Reversible severe mitral regurgitation during immunotherapy in a structurally vulnerable valve: a case report

T-cell therapy (TCT) rarely causes isolated severe valvular pathology without cardiomyopathy, but its haemodynamic effects can exacerbate mitral regurgitation (MR) in patients with subtle valvular issues, and reports describing reversible valvular dysfunction in this context remain limited.

A 48-year-old woman with a history of fenfluramine (FF) use for weight loss 10 years prior was diagnosed with B-cell acute lymphoblastic leukaemia (B-ALL). Baseline echocardiogram revealed trace MR. After her second blinatumomab (BL) cycle, she developed acute heart failure symptoms. Repeat echocardiogram showed severe MR with posterior leaflet restriction. Systemic inflammatory symptoms and end-organ damage were notably absent. BL was held, and medical therapy for heart failure with preserved ejection fraction (HFpEF) was initiated, improving MR and allowing resumption of BL.

Baseline posterior mitral leaflet restriction was likely related to prior FF use. While BL carries a low cardiotoxicity profile, it can cause heart failure via cytokine release syndrome (CRS)-dependent and potentially CRS-independent pathways. In this case, we hypothesize that transient elevations in left-sided filling pressures, possibly from unmasking subtle diastolic dysfunction in a structurally vulnerable valve, amplified her MR. Delayed disclosure of FF use underscores the importance of intentional, non-judgmental history-taking. Recognition of this interaction guided haemodynamic optimization and enabled cautious, successful reinitiation of BL therapy.

We emphasize considering prior FF use when evaluating patients with idiopathic MR. We also demonstrate how haemodynamic changes from TCT can worsen MR and show how careful haemodynamic management can enable the safe resumption of this lifesaving therapy.