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ST Segment Elevation in the Right Precordial Leads Following Administration of Class Ic Antiarrhythmic Drugs

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ST Segment Elevation in the Right Precordial Leads Following Administration of Class Ic Antiarrhythmic Drugs Heart 2001;85:e3 (http://www.heartjnl.com/cgi/content/full/85/1/e3) 1of3 CASE STUDIES Heart: first published as 10.1136/heart.85.1.e3 on 1 January 2001. Downloaded from ST segment elevation in the right precordial leads following administration of class Ic antiarrhythmic drugs M Yasuda, Y Nakazato, H Yamashita, G Sekita, Y Kawano, Y Mineda, K Nakazato, T Tokano, M Sumiyoshi, Y Nakata Abstract In 1992, Brugada and Brugada1 reported a Electrocardiographic changes were evalu- study of eight patients with idiopathic ventricu- ated retrospectively in five patients without lar fibrillation who showed ST segment eleva- previous episodes of syncope or ventricular tion in the right precordial lead (the Brugada 2–4 fibrillation who developed abnormal ST syndrome). Recent studies have reported that segment elevation mimicking the Brugada class I antiarrhythmic drugs such as flecainide, syndrome in leads V1–V3 after the admin- procainamide, and ajmaline could unmask ST istration of class Ic antiarrhythmic drugs. segment elevation in patients with “latent” Bru- Pilsicainide (four patients) or flecainide gada syndrome. In addition, we reported the first case5 of a patient who had no previous syn- (one patient) were administered orally for cope or ventricular fibrillation, but who showed the treatment of symptomatic paroxysmal electrocardiographic changes mimicking those atrial fibrillation or premature atrial con- of the Brugada syndrome after administration of tractions. The QRS duration, QTc, and JT a class Ic antiarrhythmic drug. Similar cases intervals on 12 lead surface ECG before were presented by us67and others8–10 in ensuing administration of these drugs were all years. In this article we present five such patients within normal range. After administration and evaluate retrospectively the mechanisms of of the drugs, coved-type ST segment eleva- precordial ST segment elevation on 12 lead sur- tion in the right precordial leads was face ECG in these patients. http://heart.bmj.com/ observed with mild QRS prolongation, but Division of Cardiology, there were no apparent changes in JT Department of intervals. No serious arrhythmias were Internal Medicine, Patients and method Juntendo University observed during the follow up periods. This study included five patients (four male School of Medicine, Since ST segment elevation with mild QRS and one female) without previous syncope or 2-1-1, Hongo, prolongation was observed with both pil- ventricular fibrillation who showed ST seg- Bunkyo-ward, Tokyo sicainide and flecainide, strong sodium ment elevation in the right precordial leads fol- 113-8421, Tokyo, Japan channel blocking eVects in the depolarisa- lowing administration of class Ic drugs (table on September 26, 2021 by guest. Protected copyright. M Yasuda Y Nakazato tion may have been the main factors 1). Four of the patients visited our outpatient H Yamashita responsible for the ECG changes. As the clinic because of palpitations which were G Sekita relation between ST segment elevation and caused by supraventricular arrhythmias, and Y Kawano the incidence of serious arrhythmias has the other patient was admitted to our hospital Y Mineda not yet been suYciently clarified, electro- for acute myocardial infarction between 1994 K Nakazato and 1999. Class Ic drugs were prescribed for T Tokano cardiographic changes should be closely M Sumiyoshi monitored whenever class Ic drugs are the control of supraventricular arrhythmias. Y Nakata given. There was no family history of life threatening (Heart 2001;85:e3) ventricular arrhythmias, syncope, or sudden Correspondence to: death in any of the patients. Liver function, Dr Y Nakazato renal function, and serum potassium, sodium, [email protected] Keywords: class Ic antiarrhythmic drugs; Brugada and magnesium electrolyte concentrations Accepted 16 August 2000 syndrome; ST segment elevation were within normal range in all of the patients. Table 1 Patient profiles and electrocardiographic changes Duration of Amplitude of the QRS width (secs) Underlying EF Dose treatment maximum ST Case Age/sex Arrhythmia disease (%) Drug (mg/day) (days) elevation Before After 1 70/M PACs None 68 P 100 28 2.5 mm (V1, V2) 0.09 0.11 2 62/F Paf MVR 62 P 150 14 3.9 mm (V2) 0.1 0.12 3 57/M Paf AMI, HT 40 P 200 4 5.3 mm (V3) 0.09 0.11 4 57/M Paf None 60 F 200 28 3.6 mm (V2) 0.09 0.1 5 73/M Paf SSS, HT 66 P* 150 14 2.7 mm (V1) 0.11 0.12 Paf, paroxysmal atrial fibrillation; PACs, premature atrial contractions; MVR, mitral valve replacement; AMI, acute myocardial infarction; HT, hypertension; SSS, sick sinus syndrome; EF, ejection fraction on echocardiography; P, pilsicainide; F, flecainide; *combined with digoxin. 2of3 Yasuda,Nakazato, Yamashita,et al Case 1 remained unchanged. The ST segment eleva- tion was the coved type in all cases, and the lead Heart: first published as 10.1136/heart.85.1.e3 on 1 January 2001. Downloaded from with maximum ST segment elevation varied in ABCBefore Pilsicainide After amplitude from 2.5–5.3 mm. No evidence of 100 mg/day discontinuation coronary artery spasm or other obvious causes for the ST segment elevation were evident. V1 Following discontinuation of the drugs, the ECG changes returned to within normal range. All five patients have since been attending our outpatient clinic every four weeks regularly, and serious arrhythmias or syncope have not V2 been detected so far. Discussion The main finding of this study is that abnormal ST segment elevation was presented following administration of class Ic drugs in five patients who experienced no previous syncope or V 3 ventricular fibrillation. Although the ST seg- Figure 1 Case 1. (A) Sinus rhythm with premature atrial contraction (PAC) before drug ment elevation was similar to that found in the treatment. (B) Four weeks after initiation of treatment with oral pilsicainide. ECG revealed Brugada syndrome, the relation between the abnormal ST segment elevation in leads V1–V3. (C) After discontinuation of pilsicainide ECG changes and the incidence of serious ST segment elevation returned to normal. arrhythmias has not yet been suYciently clari- The QRS duration, QTc, and JT interval on fied. The mechanism of ST segment elevation ECG were measured and compared before and in conjunction with the relevance of sodium after administration of class Ic drugs. In channel blocking eVects is discussed. addition, the ECG lead with the maximum ST Class Ic drugs are known to be eVective for segment elevation and the type of elevated ST the treatment of various arrhythmias.11 On the segment in its configuration were also evaluated. other hand, proarrhythmic eVects and other adverse eVects712 have also been reported. Results Recently, some cases of ST segment elevation Patient profiles and ECG changes are listed in in the right precordial leads following adminis- tration of class Ic drug were reported by our table 1. The QRS duration, QTc, and JT inter- 5–7 89 vals before the administration of the class Ic group and others. drugs were within normal range in all the In recent studies, the mechanisms of ST seg- patients. The QRS duration was prolonged in ment elevation in the Brugada syndrome are the five patients by 10–22% with an average thought to derive from the transmural http://heart.bmj.com/ prolongation of 17%, and the QTc was heterogeneity in repolarisation across the wall of the right ventricular (RV) outflow prolonged by 2–5.1% with an average prolon- 231213 gation of 4.3% (figs 1, 2, and 3). JT intervals tract. Also, in some patients with the Brugada syndrome, a mutation in the cardiac Case 2 Case 3 sodium channel gene SCN5A that could cause the heterogeneity has been described.414 Before Pilsicainide Before Pilsicainide In our cases, abnormal ST segment elevation 150 mg/day 200 mg/day with mild prolongation of the QRS duration on September 26, 2021 by guest. Protected copyright. and QTc was noted following administration of V1 flecainide and pilsicainide, but there were no V1 changes in the JT intervals. These drugs mainly block sodium channels resulting in a reduction of the amplitude of phase 0 of the action poten- tial. When the amplitude of phase 0 decreases in V V2 2 the subepicardium, phase 1 ends at a more negative potential, and this could bring the membrane potential to a voltage below that required for the activation of the calcium V 3 V3 current. As a result of the conduction abnor- malities and the reduction of ICa during the early phase of the action potential, ST segment elevation mimicking the Brugada syndrome could be induced. The appearance of the ST segment elevation only in the right precordial Figure 2 Case 2. (Left strip) Paroxysmal atrial fibrillation (Paf). (Right strip) Two leads in our patients is consistent with the weeks after initiation of oral pilsicainide. ECG revealed atrial flutter with 2:1 atrioventricular conduction with pronounced ST segment elevation at leads V1–V3. observation that the transient outward current Case 3. (Left strip) On the third day of acute anteroseptal myocardial infarction. ECG Ito is dominant in the right ventricular epicar- revealed sinus rhythm with abnormal Q wave and mild ST segment elevation in leads dium. In our cases, both flecainide with a V1–V6 and I, aVL. Thereafter repeated Paf episodes were noted. (Right strip) Four days after initiation of pilsicainide. ECG exhibited pronounced ST segment elevation in leads potassium channel blocking eVect and pilsicai- V1–V3. After discontinuation of pilsicainide, a combination of oral verapamil and pirmenol nide without a potassium channel blocking eVectively prevented the Paf and abnormal ST elevation was not recognised. In this case, eVect induced ST segment elevation. In addi- left ventricular aneurysm and new ischaemic episodes such as chest pain and elevations in 8 serum myocardial enzymes were not recognised during the ST segment elevation after tion, Nakamura and colleagues reported that administration of pilsicainide.
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