Abnormalities in intracellular Ca2+ regulation contribute to the pathomechanism of Tako-Tsubo cardiomyopathy

Nef, Holger; Möllmann, Helge; Troidl, Christian; Kostin, Sawa; Voss, Sandra; Hilpert, P; Behrens, Christopher B.; Rolf, Andreas; Rixe, Johannes; Weber, Michael; Hamm, Christian W.; Elsässer, Albrecht

doi:10.1093/eurheartj/ehp240

Cited by 119 publications

(89 citation statements)

References 30 publications

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“…Even though tako-tsubo was first described in the 1990s, no English language studies appeared before 2000 [4]. The two cases we present suggest that recurrence of tako-tsubo is more frequent than previously thought [2,3,[5][6][7][8][9][10][11][12]. Acute manifestation imitating acute myocardial infarction may be a part of the clinical course of the disease, which is characterized by long periods of remission and sudden onsets with doubtful prognosis of recovery [14].…”

Section: Discussionmentioning

confidence: 88%

“…Takotsubo cardiomyopathy is also known as apical ballooning syndrome (ABS). It is believed to be triggered by catecholamine stimulation of B1 and B2 receptors which causes decreased expression of regulator proteins SERCa2a and PLN depending on Ca2+ [9]. Most frequently, myocardial stunning affects the apical segments of the heart which is caused by higher affinity to adrenaline.…”

Section: Introductionmentioning

confidence: 99%

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Tako-tsubo cardiomyopathy as a recurrent disease with doubtful prognosis of recovery and heterogenic symptoms

Kubiak¹,

Jacheć²,

Kawecki³

et al. 2012

Cardiol J

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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Tako-tsubo cardiomyopathy as a recurrent disease with doubtful prognosis of recovery and heterogenic symptoms

Kubiak¹,

Jacheć²,

Kawecki³

et al. 2012

Cardiol J

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“…41 Cardioprotective AKT-1 activation is associated with physiological hypertrophy, whereas a reduction in the AKT/ mTOR pathway is associated with pathological hypertrophy. 42 Interestingly, it has been reported that β2AR-Gi signaling can modulate the cellular PI3K/AKT pathways, indicating a mechanistic link between catecholamine stress and metabolic defects in TTS.…”

Section: -72 Hoursmentioning

confidence: 99%

Pathophysiology of Takotsubo Syndrome

Wright

Tranter

Morley-Smith

et al. 2014

Circ J

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Takotsubo syndrome (TTS), also known as takotsubo cardiomyopathy, stress cardiomyopathy and apical ballooning syndrome, is an acute, reversible heart failure (HF) syndrome that has increasingly come to medical attention over the past 24 years with wider access to early diagnostic coronary angiography for patients with acute chest pain and ECG abnormalities. 1 The typical case is a postmenopausal woman with an extremely stressful emotional or physical trigger, who presents with chest pain and breathlessness, ECG changes and acute hypokinesia of the apical and middle segments of the left ventricle (LV) in a circumferential pattern extending beyond a single coronary territory, and in the absence of culprit obstructive coronary artery disease (CAD). 2,3 Providing the patient survives the acute event, the dysfunctional segments recover, at least macroscopically, within days to weeks. 4 Many other variations on this "typical case" exist, including different demographics (men, younger women), different anatomical variants (basal/inverted, mid-LV, biventricular), spontaneous cases without a triggering stressor, cases triggered by other medical, surgical or psychiatric emergencies and permanent cardiac abnormalities (permanent "new" left bundle branch block, apical transmural necrosis).One common feature appears to be an extreme surge in catecholamines in response to the triggering stress or coexisting medical condition (eg, subarachnoid hemorrhage, pheochromocytoma, and thyrotoxicosis). 5-7 Animal models can replicate the features of this HF syndrome in order to dissect its mechanisms. 8-11 In contrast to the reductionist approach in most modern pathophysiological research, the more that is understood about TTS, the more it is apparent that a number of processes may result in the final common pathway of acute apical dysfunction. There are a number of mediators that may modify the severity and course of a particular episode. Defining the precise pathophysiology is challenging, and we suggest that an integrated approach to studying the cardiovascular responses to extreme surges in catecholamines is appropriate.Here we use a novel approach to reviewing the pathophysiology of TTS. Animal and clinical studies have reported findings at different phases through the development of this condition, and it is intuitive that the observed integrated cardiovascular responses to surges in serum catecholamines and sympathetic neural outflow would change over time. We discuss the pathophysiology in a sequential fashion describing effects as they occur at different time-points, integrating the observations and explaining the negative inotropic response and potential activation of cardioprotective mechanisms.Before discussing the temporal sequence of events, it is important to note a growing body of evidence that TTS is not a form of acute myocardial infarction (MI). Firstly, the epide- Takotsubo syndrome (TTS), also known as takotsubo cardiomyopathy, is an acute heart failure syndrome that typically occurs after a period of great emotion...

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“…A rapidly accumulating body of evidence has led to very interesting insights into the possible pathophysiology of TTC. Most current hypotheses are based on cathecholamine surges in the setting of acute emotional or physical stress leading to catecholamine-related cardiac toxic effects (32,(44)(45)(46)(47)(48)(49) and was first suggested by Wittstein and colleagues (16). In this section we examine various advancements in understanding TTC pathophysiology.…”

Section: Pathogenesismentioning

confidence: 99%

Takotsubo Cardiomyopathy

Moiz¹,

Fuad²,

E.³

et al. 2012

Cardiomyopathies - From Basic Research to Clinical Management

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Abnormalities in intracellular Ca2+ regulation contribute to the pathomechanism of Tako-Tsubo cardiomyopathy

Abstract: In TTC, ventricular expression of SLN and dephosphorylation of PLN potentially result in a reduced SERCA2a activity and its Ca(2+) affinity. Thus, the TTC is associated with specific alteration of Ca(2+)-handling proteins, which might be crucial for contractile dysfunction.

Cited by 119 publications

References 30 publications

Tako-tsubo cardiomyopathy as a recurrent disease with doubtful prognosis of recovery and heterogenic symptoms

Tako-tsubo cardiomyopathy as a recurrent disease with doubtful prognosis of recovery and heterogenic symptoms

Pathophysiology of Takotsubo Syndrome

Takotsubo Cardiomyopathy

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