AI Summary & Key Takeaways
AI InsightTherefore, the very probable etiology of theprecipitated HF was inflximab toxicity.
📌 3 Key Takeaways
Özet
We present the case of a 38-year-old woman with symptoms of acute heart failure (HF). In the previous months, she received tumor necrosis factor (TNF)-α inhibitors for the treatmentof arthritis secondary to Crohn’s disease. She initially receivedetanercept (Enbrel) for nearly 1 year and subsequently receivedinflximab (Remicade) for 6 months. Echocardiograms followingthe etanercept therapy were normal. Since her disease did notrespond well to etanercept, she received 16 treatments of infliximab, at the end of which HF symptoms developed, with rapidclinical deterioration. Her echocardiogram demonstrated dilatedcardiomyopathy with severe biventricular dysfunction and leftventricular ejection fraction (LVEF) and right ventricular ejectionfraction (RVEF) <20% with severe functional mitral and tricuspidregurgitation. Her extensive diagnostic work-up, including pathological examination of endomyocardial biopsy, was normal. Despite optimal treatment of HF, her status did not improve, and aleft ventricular assist device (LVAD, HeartMate II) was implanted.The evolution was unremarkable, and she rapidly recovered inthe following months, with LVEF reaching ≥45%. Based on thepatient’s clinical improvement and LVEF recuperation, LVAD wasremoved. Her functional status and LVEF remained stable afterLVAD explantation. Therefore, the very probable etiology of theprecipitated HF was inflximab toxicity.