scholarly journals Takotsubo Syndrome — Stress-induced Heart Failure Syndrome

2015 ◽  
Vol 10 (2) ◽  
pp. 83 ◽  
Author(s):  
Mary N Sheppard ◽  

Takotsubo syndrome has been established as an entity in the past 30 years, particularly with the introduction of interventional angiography for investigation of chest pain. Typically, it occurs in middle-aged females as a response to a stressful event, such as bad news, death, accident, natural disaster, etc. but there is not always a specific trigger. Takotsubo mimics acute myocardial infarction with electrocardiogram changes and elevated troponins. On interventional angiography the coronary arteries are normal with typical apical ballooning of the left ventricle. This feature led to its descriptive name, given by Japanese cardiologists, as the left ventricle resembles a lobster trap with a narrow neck extending into a round ventricle. This leads to a reduction in cardiac function. Takotsubo is believed to be a response to catecholamine release following a stressful event resulting in temporary myocardial damage. It usually has a benign course with spontaneous return of cardiac function. However it may recur and in a small percentage of patients can result in sudden cardiac death with arrhythmia, acute myocardial infarction and cardiac rupture. It is usually treated symptomatically depending on the severity of presentation.

2021 ◽  
Author(s):  
Xiao Ma ◽  
Chengqiang Wu ◽  
Lang Li ◽  
Zhiyu Zeng ◽  
Chun Gui

Abstract Background: Myocardial angiogenesis is central to the recovery of acute myocardial infarction (AMI). Neuregulin-1 (NRG-1) plays a critical role in cardiac function, although its role in myocardial angiogenesis is still unclear. The aim of this study was to investigate the effects of NRG-1 in myocardial angiogenesis in a rat model of AMI, and elucidate the underlying mechanisms. Methods: AMI was induced by a single ligation of left anterior descending coronary artery, followed by intravenous injection of recombinant human NRG-1 or normal saline for 8 consecutive days. The cardiac function indices were measured using the catheter MPA cardiac function analysis system. Histo-pathological changes were observed by HE. Microvessel density (MVD) was measured by CD31 and α-SMA immunostaining. The expression levels of other proteins were assessed by Western blotting. Results: NRG-1 improved cardiac function and alleviated myocardial damage induced by AMI. Compared to the sham-operated group, the capillary density and arteriole density increased after AMI (P<0.05), and were augmented by NRG-1 which also significantly increased the left ventricular function (P<0.05). Furthermore, Compared with sham group, PI3K-AKT-eNOS signaling was decreased significantly (P<0.05) whereas VEGF/ VEGFR2 signaling was significantly increased(P<0.05)in AMI group and both of therm were further upregulated by NRG-1 (P > 0.05).Conclusion: NRG-1 improved cardiac function and promoted myocardial angiogenesis post AMI by up-regulating VEGF and activating the PI3K-Akt-eNOS pathway.


2018 ◽  
pp. bcr-2017-222451
Author(s):  
Rosalyn Adigun ◽  
Samantha Morley ◽  
Abhiram Prasad

Apical ballooning syndrome (ABS) is an under recognised clinical entity characterised by acute reversible left ventricular systolic dysfunction that mimics acute myocardial infarction in the absence of obstructive coronary artery disease; typically occurring in the setting of profound stress.1 ABS disproportionately affects older women and recurrences are infrequent. We, hereby, describe a rare phenomenon of recurrent ABS in an elderly male patient, 10 years apart, presenting with the same left ventricular morphological appearance following non-cardiac surgeries. The case illustrates the importance of considering ABS in the differential diagnosis of perioperative acute myocardial infarction in older men undergoing major surgery.


2006 ◽  
Vol 8 (4) ◽  
pp. 347-354 ◽  
Author(s):  
Sebastian Philipp ◽  
Jan Steffen Jürgensen ◽  
Jens Fielitz ◽  
Wanja M. Bernhardt ◽  
Alexander Weidemann ◽  
...  

2013 ◽  
Vol 6 (3) ◽  
pp. 492-498 ◽  
Author(s):  
Robin A.P. Weir ◽  
Colin J. Petrie ◽  
C. Aengus Murphy ◽  
Suzanne Clements ◽  
Tracey Steedman ◽  
...  

2014 ◽  
Vol 307 (10) ◽  
pp. H1487-H1496 ◽  
Author(s):  
Sander Land ◽  
Steven A. Niederer ◽  
William E. Louch ◽  
Åsmund T. Røe ◽  
Jan Magnus Aronsen ◽  
...  

In Takotsubo cardiomyopathy, the left ventricle shows apical ballooning combined with basal hypercontractility. Both clinical observations in humans and recent experimental work on isolated rat ventricular myocytes suggest the dominant mechanisms of this syndrome are related to acute catecholamine overload. However, relating observed differences in single cells to the capacity of such alterations to result in the extreme changes in ventricular shape seen in Takotsubo syndrome is difficult. By using a computational model of the rat left ventricle, we investigate which mechanisms can give rise to the typical shape of the ventricle observed in this syndrome. Three potential dominant mechanisms related to effects of β-adrenergic stimulation were considered: apical-basal variation of calcium transients due to differences in L-type and sarco(endo)plasmic reticulum Ca2+-ATPase activation, apical-basal variation of calcium sensitivity due to differences in troponin I phosphorylation, and apical-basal variation in maximal active tension due to, e.g., the negative inotropic effects of p38 MAPK. Furthermore, we investigated the interaction of these spatial variations in the presence of a failing Frank-Starling mechanism. We conclude that a large portion of the apex needs to be affected by severe changes in calcium regulation or contractile function to result in apical ballooning, and smooth linear variation from apex to base is unlikely to result in the typical ventricular shape observed in this syndrome. A failing Frank-Starling mechanism significantly increases apical ballooning at end systole and may be an important additional factor underpinning Takotsubo syndrome.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Irene Cuadrado ◽  
Maria Jose Garcia Miguel ◽  
Irene Herruzo ◽  
Mari Carmen Turpin ◽  
Ana Martin ◽  
...  

Extracellular matrix metalloproteinase inducer EMMPRIN, is highly expressed in patients with acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including MMP-9 and MMP-13. To prevent Extracellular matrix degradation and cardiac cell death we targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles with an EMMPRIN binding peptide AP9 conjugated (NAP9), or an AP9 scramble peptide as a negative control (NAPSC). NAP9 binds to endogenous EMMPRIN as detected by confocal microscopy of cardiac myocytes and macrophages incubated with NAP and NAPSC in vitro, and in vivo in mouse hearts subjected to left anterior descending coronary artery occlusion (IV injection 50mγ/Kg NAP9 or NAP9SC). Administration of NAP9 at the same time or 1 hour after AMI reduced infarct size over a 20% respect to untreated and NAPSC injected mice, recovered left ventricle ejection fraction (LVEF) similar to healthy controls, and reduced EMMPRIN downstream MMP9 expression. In magnetic resonance scans of mouse hearts 2 days after AMI and injected with NAP9, we detected a significant gadolinium enhancement in the left ventricle respect to non-injected mice and to mice injected with NAPSC. Late gadolinium enhancement assays exhibited NAP9-mediated left ventricle signal enhancement as early as 30 minutes after nanoprobe injection, in which a close correlation between the MRI signal enhancement and left ventricle infarct size was detected. Taken together, these results point EMMPRIN targeted nanoprobes as a new tool for the treatment of AMI.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Jianqing She ◽  
Jiahao Feng ◽  
Yangyang Deng ◽  
Lizhe Sun ◽  
Yue Wu ◽  
...  

Objective. The pathophysiologic mechanism of how thyroid function is related to the development and prognosis of acute myocardial infarction (AMI) remains under explored, and there has been a lack of clinical investigations. In this study, we investigate the relationship between triiodothyronine (T3) level and cardiac ejection fraction (EF) as well as probrain natriuretic peptide (NT-proBNP) on admission and subsequent prognosis in AMI patients. Methods. We measured admission thyroid function, NT-proBNP, and EF by echocardiography in 345 patients diagnosed with AMI. Simple and multiregression analyses were performed to investigate the correlation between T3 level and EF as well as NT-proBNP. Major adverse cardiovascular events (MACE), including new-onset myocardial infarction, acute heart failure, and cardiac death, were documented during the follow-up. 248 participants were separated into three groups based on T3 and free triiodothyronine (FT3) levels for survival analysis during a 2-year follow-up. Results. 345 patients diagnosed with AMI were included in the initial observational analysis. 248 AMI patients were included in the follow-up survival analysis. The T3 levels were found to be significantly positively correlated with EF (R square=0.042, P<0.001) and negatively correlated with admission NT-proBNP levels (R square=0.059, P<0.001), which is the same with the correlation between FT3 and EF (R square=0.053, P<0.001) and admission NT-proBNP levels (R square=0.108, P<0.001). Kaplan-Meier survival analysis revealed no significant difference with regard to different T3 or FT3 levels at the end of follow-up. Conclusions. T3 and FT3 levels are moderately positively correlated with cardiac function on admission in AMI patients but did not predict a long-time survival rate. Further studies are needed to explain whether longer-term follow-up would further identify the prognosis effect of T3 on MACE and all-cause mortality.


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