Poster 062: Fulminant Rheumatoid-Arthritis–Associated Autoimmune Myocarditis Presenting as Cardiogenic Shock in a Patient With Antiphospholipid Syndrome and Recent Catastrophic Arterial Thrombosis

Background: Rheumatoid arthritis, particularly seropositive disease, can cause fulminant immune-mediated myocarditis that mimics acute coronary syndrome or antiphospholipid syndrome–related ischemia. Early recognition is critical, as prompt immunosuppression can rapidly reverse cardiogenic shock and save lives.

Methods: A 45-year-old woman with seropositive rheumatoid arthritis and triple-positive antiphospholipid syndrome presented with acute chest pain, hypotension, and hypoxemic respiratory failure. She rapidly progressed from SCAI stage C to D cardiogenic shock with elevated lactate and troponin. Prior echocardiography three months earlier demonstrated normal left ventricular function. ECG showed inferolateral ST depression, and bedside echocardiography revealed new severe left ventricular systolic dysfunction with regional hypokinesis. Coronary angiography demonstrated non-obstructive coronary artery disease, excluding acute coronary syndrome. CTA chest excluded pulmonary embolism, and serologies for infectious and viral myocarditis evaluations were negative. Due to shock physiology and high procedural risk, cardiac MRI was deferred, and empiric pulse-dose intravenous corticosteroids were initiated alongside guideline-directed medical therapy and anticoagulation.

Outcome: Following initiation of high-dose intravenous methylprednisolone, the patient demonstrated rapid clinical improvement with normalization of lactate, decreasing vasopressor requirements, improving troponin levels, and resolution of pulmonary edema. Norepinephrine was discontinued within 24 hours. Once stabilized, cardiac MRI revealed severely reduced biventricular function, elevated T1 and T2 values, and near-circumferential subendocardial and mid-myocardial late gadolinium enhancement with a small apical thrombus. This inflammatory pattern excluded MINOCA, coronary vasospasm, and microvascular ischemia, supporting a diagnosis of autoimmune myocarditis. Endomyocardial biopsy was deferred due to institutional limitations. The patient transitioned to oral steroids with reinitiation of methotrexate for long-term disease control and was discharged on full guideline-directed heart failure therapy and therapeutic anticoagulation.

Conclusion: This case demonstrates fulminant rheumatoid arthritis–associated myocarditis presenting as cardiogenic shock in a patient with antiphospholipid syndrome. Integration of coronary angiography and cardiac MRI excluded ischemic mimics and enabled early immunosuppression, resulting in rapid shock reversal. Autoimmune myocarditis should be considered in seropositive RA patients with sudden hemodynamic collapse.