Download ST elevation is not always equivalent to acute myocardial infarction

Hong Kong Journal of Emergency Medicine
ST elevation is not always equivalent to acute myocardial infarction:
a case of Brugada syndrome
YF Choi, AYC Siu, TW Wong, CC Lau
Acute myocardial infarction (AMI) is one of the most alerting situations in emergency department.
Electrocardiogram (ECG) is one of the most important diagnostic tools and the decision about thrombolytic
therapy is usually based upon ECG findings when clinically suspicious. However, ST segment elevation is
not always equivalent to acute myocardial infarction. We present a rare syndrome whose ECG shows persistent
ST elevation not related to AMI. (Hong Kong j.emerg.med. 2003;10:121-123)
Keywords: Brugada syndrome, bundle branch block, myocardial infarction, ST elevation
Introduction
Case history
Time is muscle! This phrase always alerts emergency
doctors not only to adopt a high index of suspicion on
acute myocardial infarction (AMI) but also to start
aggressive treatment early. Owing to the fact that the
clinical presentation is often atypical and cardiac markers
level will not be available within a short time, ECG
becomes the most important diagnostic tool in
emergency departments. Currently we depend on the
typical history of chest pain and the presence of ST
elevation as the basic inclusion criteria for thrombolytic
therapy. Although ST segment elevation is a warning
signal of AMI, we need to interpret it carefully. In this
case report we present a rare syndrome whose ECG
mimicked AMI by showing persistent ST elevation.
A 66 years old man walked in complaining of dizziness,
vertigo, vomiting, chest and epigastric discomfort after
taking beef congee for lunch. His chest discomfort
lasted for two hours which was central, retrosternal
and constrictive in nature. He was a non-smoker and
enjoyed good past health. On physical examination,
there was no significant abnormal finding but from
the appearance of his coffee ground vomitus, upper
gastrointestinal bleeding was suspected.
Correspondence to:
Choi Yu Fai, MBBS(HK), FRCSEd
Pamela Youde Nethersole Eastern Hospital, Accident and
Emergency Department, 3 Lok Man Road, Chaiwan, Hong Kong
Email: [email protected]
Wong Tai Wai, FRCSEd, DCH(Ire), FHKAM(Emergency Medicine)
Lau Chor Chiu, MRCP(UK), FHKCEM, FHKAM(Emergency Medicine)
North District Hospital, Accident and Emergency Department,
9 Po Kin Road, Sheung Shui, N.T., Hong Kong
Siu Yuet Chung, Axel, MBChB(CUHK), FRCSEd, FHKAM(Emergency
Medicine)
His vital signs were all along stable and his
haemoglobin was normal. Owing to the chest
symptom, a 12 lead ECG was ordered which showed
ST elevation in chest leads V1 to V3 together
with right bundle branch block (RBBB). (Figure 1)
A coexisting acute myocardial infarction was
considered. The patient was immediately treated with
sublingual nitrate, oral aspirin and intravenous
isosorbide infusion in the emergency department.
Thrombolysis was not offered because concurrent
upper gastro-intestinal bleeding was suspected.
After admission, the patient was stable all along. The
serial cardiac enzyme levels were normal and the chest
discomfort subsided very soon. Vomiting stopped and
subsequent upper endoscopy did not show any
122
Hong Kong j. emerg. med. Vol. 10(2) Apr 2003
The syndrome was believed to be autosomal dominant
inheritance with variable expression. 4 Cases of
asymptomatic Brugada syndrome were also reported.5
In fact, our patient did not have any episode of cardiac
arrest and may be another case of asymptomatic
Brugada syndrome. Similar syndromes of unexplained
ventricular fibrillation with no structural abnormality
were reported in other series as Sudden Unexplained
Death Syndrome (SUDS) and "vagally induced
ventricular fibrillation".6,7
Figure 1.
abnormality. An interesting finding was that the serial
ECG in the next few days showed persistent ST
elevation in V1 to V3 with RBBB without any
progression. The ECG finding was considered
compatible with the diagnosis of a rare disease entity:
Brugada syndrome.
In the following weeks, the patient underwent
echocardiogram, Holter and stress electrocardiogram
which all turned out to be normal. There was no
evidence of previous ischaemic insult and no
myocardial dysplasia could be demonstrated. His close
relatives also received ECG screening and all were
normal. He is currently well with regular follow up
by the cardiology unit.
Discussion
Brugada syndrome was first described in 1992 by
Pedro Brugada and Joseph Brugada.1 They found that
a group of patients who survived aborted sudden
cardiac arrest were having similar ECG patterns,
namely, RBBB and ST elevation in V1 to V3 which
was usually either coved or saddle in appearance. They
were at risk of having recurrent cardiac arrest. In the
subsequent studies, the syndrome was characterized
by the triad of recurrent cardiac arrest, ST elevation
in V1 to V3 and RBBB. The latter two were ECG
criteria which signify a poor prognosis of having an
increased risk of sudden cardiac arrest.2 Over 90% of
these patients were male and the mean age of the first
arrhythmic incidence occurred between 22 to 65 years.3
Besides, patients with Brugada syndrome had no
previous AMI and no demonstrable myocardial
dysplasia on echocardiogram. Electrophysiology study
showed that these patients were prone to ventricular
arrhythmia and hence sudden cardiac death.
Ventricular fibrillations were reported in 73% and
syncope occurred in 27% of all 104 documented cases
of Brugada syndrome. 8 The underlying mechanism
was unknown and being investigated.9 The prevalence
of ventricular fibrillation at night and during sleep
suggested that increased nocturnal vagal activity and
withdrawal of sympathetic activity might play a role
in the pathogenesis. 10 The theory of imbalance of
autonomic activity was further substantiated by the
obser vation of the syndrome associated with
autonomic disorder. 11 Recently, it was proposed that
the syndrome was associated with a missense mutation
in the cardiac sodium channel gene SCN5A.12
Concerning the treatment of the syndrome, it is essential
to rule out other organic causes for ventricular fibrillation.
The aim of management of symptomatic patient is to
prevent sudden cardiac death. Beta-blocker and
amiodarone have been shown to be ineffective.13 Class
IC antiarrhythmic agents such as flecanide may even
exaggerate the ST segment elevation.14 Currently it is
recommended that implantable cardioverter defibrillator
is the only method which can alter the outcome of the
patients.15,16
The patient in this case report had no history of cardiac
arrest but his ECG pattern satisfied the criteria. He
belonged to the asymptomatic subgroup of the
syndrome. The treatment for asymptomatic patient
is still controversial but evaluation of inducibility of
Choi et al./Brugada syndrome
ventricular fibrillation has been suggested as an indication
of implantable cardioverter defibrillator.8,17
ST elevation is well known to be a sign of AMI and
has been used as the inclusion criteria for thrombolytic
therapy. However, it is not always the case as other
conditions may mimic ST elevation. Besides Brugada
syndrome, ST elevation can be found in acute
pericarditis and acute myocarditis.18-20 Cocaine abuse
is also an important cause of chest pain with ST
segment change and AMI 21 in the western countries.
Other causes of ST elevation include acute subarachnoid haemorrhage, antidepressant overdose, post
MI ventricular aneurysms and early repolarisation.22-25
Emergency physicians should be careful in evaluating
patients who have ECG evidence of ST elevation,
especially those with atypical presentation.
Thrombolytic therapy can benefit the patients with
AMI but can result in a disaster if the administration
is inadvertent.
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