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Annals of Otology. Rhinology & Laryngology 118(8):556-558.

2009 Annals Publishing Company. All rights reserved.

Acute Myopericarditis Complicating Acute Tonsillitis:


A Prospective Study
Yoav Talmon, MD; Reu ven Ishai, MD; Alvin Samet, MD;
Alexander Sturman, MD; Nathan Roguin, MD
Objectives: We describe a prospective study of 100 consecutive cases of acute tonsillitis tested for cardiac involvement.
There was 1 clear-cut case of acute myopericarditis and 5 more patients with pathological findings suggesting cardiac
complication.
Methods: During a 6-month period (November 2006 to April 2007), we prospectively studied 100 consecutive patients
admitted to our department with acute tonsillitis for the purpose of detecting acute myopericarditis. We obtained for each
patient a serial electrocardiogram and echocardiogram, and took blood samples. All blood samples were analyzed for the
presence of the marker troponin 1 and for cardiac enzymes.
Results: One patient (male) had a definitive diagnosis of myopericarditis, and another 5 patients (3 of whom were female) had abnormal cardiac findings suggestive of myopericarditis.
Conclusions: Otolaryngologists should be aware of the possibility of cardiac involvement in acute tonsillitis and perform
an adequate workup whenever such a possibility is suspected.
Key Words: myopericarditis, pericarditis, tonsillitis.

cal literature .2"^ Talmon et aF presented 11 cases of


acute nonrheumatic myopericarditis complicating
acute tonsillitis, all of which were in young male patients.

INTRODUCTION
The most common infectious agents clearly associated with myopericarditis are enterovirus, adenovirus, coxsackievirus, herpesvirus, and cytomegalovirus. Influenza virus and other agents have also
been mentioned.

Streptococcal toxins have been implicated as the


cause of nonrheumatic myocarditis that emerges
without the latent period typical of acute rheumatic
fever. Of the large number of intracellular products
and cellular components of group A streptococci,
only the pyrogenic toxins and hemolysins, and possibly streptococcal cell wall fragments, appear to
have toxic properties.^ Streptococci dying in large
numbers as a result of bactericidal antibiotic therapy
release toxins and cellular fragments that may cause
the myocarditis injury.^

In the past, it was widely believed that "myocarditis other than that associated with acute rheumatic fever and diphtheria is for practical purposes
non-existent."
Today, however, acute nonrheumatic nondiphtheric infectious myocarditis is a well-established clinical entity.2
In 1947, Gore and Saphir' described 12 cases of
fatal myocarditis secondary to group A streptococcal tonsillitis. In 1989, Karjalainen^ reported 2 cases
of young men with group A streptococcal tonsillitis and acute myopericarditis mimicking myocardial infarction. Dickson et aH described a case of
fatal myocarditis secondary to severe tonsillitis and
peritonsillar abscess. Several other reports of sporadic single cases of myopericarditis secondary to
streptococcal tonsillitis can be found in the medi-

The possibility that cardiac complications are


more frequent than has previously been thought motivated us to conduct this prospective study.
MATERIALS AND METHODS
During the 6-month period between November
2006 and April 2007, 100 patients with acute tonsillitis were admitted to our hospital, of whom 22
presented with peritonsillar abscess and 3 presented

From the Departments of Otolaryngology-Head and Neck Surgery (Talmon, Ishai, Samet) and Cardiology (Sturman, Roguin), Western Galilee Hospital, Nahariya, and the Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa (Talmon,
Roguin), Israel.
Correspondence: Yoav Talmon, MD, Dept of Otolaryngology-Head and Neck Surgery, Western Galilee Hospital, PO Box 2 1 , Nahariya, Israel 22100.

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Talmon et al, Myopericarditis & Tonsillitis

557

PATIENT DATA

Age
(y)
35

Sex
M

Previous
Heart
Disease
None

22

None

62

Chest pain

41

Atrial septal
defect
None

22

None

Chest pain

24

None

Complaints

Physical
Examination
Pericardial
rub
Normal
Normal
Normal
Normal
Normal

Complete
Blood
Count
Bacterial
infectious
Viral
infectious
Bacterial
infectious
Bacterial
infectious
Bacterial
infectious
Bacterial
infectious

with peritonsillitis. All patients had dysphagia and


were unable to take oral medication. There were 52
female patients and 48 male patients, ranging in age
from 12 to 62 years of age (median, 33.5 years). Forty-five patients were Jewish and 55 non-Jewish, of
whom 36 were Muslim, 17 Druze, and 2 Christian.
Upon hospitalization, all patients underwent physical examination, a tonsil smear for bacteriology, and
a blood analysis including cardiac troponin I marker
and cardiac enzymes, and we obtained a serial electrocardiogram (ECG) and echocardiogram. The cardiac troponin I marker tests were performed 8 hours
after admission. Patients whose results showed elevated troponin levels were re-tested for troponin
and were followed up until their levels returned to
normal. The serial ECG and echocardiogram were
obtained upon admission. In cases of abnormal findings, these tests were repeated and the patients were
followed up until their results returned to normal.
The tonsil smears for bacteriology were performed
even though many of the patients had received oral
antibiotics before hospitalization. All patients were
hydrated upon arrival with intravenous fluids (Ringer lactate solutions).
Only 3 patients had a history of previous systemic
or cardiac disease. Of the 3 patients who had such
a history, 1 had undergone correction for an atrial
septal defect in the past, 1 had mitral valve prolapse,
and the other had had one instance of acute myocarditis.
RESULTS
Exudative tonsillitis and cervical lymphadenitis
were found in all 100 patients, 22 patients (22%)
were judged to have peritonsillar abscess based on
clinical findings, and 3 patients (3%) had peritonsillar cellulitis.
In the majority of cases (89%), the complete blood
count was indicative of bacterial infection through

Electrocardiogram Echocardiogram
ST-T changes
Normal
ST-T changes
Normal
Normal
ST-T changes

Troponin I
(ng/mL) Culture

Pericardial
effusion
Normal

4.94

Pericardial
effusion
Pericardial
effusion
Normal

Pericardial
effusion

3.79
+

0
3.12
0

leukoeytosis (more than 10,000 mm^) and granulocytosis. Eleven patients (11%) showed blood count
results suggestive of viral infection, of whom 2 were
found to have infectious mononucleosis on srologie
tests (positive for Epstein-Barr virus). Twenty-seven
patients (27%) were found to have streptococeal infection. For technical reasons, it was impossible to
obtain the laboratory results of 12 patients (12%).
Six of the 100 patients (6%) showed cardiac involvement. One patient had a definitive diagnosis of
myopericarditis with pericardial rub, ST-T changes,
mild pericardial effusion, and a positive troponin I
test result. This patient, a man of 35 years, did not
complain of any chest pain and had no history of
heart disease. Two other patients had ST-T changes on the ECG, another had mild pericardial effusion, and 2 additional patients had a positive troponin I test result. Of these 6 patients, only 2 had
chest pains: a 62-year-old woman who showed ST-T
changes on the ECG and a 22-year-old man who had
an elevated level of troponin I in his blood sample.
All patients were treated with intravenous broadspectrum antibiotics: 4 with amoxicillin combined
with clavulanate potassium (Augmentin), 4 with
erythromycin lactobionate because of allergy to penicillin in the anamnesis, and the remaining 92 with
first-generation cephalosporin. Ten patients needed
drainage of the peritonsillar abscess under local anesthesia, but in 9 other patients, aspiration of the pus
was sufficient. Patients with cardiac involvement
were treated with aspirin and colchicine. All 6 patients completely recovered (see Table). All patients
were treated for an average of 3 days in our hospital and completely recovered without any complications.
DISCUSSION
In this prospective study, 100 patients with acute
tonsillitis were prospectively tested for signs of

558

Talmon et al, Myopericarditis & Tonsillitis

myopericarditis. We found 6 patients to have cardiac involvement: 1 had a definitive diagnosis of myopericarditis, and another 5 had findings suggestive
of myopericarditis (see Table). Of these 6 patients, 3
patients had elevated troponin I blood levels, which
is a highly sensitive and specific marker of myoeardial injury. However, a mild troponin I elevation
may also be detected in cases of sepsis, renal failure,
subarachnoid hemorrhage, or stroke, and in athletes
involved in highly strenuous activities, such as marathon runners.^ In our study, an increase in troponin
I level was attributed to myocardial involvement
rather than an infection. If the presence of troponin
I in the blood had indeed been due to infection, we
would have expected to find blood troponin I in the
more severely ill, such as those with peritonsillar abscess. In fact, none of the patients with peritonsillar
abscess showed any signs of troponin I in the blood,
and no cardiac involvement was observed.
Only 27 patients (27%) were found to have a
streptococcal infection. One probable explanation is
the intake of antibiotics prior to hospitalization, but
that requires further investigation.
We could not find any demographic or other
trends among the 6 patients who showed cardiac involvement. Three of the 6 were female. Four of the
6 were Muslim Arabs, 1 was Druze, and 1 was a
Jewish woman, who was also by far the oldest of the
6 (62 years old). Only 2 of the 6 experienced chest
pains: a male patient who had ST-T changes and a
female patient with raised levels of troponin. Streptoeoccal infection could be established in only 2 of
the 6 patients: one was the male patient who showed

the full picture of myopericarditis, and the other was


the female patient with the ST-T changes.
Laboratory tests did not show any differences
between patients with definite or suspected myopericarditis and those excluded for myopericarditis. In addition, none of the patients with peritonsillar abscess were found to have myopercarditis, so
the severity of the tonsillitis was not correlated to
the presence of myopericarditis. There is much evidence against the possibility of rheumatic carditis in
our patients.
First is the almost-simultaneous appearance of
tonsillitis and myocarditis without the typical latent period. Second is the lack of evidence in the
patient history or physical examination of previous
rheumatic activity. However, in previous reports,
acute myopericarditis has been infrequently found
in streptococcal tonsillitis .^-^ Our study shows that
this entity may be much more common than previously thought,^ and many young patients who have
acute tonsillitis may have undiagnosed cardiac complications. Otolaryngologists should take that possibility into consideration when treating acute tonsillitis. In addition, cardiologists should suspect streptococcal infection in any otherwise-healthy patient
admitted with acute myopericarditis. We are aware
that it would be impractical to suggest a full workup for myopericarditis on every patient treated for
acute strep throat. It might be adequate, however, to
check for the marker troponin I if blood analysis is
needed in the clinic or if the patient is hospitalized.
In addition, practitioners should not overlook chest
pains in young patients with acute tonsillitis.

REFERENCES
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Acute myopericarditis complicating acute tonsillitis; beware the
young male patient with tonsillitis complaining of chest pain.
Ann Otol Rhinol Laryngol 2008;117:295-7.
3. Karjalainen J. Streptococcal tonsillitis and acute nonrheumatic myopericarditis. Chest 1989;95:359-63.
4. Dickson RI, Roberts FJ, Frederick FJ. Fatal myocarditis
associated with peritonsillar abscess. Laryngoscope 1983;93:
565-7.
5. Said SA, Severin WPJ. Acute nonrheumatic myopericar-

ditis associated with group A hemolytic streptococcal tonsillitis


in a male ICU-nurse. Neth J Med 1998;53:266-70.
6. Khavandi A, Whitaker J, Elkington A, Probert J, Walker
PR. Acute streptococcal myopericarditis mimicking myocardial
infarction. Am J Emerg Med 2008;26:638.el-2.
7. Caraco J, Amon R, Raz I. Atrioventricular block complicating acute streptococcal tonsillitis. Br Heart J 1988;59:38990.
8. Putterman C, Caraco Y, Shalit M. Acute nonrheumatic
perimyocarditis complicating streptococcal tonsillitis. Cardiology 1991 ;78:156-60.
9. Ammann P, Pfisterer M, Fehr T, Rickli H. Raised cardiac
troponins. BMJ 2004;328:1028-9.

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