Subject(s)
Myocardial Infarction , Percutaneous Coronary Intervention , Coronary Angiography , Coronary Vessels , Humans , Myocardial Infarction/diagnostic imaging , Myocardial Infarction/etiology , Myocardial Infarction/therapy , Percutaneous Coronary Intervention/adverse effects , Tomography, Optical Coherence , Treatment OutcomeSubject(s)
Aged , Humans , Male , Atrioventricular Block/etiology , Pulmonary Embolism/complicationsSubject(s)
Atrioventricular Block/etiology , Pulmonary Embolism/complications , Aged , Humans , MaleSubject(s)
Endocarditis, Bacterial/complications , Fibrinolytic Agents/therapeutic use , Myocardial Infarction/drug therapy , Thrombolytic Therapy , Aged , Diagnosis, Differential , Echocardiography, Doppler, Color , Electrocardiography , Endocarditis, Bacterial/diagnostic imaging , Follow-Up Studies , Humans , Male , Myocardial Infarction/complications , Myocardial Infarction/diagnosisABSTRACT
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.
