Drugs, electrolytes and tako-tsubo cardiomyopathy: triple aetiology of acquired long QT syndrome and torsades de pointes.

Editor,

Physical or emotional stress can have unforeseen consequences. We document a 67 year-old female admitted with syncope following emotional stress. She had a history of depression and had been “crying and crying all day”. In addition, she had a history of ileostomy following severe diverticular disease. Her daily medication included ondansetron 4mg b.d. for nausea and fluoxetine 60mg for depression.

On admission, serum magnesium was low at 0.73mmol/l (0.75 – 1.25) and serum potassium was 3.9mmol/l (3.5 – 5.1). Troponin I was mildly elevated at 0.17u/l (0 – 0.04). B-type natriuretic peptide (BNP, Abbott) was grossly elevated at 2569pg/ml (normal < 100). Initial ECG (fig 1) showed new T wave inversion in ECG leads; II, III, aVf and V1 through to V6 with a prolonged corrected QT interval (QTc) of 524ms (upper limit of normal for females = 450ms). An ECG dated June 2007 was normal apart from a QTc of 509ms. She was initially treated as an anterior non-ST segment elevation myocardial infarction. Shortly after admission, she developed polymorphic ventricular tachycardia (torsades de pointes, figure 2). The risk of torsades de pointes increases substantially once QTc is > 500 ms. This was treated with a 200J DC shock, 4mmol of intravenous magnesium with oral beta-blocker, and potassium therapy. Further self-terminating runs of torsades de pointes occurred when her potassium levels dipped below 4mmol/l.

Fig 1

Leads V1 – V6 of admission 12-lead ECG showing T wave inversion resembling non-ST segment elevation MI. QTc is greatly prolonged at 524ms.

Fig 2

ECG monitor tracing shows a characteristic short (A), long (B), short (C) sequence of ventricular activity initiating polymorphic ventricular tachycardia also known as “torsades de pointes” for its twisting QRS axis about the iso-electric line.

On day two, she underwent cardiac catheterisation, which showed normal coronary arteries but marked impairment of systolic function in the apical half of the left ventricle with a characteristic “ballooning” appearance (figure 3). These findings, in association with physical or emotional strain, are diagnostic of tako-tsubo cardiomyopathy. Oral magnesium supplements and bisoprolol 5mg were added in to her medication. Ondansetron and fluoxetine both prolong the QT interval and were stopped. A cardio-defibrillator device was implanted due to continued risk of arrhythmia from electrolyte loss from the ileostomy. The QTc came down to 454ms and BNP fell to 179pg/ml at discharge.

Fig 3

Left ventriculography during diastole (A) and systole (B) demonstrate typical left ventricular apical ballooning and hyper-contractile base of tako-tsubo cardiomyopathy.

QT prolongation is the surface ECG manifestation of abnormal repolarisation of myocardial cells due to problems with cellular ion channels. The disorder is classified as either congenital or acquired. Acquired QT prolongation may be due to:

Electrolyte depletion, particularly potassium or magnesium,

Drugs that affect myocardial ion channels

A feature of tako-tsubo cardiomyopathy, a catecholamine induced metabolic disorder of myocardial cells caused by physical or emotional stress, especially seen in older females1,2.

A reference list of drugs causing QT prolongation is available from the University of Arizona () or the British National Formulary.

Initial presentation and ECGs in tako-tsubo cardiomyopathy are similar to an anterior ST or non-ST segment myocardial infarction but often with QT prolongation. A small troponin rise may be seen but coronary arteries are normal with a characteristic “apical ballooning” or Japanese octopus pot (“tako-tsubo”) pattern seen on ventriculography. Beta-blockade is a key element of treatment. The ventricular changes are mostly reversible if the patient survives the acute phase3.

Our patient had all three causes of an acquired QT prolongation – excessive secretion from her ileostomy producing hypomagnesaemia, daily ondansetron and fluoxetine therapy, and acute tako-tsubo cardiomyopathy. We believe the development of tako-tsubo cardiomyopathy exacerbated our patient's pre-existing QT prolongation to a degree where potentially fatal arrhythmias occurred.

A case of congenital long QT syndrome and tako-tsubo cardiomyopathy with torsades de pointes has been described4 but MEDLINE and PubMed searching (keywords: long QT and cardiomyopathy) revealed no acquired cases. Tako-tsubo cardiomyopathy induced by physical or emotional stress may exacerbate an underlying long QT syndrome with risk of sudden cardiac death.