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心律失常的发病机理目前尚不清楚。既往很多学者从心电生理等方面对心律失常的发病机制作了很多报道 ,但关于抗心律失常肽 (AAP)与人心律失常的关系尚未见临床报道。本文的目的是检测风湿性心脏病心房纤颤 (简称房颤 )患者、冠心病频发室性早搏 (简称室早 )患者和慢性心力衰竭患者血清中AAP的含量 ,探讨心律失常的发病机理。1998年 1~ 2月我院收住的风湿性心脏病二尖瓣狭窄房颤患者 2 5例。经多普勒血流显像技术确诊。其中男 15例 ,女 10例 ,风心病史 8~ 12年 ,房颤病史约 2~ 3年。冠心病并频发室早患者 2 1例 ,其中男 14例 ,女 7… 相似文献
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自运动性高血压的概念被提出之后,经过近40年的研究和探索,目前医学界对运动性高血压已经有了较为深入的认识,但这种认识还未引起临床医师足够多的重视。本文将就运动性高血压的定义、诊断标准、发病机制及其是否增加未来新发静息性高血压的风险,是否影响心脏结构和功能,是否增加心血管事件、脑血管事件的风险,以及是否与其他一些疾病有相关性进行综述,以期引起临床医师对运动性高血压的关注。 相似文献
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目的探讨兰尼碱(RYR2)、FK506结合蛋白12.6(FKBP12.6)及钙调蛋白依赖性蛋白激酶Ⅱ(CaMK-Ⅱ)在COPD患者肺组织中的表达及意义。方法回顾性分析2012年11月至2017年4月宁夏回族自治区人民医院心胸外科肺癌手术后患者30例,根据入院肺功能、超声心动图检查结果,将患者分为3组:慢性阻塞性肺疾病(COPD)合并肺动脉高压(PH)组、COPD组、非COPD且非PH患者对照组,取手术切除后距癌变区>5 cm的组织。测量3组肺血管组织石蜡切片中肺小动脉面积。用免疫组织化学法分别观察RYR2、FKBP12.6及CaMK-Ⅱ表达,并做相关性分析。结果(1)与对照组比较,COPD合并PH组、COPD组平滑肌面积占血管总面积百分比(WA%)、肺动脉收缩压(PASP)均增高(F=24.115、9.421,P值均<0.05),COPD合并PH组WA%和PASP高于COPD组。(2)与对照组比较,COPD合并PH组、COPD组RYR2、FKBP12.6及CaMK-Ⅱ的表达IOD均增高(F=9.219、6.143、11.337,P值均<0.05),COPD合并PH组RYR2、FKBP12.6及CaMK-Ⅱ的表达IOD高于COPD组。(3)相关性分析提示COPD合并PH组、COPD组RYR2的IOD值与WA%呈正相关(r=0.547、0.771,P值均<0.01),COPD合并PH组RYR2的IOD值与PASP呈正相关(r=0.773,P<0.01)。COPD合并PH组、COPD组FKBP12.6的IOD值与WA%呈正相关(r=0.796、0.810,P值均<0.01),COPD合并PH组FKBP12.6的IOD值与PASP呈正相关(r=0.729,P<0.01)。COPD合并PH组、COPD组CaMK-Ⅱ的IOD值与WA%呈正相关(r=0.879、0.504,P值均<0.01),COPD合并PH组CaMK-Ⅱ的IOD值与PASP呈正相关(r=0.748,P<0.01)。结论FKBP12.6和CaMK-Ⅱ可能在COPD相关的肺动脉增殖中起一定作用。 相似文献
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目的研究无症状性心肌缺血与室性心律失常的关系。方法应用动态心电图监测237例无症状性心肌缺血患乾。结果室主律失常者比无室性心律失睹 无症状性心肌缺血发作次数显著增多(P〈0.05)。缺血伴有室性心律失常死于心衰者明显高于单纯缺血者(P〈0.001)。无症状性心肌血发作次数与心昼夜时相变化相关。结论无症性心肌血伴室性心律失常同时合并有心 相似文献
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硒被认为是与人类健康息息相关的一种微量元素。越来越多的证据表明,硒与包括心血管疾病在内的多种疾病的发生、发展有关。在临床上,硒具有促进冠心病及心力衰竭恢复的特性,在发生心血管疾病的患者中常常可发现硒缺乏。研究表明,硒缺乏可通过破坏体内氧化-还原平衡、影响某些重要硒化物的含量及某些硒蛋白(如谷胱甘肽过氧化物酶)的合成、修饰与活性等参与心血管疾病的发生发展。补充硒可以重建体内氧化-还原平衡,降低体内氧化反应造成的心肌应激损伤。另外,硒在心律失常、心肌病以及心肌炎的发病过程中也起着重要的作用,但机制还尚不清楚。相信对于硒和心脏疾病研究的不断深入可最终在促进心血管疾病基础研究、药物开发以及患者营养治疗等方面起到重要作用。 相似文献
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心脏重构是多种心血管疾病的共有病理过程,包括心肌结构重构和电重构,两者互相联系。目前研究认为,Ca^2+/钙调蛋白依赖性蛋白激酶Ⅱ在心肌肥大和凋亡所致心脏重构、心律失常和心力衰竭的发生发展中起着关键信号转导作用,现就该领域近几年来的研究进展结合自己的研究结果进行扼要概述。 相似文献
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目的探讨钙释放通道稳定蛋白FK506结合蛋白12.6(FKBP12.6)基因转染对心力衰竭(简称心衰)心室肌细胞钙通道(ICaL)和钠-钙交换电流(INCX)的影响。方法用携带FKBP12.6基因的重组腺病毒Ad.FKBP12.6-GFP感染分离的心衰心室肌细胞,通过免疫荧光及激光共聚焦技术检测转基因的表达;采用全细胞膜片钳技术记录ICaL和INCX。结果①心衰心室肌细胞的FKBP12.6蛋白表达显著下调,Ad.FKBP12.6-GFP感染细胞的FK-BP12.6蛋白表达水平显著高于Ad.GFP感染细胞;②Ad.GFP组心室肌细胞的ICaL密度峰值较正常对照组显著降低(6.81±0.83pA/pFvs11.43±1.14pA/pF,P<0.01),而FKBP12.6基因转染细胞电流密度峰值较Ad.GFP组显著升高(9.60±1.09pA/pFvs6.81±0.83pA/pF,P<0.01);③Ad.GFP组心室肌细胞的INCX较正常对照组明显升高(P<0.01),FKBP12.6基因转染使心衰心室肌细胞的INCX显著降低(P<0.05)。结论FKBP12.6基因转染显著升高心衰心室肌细胞ICaL,并显著降低INCX,从而逆转心衰时上述离子通道电流的改变。 相似文献
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兰尼碱受体2调节及其与心律失常的关系 总被引:1,自引:0,他引:1
兰尼碱受体2是广泛存在于肌浆网上的Ca2+释放通道,受到多种因子的调节,兰尼碱受体2参与心肌细胞的兴奋-收缩耦联,兰尼碱受体2的结构或调节异常与心力衰竭及致死性心律失常的发生关系密切。现对兰尼碱受体2的结构、调节及其在心律失常中的作用机制作一阐述。 相似文献
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Tim Seidler Nils Teucher Kristian Hellenkamp Cornelia Grebe Hanna Schotola Friedrich A. Schöndube Lars S. Maier 《Journal of molecular and cellular cardiology》2011,50(1):33-42
Sarcoplasmic reticulum (SR) calcium (Ca) leak can be reduced by enhancing FKBP12.6 binding to SR Ca release channels (RyR2) and expression of a “sticky” FKBP12.6D37S mutant may correct reduced binding stoichiometry in RyR2 from failing hearts. Both calcium/calmodulin-dependent protein kinase IIδc (CaMKIIδc) and protein kinase A (PKA) are activated in heart failure and promote SR Ca leak at RyR2. It is possible that FKBP12.6 dissociation from RyR2 may promote remodeling and that interventions to reassociate FKBP12.6 with RyR2 reflect a future therapeutic strategy. We created transgenic (TG) mice expressing FKBP12.6D37S and tested their capacity to improve intracellular Ca handling and pathological remodeling in vivo. FKBP12.6D37S TG mice were cross-bred with CaMKIIδc TG mice, which are known to exhibit pronounced RyR2 dysfunction and heart failure. We observed a significant improvement of post-rest Ca transients and a higher SR Ca content in FKBP12.6D37S TG mice. In double-TG mice, a marked reduction of SR Ca spark frequency indicated reduced SR Ca leak but neither SR Ca transient amplitude, SR Ca content nor morphological or functional parameters improved in vivo. Likewise, FKBP12.6D37S TG mice subjected to increased afterload after aortic banding exhibited higher SR Ca load but did not exhibit any improvement in hypertrophic growth or functional decline. Enhancement of FKBP12.6-RyR2 binding markedly reduced RyR2 Ca leak in CaMKIIδc-induced heart failure and in pressure overload. Our data suggest that activation of CaMKIIδc and pressure overload confer significant resistance towards approaches aiming at FKBP12.6-RyR2 reconstitution in heart failure and maladaptive remodeling, although RyR2 Ca leak can be reduced. 相似文献
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RyR2 Common Gene Variant G1886S and the Risk of Ventricular Arrhythmias in ICD Patients with Heart Failure
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PIETRO FRANCIA CARMEN ADDUCI LORENZO SEMPRINI ROSITA STANZIONE ANDREA SERDOZ MASSIMO CAPRINOZZI DARIA SANTINI MARIA COTUGNO FRANCESCA PALANO MARIA BEATRICE MUSUMECI SPERANZA RUBATTU MASSIMO VOLPE 《Journal of cardiovascular electrophysiology》2015,26(6):656-661
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Lucia Brunello Jessica L. Slabaugh Przemys?aw B. Radwański Hsiang-Ting Ho Andriy E. Belevych Qing Lou Haiyan Chen Carlo Napolitano Francesco Lodola Silvia G. Priori Vadim V. Fedorov Pompeo Volpe Michael Fill Paul M. L. Janssen Sándor Gy?rke 《Proceedings of the National Academy of Sciences of the United States of America》2013,110(25):10312-10317
Dysregulated intracellular Ca2+ signaling is implicated in a variety of cardiac arrhythmias, including catecholaminergic polymorphic ventricular tachycardia. Spontaneous diastolic Ca2+ release (DCR) can induce arrhythmogenic plasma membrane depolarizations, although the mechanism responsible for DCR synchronization among adjacent myocytes required for ectopic activity remains unclear. We investigated the synchronization mechanism(s) of DCR underlying untimely action potentials and diastolic contractions (DCs) in a catecholaminergic polymorphic ventricular tachycardia mouse model with a mutation in cardiac calsequestrin. We used a combination of different approaches including single ryanodine receptor channel recording, optical imaging (Ca2+ and membrane potential), and contractile force measurements in ventricular myocytes and intact cardiac muscles. We demonstrate that DCR occurs in a temporally and spatially uniform manner in both myocytes and intact myocardial tissue isolated from cardiac calsequestrin mutation mice. Such synchronized DCR events give rise to triggered electrical activity that results in synchronous DCs in the myocardium. Importantly, we establish that synchronization of DCR is a result of a combination of abbreviated ryanodine receptor channel refractoriness and the preceding synchronous stimulated Ca2+ release/reuptake dynamics. Our study reveals how aberrant DCR events can become synchronized in the intact myocardium, leading to triggered activity and the resultant DCs in the settings of a cardiac rhythm disorder. 相似文献
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