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The Role of Cardiac T-Cadherin in the Indicating Heart Failure Severity of Patients with Non-Ischemic Dilated Cardiomyopathy.


  • 影响因子:1.43
  • DOI:10.3390/medicina56010027
  • 作者列表:"Baltrūnienė V","Rinkūnaitė I","Bogomolovas J","Bironaitė D","Kažukauskienė I","Šimoliūnas E","Ručinskas K","Puronaitė R","Bukelskienė V","Grabauskienė AV
  • 发表时间:2020-01-09

:Background and objectives: T-cadherin (T-cad) is one of the adiponectin receptors abundantly expressed in the heart and blood vessels. Experimental studies show that T-cad sequesters adiponectin in cardiovascular tissues and is critical for adiponectin-mediated cardio-protection. However, there are no data connecting cardiac T-cad levels with human chronic heart failure (HF). The aim of this study was to assess whether myocardial T-cad concentration is associated with chronic HF severity and whether the T-cad levels in human heart tissue might predict outcomes in patients with non-ischemic dilated cardiomyopathy (NI-DCM). Materials and Methods: 29 patients with chronic NI-DCM and advanced HF were enrolled. Patients underwent regular laboratory investigations, echocardiography, coronary angiography, and right heart catheterization. TNF-α and IL6 in serum were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, endomyocardial biopsies were obtained, and the levels of T-cad were assessed by ELISA and CD3, CD45Ro, CD68, and CD4- immunohistochemically. Mean pulmonary capillary wedge pressure (PCWP) was used as a marker of HF severity, subdividing patients into two groups: mean PCWP > 19 mmHg vs. mean PCWP < 19 mmHg. Patients were followed-up for 5 years. The study outcome was composite: left ventricular assist device implantation, heart transplantation, or death from cardiovascular causes. Results: T-cad shows an inverse correlation with the mean PCWP (rho = -0.397, p = 0.037). There is a tendency towards a lower T-cad concentration in patients with more severe HF, as indicated by the mean PCWP > 19 mmHg compared to those with mean PCWP ≤ 19 mmHg (p = 0.058). Cardiac T-cad levels correlate negatively with myocardial CD3 cell count (rho = -0.423, p = 0.028). Conclusions: Univariate Cox regression analysis did not prove T-cad to be an outcome predictor (HR = 1, p = 0.349). However, decreased T-cad levels in human myocardium can be an additional indicator of HF severity. T-cad in human myocardium has an anti-inflammatory role. More studies are needed to extend the role of T-cad in the outcome prediction of patients with NI-DCM.


背景与目的: T-cadherin (T-cad) 是一种在心脏和血管中大量表达的脂联素受体。实验研究表明,T-cad在心血管组织中隔离脂联素,并且对于脂联素介导的心脏保护至关重要。然而,没有将心脏T-cad水平与人慢性心力衰竭 (HF) 联系起来的数据。本研究的目的是评估心肌T-cad浓度是否与慢性HF严重程度相关,以及人类心脏组织中的T-cad水平是否可以预测非缺血性扩张型心肌病 (NI-DCM) 患者的预后。材料和方法: 纳入29例慢性NI-DCM合并晚期HF患者。患者定期接受实验室检查、超声心动图、冠状动脉造影和右心导管检查。采用酶联免疫吸附法 (ELISA) 检测血清中TNF-α 和IL6。此外,获得心内膜心肌活检,并通过ELISA和CD3,CD45Ro,CD68和CD4免疫组织化学评估T-cad的水平。使用平均肺毛细血管楔压 (PCWP) 作为HF严重程度的标志物,将患者分为两组: 平均PCWP> 19 mmHg vs.平均PCWP <19 mmHg。患者随访5年。研究结果是复合的: 左心室辅助装置植入、心脏移植或心血管原因死亡。结果: T-cad与平均PCWP呈负相关 (rho = -0.397,p = 0.037)。与平均PCWP ≤ 19 mmHg的患者相比,在具有更严重HF的患者中存在较低T-cad浓度的趋势,如平均PCWP> 19 mmHg所指示的 (p = 0.058)。心脏T-cad水平与心肌CD3细胞计数呈负相关 (rho = -0.423,p = 0.028)。结论: 单变量Cox回归分析没有证明T-cad是结果预测因子 (HR = 1,p = 0.349)。然而,人心肌中降低的T-cad水平可以是HF严重程度的额外指标。人心肌中的T-cad具有抗炎作用。需要更多的研究来扩展T-cad在NI-DCM患者结局预测中的作用。



作者列表:["Tadic M","Belyavskiy E","Cuspidi C","Pieske B","Haßfeld S"]

METHODS::We present the case of a 61-year-old woman with a large tumoral infiltration extending from the pelvis throughout the inferior vena cava inferior to the right atrium, protruding into the right ventricle and right ventricular outflow tract. She had been treated 10 years before for low-grade endometrial stromal sarcoma by hysterectomy and adnexectomy followed by hormone- and radio-therapy. Due to cancer recurrence, she underwent peritonectomy, appendectomy, and resection of terminal ileum.

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作者列表:["Pellicano M","Di Gioia G","Ciccarelli G","Xaplanteris P","Delrue L","Toth GG","Van Durme F","Heyse A","Wyffels E","Vanderheyden M","Bartunek J","De Bruyne B","Barbato E"]

METHODS:AIMS:Significant platelet activation after long stented coronary segments has been associated with periprocedural microvascular impairment and myonecrosis. In long lesions treated either with an everolimus-eluting bioresorbable vascular scaffold (BVS) or an everolimus-eluting stent (EES), we aimed to investigate (a) procedure-related microvascular impairment, and (b) the relationship of platelet activation with microvascular function and related myonecrosis. METHODS AND RESULTS:Patients (n=66) undergoing elective percutaneous coronary intervention (PCI) in long lesions were randomised 1:1 to either BVS or EES. The primary endpoint was the difference between groups in changes of pressure-derived corrected index of microvascular resistance (cIMR) after PCI. Periprocedural myonecrosis was assessed by high-sensitivity cardiac troponin T (hs-cTnT), platelet reactivity by high-sensitivity adenosine diphosphate (hs-ADP)-induced platelet reactivity with the Multiplate Analyzer. Post-dilatation was more frequent in the BVS group, with consequent longer procedure time. A significant difference was observed between the two groups in the primary endpoint of ΔcIMR (p=0.04). hs-ADP was not different between the groups at different time points. hs-cTnT significantly increased after PCI, without difference between the groups. CONCLUSIONS:In long lesions, BVS implantation is associated with significant acute reduction in IMR as compared with EES, with no significant interaction with platelet reactivity or periprocedural myonecrosis.

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翻译标题与摘要 下载文献
作者列表:["Dev M","Sharma M","Rana N"]

METHODS:BACKGROUND:Aortopulmonary window is an uncommon congenital heart disease, with untreated cases not surviving beyond childhood. However, very rarely it can present in adult patients with features of pulmonary hypertension. Clinically these patients cannot be differentiated from other more common conditions with left to right shunt. Transthoracic echocardiography if performed meticulously, can depict the defect in aortopulmonary septum. RESULTS:We report a case of large unrepaired aortopulmonary window in a 23 years old patient, diagnosed on transthoracic echocardiography.