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T Wave Alternans After Sotalol: Evidence for Increased Sensitivity to Sotalol After Conversion from Atrial fibrillation to Sinus Rhythm

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T Wave Alternans After Sotalol: Evidence for Increased Sensitivity to Sotalol After Conversion from Atrial fibrillation to Sinus Rhythm Heart 1998;80:303–306 303 CASE REPORT Heart: first published as 10.1136/hrt.80.3.303 on 1 September 1998. Downloaded from T wave alternans after sotalol: evidence for increased sensitivity to sotalol after conversion from atrial fibrillation to sinus rhythm H L Tan, A A M Wilde Abstract inhomogeneous distribution of repolari- A 64 year old woman with an 11 year sation controlling ion channels to induce Department of history of paroxysmal atrial fibrillation repolarisation abnormalities that may Cardiology, University of Amsterdam, presented to the emergency room because lead to torsade de pointes. Academic Medical of palpitations that had started two weeks (Heart 1998;80:303–306) Center, Amsterdam, previously. She had used sotalol 80 mg Netherlands once daily for three years without any epi- Keywords: T wave alternans; long QT syndrome; HLTan sodes of proarrhythmia or other adverse torsade de pointes; sotalol; atrial fibrillation Department of eVects. However, she developed pro- Cardiology, Heart nounced T wave alternans with giant Lung Institute, Utrecht inverted T waves and excessive QT pro- The ECG T wave reflects cardiac repolarisa- University Hospital, longation following sotalol administration tion. Its broad inscription results from the tem- Utrecht, Netherlands one day after conversion from atrial A A M Wilde poral inhomogeneity with which repolarisation fibrillation to sinus rhythm. This case proceeds through the heart. T wave changes, demonstrates bizarre T wave changes, T Correspondence to: including T wave inversion and T wave altern- Dr H L Tan, Department of wave alternans, and extreme QT prolon- ans, have been subdivided into primary and Cardiology, Academic gation following sotalol administration Medical Center, secondary forms. The latter results from a Meibergdreef 9, 1105 AZ shortly after conversion from atrial fibril- http://heart.bmj.com/ Amsterdam ZO, lation to sinus rhythm. In this situation, changed repolarisation sequence following an Netherlands. sotalol administration may be proar- altered activation sequence (such as bundle rhythmic, because it enhances repolarisa- branch block), whereas the former are caused Accepted for publication 1 24 April 1998 tion inhomogeneities based on a spatially by other factors. T wave alternans is a charac- teristic feature of congenital long QT syn- 23 0.8 *Cardioversion drome (LQTS) : it is associated with the ^Resuscitation excessive QT prolongation required for torsade de pointes4 and often precedes torsade de T wave 5 on September 26, 2021 by guest. Protected copyright. 0.7 pointes. T wave alternans also occurs in alternans LQTS induced by drugs that prolong the action potential.6 0.6 In patients receiving quinidine for atrial QTc fibrillation, torsade de pointes occurs most often shortly after conversion from atrial fibril- 0.5 lation to sinus rhythm.7 The mechanism underlying this finding is unknown. It may be caused by delayed adaptation of repolarisation 0.4 –3 yrs –6 mo –14 1 2 3 4 8 9 20 21 23 26 to the sudden change of heart rate,8 but an Day increased sensitivity to drugs that prolong the action potential in the period shortly following ***^ conversion to sinus rhythm may also play an 9 SR important role. We describe a patient who was using sotalol AF for paroxysmal atrial fibrillation for three years without proarrhythmic eVects or significant T wave changes, but she developed pronounced Sotalol 80 mg/day Sot Sotalol 80 40 mg tid T wave alternans with giant inverted T waves Digoxin and excessive QT prolongation following sota- lol administration one day after conversion Figure 1 Clinical events and ECG features. Abscissa is time scale whereby day 1 from atrial fibrillation to sinus rhythm. Figure 1 represents the day of the first presentation to the emergency room. Ordinate shows QTc duration. −3 yrs, 3 years before day 1; −6 mo, 6 months before day 1; SR, sinus rhythm; summarises the clinical events and ECG AF,atrial fibrillation; sot 80, single oral dose of 80 mg sotalol. features of this case. 304 Tan,Wilde The next day (day 2) she returned to the emergency room because she had suVered a Heart: first published as 10.1136/hrt.80.3.303 on 1 September 1998. Downloaded from transient episode of aphasia and right sided hemiparesis the night before. On presentation, her neurological dysfunctions had almost com- pletely disappeared. The ECG showed an atrial rhythm of 60 beats/min with deeper (compared to the ECG at discharge on day 1, not shown) negative T waves in V2 through V4, with a QT and QTc duration of 0.62 and U waves in all leads including the limb leads (fig 2, right panel). Although computed tomography of the brain showed no haematoma or cerebrovascu- lar accident, she was admitted to the neurology ward for observation. The next morning (day 3), two hours after taking sotalol, she suddenly experienced light- headedness, which was promptly followed by syncope. No cardiac rhythm monitoring was present, but physical examination showed severe hypotension (systolic blood pressure 60 mm Hg) and cyanosis. There were no signs of epilepsy. Chest compressions quickly re- stored blood pressure and consciousness, and the patient was referred to the coronary care unit. On admission there, the ECG showed atrial fibrillation with an average ventricular rate of 150 beats/min and positive TU waves in Figure 2 Left, ECG at presentation on day 1; Right, V2 through V5. The QT was 0.36 seconds and ECG at presentation on day 2. the QTc 0.60. Average blood pressure was 110/80 mm Hg. Sotalol was stopped and Case report digoxin was administered to control ventricular A 64 year old woman with an 11 year history of rate. The next day (day 4) the T waves in V2 paroxysmal atrial fibrillation presented to our through V4 had become deeply negative again. emergency room because of palpitations that Over the next days atrial fibrillation persisted at had started two weeks previously. She had used an average ventricular rate of 80 beats/min. No sotalol 80 mg once daily (and acenocoumarol) ventricular tachyarrhythmias occurred and the http://heart.bmj.com/ for three years without any episodes of neurological signs completely disappeared. proarrhythmia or other adverse eVects. ECGs The QT and QTc intervals gradually normal- during sinus rhythm six months and three years ised and the T waves flattened in all leads. On before presentation showed a QT interval of day 8, electrical cardioversion restored sinus 0.44 seconds and a rate corrected (Bazett) rhythm of 55 beats/min with a QT interval of QTc of 0.45; ST segments and T waves were 0.52 seconds and a QTc of 0.51. The deep normal. The voltages in the precordial leads negative T waves in V2 through V5 reappeared. met the criteria for left ventricular hypertro- Digoxin was stopped. The next day (day 9), we phy; however, this was probably due to her administered a challenge oral dose of 80 mg on September 26, 2021 by guest. Protected copyright. slender build as echocardiography showed no sotalol. The QT and QTc immediately before cardiac hypertrophy. There was no history of sotalol administration were 0.50 seconds and coronary artery disease or angina pectoris at 0.49, respectively (fig 3, left panel). Within 90 presentation or at any time during admission. minutes of sotalol administration there were ECG at presentation revealed atrial fibrillation giant negative T waves with T wave alternans with an average ventricular rate of 160 in V2 through V5 and prominent U waves in beats/min (QT 0.28 seconds, QTc 0.46). The alternate beats in all leads. QT and QTc inter- T waves were flattened in most leads (fig 2, left vals were prolonged: in V3, QT alternated panel). Physical examination and laboratory between 0.82 and 0.72 seconds, while QTc tests were normal (height 176 cm, weight alternated between 0.74 and 0.65 (fig 3, right 48 kg, average blood pressure 150/70 mm Hg, panel). This prompted us to stop sotalol. K+ 3.9 mmol/l, creatinine 44 µmol/l, INR 3.2). The next day (day 10), T wave alternans was Echocardiography showed a mildly dilated, not no longer present and over the next few days hypertrophic, left ventricle with mildly im- the T waves in the precordial leads gradually paired left ventricular function without wall became positive. On day 20, atrial fibrillation motion abnormalities. Both atria were mildly recurred with an average ventricular rate of 100 dilated and there was no thrombus in the left beats/min and positive T waves in all leads. atrium. To achieve sinus rhythm we infused Electrical cardioversion (day 21) restored sinus 100 mg flecainide. The resulting ECG showed rhythm without changing the T wave morphol- sinus rhythm of 72 beats/min with negative T ogy. Two days later (day 23) sotalol (40 mg tid) wavesinV2 through V5 (QT 0.42 seconds, QTc was readministered to prevent recurrence of 0.47). The patient was discharged and in- atrial fibrillation. Within three days, the T structed to continue taking sotalol and aceno- wavesinV2 through V3 became negative and coumarol. prominent U waves occurred in the precordial T wave alternans after sotalol 305 T WAVE CHANGES AFTER SUDDEN HEART RATE SLOWING AND THE ROLE OF IKr BLOCKADE Heart: first published as 10.1136/hrt.80.3.303 on 1 September 1998. Downloaded from T waves result from repolarisation, which occurs with temporal inhomogeneity between the transmural layers. This is based on an inhomogeneous distribution of repolarisation controlling ion channels: the transient outward current, Ito, is present in epicardium and mid-myocardium, but not in endocardium,11 12 while the slowly activating/deactivating compo- nent of the delayed rectifier current, IKs,is smaller in the mid-myocardium than in the other layers.13 Also, the activity of the inward rectifier current, IK1,diVers between these layers.14 Some conditions alter these inhomogeneities—for instance, in hypertrophic 15 16 hearts, Ito density is decreased.
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