Takotsubo cardiomyopathy is an acute, typically transient, stress-induced cardiomyopathy that can mimic acute coronary syndrome (ACS) but usually occurs without obstructive coronary disease. An uncommon variant, reverse takotsubo cardiomyopathy, is characterized by predominant basal hypokinesis with relative preservation or hyperkinesis of the apical segments. Recognizing atypical regional wall motion patterns is essential to differentiate stress cardiomyopathy from ischemic causes and to guide appropriate management.
The patient was a 69-year-old woman with a history of coronary artery disease (status post left anterior descending artery [LAD] stent), hypertension, hyperlipidemia, and chronic obstructive pulmonary disease (COPD). Additional contextual history obtained later revealed she had been experiencing ongoing grief following her sister’s death approximately 3 months earlier.
She presented in severe respiratory distress and became unresponsive, necessitating emergency endotracheal intubation. She required care in the intensive care unit for a COPD exacerbation and was managed for ventilator-dependent respiratory failure. Viral testing was positive for coronavirus OC43, which was identified during the workup of her respiratory illness.
Cardiac evaluation was prompted by rising biomarkers and electrocardiographic changes. High-sensitivity troponin increased from an initial 56 ng/L to 937 ng/L on initial testing, and later peaked at 1928 ng/L after cardiac catheterization. The electrocardiogram demonstrated ST-T changes that raised concern for an ACS-like process.
Transthoracic echocardiography revealed new segmental wall motion abnormalities with an estimated ejection fraction of 40%. The pattern of wall motion abnormality observed on imaging was not typical of a single-vessel ischemic distribution and supported consideration of a stress-induced cardiomyopathy.
Given the ACS-like presentation, the patient underwent urgent coronary angiography which demonstrated no obstructive coronary disease and confirmed the LAD stent remained patent. Left ventriculography was performed and showed severe basal hypokinesis with relatively preserved apical contraction, findings diagnostic of reverse takotsubo cardiomyopathy in the clinical context.
Although classic takotsubo is often associated with an abrupt emotional or physical trigger, this case highlights a scenario in which acute respiratory failure appeared to be the proximate precipitant while the patient also had a chronic emotional stressor—ongoing grief from her sister’s death 3 months earlier. The authors emphasize that emotional stressors contributing to stress cardiomyopathy may be chronic or nonacute and that critical illness itself can function as a primary trigger.
This case underscores several diagnostic and management points relevant to clinicians caring for critically ill patients:
In patients with ACS-like presentations during acute critical illness—including severe respiratory failure—reverse takotsubo should be considered, particularly when imaging demonstrates regional wall motion abnormalities not explained by single-vessel coronary obstruction.
Rising troponin and ST-T changes may coexist with stress cardiomyopathy; interpretation should integrate echocardiographic or ventriculographic regional wall motion patterns and coronary angiography results.
Identification of basal hypokinesis with preserved apical function on ventriculography or echocardiography can help avoid misdiagnosis of obstructive coronary disease and focus management on supportive care appropriate for stress cardiomyopathy.
The report supports the need for follow-up imaging to document recovery of systolic function, although specific timing and long-term outcomes were not detailed in the abstract.
Management described in the source was supportive in the ICU setting for respiratory failure and the cardiac condition; the abstract did not provide detailed pharmacologic treatment protocols or long-term follow-up data.
Reverse takotsubo cardiomyopathy can present during severe critical illness such as ventilator-dependent respiratory failure and may masquerade as ACS. Coronary angiography demonstrating nonobstructive coronaries together with ventriculography or echocardiography showing severe basal hypokinesis and preserved apical contraction establishes the diagnosis. Clinicians should maintain a high index of suspicion for this variant when ACS-like signs appear in the setting of respiratory failure or other critical illness, and should consider both acute physiologic triggers and chronic emotional stressors such as prolonged grief when evaluating etiology. Appropriate recognition helps avoid unnecessary revascularization strategies and supports targeted supportive management and follow-up imaging to confirm recovery of cardiac function.