Abstract

Takotsubo cardiomyopathy (TCMP), also known as stress cardiomyopathy or broken‐heart syndrome, is an increasingly recognized form of transient left ventricular (LV) dysfunction that is often completely reversible.1, 2, 3, 4 It is diagnosed in ≈1% to 2% of patients initially presenting with symptoms suggestive of acute coronary syndrome.2 It often presents with dyspnea, hypotension, syncope, elevated troponin levels, and ST elevations or T wave inversions on electrocardiography.1 Coronary angiography classically reveals normal coronary arteries with no significant stenosis, though bystander coronary disease could be present, which is often mild and not severe enough to account for the degree of ventricular dysfunction.1, 2 Complications can occur early in its course and include arrhythmia, thrombus formation, LV outlet tract obstruction, ventricular rupture, cardiogenic shock, and cardiac arrest.1, 3 An up to 8% mortality rate has been reported with excellent recovery in 95%.3 Classically it has been described following a physical and emotional event, with recurrence rates of 10% to 11% on revival of triggering factors.1 Several variants of TCMP have been described. The typical or apical variant consists of a hyperkinetic LV base with focal apical akinesis resulting in apical ballooning and reduced ejection fraction. Other variants such as the inverted or basal pattern (circumferential basal hypokinesis and apical hypercontractility), the mid LV variant (circumferential midventricular hypokinesis and both basal and apical hypercontractility), and the biventricular apical and right ventricular pattern have been described.1, 4 The exact pathogenesis is not fully understood with vast unanswered questions remaining, though a central role of catecholamines has been widely accepted. The stress related to metabolic dysfunction can be the initial trigger for the sympathetic surge found in this disorder. Several case reports have described its occurrence secondary to a number of endocrine disorders, though this has not been comprehensively evaluated. Here we have attempted to review all of the published reports of associations of endocrine conditions with TCMP and discuss some postulated mechanisms by which this may occur. This review will mainly focus on the potential association of pituitary, thyroid, adrenal, and estrogen metabolic disorders with this transient reversible cardiomyopathy and how hormones can impact cardiac function. This review suggests that hormonal dysregulation should be considered in patients presenting with cardiac abnormalities.

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