Fortschr Neurol Psychiatr 2018; 86(11): 699-710
DOI: 10.1055/a-0653-7063
Übersicht
© Georg Thieme Verlag KG Stuttgart · New York

Tako-Tsubo-Kardiomyopathie während einer EKT-Serie: Fallbericht, systematische Literaturrecherche und Diskussion spezifischer Risikofaktoren

Tako-Tsubo Cardiomyopathy during a series of Electroconvulsive Therapy (ECT) applications: A case report, systematic literature research and discussion of specific risk factors
Ralf Kudling
1   Ev. Klinikum Niederrhein, Klinik für Psychiatrie, Psychotherapie und Psychosomatik
,
Wolfgang Hartmut Schoels
2   Ev. Klinikum Niederrhein, Klinik für Kardiologie und Angiologie
,
Jens Kuhn
3   Universitätsklinikum Köln, Klinik und Poliklinik für Psychiatrie und Psychotherapie
› Author Affiliations
Further Information

Publication History

eingereicht 30 March 2017

akzeptiert 01 July 2018

Publication Date:
17 January 2019 (online)

Zusammenfassung

Hintergrund Bei der Tako-Tsubo-Kardiomyopathie (TTK) handelt es sich um eine akute reversible Erkrankung des Herzmuskels. Sie wird ursächlich mit einem Überschuss an Adrenalin, Noradrenalin und Dopamin in Zusammenhang gebracht. Als bekannte Risikofaktoren gelten psychischer und physischer Stress. Es existieren Fallberichte über das Auftreten von TTK nach Krampfanfällen sowie EKT-Behandlungen.

Methoden Es wird der Fall eines 63 Jahre alten Patienten vorgestellt, bei dem es im Verlauf einer zweiten EKT-Serie unter Etomidat-Narkose und laufender antidepressiver Medikation mit Tranylcypromin zu einer TTK kam. Mögliche pathophysiologische Zusammenhänge werden anhand der zur Verfügung stehenden Literatur diskutiert. In Anbetracht eines erhöhten Rezidivrisikos wird der Frage nachgegangen, ob die Wiederaufnahme der EKT-Behandlung nach Abklingen der TTK verantwortbar ist.

Ergebnisse Depressive Störungen, EKT-Behandlungen mit konvulsiven Anfällen, der Einsatz von Etomidat als Narkotikum sowie eine Behandlung mit Tranylcypromin könnten eine theoretische Rolle als Risikofaktoren für die TTK spielen. Die durch Etomidat vermittelten Effekte könnten auf die substanzbedingte Störung der Kortisolsynthese und einer daraus resultierenden sympathomimetischen und pro-inflammatorischen Wirkung zurückgeführt werden. Es konnten 19 publizierte TTK-Fälle im Zusammenhang mit EKT gefunden werden. Einschließlich des hier vorgestellten Patienten wurde in 8 Fällen von einer erfolgreichen und komplikationslosen Wiederaufnahme der EKT-Behandlung berichtet.

Diskussion Das Auftreten der TTK scheint letztlich multifaktoriell begründet zu sein. Die Konstellation unseres Falles sowie die analysierte medizinische Literatur erlauben keinen Rückschluss, dass einer der genannten Faktoren alleine für die Entstehung der TTK verantwortlich gemacht werden kann. Angesichts der theoretischen Überlegungen und Teilbefunde über die mögliche Rolle eines relativen Kortisol-Defizits für die TTK wären gezielte Untersuchungen wünschenswert. Die Wiederaufnahme der EKT-Behandlung nach einem TTK-Fall ist, unter Risikoabwägung und Berücksichtigung besonderer Vorsichtsmaßnahmen, nicht ausgeschlossen.

Abstract

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.

 
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