Is Takotsubo cardiomyopathy still looking for its own nosological identity?

Table 1 Characterizing the differences between Takotsubo cardiomyopathy and myocardial infarction with non-obstructive coronary arteries

	Takotsubo cardiomyopathy	MINOCA
Clinical findings	A more aggressive acute phase despite a better long-term cardiovascular prognosis	A less aggressive acute phase despite a worse long-term cardiovascular prognosis
Main pathophysiologic mechanisms	Sympathetic hyperactivity and a direct effect of catecholamines on β-adrenergic receptors of cardiomyocytes	Coronary plaque disruption; Coronary vasospasm; Spontaneous coronary artery dissection; Microvascular dysfunction; Coronary thromboembolism
Histopathologic lesions	Areas of myofibrillar damage with hypercontracted sarcomeres and mononuclear infiltrates	Absence of myofibrillar damage with atonic sarcomeres and polymorphonuclear infiltrates
Location of myocardial lesions	Around intracardiac nervous terminals	Around cardiac vessels
Inflammatory patterns	Increased levels of anti-inflammatory interleukins, able to remove damaged cells and preserve healthy myocardial tissue	Increased levels of pro-inflammatory interleukins, able to promote coronary plaque disruption and microvascular impairment
CMR findings	Transient and reversible transmural myocardial edema on T2-weighted imaging in the absence of late gadolinium enhancement	Late gadolinium enhancement (either subendocardial or transmural) with or without myocardial edema on T2-weighted imaging

CMR: Cardiac magnetic resonance; MINOCA: Myocardial infarction with non-obstructive coronary arteries.