To the Editor: Abdulla and Ward’s excellent article on tako-tsubo cardiomyopathy (TTC)1 raises two important issues.

The first issue is the diagnostic dilemma faced by emergency physicians and cardiologists in differentiating TTC from ST-elevation myocardial infarction (STEMI) in centres that lack coronary angiogram capabilities.

In patients presenting with chest pain and ST elevation on electrocardiography, the diagnosis of TTC might be suspected on recognition of risk factors and the common psychological, physical and emotional stressors that precipitate TTC.1 Supporting evidence can be obtained by demonstration of basal hyperkinesis and apical or midventricular hypokinesis on transthoracic echocardiography. This modality is now available in many centres without coronary angiography.

However, if the diagnosis is incorrectly made as STEMI rather than TTC, the patient runs the risk of unnecessary thrombolysis. Alternatively, after risk–benefit analysis, the clinicians may transfer the patient to a facility with coronary angiography to confirm TTC.

The second issue is the therapeutic dilemma facing intensivists treating TTC-related shock with adrenergic inotropes. Although cardiogenic shock in TTC is uncommon, it can still occur (4.2%).2 As increased endogenous catecholamines are thought to be central to the pathophysiology of TTC,3 treating shock with inotropes puts the clinician in a quandary.

Agents such as adrenaline, dobutamine, dopamine, milrinone and noradrenaline increase cyclic AMP within the myocardial cell, and are commonly used to restore blood pressure and cardiac output. However, in TTC, inotropes may theoretically delay resolution of the apical ballooning. A recent echocardiographic study showed no improvement in apical and midventricular akinesis with the use of low-dose dobutamine.4

Levosimendan is a calcium sensitiser that has been used successfully to stabilise shock secondary to TTC (with and without use of an intra-aortic balloon pump).5 Levosimendan is non-adrenergic and allows earlier introduction of β-blockers than would be possible with adrenergic inotropes.

I agree that prospective trials are needed to guide management in this intriguing condition.

In reply: I thank Padayachee for his interest in our review.1 We read Padayachee’s published case series of the use of levosimendan to help recovery of left ventricular dysfunction in tako-tsubo cardiomyopathy (TTC)2 after our review was published.

I agree that levosimendan is the inotropic agent of choice in this situation, and this approach has been used successfully in my hospital on two occasions. This is, in fact, what we meant by “In our experience, β-blockade in conjunction with non-adrenergic inotropes can prevent this vicious cycle and allow the ventricle to recover (unpublished data)”.

As Padayachee rightly points out, definitive evidence on this point would require a proper randomised trial, which would be very difficult to organise, given the low incidence of tako-tsubo cardiomyopathy and the small fraction of patients who develop cardiogenic shock requiring inotropic support. I think that it is probably better to simply state that levosimendan therapy works and makes scientific sense, so “just do it”.

However, Padayachee also surmises that, if the patient has a typical wall-motion abnormality and a typical history, it might be possible to avoid unnecessary thrombolytic therapy in cases of TTC. Unfortunately, my understanding is that this is not the case. Occlusion of the left anterior descending artery (LAD) may result in the classic TTC wall-motion abnormality if the LAD extends far beyond the apex (usually with a non-dominant right coronary). As myocardial infarction can be precipitated by stressful events, and the evolution of electrocardiographic changes in TTC is similar to that seen with an anterior infarct after thrombolysis, there is still no clear way to discriminate between the two diagnoses apart from immediate coronary angiography. Whether computed tomography (CT) angiography can accurately discriminate remains to be seen — this might be useful in centres that have CT but not a cardiac catheterisation laboratory. Until then, I believe it is probably less harmful to give TTC patients thrombolysis than to withhold thrombolysis from patients with large anterior infarcts.

Lastly, I invite Padayachee and other interested clinicians who frequently manage these patients to participate in an ongoing study of genetic predisposition to TTC for which we are currently enrolling participants.