a computed tomography scan excluded pulmonary thromboembolism.
A transthoracic echocardiogram demonstrated preserved left
ventricular function without valvular dysfunction or pericardial effusion.
The patient was admitted to the cardiology ward, and
cardiac magnetic resonance imagery (CMRI) established
a diagnosis of acute myocarditis, with preserved biventricular
function with inferolateral and anterolateral subepicardial
enhancement in short T1 inversion recovery (STIR) sequences
(Fig. 2). Gadolinium CMRI revealed delayed subepicardial
contrast enhancement that matched the STIR sequences,
indicating a potentially reversible lesion. No pericardial effusion or thickening was present.
Skin lesion and blood cultures were negative for bacteria
and fungi, and blood tests were negative for HIV and hepatitis
C. Immunologic studies (antinuclear antibody, antineutrophil
cytoplasmic antibody, rheumatoid factor) and antistreptolysin
O (ASO) test were normal. A skin biopsy showed classical
ndings of erysipelas.

Received for publication October 28, 2012. Accepted December 22, 2012.
Corresponding author: Dr Pablo Garcia-Pavia, Department of Cardiology, Hospital Universitario Puerta de Hierro, Manuel de Falla, 2, 28222
Madrid, Spain.
E-mail: pablogpavia@yahoo.es
See page 1138.e4 for disclosure information.

0828-282X/$ - see front matter 2013 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.cjca.2012.12.021

1138.e4

Canadian Journal of Cardiology


Volume 29 2013

Figure 1. Erysipelas in the lower left limb.

No further complications were observed, and the patient


was discharged after 6 days. The skin lesion improved after
treatment with amoxicillineclavulanic acid. At outpatient
visits 2 and 6 months after discharge, the patient remained
asymptomatic. CMRI 6 months after the initial visit was
normal.
Discussion
The clinical presentation of myocarditis is highly variable,
with divergent ECG and echocardiographic ndings. CMRI
has become an essential test for accurate diagnosis1,2 and is
highly valuable for predicting clinical outcome.3
Erysipelas is mainly caused by infection with group A
b-hemolytic Streptococcus. Diagnosis is based on the typical
clinical presentation. ASO is elevated in only 40% of patients,
and blood cultures are positive in only 5%. Systemic

involvement is usually mild. Although microbiological tests


are usually negative, a common causative agent is group A
b-hemolytic Streptococcus, which has also been linked to the
development of myocarditis when infection affects the upper
respiratory tract.4
Streptococcal infection can damage the heart through
a variety of mechanisms. First, myocarditis can occur in the
setting of rheumatic fever. However, our patient did not
show any of the other Jones criteria, and the typical latency
between streptococcal infection and carditis was absent.
Moreover, the lack of streptococcal antibodies supports
a noneimmune-mediated process. Myocarditis can also
occur with invasive streptococcal infection or toxic-shock
syndrome, typically fulminant, with a rapid onset and
severe skin manifestations, which were not present in this
case. Toxin-mediated myocarditis seems to be the most
popular explanation for previously described cases of
myocarditis associated with streptococcal pharyngitis4,5 and
has been related histopathologically to nonspecic myocarditis in the absence of direct streptococcal bacterial invasion.
Although we did not perform endomyocardial biopsy, toxininduced myocarditis is the most probable explanation of our
case, in view of the positive clinical outcome. This case is, to
our knowledge, the rst description of erysipelas complicated
by myocarditis.
Funding Sources
This work was partially supported by the Instituto de Salud
Carlos III [grant PI11/0699] and the Spanish Ministry of
Health [Red Cooperativa de Insuciencia Cardiaca (REDINSCOR) RD06/03/0018].
Disclosures
The authors have no conicts of interest to disclose.

Figure 2. Cardiac magnetic resonance imaging. (A) Short-axis view of the left ventricle in T2-weighted sequence. Increased signal (> 2 SD from the
normal myocardium) is seen in the anterolateral subepicardial area (white arrow). (B) Short-axis view with the delayed enhancement technique.
Gadolinium deposits are found at the same location (black arrow).

Domnguez et al.
Erysipelas and Acute Myocarditis

References
1. Garcia-Pavia P, Aguiar-Souto P, Silva-Melchor L, et al. Cardiac magnetic
resonance imaging in the diagnosis of myocarditis mimicking myocardial
infarction. Int J Cardiol 2006;112:e27-9.
2. Friedrich MG, Sechtem U, Schulz-Menger J, et al. Cardiovascular
magnetic resonance in myocarditis: a JACC white paper. J Am Coll
Cardiol 2009;53:1475-87.

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3. Grn S, Schumm J, Greulich S, et al. Long-term follow-up of biopsyproven viral myocarditis predictors of mortality and incomplete recovery.
J Am Coll Cardiol 2012;59:1604-15.
4. Chaudhuri A, Woods ML, Dooris M. Non-rheumatic streptococcal myocarditisdwarm hands, warm heart. J Med Microbiol 2013;62(pt 1):169-72.
5. Gill MV, Klein NC, Cunha BA. Nonrheumatic poststreptococcal
myocarditis. Heart Lung 1995;24:425-6.

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