Is everything clear about Tako-Tsubo syndrome?

Abstract

IntroductIon: tako-tsubo syndrome is a novel cardio-vascular disease affecting predominantly postmenopausal women exposed to unexpected strong emotional or physical stress, in the absence of significant coronary heart disease. It is characterized by acute onset of severe chest pain and/or acute left ventricular failure, eCg-changes, typical left ventricular angiographic findings, good prognosis and positive resolution of the morphological and clinical manifestations. First described in 1990 in Japan by Sato, Tako

Women's experiences of Takotsubo cardiomyopathy in a short‐term perspective – a qualitative content analysis

“…Treatment is considered relative to the severity of the heart failure, which can range from moderate symptoms to cardiogenic shock. Patients require monitoring for complications such as left ventricular failure, pulmonary oedema, arrhythmias and apical thrombus formation . The relationship between sudden death and TTC is uncertain.…”

“…The aetiology and pathophysiology of TTC remain uncertain. Theories put forth are related to catecholamine excess, multivessel epicardial or microvascular spasm or dysfunction . Better understanding of these mechanisms appears to be the focus of current research, whilst knowledge regarding patients' own experience of TTC is scarce.…”

Późna postać zespołu takotsubo w przebiegu zatorowości płucnej

“…In the presented case the symptoms of an acute pulmonary embolism constituted both emotional and physical stressors. Usually, TTS develops within 1-5 days after the occurrence of the stress factor but there are a few described in literature cases of so-called late TTS which developed even up to 14 days after the stressor [5,6]. One of the most characteristic features of TTS is the spontaneous withdrawal of the left ventricle dysfunction [7] (Table 2, Figure 1).…”

Arrhythmias and Their Electrophysiological Mechanisms in Takotsubo Syndrome: A Narrative Review

“…QTc prolongation is widely reported to be associated with ventricular arrhythmias in TTS [32]. It reflects prolonged repolarisation, likely via elevated cyclic adenosine monophosphate (cAMP) levels and decreased potassium channel activity [33]. In TTS, the QTc is often in the interval of .460 ms [34], but can be markedly prolonged (600-650 ms) when associated with TdP [35], which is often associated with predisposing conditions such as bradycardia, electrolyte disturbance and medications [36].…”