Abstract
Introduction Takotsubo cardiomyopathy (TTC) is a stress-induced, reversible left-ventricular dysfunction attributed to catecholamine excess. Serotonin-norepinephrine reuptake inhibitors (SNRIs) such as duloxetine increase sympathetic tone and have been implicated in TTC. We report a case of TTC temporally associated with duloxetine?initiation in a lung transplant recipient who also had prolonged QTc. Case Description A 74-year-old woman with idiopathic pulmonary fibrosis status post bilateral lung transplant presented after out-of-hospital cardiac arrest. She was intubated and resuscitated with vasopressor support. ECG showed new T-wave inversions and QTc of 560 ms; high-sensitivity troponin was elevated. Echocardiography revealed apical akinesis with LVEF 35-40%, and coronary angiography showed no obstructive disease. Duloxetine 20 mg daily, started one month earlier for neuropathic pain, was discontinued. She received guideline-directed heart failure therapy with gradual recovery of LVEF to 55-60% over six weeks. Discussion The temporal relationship between duloxetine use and TTC onset, absence of ischemic or infectious etiologies, and functional recovery after drug withdrawal support duloxetine as a probable trigger. SNRIs increase synaptic norepinephrine and augment β-adrenergic stimulation, central to TTC pathophysiology. Duloxetine and co-medications such as azithromycin can prolong QT by blocking IKr channels, potentially amplifying repolarization heterogeneity and triggering ventricular arrhythmias that may mimic or precipitate stress cardiomyopathy. Post-transplant patients may be predisposed through autonomic denervation, calcineurin-inhibitor-induced sympathoexcitation, and recurrent vasopressor exposure. Recognition of drug-induced QT prolongation and avoidance of multiple QT-prolonging agents are critical. TTC typically resolves with supportive care and withdrawal of the offending agent. This abstract is funded by: None