Tako-tsubo cardiomyopathy: how stress can mimic acute coronary occlusion
Author: Laven Padayachee
Published online: 17 March 2008
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.
References
- Abdulla I, Ward MR. Tako-tsubo cardiomyopathy: how stress can mimic acute coronary occlusion. Med J Aust 2007; 187: 357-360.
- Gianni M, Dentali F, Grandi AM, et al. Apical ballooning syndrome or takotsubo cardiomyopathy: a systemic review. Eur Heart J 2006; 27: 1523-1529. 0_i1091836
- Wittstein IS, Thiemann DR, Lima JA, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005; 352: 539-548. 0_i1091839
- Fujiwara S, Takeishi Y, Isoyama S, et al. Responsiveness to dobutamine stimulation in patients with left ventricular apical ballooning syndrome. Am J Cardiol 2007; 100: 1600-1603. 0_i1091841
- Padayachee L. Levosimendan: the inotrope of choice in cardiogenic shock secondary to takotsubo cardiomyopathy? Heart Lung Circ 2007; 16 Suppl 3: S65-S70. 0_i1091844