Ortega-Carnicer Julián, Benezet Juan, Ruiz-Lorenzo Francisco, Alcázar Roberto
Intensive Care Unit and Nephrology Service, Hospital Alarcos, Av Pio XII s/n, 13002 Ciudad Real, Spain.
Resuscitation. 2002 Nov;55(2):215-9. doi: 10.1016/s0300-9572(02)00210-1.
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.
Brugada综合征（BRS）是一种遗传性心脏疾病（其特征是基因突变影响钠通道功能），通过右胸前导联中QRS波群终末部分抬高（显著J波），随后ST段抬高下降并以负向T波结束，以及在无明显结构性心脏病的患者中出现恶性快速性心律失常来识别。我们报告了一名既往有癫痫病史且接受过具有钠通道阻滞作用的精神药物治疗以及慢性肾衰竭并接受血液透析的患者，该患者出现了高钾血症（6.6 mmol/L）且心电图表现类似于BRS。这种情况表现为右胸前导联中显著的J波、穹窿型ST段抬高和负向T波。血液透析后血钾恢复正常时，这些心电图改变消失。随后，氟卡尼试验未再现ST段抬高。我们得出结论，与心脏膜活性药物相关的高钾血症可能导致模仿Brugada综合征的心电图改变。
