Background: Blinatumomab and inotuzumab ozogamicin (InO) are B-cell targeted agents used in the frontline and relapsed/refractory treatment of B-cell acute lymphoblastic leukaemia (B-ALL). Blinatumomab, a bispecific T-cell engager that targets CD19 and CD3, and InO, an antibody-drug conjugate targeting CD22, have both shown efficacy. However, recent reports have noted lineage conversion as a complication when these agents are used individually or sequentially. We present a rare case of this phenomenon in a 79-year-old male patient. Case description: A 79-year-old male with refractory B-ALL underwent a lineage switch to acute myeloid leukaemia following treatment with blinatumomab and InO. The patient initially achieved remission after initial therapy but relapsed and was subsequently treated with blinatumomab. Due to adverse effects, the treatment was discontinued. He was then treated with InO but again relapsed. A subsequent bone marrow biopsy revealed morphologic evidence of residual B-ALL, but with the presence of acute monocytic leukaemia. Fluorescence in situ hybridisation (FISH) analysis demonstrated an additional copy of KMT2A in a large percentage of cells which was a feature present since the initial diagnosis. Unfortunately, the patient’s condition deteriorated, and he died. Conclusion: This case underscores potential complication of lineage switch following treatment with B-cell directed therapies. Although such therapies have improved outcomes in B-cell malignancies, clinicians should remain aware of rare risks such as lineage transformation. Timely recognition is essential to guide appropriate clinical management.

Background/Objectives: Left ventricular free wall rupture is a rare but catastrophic complication of acute myocardial infarction with extremely high mortality. Deaths occurring in water environments present unique forensic challenges requiring systematic evaluation of drowning, intoxication, trauma, and natural disease. This case report describes a fatal left ventricular free wall rupture occurring shortly after successful percutaneous coronary intervention (PCI), emphasizing the medicolegal differential diagnosis and the importance of comprehensive postmortem evaluation. Results: A 58-year-old man with non-ST-elevation myocardial infarction underwent successful PCI with three drug-eluting stents and was discharged home. Six hours later, he developed severe back pain and was found unresponsive in a bathtub. Autopsy demonstrated a 2.6 cm transmural rupture of the anterolateral left ventricular free wall with 150 mL of hemopericardium. Postmortem computed tomography (PMCT), performed as part of routine forensic evaluation, had identified hemopericardium prior to autopsy. Histology showed coagulative necrosis with neutrophilic infiltration. The rupture site was remote from stented vessels with no procedural injury. Toxicology revealed therapeutic medication levels. Pulmonary and scene findings did not support drowning as a cause of death. Conclusions: Ventricular free wall rupture remains a relevant cause of sudden death following myocardial infarction despite successful revascularization. Comprehensive forensic evaluation integrating scene investigation, macroscopic autopsy findings, histopathology, and toxicology is essential to distinguish natural disease progression from accidental or iatrogenic causes in deaths occurring in water environments. This case highlights that ventricular free wall rupture can occur shortly after apparently successful PCI and underscores the importance of comprehensive forensic evaluation in water-associated deaths.