Tako-tsubo cardiomyopathy (TC) typically presents with chest pain, ST changes, and transient left ventricular (LV) apical ballooning in the absence of epicardial coronary artery disease (CAD). This process is reversible and usually benign. An unusual manifestation is that of left ventricular outflow tract (LVOT) obstruction with systolic anterior motion of the mitral valve. Recognition of this finding is critical in patient management especially in the setting of cardiogenic shock, as inotropes are likely to aggravate and worsen the clinical condition. We provide a systematic review and an illustrative case, and discuss treatment strategies.Key words: tako-tsubo cardiomyopathy, left ventricular outflow tract obstruction, coronary vasospasm, left ventricular apical ballooning Tako-tsubo cardiomyopathy (TC) mimics acute myocardial infarction (MI) and should be considered in all patients, especially post-menopausal women who present with transient left ventricular (LV) dysfunction in the absence of obstructive coronary artery disease (CAD). Approximately 2% of all patients presenting with a presumed diagnosis of ST segment elevation MI have this syndrome, 1 and 87% of the reported cases of TC are post-menopausal women with a mean age of 68. 2 While TC frequently presents with substernal chest pain, these patients might present with electrocardiogram (ECG) changes alone, shortness of breath, or cardiogenic shock. 3 The ECG changes include ST elevation, ST depression, Twave inversion, pathologic Q waves, and QT prolongation. New left and right bundle branch blocks have been reported, 4 but the most common ECG changes are ST elevation (68%), which is most commonly seen in the precordial leads and diffuse T-wave inversions (97%). 2,4 The frequency of ST depression and Q waves is ∼10% and 27%, respectively. 3 -5 There is usually mild elevation of troponin, and less commonly, creatine kinase (CK) and its isoenzyme CK-MB, but the pattern differs from that seen following MI. In fact, cardiac enzyme levels peak at the onset of symptoms, and they do not slowly rise and fall as in MI.2,4 Troponin and CK-MB levels are elevated in 86% and 74% of the cases, respectively.
6Several LV wall motion abnormalities have been described in the setting of TC. The classic abnormality involves ballooning of the distal LV segments and apex as a result of severe hypokinesia, akinesia, or dyskinesia. At the same time, there is compensatory basal hyperkinesia. A less common variant involving mid-LV dyskinesia has also been described. 7 These transient LV wall motion abnormalities can be detected by left ventriculography, 2-Dimensional echocardiography (2DE), gated single photon emission computed tomography (SPECT), and magnetic resonance imaging (MRI), and usually involve multiple vascular territories. 8 The pathophysiology behind TC is poorly understood. However, according to a recent large systematic review of 542 cases, physical or emotional stress precipitated the reversible LV dysfunction in ∼80% of the cases.
2Excessive sympathetic stim...