Abstract Body (Do not enter title and authors here): Case Descriptions
Takotsubo Syndrome (TTS) typically occurs in postmenopausal women who experience acute transient left ventricular (LV) systolic dysfunction that is most commonly apical, but may occur with other patterns such as a basal and midventricular “reverse” type. TTS pathophysiology has been attributed to catecholamine cardiotoxicity, microvascular dysfunction, and estrogen deficiency, although the mechanisms for reverse TTS (rTTS) remain to be elucidated. Here, we share rTTS cases of premenopausal women who underwent recent in vitro fertilization (IVF), suggesting a link between altered hormone milieu and basal LV dysfunction in the setting of TTS.

Patient 1: A 35-year-old G0P0 woman presented immediately after IVF egg retrieval for hypotension and hemoperitoneum. TTE revealed EF 18% with basal-mid LV akinesis and preserved LV apical contraction. After 5 days of diuresis and vasopressor weaning, TTE showed improved EF 38%. TTE 15 days later demonstrated recovery of wall motion, EF 50%.

Patient 2: A 36-year-old G3P1011 woman at 16 weeks gestation from IVF pregnancy was admitted with acute respiratory failure. TTE showed EF <20% with basal-mid LV hypokinesis and apical sparing. Her worsening respiratory failure required intubation and ultimately ECMO. TTE 6 days later showed EF 63% without wall motion abnormalities.

Discussion
Previous studies suggest that rTTS has higher prevalence in pregnant and younger women compared to apical TTS. Hypotheses of contributing mechanisms are two-fold: 1) estrogen is protective against catecholamine surges, and 2) estrogen receptors have increased concentration towards the LV apex. IVF and pregnancy are both associated with high estrogen levels. As such, our cases provide additional support for estrogen’s cardioprotective role, which may disproportionately assist the LV apex, favoring the rTTS variant. Both cases had emotional and/or physical stressors, no EKG ST elevation, and no coronary artery lesions or preexisting heart disease. Estrogen and catecholamine levels were not drawn, thus limiting our understanding. Although these cases suggest a hormonal influence on rTTS variant, the pathophysiology of TTS variants remains elusive and is likely multifactorial.