Amiodarone-Induced Torsade De Pointes in a Patient with Wolff
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Hellenic J Cardiol 2009; 50: 224-226 Case Report Amiodarone-Induced Torsade de Pointes in a Patient with Wolff-Parkinson-White Syndrome 1 1 1,2 3 AAREF BADSHAH , BAKHTIAR MIRZA , MUHAMMAD JANJUA , RAJIV NAIR , 3 3 RUSSELL T. STEINMAN , JOHN F. COTANT 1Department of Internal Medicine, Saint Joseph Mercy-Oakland Hospital, Pontiac, Michigan, 2Department of Internal Medicine, William Beaumont Hospital, Royal Oak, Michigan, 3Department of Cardiology, Saint Joseph Mercy-Oakland Hospital, Pontiac, Michigan, USA Key words: Amiodarone is generally regarded to have a high safety profile with a low incidence of arrhythmias. However, Atrial fibrillation, there have been reports of torsades de pointes under certain conditions, such as electrolyte imbalance or amiodarone, T-wave alternans, Wolff- concomitant antiarrhythmic therapy. We describe a case of amiodarone-induced torsade de pointes early Parkinson-White after initiation of intravenous amiodarone in the setting of T-wave alternans. syndrome, torsade de pointes. miodarone is generally regarded to mate total dose of 1 g), sinus rhythm was have a high safety profile with a low restored. The analysis of the ECG upon A incidence of arrhythmias. How- cardioversion revealed a short PR interval ever, there have been reports of torsades with QT interval prolongation (QTm 582 de pointes under certain conditions, such as ms, QTc 582 ms) with evidence of pre-ex- Manuscript received: electrolyte imbalance or concomitant an- citation (delta waves) in the precordial December 25, 2008; tiarrhythmic therapy. We describe a case of leads (Figure 2) and macroscopic T-wave Accepted: amiodarone-induced torsade de pointes ear- alternans. In light of his electrocardiogra- March 3, 2009. ly after the initiation of intravenous amio- phic findings, it was suspected that the pa- darone in the setting of T-wave alternans. tient had experienced atrial fibrillation due to rapid anterograde conduction over Address: the accessory pathway. Intravenous amio- Case presentation Aaref Badshah darone was continued and an electrophys- Saint Joseph Mercy An approximately 60-year-old African iological study with possible catheter abla- Oakland American male was evaluated for com- tion was planned. However, that night the 44405 Woodward plaints of palpitations and dyspnea of 2 days’ patient’s telemeter monitoring recorded Avenue Pontiac, duration. The electrocardiogram revealed frequent asymptomatic multifocal prema- MI 48341-5023 USA wide complex tachycardia (Figure 1) with ture ventricular complexes (PVCs). Even- e-mail: intermittent loss of atrioventricular con- tually, the patient complained of “not feel- [email protected] duction, best seen in lead V1 (arrows). The ing well” and was found to be pale, light duration of the QRS complex was prolong- headed and shivering. Telemetry record- ed, measuring approximately 155 ms, with ings at this time showed a short run of sus- positive concordance in the precordial tained polymorphic ventricular tachycar- leads. The patient was transferred to the dia with undulation of the QRS complex coronary care unit on intravenous amio- compatible with torsade de pointes (Figure darone at 1 mg/min following a loading 3). Serum electrolytes and magnesium lev- dose of 150 mg. After 24 hours of intra- els were all within normal limits. Intra- venous amiodarone exposure (approxi- venous amiodarone was discontinued and 224 ñ HJC (Hellenic Journal of Cardiology) Amiodarone-Induced Torsade de Pointes Figure 1. Presenting 12-lead ECG with wide-QRS complex tachycardia. There is intermittent loss of atrioventricular con- duction best seen in lead V1 (arrows). The QRS width was measured to be approxi- mately 155 ms with positive concordance in the pre-cordial leads. Figure 2. A 12-lead ECG after intrave- nous amiodarone cardioversion demon- strates sinus rhythm with a short PR inter- val and QRS prolongation. Also present is shortening of the PR interval with slurred slow rising onset to the QRS or the delta waves in leads V1-V4 (arrows). Significant macroscopic T-wave alternans is also evi- dent on the chest leads (V2-V4). the patient was promptly taken to the electrophysiol- tiarrhythmic agent. Amiodarone has certain unique ogy laboratory where mapping confirmed a left lateral pharmacological properties that differentiate it from accessory pathway, which was ablated successfully. At other anti-arrhythmics,1 such as the ability to block the 6 months of follow up, he was clinically stable with the fast sodium channel and the slow ICa current mediated 2 QT interval prolongation no longer present (QT ~ 418 through the L-calcium channel. This calcium-channel ms, QTc ~ 438 ms). Nor was any delta wave visible at blocking action is an important factor explaining the this time. relatively low incidence of torsade de pointes associated with amiodarone. However, electrophysiological chang- es and ventricular tachyarrhythmia have sometimes Discussion been observed during high-dose amiodarone loading This case illustrates the proarrhythmic potential of within the first day of therapy under certain clinical amiodarone, a commonly prescribed and potent an- conditions.3,4 This appears to be the case with our pa- (Hellenic Journal of Cardiology) HJC ñ 225 A. Badshah et al Figure 3. Telemetry strip revealing bradycardia with a long QT interval preceding a run of polymorphic ventricular tachycardia with undu- lation on the QRS axis (torsade de pointes). The rhythm self-resolved before any medical therapy could be initiated. tient, who was started on a maintenance dose of amio- be aware of the importance of careful patient monitor- darone (1 mg/ min) following a bolus (150 mg). Upon ing during amiodarone therapy, even with short-term conversion, his ECG revealed certain highly arrhyth- use, in high risk patients. mogenic milieus that significantly increased his risk for the development of ventricular arrhythmias. These in- cluded QT interval prolongation and rare macroscopic References T-wave alternans. Continuation of intravenous amio- 1. Podrid PJ. Amiodarone: reevaluation of an old drug. Ann In- darone despite these changes eventually led to torsade tern Med. 1995; 122: 689-700. in our patient. He had no history of ventricular tachy- 2. Nattel S, Talajic M, Quantz M, DeRoode M. Frequency-depen- dent effects of amiodarone on atrioventricular nodal function cardia before amiodarone administration and devel- and slow-channel action potentials: evidence for calcium chan- oped torsade within 24 hours of initiation of intravenous nel blocking activity. Circulation. 1987; 76: 442-449. therapy. Our case illustrates the importance of recog- 3. Lim HE, Pak HN, Ahn JC, Song WH, Kim YH. Torsade de nizing the proarrhythmic properties of amiodarone in pointes induced by short-term oral amiodarone therapy. certain high-risk situations. In our patient it was the Europace. 2006; 8: 1051-1053. 4. Tomcsányi J, Merkely B, Tenczer J, Papp L, Karlócai K. Ear- highly arrhythmogenic combination of prolonged QT ly proarrhythmia during intravenous amiodarone treatment. interval and T-wave alternans. Clinicians must therefore Pacing Clin Electrophysiol. 1999; 22: 968-970. 226 ñ HJC (Hellenic Journal of Cardiology) .