Profound hypokalaemia mimicking acute myocardial infarction.

Incidence and clinical significance of left ventricular thrombus in tako-tsubo cardiomyo-pathy assessed with echocardiography. Profound hypokalaemia mimicking acute myocardial infarction Sir, A 70-year-old female, recently diagnosed with metastatic rectal carcinoma requiring a de-functioning colostomy, presented to her local emergency department with chest pain in keeping with myocar-dial ischaemia. An initial electrocardiogram (ECG) demonstrated lateral ST-segment elevation and she was urgently transferred to the regional percuta-neous coronary intervention (PCI) centre. On arrival her pain had settled. Emergency coronary angiogra-phy revealed single vessel disease in the form of a heavily calcified non-flow limiting stenosis in the mid-portion of the right coronary artery. Echocardiography demonstrated a lateral wall motion abnormality with no evidence of malignant invasion of the pericardium or a pericardial effusion. Troponin I was raised at 1.9 mg/l confirming a myo-cardial infarction and routine biochemistry revealed a plasma potassium concentration of 2.9 mmol/l, for which she was commenced on an intravenous potassium chloride infusion. The following day she developed recurrent episodes of ventricular tachy-cardia (VT) and repeat ECG demonstrated gross global ST-segment elevation (Figure 1). She was immediately taken back to the catheterization laboratory, but angiographic appearances were unchanged from the previous day. Biochemistry now revealed profound hypokalaemia (2.1 mmol/l) despite replacement and hypocalcaemia (corrected 1.75 mmol/l). On further questioning she had noticed greatly increased output from her stoma over the previous week. Her rhythm stabilized and the ECG changes resolved over 24 h following aggressive intravenous replacement of electrolytes up to normal levels. This lady initially presented with ischaemic chest pain, lateral ECG changes and a correlating wall motion abnormality on echocardiography. Coronary artery disease was confirmed at angiogra-phy, but there was no evidence of an acute flow limiting lesion. Whether this was due to coronary vasospasm secondary to electrolyte disturbance or a self-resolving plaque rupture is unclear. Her deterioration the following day with the development of Figure 4. Echocardiogram (apical four chamber view) 4 weeks later demonstrating normal left ventricular ejection fraction.