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• True pseudo-myocardial infarction?
  Robert J Huggett
  Published on: 6 September 2005

• Published on: 6 September 2005

  True pseudo-myocardial infarction?

  • Robert J Huggett, SpR Cardiology
  • Other Contributors:
    • Dr Gillian E Payne

  Dear Editor,

  In the recent issue of Heart, Egred et al.[1] reported an important example of pseudo-myocardial infarction in a patient with diabetic ketoacidosis. This was presumably related to hyperkalaemic effects on the ECG.

  However, in the current case report it is not mentioned why the patient developed ketoacidosis and in the context of a sepsis syndrome other factors may be at play to orchestrate the...

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  Dear Editor,

  In the recent issue of Heart, Egred et al.[1] reported an important example of pseudo-myocardial infarction in a patient with diabetic ketoacidosis. This was presumably related to hyperkalaemic effects on the ECG.

  However, in the current case report it is not mentioned why the patient developed ketoacidosis and in the context of a sepsis syndrome other factors may be at play to orchestrate these changes. Indeed whilst hyperkalaemia has been previously shown to cause ST elevation, this has been often in the context of other pathology.[1-6]

  It has also been suggested that IV potassium replacement in hypokalaemic patients may also cause a pseudo-infarct ECG pattern.[5] In addition, we have recently seen a case of a 30 year old female IV drug user who presented with sepsis and pulmonary embolism. On admission to the high dependency unit her ECG showed similar ECG changes to that reported by Egred et al. of tall peaked T waves (Panel A) but conversely the potassium was 3.1 mmol/l, corrected calcium 2.01 mmol/l, phosphate 0.6 mmol/l and magnesium 0.9 mmol/l. She was therefore given gradual IV potassium replacement.

  On day 2 of her stay she developed again remarkably similar ECG changes as that reported by Egred et al. (Panel B) and whilst fibrinolytic therapy was considerd; this was rejected on the lack of ischaemic symptoms and the bizarre nature to these ECG changes. Of particular note was normal serial troponin levels and lack of wall motion abnormalities on echocardiography. Also serial ECGs revealed a gradual improvement in these changes as the patient’s electrolyte abnormalities and sepsis improved.

  We feel, therefore, that there are other possible alternative explanations to these ECG changes including sepsis with intracellular shifts in potassium, pulmonary embolism and even adrenergic hyperstimulation which could all lead to a picture of ‘sick’ cardiomyocytes with alteration in their action potential mimicking an injury current seen in myocardial necrosis.

  Yours faithfully,

  Robert J Huggett*
  Gillian E Payne†

  SpR Cardiology*
  Consultant Cardiologist†

  Competing interests: None declared.

  1. M Egred, W L Morrison. Diabetic keto-acidosis and hyperkalaemia induced pseudo-myocardial infarction Heart 2005;91;1180.

  2. Levine HD, Wanzer SH, Merrill JP. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Circulation 1956;13:29-36.

  3. Boulmier D, Bazin P. Myocardial pseudo-infarction: "stress"- associated catecholamine-induced acute cardiomyopathy or coronary spasm? Ann Cardiol Angeiol 2000;49:449-54.

  4. Lim YH, Anantharaman V. Pseudo myocardial infarct-- electrocardiographic pattern in a patient with diabetic ketoacidosis. Singapore Med J. 1998;39:504-6.

  5. Madias JE, Madias NE. Hyperkalemia-like ECG changes simulating acute myocardial infarction in a patient with hypokalemia undergoing potassium replacement. J Electrocardiol. 1989;22:93-7.

  6. Hung SC, Chiang CE, Chen JD, Ding PY Images in cardiovascular medicine: pseudo-myocardial infarction.Circulation. 2000;101:2989-90.

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  Conflict of Interest:
  None declared.

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