Iatrogenic epinephrine-induced reverse Takotsubo cardiomyopathy: direct evidence supporting the role of catecholamines in the pathophysiology of the “broken heart syndrome”

Abstract

Sirs Stress-induced transient cardiomyopathy (also known as Takotsubo cardiomyopathy) has been recognized as a disease entity since 1991 and accounts for 1% of acute coronary syndromes (ACS) that present with elevated cardiac biomarkers [1, 2]. About 80% of Takotsubo cardiomyopathy occurs in postmenopausal women [3]. The diagnosis depends on four criteria: (1) ST-segment changes or Twave inversions on the electrocardiogram, (2) transient wall motion abnormalities that are often inconsistent with coronary anatomy, (3) absence of obstructive coronary artery disease or evidence of acute plaque rupture, and (4) absence of significant head trauma, intracranial hemorrhage, pheochromocytoma, or other causes of myocardial dysfunction [3, 4]. The cardiomyopathy can be classified into a left ventricular (LV) apical ballooning variant (classic Takotsubo cardiomyopathy—most common), an inverted or reverse Takotsubo variant (basal akinesis with hyperdynamic apex), or a midventricular Takotsubo variant. The condition is often associated with catastrophic life events and severe psychological or physical stress. Due to this association with psychological stress, the cardiomyopathy is often referred to as the ‘‘Broken Heart Syndrome’’. Although the pathophysiology of stress-induced cardiomyopathy is not fully understood, it is thought that intense psychological or physical stress results in a catecholamine surge that adversely affects myocardial contractility, where postmenopausal women appear to be at a higher risk for developing the disease. The evidence for this was obtained from observational and case-control studies that have found an association between elevated catecholamine levels and disease onset [1, 4, 9]. In this paper, we present a case of iatrogenic epinephrine-induced reverse Takotsubo cardiomyopathy in a young 24-year-old female with no previous history of cardiac disease. While this case is unfortunate, it provides a unique opportunity to observe the triggering of stress-induced transient cardiomyopathy and provides evidence to support the role of epinephrine in the pathogenesis of this disease.