Because earlier studies used left ventriculography to detect and diagnose TTS, right ventricular involvement had not been reported until 2006, when two studies from the USA and EU reported right ventricular involvement in TTS [33,34]. are still uncertain, observational data suggest favorable impact of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Finally, in the era of COVID-19, we should pay attention to a variety of cardiovascular conditions related to COVID-19. TTS is usually one of these conditions that can be brought on by both emotional and physical impact of the COVID-19 pandemic. strong class=”kwd-title” Keywords: Takotsubo syndrome, Echocardiography, COVID-19 Introduction Since the initial reports from Japan [[1], [2], [3], [4]], takotsubo cardiomyopathy or takotsubo syndrome (TTS) has become globally recognized as a unique syndrome mimicking acute coronary syndrome brought on by emotional or physical stress [5]. Initially, emotional stress was considered as essential for TTS and thus TTS was also named as stress-induced cardiomyopathy. SRT 2183 However, emotional stress was documented in only 20-39% and physical stress in 35-55% of cases [6]. Interestingly, not only unfavorable emotional stress but also positive emotional stress could be a trigger of TTS, and it has been called happy heart syndrome [7]. Natural disasters may cause a variety of cardiovascular diseases, such as acute myocardial infarction [8,9], stroke [10], deep vein thrombosis [10,11], and TTS [12,13]. Currently, the pandemic of COVID-19 affects the health status of people all over the world. SARS-CoV-2 is usually a newly found corona virus that sometimes causes catastrophic respiratory failure requiring respirator and/or extracorporeal membrane oxygenation. In this review, a current update of TTS in the era of COVID-19 pandemic is usually summarized. Pathophysiology and mechanisms of TTS Although catecholamine has been suspected to play some role during the development of TTS, exact mechanisms of TTS are still uncertain. In TTS patients, plasma catecholamine (epinephrine, norepinephrine, and dopamine) levels at presentation were markedly higher than among those with Killip class III myocardial infarction [14]. We further compared catecholamine levels at the aortic root and coronary sinus and exhibited local release of catecholamine levels (norepinephrine) in TTS [15]. Akashi et al. reported increased iodine-123-meta-iodobenzylguanidine uptake and increased washout ratio in the acute phase of TTS, suggesting the presence of cardiac sympathetic hyperactivity [16]. Paur et al. reported interesting results of an in vivo rat model of TTS. They suggested that high-dose epinephrine can induce direct cardiomyocyte cardiodepression and cardioprotection in a 2-adrenergic receptor (AR)CGi-dependent manner [17]. At higher concentrations, epinephrine stimulates a negative inotropic effect on myocardial contraction by switching 2-AR coupling from Gs protein to Gi protein [18]. Stimulation of the 2-AR-Gi protein pathway then produces negative inotropic action resulting in akinesis CENPA of the involved segments. Location and the extent of wall motion abnormalities in TTS may be explained by the distribution of the 2-AR [18]. More recently, we exhibited in vivo evidence of -AR alteration [19]. Left ventricular biopsy samples from patients with TTS exhibited more abundantly expressed G protein coupled receptor kinase 2 (GRK2) and -arrestin2, both of which are known to desensitize -AR, than in samples from dilated cardiomyopathy. Desensitization of 1-AR causes decreased left ventricular contraction of the involved segments. In cases with apical TTS, apical segments may be more involved, although exact mechanisms of the segment specific changes in desensitization of the 1-AR are unclear. Desensitization of 1-AR together with switching of the coupling G protein from Gs to Gi in 2-AR could explain apical involvement because of its apical dominant distribution [[17], [18], [19]] (Fig. 1 ). Open in a separate window Fig. 1 Proposed mechanisms of wall motion abnormalities in patients with takotsubo syndrome. (A) With superphysiological catecholamine levels, -arrestin2 internalization the 1-AR and GRK2 induces 1-AR uncoupling, resulting in desensitization and SRT 2183 suppression of myocardial contraction. Adapted from Nakano et al. [19]. (B With superphysiological catecholamine levels, stimulation of 2-AR suppress myocardia contraction by switching Gs protein to Gi protein. Adapted from Paur et al. [17]. New classification and diagnostic criteria of TTS Originally, only those who presented left ventricular apical ballooning or takotsubo-like wall motion were.A recent Japanese nationwide survey including 5274 patients with TTS revealed that 3255 (61.7%) underwent coronary angiography and 2019 (38.3%) did not [64]. prognosis of TTS are still uncertain, observational data suggest favorable impact of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Finally, in the era of COVID-19, we should pay attention to a variety of cardiovascular conditions related to COVID-19. TTS is usually one of these conditions that can be brought on by both SRT 2183 emotional and physical impact of the COVID-19 pandemic. strong class=”kwd-title” Keywords: Takotsubo syndrome, Echocardiography, COVID-19 Introduction Since the initial reports from Japan [[1], [2], [3], [4]], takotsubo cardiomyopathy or takotsubo syndrome (TTS) has become globally recognized as a unique syndrome mimicking acute coronary syndrome brought on by emotional or physical stress [5]. Initially, emotional stress was considered as essential for TTS and thus TTS was also named as stress-induced cardiomyopathy. However, emotional stress was documented in only 20-39% and physical stress in 35-55% of cases [6]. Interestingly, not only negative emotional stress but also positive emotional stress could be a trigger of TTS, and it has been called happy heart syndrome [7]. Natural disasters may cause a variety of cardiovascular diseases, such as acute myocardial infarction [8,9], stroke [10], deep vein thrombosis [10,11], and TTS [12,13]. Currently, the pandemic of COVID-19 affects the health status of people all over the world. SARS-CoV-2 is usually a newly found corona virus that sometimes causes catastrophic respiratory failure requiring respirator and/or extracorporeal membrane oxygenation. In this review, a current update of TTS in the era of COVID-19 pandemic is usually summarized. Pathophysiology and mechanisms of TTS Although catecholamine has been suspected to play some role during the development of TTS, exact mechanisms of TTS are still uncertain. In TTS patients, plasma catecholamine (epinephrine, norepinephrine, and dopamine) levels at presentation were markedly higher than among those with Killip class III myocardial infarction [14]. We further compared catecholamine levels at the aortic root and coronary sinus and exhibited local release of catecholamine levels (norepinephrine) in TTS [15]. Akashi et al. reported increased iodine-123-meta-iodobenzylguanidine uptake and increased washout ratio in the acute phase of TTS, suggesting the presence of cardiac sympathetic hyperactivity [16]. Paur et al. reported interesting results of an in vivo rat model of TTS. They suggested that high-dose epinephrine can induce direct cardiomyocyte cardiodepression and cardioprotection in a 2-adrenergic receptor (AR)CGi-dependent manner [17]. At higher concentrations, epinephrine stimulates a negative inotropic effect on myocardial contraction by switching 2-AR coupling from Gs protein to Gi protein [18]. Stimulation of the 2-AR-Gi protein pathway then produces negative inotropic action resulting in akinesis of the involved segments. Location and the extent of wall motion abnormalities in TTS may be explained by the distribution of the 2-AR [18]. More recently, we exhibited in vivo evidence of -AR alteration [19]. Left ventricular biopsy samples from patients with TTS exhibited more abundantly expressed G protein coupled receptor kinase 2 (GRK2) and -arrestin2, both of which are known to desensitize -AR, than in samples from dilated cardiomyopathy. Desensitization of 1-AR causes decreased left ventricular contraction of the involved segments. In cases with apical TTS, apical segments may be more involved, although exact mechanisms of the segment specific changes in desensitization of the 1-AR are unclear. Desensitization of 1-AR together with switching of the coupling G protein from Gs to Gi in 2-AR could explain apical involvement because of its apical dominant distribution SRT 2183 [[17], [18], [19]] (Fig. 1 ). Open in a separate window Fig. 1 Proposed mechanisms of wall motion abnormalities in individuals with takotsubo symptoms. (A) With superphysiological catecholamine amounts, -arrestin2 internalization the 1-AR and GRK2 induces 1-AR uncoupling, leading to desensitization and suppression of myocardial contraction. Modified from Nakano et al. [19]. (B With superphysiological catecholamine amounts, excitement of 2-AR suppress myocardia contraction by switching Gs proteins to Gi proteins. Modified from Paur et al. [17]. New classification and diagnostic requirements of TTS Originally, just those who shown remaining ventricular apical ballooning or takotsubo-like wall structure motion had been diagnosed as having takotsubo cardiomyopathy or TTS, because just remaining ventriculography was utilized.
Because earlier studies used left ventriculography to detect and diagnose TTS, right ventricular involvement had not been reported until 2006, when two studies from the USA and EU reported right ventricular involvement in TTS [33,34]
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