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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. References 1. 2. 3. 4. 5. 6. 7. 8. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992;20(6):1391-6. Brugada P, Brugada J. 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