Document Type

Conference Proceeding

Publication Date

5-1-2026

Abstract

Introduction Takotsubo cardiomyopathy (TC) is characterized by transient left ventricular (LV) dysfunction following a stressor in the absence of obstructive coronary artery disease. We present a case of a less common variant with right ventricular involvement. Hospital course A 45-year-old woman with sickle cell disease and asthma presented with nausea, vomiting, abdominal pain, and fevers, one week after the death of her father. Examination revealed an irregular tachycardia. Labs demonstrated leukocytosis, elevated lactate, and markedly increased troponin. Chest imaging showed bilateral basilar opacities. ECG demonstrated atrial flutter with rapid ventricular response. She developed progressive respiratory failure requiring intubation. Repeat ECG showed anterolateral ST-segment elevation with reciprocal ST-segment depression in the inferior leads. Emergent coronary angiography demonstrated nonobstructive, small-caliber coronary arteries. Right heart catheterization revealed cardiogenic shock, with a right atrial pressure of 19 mm Hg, pulmonary capillary wedge pressure of 20 mm Hg, cardiac output of 2.3 L/min, cardiac index of 1.5 L/min/m², and a pulmonary artery pulsatility index of 0.1. Echocardiography and left ventriculography demonstrated severe global LV systolic dysfunction with apical ballooning and basal hyperkinesis (LV ejection fraction ≈10%), and reduced right ventricular (RV) systolic function. She was treated with milrinone and dobutamine. Coxsackie B serologies subsequently returned positive, prompting consideration of viral myocarditis. Serial echocardiography showed gradual improvement in LV systolic function, with recovery of the ejection fraction to 40–45%. Cardiac magnetic resonance (CMR) imaging demonstrated LV systolic dysfunction with apical ballooning and myocardial edema on STIR sequences, without definitive late gadolinium enhancement, supporting a diagnosis of TC. Additional findings included RV dysfunction with focal free-wall segmental dilation and dyssynchronous contraction, raising concern for right ventricular involvement in TC. The patient was transitioned to guideline-directed medical therapy for heart failure and managed for atrial flutter, with overall clinical stabilization and improvement in biventricular function. Discussion TC is thought to result from an acute sympathetic surge producing catecholamine-mediated myocardial stunning, microvascular dysfunction, oxidative stress, and inflammation. The LV apex is classically most affected due to higher βadrenergic receptor density, although multiple morphologic variants exist. RV involvement occurs in approximately one-third of TC cases and may be seen as biventricular (apical with RV involvement), isolated RV, or global patterns. In our patient, biventricular TC was favored by (1) the typical segmental and transient ventricular dysfunction pattern, (2) the absence of obstructive, fixed coronary lesions on angiography, and (3) CMR findings demonstrating regional dysfunction and myocardial edema without a definitive ischemic or myocarditic LGE pattern. Although the absence of LGE argues against frank necrosis and supports stress cardiomyopathy, this finding does not completely exclude myocarditis, as CMR sensitivity may vary with timing and multiparametric tissue mapping, and therefore the clinical context (temporal relation to emotional stress, biomarker pattern, ECG, and angiography) remains essential for differentiation. Clinically, RV dysfunction should prompt closer hemodynamic monitoring and early consideration of targeted supportive therapies, as RV involvement in TC is associated with higher rates of in-hospital cardiogenic shock. Additionally, RV involvement identifies a high-risk subgroup with increased long-term all-cause mortality.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter 2026 Resident and Medical Student Day, May 1, 2026, Troy, MI

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