The focal takotsubo syndrome presenting with the snail-like left ventricle.
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ABSTRACT:
SUBMITTER: Genc A
PROVIDER: S-EPMC8277007 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Publications
The focal takotsubo syndrome presenting with the snail-like left ventricle.
Genc Alicja A Sobolewski Jakub J Bachorski Witold W Pisowodzka Izabela I Jaguszewski Miłosz M Fijałkowski Marcin M
Cardiology journal 20210101 4
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Project description:Accumulating evidence indicates alteration of the β-adrenoceptor (AR), such as desensitization and subtype switching of its coupling G protein, plays a role in the protection against catecholamine toxicity in heart failure. However, in human takotsubo syndrome (TTS), which is associated with a surge of circulating catecholamine in the acute phase, there is no histologic evidence of β-AR alteration. The purpose of this study was to investigate the involvement of alteration of β-AR signaling in the mechanism of TTS development. Left ventricular (LV) biopsied samples from 26 patients with TTS, 19 with normal LV function, and 26 with dilated cardiomyopathy (DCM) were studied. G protein-coupled receptor kinase 2 (GRK2) and β-arrestin2, which initiate the alteration of β-AR signaling, were more abundantly expressed in the myocardium in acute-phase TTS than in those of DCM and normal control as indicated by immunohistochemistry. The percentage of cardiomyocytes that showed positive membrane staining for GRK2 and β-arrestin2 was also significantly higher in acute-phase TTS. Sequential biopsies in the recovery-phase for two patients with TTS revealed that membrane expression of GRK2 and β-arrestin2 faded over time. This study provided the first histologic evidence of the involvement of alteration of β-ARs in the development of TTS.
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Project description:Background Left bundle branch block (LBBB) causes left ventricular dyssynchrony, and its presence with concomitant left ventricular dysfunction has been proven to play a synergistic role, worsening ventricular function. Our study seeks to further explore the association between LBBB and various in-hospital outcomes in patients with takotsubo syndrome (TTS). Methods The national inpatient sample was queried from 2016 to 2019 to identify all admissions with a primary diagnosis of TTS. International classification of diseases, tenth revision codes were used to divide patients based on the presence or absence of LBBB. Multivariate regression analysis was performed to assess the effect of LBBB among all the pre-specified outcomes. Results A total of 26,615 admissions were included in the analysis. Admissions with LBBB were more likely to be older (72.2 vs. 66.2 years) and have a higher burden of comorbidities. The presence of a LBBB was associated with ventricular arrhythmias (OR = 1.97, 95% CI 1.08–3.61, p = 0.028) but not with sudden cardiac arrest (SCA), acute heart failure, cardiogenic shock, and all-cause intra-hospital mortality. Conclusions Intraventricular dyssynchrony appears to play a significant role in ventricular arrhythmogenesis and SCA, as several trials have demonstrated that cardiac resynchronization therapy alone without defibrillator function reduces the rate of ventricular arrhythmias and SCA in patients with heart failure with systolic dysfunction and a widened QRS complex. The most likely mechanism of arrhythmia development in TTS is related to the elevated plasma levels of catecholamines and their proarrhythmic effects in the ventricular myocardium.
| S-EPMC9513099 | biostudies-literature
Project description:Takotsubo syndrome (TS) is a reversible form of cardiomyopathy characterized by transient systolic dysfunction with regional wall motion abnormalities and absence of coronary artery obstruction, which can be precipitated by severe emotional or physical stress. Its clinical presentation is similar to that of acute coronary syndrome. However, TS presenting with atrioventricular (AV) block with ventricular asystole is rarely reported. In this article, we describe the case of a postmenopausal woman who experienced near cardiac arrest due to high-degree AV block. Although transthoracic echocardiography revealed left ventricular dysfunction with severe global hypokinesia, coronary angiography and cardiac magnetic resonance imaging showed normal coronary arteries without myocardial scarring. The patient's condition improved after permanent pacemaker implantation and medical treatment for heart failure. Echocardiography and pacemaker analysis at two-month follow-up revealed normalization of heart function and cardiac rhythm, and the patient was finally diagnosed with TS. <Learning objective: Takotsubo syndrome can present with conduction abnormalities such as a high-degree atrioventricular block in case of left ventricular basal segment involvement. Cardiac magnetic resonance imaging is useful for distinguishing stress-induced cardiomyopathy from other myocardial diseases with non-obstructive coronary arteries.>.
| S-EPMC8888725 | biostudies-literature
Project description:BackgroundMatrix metalloproteinase 8 (MMP-8) is the most potent type-I collagen protease. Such collagen mainly constitutes the transient fibrosis in takotsubo cardiomyopathy (TTC) endomyocardial biopsies. High MMP-8 and tissue-inhibitor of matrix metalloproteinase-1 (TIMP-1) levels are implicated in acute coronary syndrome (ACS). We compared MMP-8 and TIMP-1 levels in consecutive TTC and ACS patients, and their association to TTC severity.Methods and resultsIn 45 acute serum samples of TTC, 2072 ACS and 1000 controls, TIMP-1 differed between ACS 146.7ng/mL (115.0-186.3) (median (interquartile range)), TTC 115.7 (94.3-137.7) and controls 80.9 (73.2-90.4), (p<0.0001). MMP-8 levels were similar between ACS and TTC. In receiver-operating characteristics analysis, TIMP-1 differentiated TTC from ACS with an area under the curve (AUC) of 0.679 (p<0.0001) surpassing troponin T (TnT) at 0.522 (p = 0.66). Compared to other differing factors (age, sex, smoking), TIMP-1 improved diagnostic specificity and sensitivity from AUC of 0.821 to 0.844 (p = 0.007). The MMP8/TIMP-1 molar ratio differentiated normal ejection fraction (EF) at 0.27 (0.13-0.51) from decreased EF<50% at 0.08 (0.05-0.20), (p = 0.04) in TTC, but not in ACS.ConclusionsEven with other differing factors considered, TIMP-1 differentiated TTC from ACS better than TnT. In TTC, the low MMP-8/TIMP-1 molar ratio may reflect decreased proteolysis and increased transient fibrosis, perhaps in part explaining the left-ventricle impairment.
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Project description:In cases of fetal aortic stenosis and evolving Hypoplastic Left Heart Syndrome (feHLHS), aortic stenosis is associated with specific abnormalities such as retrograde or bidirectional systolic transverse arch flow. Many cases progressed to hypoplastic left heart syndrome (HLHS) malformation at birth, but fetal aortic valvuloplasty can prevent the progression in many cases. Since both disease and intervention involve drastic changes to the biomechanical environment, in-vivo biomechanics likely play a role in inducing and preventing disease progression. However, the fluid mechanics of feHLHS is not well-characterized. Here, we conduct patient-specific echocardiography-based flow simulations of normal and feHLHS left ventricles (LV), to understand the essential fluid dynamics distinction between the two cohorts. We found high variability across feHLHS cases, but also the following unifying features. Firstly, feHLHS diastole mitral inflow was in the form of a narrowed and fast jet that impinged onto the apical region, rather than a wide and gentle inflow in normal LVs. This was likely due to a malformed mitral valve with impaired opening dynamics. This altered inflow caused elevated vorticity dynamics and wall shear stresses (WSS) and reduced oscillatory shear index at the apical zone rather than mid-ventricle. Secondly, feHLHS LV also featured elevated systolic and diastolic energy losses, intraventricular pressure gradients, and vortex formation numbers, suggesting energy inefficiency of flow and additional burden on the LV. Thirdly, feHLHS LV had poor blood turnover, suggesting a hypoxic environment, which could be associated with endocardial fibroelastosis that is often observed in these patients.
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Project description:Currently, there are 2 proposed causes of acute left ventricular ballooning. The first is the most cited hypothesis that ballooning is caused by direct catecholamine toxicity on cardiomyocytes or by microvascular ischemia. We refer to this pathogenesis as Takotsubo syndrome. More recently, a second cause has emerged: that in some patients with underlying hypertrophic cardiomyopathy, left ventricular ballooning is caused by the sudden onset of latent left ventricular outflow tract obstruction. When it becomes severe and unrelenting, severe afterload mismatch and acute supply-demand ischemia appear and result in ballooning. In the context of 2 causes, presentations might overlap and cause confusion. Knowing the pathophysiology of each mechanism and how to determine a correct diagnosis might guide treatment.
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