Published: August 29, 2025 | Updated: September 17, 2025
A 48-year-old male with a past medical history significant for malignant thymoma status post thymectomy and right lower lobe lobectomy, and myasthenia gravis, presented to Norton Women’s & Children’s Hospital emergency department with dyspnea on exertion (DOE). His CT was concerning for possible pulmonary embolism. His labs on this admission showed B-type natriuretic peptide 2,400pg/mL and high-sensitivity troponin 5,000ng/L. He was admitted for further evaluation of his dyspnea. Notably, the patient was admitted the month prior with aspiration pneumonia, during which an echocardiogram showed a preserved left ventricular ejection fraction (EF) or 50 to 55%.
During this admission, the patient began to experience worsening shortness of breath, hypotension, and a lactic acid of 4mmol/L. Repeat echocardiogram showed new onset systolic dysfunction with EF 15%, with evidence of biventricular failure. The cardiogenic shock team was activated, and the patient was transferred to Norton Audubon Hospital for further evaluation and management. A right and left heart catheterization revealed normal coronary arteries, elevated filling pressures, and a severely reduced cardiac output. He was started on an intravenous milrinone drip and supported with intra-aortic balloon pump.
The team had concerns for acute myocarditis due to the combination of his echocardiogram findings, significantly elevated troponin levels in the setting of normal coronaries, and his frequent ectopy on telemetry. He was taken back to the cath lab for an endomyocardial biopsy which confirmed the diagnosis of giant cell myocarditis. Giant cell myocarditis is exceedingly rare—only a few dozen confirmed cases have been collected in major registries and only isolated case reports beyond that. While not precisely tallied, the total documented cases since 1905 is likely in the low hundreds. Patients with giant cell myocarditis often show clinical features that may resemble those seen in acute coronary syndrome or forms of decompensated heart failure. The 1 year mortality for giant cell myocarditis, without treatment, is roughly 70%.
High dose IV corticosteroids were initiated which were later transitioned to oral therapy with the addition of mycophenolate. The patient began to exhibit resolution of his cardiogenic shock. He was successfully weaned from mechanical support and started on guideline-directed medical therapy for his acute systolic heart failure. He continued to improve and was able to transfer to an acute rehabilitation facility for further physical therapy.
Kelly C. McCants, M.D.
Executive Director, Norton Heart & Vascular Institute Advanced Heart Failure & Recovery Program
Bassel Alkhalil, M.D.
Heart Failure Cardiology
Medical Director, Mechanical Circulatory Support Program
Norton Heart & Vascular Institute
Emily E. Corsentino, APRN
Anna Gibson, APRN
Pulmonology/Critical Care Medicine
Norton Neuroscience Institute- Neurology Audubon