CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 4, May 2013
e4
AFRICA
Case Report
Acute myocardial infarction after prednisolone
administration for the treatment of anaphylaxis caused
by a wasp sting
ZEKERIYA ARSLAN, ATILA IYISOY, MURAT TAVLASOGLU
Abstract
Background:
Wasp stings have been demonstrated to cause
a wide spectrum of allergic reactions from localised reac-
tions to anaphylaxis. Acute coronary syndromes have been
described as potential complications of anaphylactic reac-
tions or some of the drugs used for the treatment of anaphy-
laxis. We know of only a few cases reported of acute myocar-
dial infarction (MI) following corticosteroid administration
or anaphylaxis in subjects with normal coronary arteries. If
it exists, underlying subclinical coronary atherosclerosis may
become clinically evident.
Case
report:
A 20 year-old male with anaphylaxis due to a
wasp sting, complicated by acute ST-elevation MI after intra-
venous methyl prednisolone administration, is the subject of
this report. He was admitted to our emergency service for
dizziness, blurred vision, presyncope and mild respiratory
distress 10 minutes after the wasp had stung him on the nape
of the neck. Six to seven minutes after administration of
prednisolone, the patient complained of typical chest pains.
A high posterolateral MI with mild mitral regurgitation were
seen on examination. He was treated conservatively with
aspirin and heparine. Coronary angiography and intravascu-
lar ultrasound imaging, performed 10 days later, showed no
evidence of obstructive coronary artery disease.
Conclusion:
Although reduced coronary perfusion, local
histamine release-induced coronary vasospasm or severe
hypoxia have been suggested, the pathophysiology remains
unclear.Acute STEMI may be a rare but clinically important
complication of a wasp sting, anaphylaxis or the corticoster-
oid used for its treatment, even in young adults with normal
coronary arteries. Therefore, physicians should be aware of
such serious complications in order to diagnose them early.
Keywords:
acute myocardial infarction, wasp sting, anaphylactic
reaction, prednisolone administration
Submitted 2/4/12, accepted 13/3/13
Cardiovasc
J Afr
2013;
24
: e4–e6
DOI: 10.5830/CVJA-2013-013
Acute coronary syndromes may occur as a result of anaphylactic
reaction or the drugs used for its treatment. Rare reports
have revealed acute myocardial infarction (MI) following
anaphylaxis in subjects with normal coronary arteries,
1-6
or in
subjects with underlying ischaemic heart disease.
7-9
Although
coronary vasospasm, plaque activation and systemic hypotension
have been suggested,
10
its pathophysiology remains unclear.
Corticosteroids have many side effects on the cardiovascular
system and may provoke acute MI.
11
We present a case of acute ST-elevation MI (STEMI) after
intravenous methyl prednisolone administration for the treatment
of anaphylaxis following a wasp sting in a young patient with
normal coronary arteries. The medical literature that pertains to
this phenomenon is discussed.
Case report
A 20-year-old male was admitted to our emergency service with
the symptoms of dizziness, blurred vision and mild respiratory
distress 10 minutes after a wasp sting on the nape of the neck.
There was only minimal local reaction and he was not in cardiac
distress. He had no allergic history or any other cardiovascular
risk factors, such as hypertension, diabetes, hyperlipidaemia,
overweight, or family history of heart disease, but had been
smoking for seven years. His blood pressure was 140/80 mmHg,
heart rate was 88 beats per minute and oxygen saturation was
93% in room air. His white blood cell count was also normal [7.3
×
10
3
(with 3.6% eosinophils;
n
<
4%)].
Considered as an allergic reaction, 40 mg methyl prednisolone
and 10 mg chlorpheniramine maleate were administered
intravenously in a slow infusion. However, the patient’s condition
deteriorated six to seven minutes later. He had typical chest pains
and an ECG showed ST elevation with a reciprocal depression
(Fig. 1a). His blood pressure also decreased markedly to 80/60
mmHg, the heart rate increased up to 100 beats per minute but
O
2
saturation was normal.
Conservative therapy including aspirin, heparine, and volume
replacement was administered but nitrates or calcium channel
blockers could not be used due to hypotension at that time. The
first bedside echocardiography revealed left ventricular posterior,
lateral and apical wall movement abnormalities and mild mitral
regurgitation (Fig. 2a). Left ventricular ejection fraction (LVEF),
estimated by the modified Simpson method, was 35%.
The symptoms and clinical findings began to improve in
approximately 25 minutes and the ST deviations resolved (Fig.
Department of Cardiology, Gelibolu Military Hospital,
Canakkale, Turkey
ZEKERIYA ARSLAN, MD,
ATILA IYISOY, MD
MURAT TAVLASOGLU, MD
