Abstract
ABSTRACT
Citrate anticoagulation during therapeutic plasma exchange (TPE) chelates divalent cations and can precipitate torsades de pointes (TdP) in patients with pre‐existing repolarization vulnerability. We report a 44‐year‐old woman with genetically determined long QT syndrome Type 2 (LQT2) presenting in myasthenic crisis due to anti‐MuSK‐positive myasthenia gravis. TPE was initiated urgently before confirmatory antibody results were available, as alternative rapid immunomodulatory options were not immediately accessible. Despite prophylactic electrolyte supplementation, the corrected QT interval (QTc) progressively prolonged, rising from a baseline of 493 to 509 ms—exceeding the 500 ms high‐risk threshold—immediately before TdP onset during the second TPE. TPE was discontinued and replaced with double‐filtration plasmapheresis (DFPP) using albumin‐based replacement, which reduces citrate exposure by retaining the patient's own albumin. Five subsequent DFPP sessions were completed without arrhythmia recurrence. This case highlights the apheresis‐related arrhythmia risk in LQT2 and the mechanistic rationale for DFPP as a safer alternative.