American Journal of Therapeutics 21, 540–541 (2014)
Brugada Electrocardiogram Pattern “Unmasked” by Amiodarone Infusion Sharad Bajaj, MD,1 Constantinos Costeas, MD,2 and Fayez Shamoon, MD, FACC, FSCAI1*
Brugada syndrome predisposes individuals to ventricular arrhythmias and sudden cardiac death, in the absence of structural heart disease. The typical Brugada electrocardiogram (ECG) phenotype is often concealed in affected population, and the existing genetic testing is capable of detecting just about 20% of cases. Therefore, the diagnosis largely requires various pharmacological provocative agents like class I antiarrhythmic drugs to unmask the unique features of Brugada ECG phenotype. We report an unusual case of “unmasking” of Brugada ECG pattern with ventricular tachycardia brought out by amiodarone infusion. Keywords: Brugada syndrome, Brugada ECG pattern, amiodarone, sudden cardiac death, ventricular tachycardia
CASE REPORT A 64-year-old African American man with past medical history significant for hypertension, diabetes mellitus, peripheral arterial disease, and end-stage renal disease presented to our institution with non-ST elevation myocardial infarction. He underwent successful coronary artery bypass grafting for severe triple-vessel coronary artery disease. Postoperatively, amiodarone infusion was initiated for atrial fibrillation prophylaxis. Thereafter, he started having episodes of nonsustained ventricular tachycardia (VT) and had a sudden cardiac arrest secondary to sustained VT. He was resuscitated using multiple defibrillations. Lidocaine infusion was then added to the existing amiodarone infusion, but VT continued to recur. The electrocardiogram (ECG) at that point started demonstrating a pattern consistent
Departments of 1Cardiovascular Diseases and 2Electrophysiology, St. Michael’s Medical Center, Newark, NJ. The authors have no conflicts of interest to declare. *Address for correspondence: Program Director, Cardiology Fellowship, Department of Cardiology, St. Michael’s Medical Center, 111 Central Avenue, Newark, NJ 07102. E-mail: [email protected] 1075–2765 Ó 2014 Lippincott Williams & Wilkins
with both Brugada type 3 and type 1 phenotypes (Figure 1B). Decision was made to discontinue both amiodarone and lidocaine infusions. Thereafter, no further episodes of VT were recorded during rest of the hospital stay. Over the next few days, the Brugadaspecific ECG changes resolved, and the patient was
FIGURE 1. (A) Electrocardiogram at the time of admission. (B) Postoperative electrocardiogram showing Brugada type 3 and Brugada type 1 patterns. (C) V1 rhythm strip showing Brugada type 1 pattern. (D) Electrocardiogram at the time of discharge. www.americantherapeutics.com
Amiodarone Use Unmasking Brugada ECG Pattern
discharged from the hospital. No further arrhythmic events were reported during follow-ups. Brugada syndrome (BS) is an autosomal dominant entity that predisposes individuals without overt structural heart disease to ventricular arrhythmias and sudden cardiac death.1 The available genetic testing is capable of detecting just about 20% of cases with mutations involving the SCN5A gene.1 For this reason, the diagnosis of BS largely requires various pharmacological provocative agents like class I antiarrhythmic drugs (procainamide, flecainide, and ajmaline) as they unmask the unique features of Brugada ECG phenotype.2 The mechanism of arrhythmogenesis in BS is suggested to be phase II reentry.3 Amiodarone is essentially a potassium ion channel-blocking agent with multiple active metabolites that have been shown to possess the electrophysiological characteristics of all 4 classes of antiarrhythmic agents. They block rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs), Na+ current (INa), L-type Ca2+ current (ICaL), and adrenergic receptors.2 On the contrary, isoproterenol, via its beta-adrenergic stimulatory effect, augments inward calcium current and reduces the outward current, thereby effectively terminating VT storm among patients with BS.3 Quinidine, a class Ia antiarrhythmic agent, due to its Ito channel-blocking properties has been acknowledged to have a therapeutic effect on the ventricular arrhythmias in BS.4 There are only 2 other cases reported in the literature that demonstrated “unmasking” of Brugada ECG phenotype after amiodarone infusion. Paul et al1 described a 51-year-old female who developed type 1 Brugada ECG pattern after receiving amiodarone infusion that
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541
subsequently resolved after discontinuation of the drug. D’Aloia et al2 described a 32-year-old male admitted after an episode of “at-home resuscitated ventricular fibrillation cardiac arrest,” who started displaying type 1 Brugada ECG changes after amiodarone infusion. This case emphasizes that antiarrhythmic drugs, regardless of their delegated classifications, are in reality a diverse group of compounds commonly influencing more than 1 ion channel. In a clinical setting, the underlying mechanisms responsible for antiarrhythmic and proarrhythmic effects of these agents are more complex than expected. It is increasingly recognized that several drugs can “unmask” Brugada-like ECG pattern or induce arrhythmias and should be avoided in these patients (www.brugadadrugs.org).
REFERENCES 1. Paul G, Yusuf S, Sharma S. Unmasking of the Brugada syndrome phenotype during the acute phase of amiodarone infusion. Circulation. 2006;114:489–491. 2. D’Aloia A, Vizzardi E, Bugatti S, et al. Brugada syndrome phenotype cardiac arrest in a young patient unmasked during the acute phase of amiodarone infusion: disclosure and aggravation of Brugada electrocardiographic pattern. J Electrocardiol. 2012;45:411–413. 3. Tanaka H, Kinoshita O, Uchikawa S, et al. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1293–1294. 4. Viskin S, Wilde AA, Tan HL, et al. Empiric quinidine therapy for asymptomatic Brugada syndrome: time for a prospective registry. Heart Rhythm. 2009;6:401–404.
American Journal of Therapeutics (2014) 21(6)
Brugada Electrocardiogram Pattern “Unmasked” by Amiodarone Infusion Sharad Bajaj, MD,1 Constantinos Costeas, MD,2 and Fayez Shamoon, MD, FACC, FSCAI1*
Brugada syndrome predisposes individuals to ventricular arrhythmias and sudden cardiac death, in the absence of structural heart disease. The typical Brugada electrocardiogram (ECG) phenotype is often concealed in affected population, and the existing genetic testing is capable of detecting just about 20% of cases. Therefore, the diagnosis largely requires various pharmacological provocative agents like class I antiarrhythmic drugs to unmask the unique features of Brugada ECG phenotype. We report an unusual case of “unmasking” of Brugada ECG pattern with ventricular tachycardia brought out by amiodarone infusion. Keywords: Brugada syndrome, Brugada ECG pattern, amiodarone, sudden cardiac death, ventricular tachycardia
CASE REPORT A 64-year-old African American man with past medical history significant for hypertension, diabetes mellitus, peripheral arterial disease, and end-stage renal disease presented to our institution with non-ST elevation myocardial infarction. He underwent successful coronary artery bypass grafting for severe triple-vessel coronary artery disease. Postoperatively, amiodarone infusion was initiated for atrial fibrillation prophylaxis. Thereafter, he started having episodes of nonsustained ventricular tachycardia (VT) and had a sudden cardiac arrest secondary to sustained VT. He was resuscitated using multiple defibrillations. Lidocaine infusion was then added to the existing amiodarone infusion, but VT continued to recur. The electrocardiogram (ECG) at that point started demonstrating a pattern consistent
Departments of 1Cardiovascular Diseases and 2Electrophysiology, St. Michael’s Medical Center, Newark, NJ. The authors have no conflicts of interest to declare. *Address for correspondence: Program Director, Cardiology Fellowship, Department of Cardiology, St. Michael’s Medical Center, 111 Central Avenue, Newark, NJ 07102. E-mail: [email protected] 1075–2765 Ó 2014 Lippincott Williams & Wilkins
with both Brugada type 3 and type 1 phenotypes (Figure 1B). Decision was made to discontinue both amiodarone and lidocaine infusions. Thereafter, no further episodes of VT were recorded during rest of the hospital stay. Over the next few days, the Brugadaspecific ECG changes resolved, and the patient was
FIGURE 1. (A) Electrocardiogram at the time of admission. (B) Postoperative electrocardiogram showing Brugada type 3 and Brugada type 1 patterns. (C) V1 rhythm strip showing Brugada type 1 pattern. (D) Electrocardiogram at the time of discharge. www.americantherapeutics.com
Amiodarone Use Unmasking Brugada ECG Pattern
discharged from the hospital. No further arrhythmic events were reported during follow-ups. Brugada syndrome (BS) is an autosomal dominant entity that predisposes individuals without overt structural heart disease to ventricular arrhythmias and sudden cardiac death.1 The available genetic testing is capable of detecting just about 20% of cases with mutations involving the SCN5A gene.1 For this reason, the diagnosis of BS largely requires various pharmacological provocative agents like class I antiarrhythmic drugs (procainamide, flecainide, and ajmaline) as they unmask the unique features of Brugada ECG phenotype.2 The mechanism of arrhythmogenesis in BS is suggested to be phase II reentry.3 Amiodarone is essentially a potassium ion channel-blocking agent with multiple active metabolites that have been shown to possess the electrophysiological characteristics of all 4 classes of antiarrhythmic agents. They block rapidly and slowly activating delayed rectifier K+ currents (IKr and IKs), Na+ current (INa), L-type Ca2+ current (ICaL), and adrenergic receptors.2 On the contrary, isoproterenol, via its beta-adrenergic stimulatory effect, augments inward calcium current and reduces the outward current, thereby effectively terminating VT storm among patients with BS.3 Quinidine, a class Ia antiarrhythmic agent, due to its Ito channel-blocking properties has been acknowledged to have a therapeutic effect on the ventricular arrhythmias in BS.4 There are only 2 other cases reported in the literature that demonstrated “unmasking” of Brugada ECG phenotype after amiodarone infusion. Paul et al1 described a 51-year-old female who developed type 1 Brugada ECG pattern after receiving amiodarone infusion that
www.americantherapeutics.com
541
subsequently resolved after discontinuation of the drug. D’Aloia et al2 described a 32-year-old male admitted after an episode of “at-home resuscitated ventricular fibrillation cardiac arrest,” who started displaying type 1 Brugada ECG changes after amiodarone infusion. This case emphasizes that antiarrhythmic drugs, regardless of their delegated classifications, are in reality a diverse group of compounds commonly influencing more than 1 ion channel. In a clinical setting, the underlying mechanisms responsible for antiarrhythmic and proarrhythmic effects of these agents are more complex than expected. It is increasingly recognized that several drugs can “unmask” Brugada-like ECG pattern or induce arrhythmias and should be avoided in these patients (www.brugadadrugs.org).
REFERENCES 1. Paul G, Yusuf S, Sharma S. Unmasking of the Brugada syndrome phenotype during the acute phase of amiodarone infusion. Circulation. 2006;114:489–491. 2. D’Aloia A, Vizzardi E, Bugatti S, et al. Brugada syndrome phenotype cardiac arrest in a young patient unmasked during the acute phase of amiodarone infusion: disclosure and aggravation of Brugada electrocardiographic pattern. J Electrocardiol. 2012;45:411–413. 3. Tanaka H, Kinoshita O, Uchikawa S, et al. Successful prevention of recurrent ventricular fibrillation by intravenous isoproterenol in a patient with Brugada syndrome. Pacing Clin Electrophysiol. 2001;24:1293–1294. 4. Viskin S, Wilde AA, Tan HL, et al. Empiric quinidine therapy for asymptomatic Brugada syndrome: time for a prospective registry. Heart Rhythm. 2009;6:401–404.
American Journal of Therapeutics (2014) 21(6)
