Fortschritte der Neurologie-Psychiatrie · 2019
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Клинический случайСтатьяСистематический обзорНазвание и аннотация: Перевод пока не подготовлен
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Kudling Ralf, Hartmut Schoels Wolfgang, Kuhn Jens
Аннотация
BACKGROUND: Tako-Tsubo Cardiomyopathy (TTC) is an acute, reversible disease of the myocardium. It seems to be caused by an excess of epinephrine, norepinephrine and dopamine. Psychological or physiological stress is considered as a risk factor. Several cases of Tako-Tsubo cardiomyopathy in the context of seizures and electroconvulsive therapy have been reported.
METHODS: We describe the case of a 63-year-old patient who developed TTC during a second series of ECT applications with etomidate anaesthesia and continued antidepressant medication with tranylcypromine. Potential pathophysiological correlations are discussed on the basis of the available literature. Given the increased risk of TTC recurrence, the question on reinitiation of ECT treatment after remission of the heart disease is also addressed.
RESULTS: At least in theory, depressive disorders, ECT applications with seizures, the application of the anaesthetic etomidate, as well as tranylcypromine treatment may all be causally related to the development of TTC. Etomidate is known to interfere with cortisol synthesis, resulting in sympathomimetic and pro-inflammatory effects. To date, 19 cases of TTC in conjunction with ECT applications have been published. As in our patient, ECT was reinitiated successfully without complications in eight of them.
DISCUSSION: ECT-related TTC seems to be caused by multiple factors. Circumstantial evidence in our case as well as published data does not support the conclusion that a single risk factor can be held responsible for the development of TTC. Based on theoretical considerations and preliminary findings on a potential role of a relative cortisol deficit, future studies should be encouraged to provide relevant evidence. If careful risk-benefit considerations are done and specific precautions are taken, previous TTC does not exclude reinitiation of ECT.
METHODS: We describe the case of a 63-year-old patient who developed TTC during a second series of ECT applications with etomidate anaesthesia and continued antidepressant medication with tranylcypromine. Potential pathophysiological correlations are discussed on the basis of the available literature. Given the increased risk of TTC recurrence, the question on reinitiation of ECT treatment after remission of the heart disease is also addressed.
RESULTS: At least in theory, depressive disorders, ECT applications with seizures, the application of the anaesthetic etomidate, as well as tranylcypromine treatment may all be causally related to the development of TTC. Etomidate is known to interfere with cortisol synthesis, resulting in sympathomimetic and pro-inflammatory effects. To date, 19 cases of TTC in conjunction with ECT applications have been published. As in our patient, ECT was reinitiated successfully without complications in eight of them.
DISCUSSION: ECT-related TTC seems to be caused by multiple factors. Circumstantial evidence in our case as well as published data does not support the conclusion that a single risk factor can be held responsible for the development of TTC. Based on theoretical considerations and preliminary findings on a potential role of a relative cortisol deficit, future studies should be encouraged to provide relevant evidence. If careful risk-benefit considerations are done and specific precautions are taken, previous TTC does not exclude reinitiation of ECT.