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Cardiovascular Disease |

Amiodarone Use Unmasking Brugada ECG Pattern

Sharad Bajaj*, MD; Nishant Gupta, MD; Yazan Alkhoury, MD; Constantinos Costeas, MD; Fayez Shamoon, MD
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St. Michael's Medical Center, Seton Hall University, Newark, NJ


Chest. 2012;142(4_MeetingAbstracts):92A. doi:10.1378/chest.1390815
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Abstract

SESSION TYPE: Cardiovascular Cases

PRESENTED ON: Wednesday, October 24, 2012 at 11:15 AM - 12:30 PM

INTRODUCTION: Brugada syndrome, first described in 1992, is primarily an autosomal-dominant condition that predisposes individuals with structurally normal hearts to ventricular arrhythmias and sudden cardiac death. It is associated with various channelopathies, with mutations affecting sodium channel being the commonest. It is characterized by its typical ECG pattern with ST-segment elevation in the precordial leads V1-V3, with QRS morphology mimicking RBBB. We report a case of unmasking of Brugada ECG pattern and VT storm brought on by amiodarone infusion.

CASE PRESENTATION: A 64-year old African-American gentleman with past medical history significant for hypertension, diabetes mellitus, peripheral arterial disease and end-stage renal disease on hemodialysis was admitted to our institution with a diagnosis of non-ST elevation myocardial infarction. Cardiac catheterization revealed severe triple vessel coronary artery disease with mild left ventricular systolic dysfunction. He subsequently underwent successful coronary artery bypass grafting for the same. Post operatively, he was started on amiodarone infusion for atrial fibrillation prophylaxis. Two days after his surgery, he suddenly went into cardiac arrest secondary to electrical storm with multiple episodes of ventricular tachycardia and ventricular fibrillation requiring multiple defibrillations. Subsequently, over the next three days, inspite of continuous amiodarone and lidocaine infusion patient continued to have multiple episodes of non-sustained as well as sustained, monomorphic as well as polymorphic ventricular tachycardia, requiring ICD implantation. To our surprise, the day after the ICD implantation patient started demonstrating an ECG pattern consistent with both Brugada type 1 and 2 phenotypes. Decision was made to discontinue both amiodarone and lidocaine. Thereafter, no further episodes of ventricular tachycardia were recorded during the rest of the hospital stay. And over a few days period even the Brugada specific ECG changes resolved and patient was discharged from the hospital.

DISCUSSION: Amiodarone is predominantly a potassium ion channel blocking agent (Vaughan Williams class III). However, it has also been shown in-vitro to have sodium ion channel blocking properties, especially in the acute phase of its administration. This provides a probable justification for this unusual observation in the present case. To our knowledge, there are only two case reports ever reported in the literature illustrating this phenomenon as a result of acute amiodarone therapy.

CONCLUSIONS: This particular case highlights the need to explore and understand various mechanisms that are responsible for pro-arrhythmic effects of commonly used anti-arrhythmic drugs.

1) Unmasking of the Brugada Syndrome Phenotype During the Acute Phase of Amiodarone Infusion. Gideon Paul, Shamil Yusuf and Sanjay Sharma. Circulation 2006, 114:e489-e491

DISCLOSURE: The following authors have nothing to disclose: Sharad Bajaj, Nishant Gupta, Yazan Alkhoury, Constantinos Costeas, Fayez Shamoon

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St. Michael's Medical Center, Seton Hall University, Newark, NJ

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