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. 2021 Jan 28;10(3):479. doi: 10.3390/jcm10030479

Table 1.

Heart Failure Association diagnostic criteria for takotsubo syndrome (TTS).

Diagnostic criteria
1 Transient regional wall motion abnormalities of left ventricle (LV) or right ventricle (RV) myocardium which are frequently, but not always, preceded by a stressful trigger (emotional or physical).
2 The regional wall motion abnormalities usually a extend beyond a single epicardial vascular distribution and often result in circumferential dysfunction of the ventricular segments involved.
3 The absence of culprit atherosclerotic coronary artery disease including acute plaque rupture, thrombus formation, and coronary dissection or other pathological conditions to explain the observed pattern of temporary LV dysfunction (e.g., hypertrophic cardiomyopathy and viral myocarditis).
4 New and reversible electrocardiography (ECG) abnormalities (ST-segment elevation, ST depression, left bundle branch block (LBBB) b, T-wave inversion, and/or QTc prolongation) during the acute phase (3 months).
5 Significantly elevated level of serum natriuretic peptide (B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP)) during the acute phase.
6 Positive but relatively small elevation in cardiac troponin measured with a conventional assay (i.e., disparity between the troponin level and the amount of dysfunctional myocardium present). c
7 Recovery of ventricular systolic function on cardiac imaging at follow-up (3–6 months) d.

a Acute, reversible dysfunction of a single coronary territory has been reported. b Left bundle branch block may be permanent after takotsubo syndrome but should also alert clinicians to exclude other cardiomyopathies. T-wave changes and QTc prolongation may take many weeks to months to normalize after recovery of LV function. c Troponin-negative cases have been reported but are atypical. d Small apical infarcts have been reported. Bystander subendocardial infarcts, involving a small proportion of the acutely dysfunctional myocardium, have been reported. These infarcts are insufficient to explain the observed acute regional wall motion abnormality.