Herz

, Volume 35, Issue 4, pp 258–265

Historische und gegenwärtige pathophysiologische Konzepte der Tako-Tsubo-Kardiomyopathie

  • S. Szardien
  • H. Möllmann
  • A. Elsässer
  • C.W. Hamm
  • H.M. Nef
Schwerpunkt/CME

Zusammenfassung

Die vor wenigen Jahren erstmals beschriebene Tako-Tsubo-Kardiomyopathie (TTC) oder Stresskardiomyopathie (SCM) ist durch eine plötzlich auftretende, reversible kontraktile Dysfunktion gekennzeichnet und weist eine Prävalenz von 1–2% aller akuten Koronarsyndrome auf. In den meisten Fällen gehen der Erkrankung extreme emotionale oder körperliche Stresssituationen voraus, die überwiegende Zahl der betroffenen Patienten sind zudem postmenopausale Frauen.

Seit der Erstbeschreibung der TTC werden diverse pathophysiologische Hypothesen diskutiert. Vielfach wurden in diesem Zusammenhang multiple koronare Vasospasmen als ursächlich erachtet. Aufgrund widersprüchlicher Daten und geringer Fallzahlen in Registerstudien muss jedoch derzeit davon ausgegangen werden, dass koronare Vasospasmen eine untergeordnete Rolle in der Pathogenese der TTC spielen. In mehreren Arbeiten konnten Störungen der myokardialen Mikrozirkulation und des myokardialen Energiestoffwechsels dokumentiert werden. Anhand der aktuellen Datenlage kann jedoch nicht sicher differenziert werden, ob diese Veränderungen Ursache oder lediglich Folge der TTC sind.

Eindeutig dokumentiert sind hingegen eine übermäßige Ausschüttung von Katecholaminen bei Patienten mit TTC und morphologische Veränderungen, welche denen einer katecholamininduzierten Kardiomyopathie gleichen. Auch im Tierversuch konnte ein Zusammenhang zwischen erhöhten Katecholaminkonzentrationen und myokardialen Funktionsstörungen analog zur TTC aufgezeigt werden.

Zusammenfassend muss daher davon ausgegangen werden, dass die TTC durch hohe lokale toxische Katecholaminkonzentrationen verursacht wird. Das typische Kontraktionsmuster des linken Ventrikels kann durch eine erhöhte Konzentration von Adrenozeptoren im Apex erklärt werden, woraus eine lokal erhöhte Sensitivität gegenüber erhöhten Katecholaminspiegeln resultiert. Individuelle anatomische Unterschiede in der sympathischen Innervation oder der Verteilung von β-Adrenozeptoren sind vermutlich für die interindividuelle Ausprägung der Wandbewegungsstörungen bei der TTC verantwortlich.

Schlüsselwörter

Stresskardiomyopathie Kontraktile Dysfunktion Katecholamine 

Historical and current pathophysiological concepts of stress (Tako-Tsubo) cardiomyopathy

Abstract

Tako-Tsubo cardiomyopathy (TTC), also referred to as stress cardiomyopathy (SCM), was first described in the 1990s and is characterized by transient left ventricular dysfunction. Its incidence represents 1–2% of all acute coronary syndromes (ACS). In most cases extreme emotional or physical stress precedes this syndrome. The majority of patients affected are postmenopausal women.

Since its first description, various hypotheses regarding the pathophysiology of TTC have been discussed. From a historical perspective, coronary vasospasm has often been proposed as a possible cause of this disorder. However, reviews from numerous registries were able to demonstrate that coronary vasospasm plays only a minor role in the pathogenesis of TTC. Several groups showed disturbances in myocardial microcirculation and energy metabolism in the acute phase of TTC. Nevertheless, with regard to the data currently available, it cannot be differentiated whether these changes are the cause or rather the result of TTC.

However, recent concepts include an excessive catecholamine overload and morphological changes which are unequivocally documented in TTC. The relation between elevated catecholamine levels and myocardial dysfunction analogous to TTC could be confirmed in animal experiments.

In summary, it can be assumed that TTC is caused by an excessive cardiotoxic release of catecholamines. Ventricular dysfunction can be explained by increased numbers of β-adrenergic receptors in the apex, leading to greater vulnerability to catecholamine overload. Individual anatomical differences in the sympathoadrenergic system and distribution from β-adrenergic receptors are presumably responsible for the interindividual occurrence of wall motion abnormalities in TTC.

Keywords

Stress cardiomyopathy Contractile dysfunction Catecholamines 

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Copyright information

© Urban & Vogel, Muenchen 2011

Authors and Affiliations

  • S. Szardien
    • 1
  • H. Möllmann
    • 1
  • A. Elsässer
    • 1
  • C.W. Hamm
    • 1
  • H.M. Nef
    • 1
  1. 1.Abteilung KardiologieKerckhoff-Klinik Herz- und ThoraxzentrumBad NauheimDeutschland

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