• Claudio Marabotti, Elio Venturini, Alberto Marabotti, and Alessandro Pingitore.
• CNR Institute of Clinical Physiology, Pisa, Italy; EXTREME CENTRE, Scuola Superiore Sant'Anna, Pisa, Italy. Electronic address: c.marabotti@alice.it.
• Heart Lung. 2014 May 1; 43 (3): 225-30.

AbstractStress-induced cardiomyopathy is an acute disease characterized by a large left ventricular apical dyskinesia ("apical ballooning"), triggered by intense emotional or physical stress, acute illnesses or, rarely, by alcohol or opiates withdrawal. Connection to stress and apical asynergy suggest a catecholamine-mediated pathogenesis. We recently observed a typical apical stress-induced cardiomyopathy, arising two weeks after a long-lasting antidepressant treatment withdrawal and recurring, a week later, with evidence of inferior wall akinesia. The reported case has several unusual features: 1) both episodes were not preceded by relevant triggering event (except antidepressant discontinuation); 2) early heterozonal relapse was observed; 3) the latency between antidepressant discontinuation and stress-induced cardiomyopathy onset is unusually long. The lack of relevant triggering stress and the evidence of multifocal asynergies could support the hypothesis of a non-catecholaminergic pathogenesis. Moreover, the long latency after antidepressant withdrawal may suggest that prolonged antidepressant treatments may have delayed pathological consequences, possibly related to their known neuroplastic effects.Copyright © 2014 Elsevier Inc. All rights reserved.

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