JACC. Case reports · 2026
Bortezomib-Induced Myocarditis in a Patient With Multiple Myeloma.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Domínguez-Linares Adriana, Nieto-Dolores Ana Karen, Garcia-Cardenas Mauricio, Gonzalez-Trejo Alfonso, Ayala-Bustamante Estela, Valencia-Hernandez Hugo Armando, Viñas-Mendieta Adriana, Ruiz-Mori Enrique, Espinola-Zavaleta Nilda
Аннотация
BACKGROUND: Bortezomib is a reversible proteasome inhibitor used as first-line therapy for multiple myeloma and mantle cell lymphoma. Although effective, it can in rare cases cause cardiotoxicity, including myocarditis.
CASE SUMMARY: A 58-year-old man with multiple myeloma (MC I, lambda light chain type) developed progressive dyspnea and edema after VTD (bortezomib, thalidomide, dexamethasone) therapy. Echocardiography showed severe left ventricular systolic dysfunction (left ventricular ejection fraction: 35%, global longitudinal strain: -10%) with elevated troponin I (3,176 ng/L). Coronary computed tomography angiography ruled out ischemia, and cardiac magnetic resonance imaging confirmed extensive acute myocarditis. Bortezomib was discontinued and guideline-directed heart failure therapy was initiated, resulting in complete clinical and echocardiographic recovery (left ventricular ejection fraction: 52%, global longitudinal strain: -17%) within 3 weeks.
DISCUSSION: Bortezomib-induced myocarditis is extremely rare. Proposed mechanisms include proteasome inhibition-induced endoplasmic reticulum stress, mitochondrial dysfunction, and impaired NF-κB signaling.
TAKE-HOME MESSAGE: Early recognition, prompt drug withdrawal, and timely heart failure therapy are essential to ensure full recovery.
CASE SUMMARY: A 58-year-old man with multiple myeloma (MC I, lambda light chain type) developed progressive dyspnea and edema after VTD (bortezomib, thalidomide, dexamethasone) therapy. Echocardiography showed severe left ventricular systolic dysfunction (left ventricular ejection fraction: 35%, global longitudinal strain: -10%) with elevated troponin I (3,176 ng/L). Coronary computed tomography angiography ruled out ischemia, and cardiac magnetic resonance imaging confirmed extensive acute myocarditis. Bortezomib was discontinued and guideline-directed heart failure therapy was initiated, resulting in complete clinical and echocardiographic recovery (left ventricular ejection fraction: 52%, global longitudinal strain: -17%) within 3 weeks.
DISCUSSION: Bortezomib-induced myocarditis is extremely rare. Proposed mechanisms include proteasome inhibition-induced endoplasmic reticulum stress, mitochondrial dysfunction, and impaired NF-κB signaling.
TAKE-HOME MESSAGE: Early recognition, prompt drug withdrawal, and timely heart failure therapy are essential to ensure full recovery.