Key result
Immunochemotherapy normalizes native T1 in cardiac DLBCL, but residual fibrosis triggers recurrent ventricular tachycardia.
Why the study?
Cardiac involvement by diffuse large B-cell lymphoma is rare and frequently presents with non-specific cardiac findings. Diffuse myocardial infiltration may resemble hypertrophic cardiomyopathy, leading to delayed diagnosis and treatment.
Case Report (n=1)
No
Answers are grounded in this paper and cite their sources.
This case demonstrates that secondary cardiac involvement by diffuse large B-cell lymphoma can masquerade as hypertrophic cardiomyopathy for years and that persistent post-chemotherapy myocardial fibrosis carries a long-term risk of ventricular arrhythmias warranting ICD consideration.
Background Cardiac involvement by diffuse large B‑cell lymphoma (DLBCL) is rare and frequently presents with non‑specific cardiac findings. Diffuse myocardial infiltration may resemble hypertrophic cardiomyopathy (HCM), leading to delayed diagnosis and treatment. Case presentation A 57-year-old man presented with postprandial left upper abdominal discomfort and a low-grade fever. Endoscopic ultrasound-guided pancreatic biopsy established non-Hodgkin lymphoma, consistent with DLBCL of the germinal-center B-cell (GCB) subtype. Retrospective review revealed a history of unexplained pericardial effusion, progressive electrocardiographic changes, and progressive ventricular wall thickening that had been diagnosed as HCM. At admission, cardiac troponin I (cTnI) was markedly elevated. Echocardiography showed diffuse hypoechoic thickening of both ventricles, a right atrioventricular-groove mass, reduced left ventricular ejection fraction (LVEF), and severe impairment of global longitudinal strain (average GLS − 2.8%). ¹⁸F‑FDG PET/CT demonstrated intense uptake in the pancreas and myocardium. Cardiac magnetic resonance (CMR) strongly suggested extensive myocardial infiltration. After eight cycles of R‑COEP chemotherapy, multimodality imaging suggested the resolution of the pancreatic lesion and partial regression of myocardial involvement. Subsequently, a single cycle of bridging chemotherapy with gemcitabine and oxaliplatin was administered, followed by three cycles of Pola‑R‑GEMOX and one year of lenalidomide maintenance therapy, which resulted in regression of the myocardial lesions and normalization of cardiac biomarkers. However, apical fibrosis and left ventricular systolic dysfunction persisted. Three years after the index admission, the patient experienced two episodes of asymptomatic self-terminating ventricular tachycardia (VT) of undocumented duration and underwent implantable cardioverter-defibrillator (ICD) implantation. Conclusions Lymphomatous cardiac infiltration should be considered in patients with unexplained progressive myocardial thickening, especially when accompanied by pericardial effusion, biomarker elevation, and electrocardiographic abnormalities. Multimodality imaging can identify an infiltrative phenotype, guide biopsy, and monitor treatment response. Persistent myocardial fibrosis may confer long‑term arrhythmic risk despite substantial tumor regression.
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Chen et al. (2026) conducted a case report in Cardiac involvement by diffuse large B-cell lymphoma (DLBCL) mimicking hypertrophic cardiomyopathy (n=1). R-COEP chemotherapy, gemcitabine/oxaliplatin, Pola-R-GEMOX, lenalidomide maintenance, and ICD implantation was evaluated on Myocardial tumor regression, native T1 mapping normalization, and arrhythmic outcomes. Sequential immunochemotherapy normalized cardiac native T1 from 1536 ms to 1219 ms in cardiac DLBCL mimicking HCM, though residual fibrosis led to recurrent VT requiring ICD implantation at 3 years.
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