Case report

Transient Brugada-type electrocardiographic abnormalities in renalfailure reversed by dialysis

Julian Ortega-Carnicer *, Juan Benezet, Francisco Ruiz-Lorenzo, Roberto Alcazar

Intensive Care Unit and Nephrology Service, Hospital Alarcos, Av. Pio XII s/n, 13002 Ciudad Real, Spain

Received 20 January 2002; received in revised form 25 February 2002; accepted 11 June 2002

Abstract

The Brugada syndrome (BRS) is a hereditary cardiac condition (characteristically with a gene mutation affecting sodium channel

function) identified by an elevated terminal portion of the QRS complex (prominent J wave) followed by a descending ST-segment

elevation ending in a negative T wave in the right precordial leads, and malignant tachyarrhythmias in patients without

demonstrable structural heart disease. We report a patient with a previous history of epilepsy treated with psychotropic drugs (with

a sodium channel blocking effect) and chronic renal failure on haemodialysis who developed hyperkalaemia (6.6 mmol/l) and ECG

findings resembling BRS. This condition was manifested by the prominent J wave, the coved-type ST-segment elevation and the

negative T wave in the right precordial leads. These ECG changes disappeared after haemodialysis when the potassium became

normal. Subsequently, a flecainide test did not reproduce ST-segment elevation. We conclude that hyperkalaemia associated with

cardiac membrane active drugs may cause ECG changes mimicking the Brugada syndrome.

# 2002 Elsevier Science Ireland Ltd. All rights reserved.

Keywords: Brugada syndrome; Hyperkalaemia; Haemodialysis; ST-segment elevation; J wave; Peaked T wave; Psychotropic drugs

Resumo

O Sındrome de ‘‘Brugada’’ (BRS) e uma doenca cardıaca hereditaria (mutacao genetica que afecta o funcionamento dos canais de

sodio) caracterizada pela elevacao da porcao terminal do QRS (onda J proeminente) seguida de elevacao do segmento ST

terminando com uma onda T invertida nas derivacoes pre-cordiais direitas e taquiarritmias malignas em doentes sem doenca

cardıaca estrutural. Descrevemos o caso clınico de um doente com antecedentes de epilepsia em tratamento com psicotropico (com

efeito bloqueador dos canais de sodio) e insuficiencia renal cronica em hemodialise. Este doente desenvolveu hiperkalemia (6.6

mmol/l) e alteracoes electrocardiograficas semelhantes a BRS. Verificou-se onda J proeminente seguida de elevacao do segmento ST

terminando com uma onda T negativa nas precordiais direitas. Estas alteracoes electrocardiograficas desapareceram apos a dialise

quando o potassio normalizou. Fez-se um teste com Flecainida que nao reproduziu as alteracoes. Concluimos que a hiperkalemia

associada a farmacos com papel activo na membrana miocardica podem provocar alteracoes electrocardiograficas que mimetizam o

BRS.

# 2002 Elsevier Science Ireland Ltd. All rights reserved.

Palavras chave: Sındrome de ‘‘Brugada’’; Hipercalemia; Hemodialise; Supradesnivelamento ST; Onda J; Ondas T ponteagudas; Farmacos

psicotropicos

Resumen

El sındrome de Brugada (BRS) es una condicion cardıaca hereditaria (caracterısticamente con una mutacion genetica que afecta la

funcion de los canales de sodio), identificada por una elevacion en la porcion terminal del complejo QRS (onda J prominente)

seguida por una elevacion descendente del segmento ST terminando en una onda T negativa en la derivaciones precordiales

* Corresponding author. Tel.: �/34-926-213-444; fax: �/34-926-210-298

E-mail address: jortegacar@nexo.es (J. Ortega-Carnicer).

Resuscitation 55 (2002) 215�/219

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PII: S 0 3 0 0 - 9 5 7 2 ( 0 2 ) 0 0 2 1 0 - 1

derechas, y la presencia de taquiarritmias malignas en pacientes sin enfermedad cardıaca estructural demostrable. Reportamos el

caso de un paciente con una historia previa de epilepsia tratado con drogas sicotropicas (con efecto bloqueador de los canales de

sodio) y con falla renal cronica en hemodialisis, quien desarrollo hipercalemia (6.6 mmol/l) y hallazgos electrocardiograficos que

simulaban un BRS. Esta condicion se manifesto por una onda J prominente, una elevacion descendente de segmento ST curvado y

una onda T negativa en las derivaciones precordiales derechas. Estos cambios del ECG desaparecieron despues de la hemodialisis

cuando el potasio se hizo normal. Subsecuentemente, una prueba de flecainamida no reprodujo la elevacion del segmento ST.

Concluimos que la hipercalemia asociada con drogas activas en la membrana cardıaca puede producir cambios en el ECG que

imitan el sındrome de Brugada.

# 2002 Elsevier Science Ireland Ltd. All rights reserved.

Palabras clave: Sındrome de Brugada; Hipercalemia; Hemodialisis; Elevacion del segmento ST; Onda J; Onda T picuda; Drogas psicotropicas

1. Introduction

The Brugada syndrome (BRS) is a hereditary cardiac

condition (characteristically with a gene mutation af-

fecting sodium channel function) identified by an

elevated terminal portion of the QRS complex (promi-

nent J wave) followed by a descending ST-segmentelevation ending in a negative T wave in the right

precordial leads, and malignant tachyarrhythmias in

patients without demonstrable structural heart disease

[1�/4]. Although Gussak et al. [3] in a recent literature

review of the BRS listed hyperkalaemia as a cause of ST-

segment elevation in the right precordial leads, clinical

cases of hyperkalaemia-induced ECG abnormalities

simulating the BRS have not been specifically men-tioned in the literature. We report a patient with

hyperkalaemia and psychotropic drugs intake who had

ECG findings mimicking the BRS.

2. Case report

A 34-year-old man was admitted to the hospital

because of prolonged and repetitive episodes of tonic�/

clonic contractions of the right arm with secondarygeneral seizures. During monitoring, these seizures were

not accompanied by ventricular arrhythmias. He was

treated with intravenous diazepan and phenytoin, but

the seizures continued and the patient was transferred to

the Intensive Care Unit (ICU). His medical history

included alcohol abuse, peripheral obliterating arterio-

pathy, epilepsy and malignant hypertension with

chronic renal insufficiency treated by haemodialysis.There was no history of chest pain or syncope. Cardiac

events or sudden death were not recorded in members of

his family. His medication included carbamazepine (800

mg/day), phenytoin (200 mg/day), risperidone (2 mg/

day), ticlopidine (250 mg/day), calcium carbonate (2.5

mg/day) and folic acid (5 mg/day).

On physical examination, the patient was lethargic,

with a blood pressure of 135/85 mmHg, a pulse rate of100/min, and a temperature of 37.5 8C. Cardiopulmon-

ary examination revealed normal breath sounds and soft

heart sounds without murmurs. Serum biochemistry

revealed a creatinine of 1096 mmol/l and hyperkalaemia

of 6.6 mmol/l (Table 1). The phenytoin plasma concen-

tration was 8.5 mg/ml (upper limit of therapeutic

concentration in renal insufficiency: 10 mg/ml). Serial

creatine phosphokinase values peaked at 560 U/l (MB

fraction of 20 U/l), which was interpreted as presumably

due to the patient’s seizures. Chest X-ray was normal.

The ECG (Fig. 1) showed sinus tachycardia at 105

beats/min with PR-interval of 0.16 s, and mean electrical

QRS axis of 08. There was a prominent J wave followed

by a coved type ST-segment elevation ending in a

negative T wave in leads V1 and V2 resembling the

BRS. There was also a saddle-back type ST-segment

elevation in lead V3 and a peaked T wave in leads V3 to

V5 characteristic of potassium intoxication.Treatment with a midazolam infusion at 0.5 mg/kg

per h resulted in complete remision of seizures. Intrave-

nous nitroglycerin had no effect on the ST-segment

elevation. Sodium bicarbonate administration decreased

the serum potassium to 5.9 mmol/l, and a concomitant

ECG revealed a reduction of the magnitude of the J

wave, ST-segment elevation, and T wave. The patient

Table 1

Laboratory tests on admission

White blood cells (109/l): 7.3

Neutrophils (%) 76

Red blood cells (1012/l) 3.4

Haematocrit (l/l) 0.34

Haemoglobin (g/l) 113

Platelet count (109/l) 141

Total protein (g/l) 67

Creatinine (mmol/l) 1096

Glucose (mmol/l) 6

Sodium (mmol/l) 139

Potassium (mmol/l) 6.6

Calcium (mmol/l) 2.2

Magnesium (mmol/l) 0.91

CK (UI/l) 281

CK-MB (UI/l) 9.6

Arterial blood gases (FiO2: 0.21):

pH 7.33

PO2 (kPa) 59

PCO2 (kPa) 29

Bicarbonate (mmol/l) 15.5

J. Ortega-Carnicer et al. / Resuscitation 55 (2002) 215�/219216

was dialyzed. After the procedure, the ECG changes

disappeared coinciding with a serum potassium value of

3.4 mmol/l (Fig. 2). An echocardiogram was normal.

The flecainide test (2 mg/kg) did not reproduce ST-

segment elevation. The patient remained seizure free and

midazolam was discontinued without complications.

3. Discussion

In 1956, Levine et al. [5] described a ‘dialyzable’

current of injury in potassium intoxication resembling

acute myocardial infarction or pericarditis. Since then,

ST-segment elevation (with or without associated right

bundle branch block) has been noted rarely in associa-

tion with hyperkalaemia, usually secondary to diabeticketoacidosis, renal failure or potassium replacement [6�/

10]. This patient had moderate hyperkalaemia (probably

caused by a composite effect of chronic renal failure and

rhabdomyolysis from seizures) and atypical ECG find-

ings resembling the BRS [1�/4], as evidenced by the

prominent J wave, the coved-type ST-segment elevation

and the negative T wave in the right precordial leads.

There was also symmetrically peaked T waves in leadsV3 to V5 characteristic of potassium. All ECG changes

disappeared after haemodialysis when the potassium

was returned to normal. Subsequently, the flecainide test

performed to unmask a ‘latent’ BRS did not reproduce

the ST-segment elevation [11].

A similar ST-segment elevation has been noted in the

case of anteroseptal or right myocardial infarction [12],

but the absence of evolutionary ECG changes (new Q orinverted T waves) and the normal cardiac isoenzyme

determinations and echocardiographic evaluation ex-

cluded the presence of myocardial infarction. Although

Fig. 1. The ECG recorded with a serum potassium of 6.6 mmol/l

shows prominent J wave and coved type ST-segment elevation ending

in a negative T wave in leads V1 and V2 resembling the Brugada

syndrome. There is also a saddle-back type ST-segment elevation in

lead V3, and a peaked T wave in leads V3 to V5 characteristic of

potassium intoxication.

Fig. 2. The ECG obtained immediately after haemodialysis, coincid-

ing with a serum potassium of 3.4 mmol/l, reveals complete resolution

of both the ST-segment elevation in leads V1 to V3 and the peaked T

wave in leads V3 to V5.

J. Ortega-Carnicer et al. / Resuscitation 55 (2002) 215�/219 217

a vasospastic angina has been reported in patients with

Brugada-type ECG abnormalities [13], the presence of a

coronary vasospasm was unlikely because the ST-

segment did not show any change despite the nitrogly-

cerin infusion.

Recently, Littmann et al. [14] and one of us [15]

reported two patients with cocaine-induced transient

ECG changes simulating BRS. Although toxicology

studies were not performed in this case,, we believe

that cocaine was not involved because this well known

chronic renal patient and his family denied cocaine use.

The electrophysiological mechanism for these ECG

abnormalities in the right precordial leads is unclear. As

in acute ischaemia, hyperkalaemia causes a decrease in

the resting membrane potential, which in turn leads to

inactivation of sodium channels and slowing of conduc-

tion in all cardiac tissues [16,17]. Some myocardial

regions (usually the anteroseptal wall) appear to be the

most sensitive to these effects due to greater accumula-

tion of potassium in their extracellular space [18]. Right

precordial ST-segment elevation secondary to regional

hyperkalaemia have been observed experimentally by

direct myocardial application of potassium [19], and

after injection of potassium salts into the coronary

arteries [20] and into subepicardium [21]. This hetero-

geneous sensivity may cause a voltage gradient between

normal and hyperkalaemic zones causing ST-segment

elevation secondary to a diastolic current of injury (due

to depolarization of resting membrane potential) or to a

combination of diastolic and systolic current of injury

(due to a reduction of action potential amplitude)

[22,23]. In our case, there was also a large, terminal,

negative T wave following ST-segment elevation in V1�2

leads. This ECG finding may occur when activation of

hyperkalaemic cells are considerably delayed, and

repolarization in the hyperkalaemic area occurred later

than in non-hyperkalaemic myocardium [10,21].

Although there is no precise clinical correlation

between the surface ECG and the serum potassium level

[24], absolute hyperkalaemia cannot explain totally the

ECG changes observed in our case. The administration

of antiarrhythmic agents Class I [25] and psychotropic

drugs [26,27] may cause transient anteroseptal ST-

segment elevation similar to that observed in patients

with the BRS. Since this patient had taken carbamaze-

pine and phenytoin (with sodium channel blocking

effect) and risperidone (with QT-interval prolongation

effect), the coadministration of these drugs could

increase the toxicity of hyperkalaemia because they

may facilitate a loss of the epicardial action potential

dome. In such circumstances, the ECG display ECG

changes simulating the BRS. Although Class IB sodium

channel blockers have no effect on the ST segment

elevation, phenytoin may also slow conduction at high

potassium concentrations [28].

We conclude that moderate hyperkalaemia associated

with cardiac membrane active drugs may cause ECG

changes simulating the BRS.

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