Reverse Takotsubo Syndrome Triggered by COVID-19-Associated Cytokine Storm: Unveiling a Novel Pattern of Myocardial Dysfunction in SARS-CoV-2 Infection.

BACKGROUND Reverse takotsubo cardiomyopathy (rTTC) is a rare variant of stress-induced cardiomyopathy typically associated with neurological triggers. Recent evidence suggests that hyperinflammatory states, such as cytokine storm as seen in some COVID-19 cases, may precipitate rTTC. We present a unique case of rTTC occurring during SARS-CoV-2 infection with the omicron variant, highlighting diagnostic and therapeutic implications. CASE REPORT A 48-year-old Hispanic woman with morbid obesity, hypertension, and rheumatoid arthritis, fully vaccinated against COVID-19, presented with chest pain, fever, and respiratory symptoms. SARS-CoV-2 infection was confirmed by RT-PCR. Initial laboratory test results showed hyperferritinemia (peak: 14 707 ng/mL). On Day 4, cardiac biomarkers were elevated (troponin T: 28 ng/L; NT-proBNP: 1582 pg/mL). Transthoracic echocardiography revealed basal hypokinesia with preserved apical contractility and moderately reduced left ventricular ejection fraction (LVEF) (45%), consistent with reverse takotsubo cardiomyopathy. She received colchicine and spironolactone as anti-inflammatory therapy. Gradual clinical and echocardiographic improvement followed. At her 6-month follow-up, her LVEF had normalized to 63%, and she remained asymptomatic. No cardiac sequelae were detected at 12 months. CONCLUSIONS This case illustrates how COVID-19-associated cytokine storm can precipitate rTTC in the absence of obstructive coronary disease, even in vaccinated individuals. The temporal alignment between inflammatory marker peaks and left ventricular dysfunction supports a transient, inflammation-mediated myocardial stunning. Clinicians should consider rTTC in COVID-19 patients presenting with atypical chest pain and modest biomarker elevation. Early echocardiography and targeted anti-inflammatory therapy may facilitate diagnosis and promote full recovery.