A 23-year-old man developed reversible nonischemic cardiomyopathy during ECT likely triggered by paroxysmal sympathetic hyperactivity, despite no prior cardiac history.
Electroconvulsive therapy may rarely induce reversible nonischemic cardiomyopathy and left ventricular diastolic dysfunction in young, cardiac-stable patients, potentially exacerbated by underlying paroxysmal sympathetic hyperactivity.
Electroconvulsive therapy (ECT) is an effective and lifesaving treatment for severe mental illnesses. It is also considered safe with limited side effects and few deaths. Cardiac deaths occur in <30% of all ECT-related deaths and primarily occur in the elderly. It is unusual for a young man with no previous cardiac history to experience cardiac comorbidities while undergoing ECT. We present the case of a 23-year-old man who presented with treatment-resistant catatonia. He had undergone a series of bifrontal ECT with limited improvement and was then trialed on bitemporal ECT. During his second round of ECT, he developed left ventricular diastolic dysfunction and a resultant nonischemic cardiomyopathy. This cardiomyopathy resolved with the cessation of ECT treatments. We hypothesize that paroxysmal sympathetic hyperactivity syndrome following concussion may have predisposed him to cardiomyopathy. This case is unique given the rarity of cardiac effects of ECT, and especially in cardiac stable individuals. In our discussion, we will touch on physiological effects of ECT on the parasympathetic and sympathetic systems, compounded with paroxysmal sympathetic hyperactivity syndrome that likely caused the left ventricular dysfunction.
Shapiro-Krew et al. (2026) studied this question. A 23-year-old man developed reversible nonischemic cardiomyopathy during ECT likely triggered by paroxysmal sympathetic hyperactivity, despite no prior cardiac history.
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