Propafenone induced Brugada-like ECG changes mistaken as acute myocardial infarction

Abstract

Brugada syndrome is one of the important causes of sudden cardiac death in young adults. The condition is associated with typical electrocardiogram (ECG) changes in anteroseptal leads V1 and V2 that can be unmasked by various medications, electrolyte disturbances, and even by the febrile state in susceptible individuals. The case history is reported of a patient with atrial flutter and atrial fibrillation who developed Brugada-like ECG changes when treated with propafenone. He was mistakenly diagnosed as having acute myocardial infarction when he presented to the emergency room with acute precordial chest pain. Cardiac catheterisation revealed normal coronary arteries and normal left ventricular systolic function. A review of previous ECGs showed the temporal relationship of ECG changes to initiation of propafenone a few years earlier. The ECG changes resolved with discontinuation of propafenone and re-emerged when he was rechallenged with oral propafenone. This case highlights the importance of recognising the characteristic ECG changes of Brugada syndrome and being able to differentiate them from those of acute myocardial infarction and other conditions manifesting with similar changes

BACKGROUND

The Brugada syndrome, first described as a clinical entity in 1992, is now recognised as one of the important causes of sudden death in young adults. The electrocardiogram (ECG) manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked by class IC antiarrhythmic drugs, a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalaemia, hypercalcaemia, alcohol and cocaine. We present the case of a patient who was mistakenly diagnosed with acute myocardial infarction when he presented to the emergency room with chest pain and found to have ST segment elevation in leads V1 and V2. After the documentation of normal coronary arteries on cardiac catheterisation, a review of older ECGs showed that the changes coincided with the initiation of propafenone used for treatment of atrial flutter and atrial fibrillation.

Differentiation of either primary or drug induced Brugada-like ECG changes from those of acute myocardial infarction is of utmost importance in the emergency room setting.

CASE PRESENTATION

A 66-year-old Caucasian man with a history of atrial flutter/atrial fibrillation, hypertension, tobacco use and hypercholesterolaemia presented to the emergency room with acute precordial chest pain. The ECG on admission showed ST segment elevation in the anteroseptal leads (fig 1) and the patient underwent emergency cardiac catheterisation for a diagnosis of acute myocardial infarction. Coronary angiography showed normal coronary arteries and left ventriculography showed normal wall motion and ejection fraction.

Figure 1.

Electrocardiogram on presentation showing ST elevation in leads V1 to V3 mistaken for anteroseptal myocardial infarction.

On further investigation it was discovered that the patient had been started on propafenone for treatment of atrial fibrillation/flutter many years ago. Review of an ECG before initiation of propafenone showed typical atrial flutter with no significant ST segment or T wave abnormalities. Analysis of ECGs since then showed different types of typical Brugada-like changes over a period of many years.

Treatment with propafenone was stopped and the ECG changes completely resolved. No ventricular tachycardia or fibrillation could be induced during an electrophysiology study. Procainamide challenge during the procedure also failed to induce Brugada-like ECG changes. The patient was rechallenged with oral propafenone under monitored conditions and typical Brugada-like ECG changes were again induced. On follow-up a few months later he presented with atrial flutter and fibrillation for which he underwent radiofrequency ablation. He has been in sinus rhythm for the last 2 years, is off all antiarrhythmic medications, and has no ECG abnormalities.

DISCUSSION

In 1992 Brugada and Brugada described eight patients with a history of cardiac arrest and ECG findings of right bundle branch block and ST segment elevation in the right precordial leads in the absence of long QT intervals or structural heart disease.¹ The Brugada syndrome is now recognised as a clinical entity and accounts for 40–60% of all cases of idiopathic ventricular fibrillation. The syndrome has been linked to mutations in the cardiac sodium channel gene that leads to transmural heterogeneity and the associated ECG changes. Brugada-like ECG changes unrelated to the actual syndrome are being recognised more frequently and reported in the literature.

The Brugada syndrome is characterised by ECG abnormalities and diagnostic criteria have been proposed.² In some patients, complete or incomplete right bundle branch block is present. In others, the high takeoff ST segment mimics the pattern of right bundle branch block, but the wide S waves in leads I, aVL and V6 that are typically seen in right bundle branch block are absent. ST segment elevation is primarily limited to leads V1 and V2 and can have a saddleback shape, but in typical cases the ST segment begins from the top of the R′ wave, is downsloping, and ends with an inverted T wave. This pattern is so distinctive that it should not be mistaken for acute infarction.³ In anteroseptal infarction complicated by right bundle branch block, the downstroke of the R′ wave and the beginning of the ST segment have a distinct transition, and the ST segment is horizontal or upsloping, not downsloping. The ECG changes in the Brugada syndrome may be present continuously or intermittently. Sodium channel blockers such as ajmaline, flecainide, procainamide, propafenone⁴ and cocaine can unmask or accentuate the ECG pattern, as can the febrile state, electrolyte abnormalities, vagotonic agents, and antihistamines.

An ECG pattern similar to that of the Brugada syndrome has been observed in arrhythmogenic right ventricular dysplasia, another condition associated with ventricular arrhythmias and sudden death, pulmonary embolism, and hyperkalaemia, and it has also been reported in a patient with compression of the right ventricular outflow tract by a mediastinal tumour.

In conclusion, asymptomatic Brugada-like ECG changes can be induced by a spectrum of drugs, and presentation with such changes in the appropriate setting, if not recognised, can lead to an erroneous diagnosis of acute myocardial infarction and unnecessary invasive testing. This case highlights the importance of the recognition and awareness of the drug induced Brugada-like ECG changes and is especially important in the emergency room setting where patients may present initially.

LEARNING POINTS

• Brugada syndrome causes sudden cardiac death in adults; on ECG there is ST elevation in leads V1 and V2.

• Brugada syndrome can be unmasked by fever, and by drugs including tricyclic antidepressants and β-blockers.

• In this case reported here, Brugada syndrome was unmasked by propafenone.