Golimumab-Associated Myocarditis with Progressive Eosinophilia after Route Switch in Rheumatoid Arthritis

Tumour necrosis factor-alpha (TNF-α) inhibitors are cornerstone therapies in rheumatoid arthritis (RA) and generally reduce cardiovascular events. Drug-induced myocarditis associated with TNF-α inhibitors is not well-established in pharmacovigilance databases.

A 51-year-old male with seropositive RA receiving intravenous golimumab presented with acute chest pain, dyspnoea, and left arm numbness without viral prodrome. He had been switched from subcutaneous to intravenous golimumab 6 months prior, producing a 14-fold increase in peak serum concentration. High-sensitivity troponin I peaked at 32,419 ng/l with mildly reduced left ventricular ejection fraction (45-49%) and global hypokinesis. Coronary angiography revealed non-obstructive arteries. Comprehensive viral serology was negative for acute infection. Inflammatory markers were normal. Progressive eosinophilia developed during hospitalization (0.12 → 0.54 ×10³/μl). Cardiac magnetic resonance imaging was unavailable at our institution. Despite not initiating prescribed sacubitril/valsartan (continuing only metoprolol), repeat echocardiography at 4 weeks demonstrated complete normalization of left ventricular function; coinciding with near-complete drug elimination. Golimumab was permanently discontinued.

This case meets criteria for clinically suspected myocarditis per the 2024 American College of Cardiology Expert Consensus Decision Pathway. The absence of viral prodrome, negative viral serology, progressive eosinophilia, normal inflammatory markers, and complete functional recovery paralleling drug elimination support drug-induced hypersensitivity myocarditis. Causality assessment yields "probable" by both the World Health Organization - Uppsala Monitoring Centre system and the Naranjo algorithm (score 6 to 8). This case contributes to the limited literature on TNF-α inhibitor cardiotoxicity and emphasizes the need for continued pharmacovigilance.

Tumour necrosis factor-alpha inhibitor-associated myocarditis is exceptionally rare; clinicians should consider this diagnosis in patients presenting with acute troponinemia and non-obstructive coronary arteries while receiving biologic therapy.Switching from subcutaneous to intravenous golimumab produces an approximately 14-fold increase in peak serum concentration (C_max 44.4 vs. 3.2 μg/ml), which may theoretically contribute to immune sensitization and delayed hypersensitivity myocarditis.Progressive peripheral eosinophilia in the setting of acute myocardial injury without viral prodrome should raise suspicion for drug-induced hypersensitivity myocarditis, even when the offending agent was administered weeks prior.