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加强经导管射频消融治疗室性心律失常的临床研究
室性心律失常是器质性心脏病患者致死的主要原因,也是心脏结构正常者心脏性猝死的主要死因.故加深对其发病机制的研究,加强对其防治学的探讨具有十分重要的意义.
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特发性室性心律失常经导管射频消融治疗的临床意义与进展
室性心律失常在临床上很常见,也是心脏性猝死的主要原因.频发室性早搏(室早)、室性心动过速(室速)和心室颤动(室颤)不仅发生于器质性心脏病患者,同样也可见于心脏结构正常的人群.此类未发现器质性心脏病患者的室性心律失常我们称之为特发性室性心律失常,尽管多数预后是良好的,但少数患者依然有猝死的潜在风险,越来越受到临床的重视.有资料显示,发生在医院外猝死幸存者中5%~10%为无器质性心脏病和体表心电图异常改变的原发性室颤所致.
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室性心律失常的一些研究进展
继心房颤动(房颤)之后,室性心律失常再度成为心律学领域的研究热点.近年取得许多进展,可能影响或改变今后的临床实践.
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室性心律失常的治疗进展
室性心律失常(VA)是临床常见的心律失常,包括室性早搏(PVC)、室性心动过速(VT)、心室扑动与颤动(VF).VA严重威胁人类的健康,尤其是发作时伴有血流动力学障碍的VT和VF,严重者甚至可危及患者生命.VA不仅可以发生于冠心病、非缺血性心肌病、致心律失常性右心室心肌病(ARVC)与心力衰竭等器质性心脏病患者,也可发生于无器质性心脏病患者,如原发性VA.近年来,一些遗传性VA如长QT综合征、短QT综合征、Brugada综合征和儿茶酚胺敏感性多形VT等,越来越受到电生理学者的关注.VA治疗是当今心血管领域研究的重点与热点.目前VA治疗措施主要包括抗心律失常药物(AADs)、植入型心律转复除颤器(ICD)和导管消融等.
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第三届全国室性心律失常专题会议纪要
由中华医学会心电生理与起搏分会和南京医科大学第一附属医院共同举办的"第三届全国室性心律失常专题会议"于2011年3月4日至6日在美丽的古都南京举行.此次会议邀请到国内外知名专家与参会人员近800人,共同研讨室性心律失常的发病机制与治疗策略.
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CRT-D治疗重度心功能不良伴恶性室性心律失常的初步观察
大规模临床试验证明,对于药物治疗无效伴有收缩功能不同步的严重心功能不良患者,不论有无室性心律失常,心脏再同步治疗加心脏复律除颤器(cardiac resynchronization therapy device and defibrillator,CRT-D)均能有效地改善患者症状、提高生活质量、减少心力衰竭住院次数、延长寿命和防止心脏性猝死.由于经济等多方面的原因,国内CRT-D治疗病例不多,现报道本中心2007年1月至7月间3例植入CRT-D患者的初步临床观察.
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急性心肌梗死合并室性心律失常病人的护理
急性心肌梗死(AMI)是指由于冠状动脉急性狭窄或闭塞所产生的心肌严重缺血和坏死.多是由于冠状动脉粥样硬化斑块破裂和血栓形成,导致冠状动脉急性狭窄或闭塞.AMI主要死因是室性心律失常.为探讨急性心肌梗死合并室性心律失常的有效护理方法,我院对急性心肌梗死合并室性心律失常的病人采取严格的临床治疗与护理,现介绍如下.
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胺碘酮治疗室性心律失常的观察与护理
胺碘酮是迄今认为有效的抗心律失常药,对预防致命性室性心动过速、复发性心房仆动、心房颤动、阵发性室上性收动过速以及预激综合征伴发的快速性心律失常均有效[1].
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急性心肌梗死并发高危室性心律失常早期识别的研究进展
急性心肌梗死(AMI)是指心肌的急性、持续性缺血、缺氧所引起的心肌坏死,可出现心律失常、休克或心力衰竭等并发症,严重时危及患者生命。当前,国内外AMI发病率均呈明显上升趋势,而且治疗后发生再梗死或多次梗死患者增多,因此对本病的及时诊断、治疗以及并发症的防治应予以高度重视。高危心律失常是指:某些心律失常能够引起血流动力学的明显变化,若不及时处理会急剧恶化;或是在原有严重器质性心脏疾病的基础上发生的心律失常,使得原有的心脏疾病明显加重、恶化,使病情处于非常不稳定的状态。高危心律失常进一步恶化可发展为心室颤动,甚至引起猝死[1‐2]。室性心律失常是急性心肌梗死常见的并发症[3]。在急性心肌梗死幸存的人群中,50%以上仍死于致命的高危室性心律失常。目前对室性心律失常已建立相关的诊治策略[4],随着急性心肌梗死综合治疗水平的不断提高,室性心律失常的发生、组成、与冠状动脉病变特点的关系及对患者预后的影响也将有变化[5]。因此急性心肌梗死后高危心律失常的早期识别对于挽救患者生命,降低病死率有着重要的意义。
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Objective:Glucose-insulin-potassium(GIK) is clinically used for reducing mortality in acute myocardial infarction(MI). It is known that ventricular arrhythmia, left ventricular dysfunction and impaired baroreflex sensitivity(BRS) are the three major determinants for predicting the mortality after acute MI. The present work was designed to study the effects of GIK on BRS, ventricular arrhythmia, and left ventricular function in rats with coronary artery ligature. Sprague-Dawley rats were used and the myocardial infarction was produced by ligature of the left anterior descending artery. Five weeks after coronary artery ligation, BRS was measured in conscious state with a computerized blood pressure monitoring system and left ventricular function and electrocardiogram were determined in the anaesthetized state in the subacute phase of myocardial infarction. It was found that GIK did not affect the blood pressure and heart period in both conscious and anaesthetized rats. GIK did not enhance BRS, but reduced ventricular arrhythmia and improved left ventricular function by reducing left ventricular end diastolic pressure in anaesthetized rats with MI. It is proposed that reducing ventricular arrhythmia and improving left ventricular function contribute to the effect of GIK on reducing the mortality after MI.
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恶性室性心律失常的现代诊治概念
恶性室性心律失常(malignant ventricular arrhythmia,MVA)系指引起严重血流动力学障碍的室性心律失常.
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连续静滴芬太尼、利多卡因和琥珀胆碱复合液用于小儿全麻的观察
我院将芬太尼、利多卡因和琥珀胆碱复合剂用于小儿全麻,观察50例,发现患儿用该法麻醉血流动力学平稳和基本平稳者占80%,大部分患儿在停用该复合剂三十分钟后自主呼吸恢复,且该法有镇痛强、作用快等作用.文中还就复合剂中药物的使用及注意事项作了说明,供临床参考.
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AIM:To investigate the regulation mechanism for insufficient KChIP 2 expression induces Ito,f downregulation and arrhythmogene-sis in cardiac hypertrophy .METHODS:Bidirectional manipulations of MG 53 expression were performed by adenoviral overexpression of MG53 or knockdown of MG53 with RNA interference in neonatal rat ventricular myocytes with or without PE stimulation .Ito,f was re-corded with patch clamp in whole-cell mode 48 h after adenoviral transfection .Then the WT or MG53 knockout ( MG53 -/-) mouse model of left ventricular hypertrophy induced by transverse aortic constriction ( TAC) were used to detect the susceptibility to ventricu-lar arrhythmia.RESULTS: Here, we show muscle-specific MG53 regulates KChIP2 expression and Ito,f densities, where they are downregulated in hearts from MG53 knockout mice and MG53 knockdown rat cardiomyocytes , but upregulated in MG53 overexpressed cells.MG53 expression is decreased in phenylephrine ( PE)-induced cardiomyocyte hypertrophy and restoration of MG 53 rescues PE-induced downregulation of KChIP2 and Ito,f.Furthermore, MG53 is decreased in a mouse model of hypertrophy induced by transverse aortic constriction and ablation of MG 53 increases the susceptibility to ventricular arrhythmia by exaggerating Ito,f remodeling.CON-CLUSION:These findings establish MG53 as a novel regulator of Ito,f and its central role in arrhythmogenesis in hypertrophy .