A 59-year-old transgender female on estrogen therapy presented with spontaneous coronary artery dissection, highlighting the potential role of exogenous estrogen in coronary susceptibility to injury.
Case Report (n=1)
This case highlights a potential link between exogenous estrogen therapy and spontaneous coronary artery dissection in transgender women, emphasizing the need for vigilance regarding non-atherosclerotic acute coronary syndromes in this population.
Abstract Introduction Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of acute coronary syndrome (ACS). While this condition predominantly affects women and is associated with hormonal changes, the link is still being investigated. Cases of SCAD occurring in transgender women on estrogen therapy are exceedingly rare, and this particular patient population may provide a unique insight into the influence of exogenous hormones on coronary injury. Case Presentation A 59-year-old transgender female with a history of a right central retinal artery occlusion, dyslipidemia, and asthma, presented to the emergency department with sudden severe substernal chest pain radiating to the neck, along with dyspnea and nausea. Electrocardiography revealed ST-segment elevations in the lateral leads. An initial high-sensitivity cardiac troponin I was 16 ng/L, which subsequently increased to 23,000 ng/L. The patient was taken for emergent left heart catheterization, and coronary angiography demonstrated SCAD of the mid-left anterior descending artery with consequent 90% luminal narrowing with preserved TIMI grade III flow. There was no evidence of coronary disease elsewhere. Transthoracic echocardiography demonstrated an ejection fraction of 40% with anterolateral and apical wall motion abnormalities. Given preserved flow and hemodynamic stability, conservative medical management was pursued with aspirin, short-term clopidogrel, and metoprolol. Atorvastatin was discontinued based on data suggesting a potential association with SCAD recurrence. The patient’s hypertriglyceridemia (239 mg/dL) was therefore managed with fenofibrate. Given the patient’s history of retinal artery occlusion, family history of aortic dissection, and phenotypic features suggestive of a connective tissue disorder (e.g., Marfanoid habitus), further evaluation for an underlying arteriopathy was pursued. A computed tomographic angiography of the head, neck, chest, abdomen, and pelvis revealed no evidence of fibromuscular dysplasia, aneurysms, or other vascular abnormalities. Given the suspected link between exogenous estrogen and SCAD, estradiol therapy was discontinued, and the patient was scheduled to follow up with endocrinology for alternative hormonal strategies. Discussion This rare case of SCAD in a transgender woman on estrogen therapy emphasizes the potential role of exogenous estrogen in coronary susceptibility to injury and consequent dissection. Recognition of non-atherosclerotic etiologies of ACS in transgender individuals is essential, as management differs significantly from traditional plaque rupture-related events. With the growing use of gender-affirming hormone therapy, clinicians must maintain vigilance for rare cardiovascular complications and pursue individualized, multidisciplinary care strategies. This abstract is funded by: None
Shah et al. (Fri,) conducted a case report in Spontaneous coronary artery dissection (SCAD) (n=1). Estrogen therapy was evaluated. A 59-year-old transgender female on estrogen therapy presented with spontaneous coronary artery dissection, highlighting the potential role of exogenous estrogen in coronary susceptibility to injury.