起搏心电图的房室间期分析方法

起搏心电图在房室间期主要分为两种,一种是起搏类型,一种是感知类型,由于起搏心电器的相应的程控的不一样,导致心房的感知功能的不良、心室安全起搏,非竞争性心房起搏、起搏器特殊程序模式等原因。所以通过了解起搏器的特殊功能对了解起搏心电图房室间期具有一定的作用。     

频率响应心脏起搏系统

一、频率响应心脏起搏系统在起搏治疗中的地位临床研究表明,就改善心功能、增加心排血量而言,适时地增加起搏频率较保持房室顺序收缩更为重要,特别是在运动负荷条件下更是如此。根据机体代谢情况而改变起搏频率即频率响应心脏起搏系统,是近年发展起来,并受到普遍重视的一种单腔(或双腔)生理型起搏方式。它应用不同的生理、生化指标,经过相应地传感器,从而对起搏频率进行自动控制。     

脉冲多普勒超声心动图对高原人室性早搏时血液动力学定量研究

高原由于高寒缺氧 ,心律失常 ,特别是室性早博的发生率较高。对于室性早博时血液动力学的定量研究国内尚较少报道。本研究应用脉冲多普勒超声心动图进行分析 ,以探讨室性早博时对心脏排血和充盈的血液动力学变化的影响及高原人室性早博血液动力学变化的特点。1　资料和方法(1)病历选择　 1998年 6月至 1998年 12月 ,收住我院 35例室性早博患者 ,其中男性 2 3例、女性 12例 ,年龄 2 4～ 6 8岁。经体检和实验室及器械检查 ,排除器质性心脏病。心功能在正常范围 (ＮＹＨＡ心功能Ｉ级 ) ,心电图及 2 4ｈＨｏｌｔｅｒ诊断明确 ,排除间断、成对室…     

探讨超声心动图对心肌致密化不全的诊断及指导治疗价值

目的研究心肌致密化不全的心内结构及心功能的改变,探讨超声心动图对心肌致密化不全的诊断及指导治疗的价值。方法常规检查各切面,主要测量房室内径、室壁厚度及运动幅度、瓣膜血流情况、心功能指数,重点了解室壁心肌结构及舒张末期左室内径、左心室射血分数,观察房室腔内是否有血栓形成。结果 3例患者中有2例单独左心室受累,1例累及双心室。3例患者超声心动图上均有特征性改变,心室内均见异常隆突的肌小梁和深陷其间的隐窝,彩色多普勒超声见肌小梁隐窝内的血流信号与心室腔相通。病变好发于左室心尖部、侧壁、下后壁,伴或不伴心功能不全、心律失常。结论对心肌致密化不全超声心动图具有特征性声像图表现,其检查能够对心肌致密化不全进行房室结构及功能的全面评价,是发现心肌致密化不全的首要方法,也是定期观察治疗后心功能改善的必要手段。     

右室间隔部起搏患者起搏QRS 波时限与心功能的关系

目的:探讨右室间隔部起搏患者起搏QRS波时限与心功能的关系。方法:回顾性分析植入右室间隔部起搏的双腔起搏器患者(111例),起搏器平均植入时间(4.52±3.65)年,通过常规体表心电图测得完全起搏时QRS波时限分为四组:A组为QRS≤120ms(21例);B组为120ms180ms(26例),行心脏彩色多普勒检查获取左房内径(LAD)、收缩末期左室内径(LVESD)、舒张末期左室内径(LVEDD)、室间隔厚度(IVST)、左室后壁厚度(LVPWT)及LVEF,同时检测患者的血清氨基末端脑肭肽前体(NT-proBNP),分析起搏QRS波时限与以上各指标的关系。结果:D组患者LAD、LVEDD、LVESD、IVST及IVPWT较其他三组明显增大,同时LVEF显著下降,NT-proBNP明显升高,有统计学意义(P<0.05)。同时发现随起搏QRS时限的不断增宽,不同组别的LVEF是依次降低(中位值分别为66.5%、60.3%、52.7%和45.8%),而血清NT-proBNP水平是依次增大(中位值分别为143.7 pg/ml、261.8 pg/ml、599.4 pg/m和971.2 pg/ml)。直线相关性分析示起搏QRS波时限与LAD(r=0.141,P<0.05)、LVEDd(r=0.678,P<0.05)、LVEDs(r=0.439,P<0.05)、IVST(r=0.165,P<0.05)及LVPWT(r=0.189,P<0.05)有显著线性关系,呈正相关。起搏QRS波时限与LVEF负相关(r=-0.684,P<0.05),起搏QRS波时限与NT-proBNP的对数正相关(r=0.368,P=0.029)。结论:对于右室间隔部起搏的双腔起搏患者,起搏QRS波时限是一个可初步判断心脏结构和功能的指标,其起搏QRS波时限延长可能会恶化患者的心脏结构及功能,可结合NT-proBNP进行动态观察,对起搏器植入患者的心功能恶化和心衰的预防有一定的临床实用价值。     

双腔及双腔频率应答起搏器的临床探讨

本文通过２１例双腔（ＤＤＤ）及双腔频率应答式起搏器（ＤＤＤＲ）的按置和随地治疗适应症,起搏导按置方法及体外程摈调节等进行了初步探讨。     

非侵入性起搏器负荷超声心动图对永久起搏器植入术后合并冠脉病变的临床诊断意义

目的：探讨非侵入起搏器负荷超声心动图对永久起搏器植入术后合并冠脉病变的临床诊断意义。方法：采用前瞻性研究,实验对象为24名因房室传导阻滞或慢性心房纤颤而植入永久起搏器的患者（男12人,女12人,平均年龄70.2±6.1岁）,所有患者均因不典型心绞痛入院和完全起搏依赖,心电图改变无法判断是否存在心肌缺血。通过体外程控进行非侵入性起搏器负荷超声心动图检测室壁运动幅度如左室射血分数评估心功能,检测后行冠脉造影术评估冠脉狭窄情况,及实验前后测定B型脑钠肽的变化。结果：24例患者中,有13例通过起搏器负荷超声心动图应激实验测得LVEF随起搏心率增加而降低,这其中又有11例患者通过冠状动脉造影证实其冠脉存在不同程度的狭窄,诊断的准确性84.62%;11例冠脉造影结果阳性的患者实验后30分钟测得的BNP水平较实验前明显升高。结论：非侵入性起搏器负荷超声心动图应激实验作为一种简单、快速、安全及具有诊断意义的方法,可用来评价植入起搏器术后完全起搏依赖,心电图继发性ST-T改变难以判断的心肌缺血,为进一步检查及治疗提供可靠临床数据。     

起搏器术后新发房性心律失常的影响因素分析

目的:探讨起搏器术后新发房性心律失常的发生情况及其相关影响因素。方法:选择2006年1月至2007年12月于沈阳军区总医院首次植入永久起搏器的107例患者,男性50例,平均年龄65.0±11.9岁,术前通过追问病史及相关检查均排除房性心律失常(房颤、房扑、房速),术后平均随访3.9年,观察新发房性心律失常情况。按术后是否出现房性心律失常,将患者分为新发房性心律失常组和无房性心律失常组,比较两组患者术前和术后心脏超声结果的变化、心室起搏比例、起搏部位及起搏模式,并通过logistic回归分析起搏器术后发生房性心律失常的影响因素。结果:新发房性心律失常组26例(24.3%),其中房颤17例(15.9%),房扑2例(1.9%),房速7例(6.5%);无房性心律失常组81例。与无房性心律失常组比较,新发房性心律失常组左房内径明显增加(P=0.040)、二尖瓣返流程度较重(P=0.032)及左室射血分数明显下降(P=0.001),心室起搏百分比(VP%)显著升高(P=0.017)。心尖部起搏患者房性心律失常的发生率明显高于间隔部起搏(33.3%vs 16.9%,P<0.05),双腔起搏组患者房性心律失常发生率明显低于单腔起搏器组(18.7%vs 37.5%,P<0.05)。Logistic回归分析显示术后新发房性心律失常的发生与高比例的心室起搏(P=0.006)、VVI(R)起搏模式(P=0.014)及右心室起搏电极导线植于心尖部(P=0.024)显著相关。结论:起搏模式、心室起搏百分比、起搏部位是起搏器术后发生房性心律失常的影响因素。     

raldh2基因阻抑导致斑马鱼心脏发育畸形的机制

目的通过显微注射吗啡啉修饰的反义寡核苷酸(MO)阻抑视黄醛脱氢酶2(raldh2)基因表达,探讨raldh2基因阻抑对斑马鱼胚胎心脏发育的影响及可能的分子机制。方法根据斑马鱼raldh2基因起始密码区域序列设计合成吗啡啉修饰的反义寡核苷酸,采用显微注射方法阻抑斑马鱼胚胎raldh2基因表达。构建raldh2-EG-FP重组质粒进一步验证MO的特异性和有效性。分析raldh2基因阻抑后对胚胎发育,尤其心脏表型和功能的影响。通过胚胎整体原位杂交,分析心脏相关nppa和tbx20基因表达模式以及raldh2阻抑后对其表达的影响。结果显微注射raldh2-MO能有效地特异地阻抑斑马鱼胚胎raldh2基因表达,raldh2-MO对胚胎发育影响呈剂量依赖性。raldh2基因阻抑可导致胚胎心脏发育畸形,干扰正常的房室分化和向右环化,导致房室瓣血液反流。与野生型胚胎比较,raldh2基因阻抑组胚胎心率和心室收缩分数降低(P<0.05),心功能受损。整体原位杂交结果显示raldh2基因阻抑后nppa基因表达改变,心室部位nppa表达清晰,而心房部位表达减弱。tbx20基因在心脏、运动神经元、顶盖及视网膜表达,raldh2基因阻抑后,tbx20表达下调,在心脏表达减弱,以心房和流出道部位更显著。结论 raldh2基因在心脏早期发育的多个环节发挥重要作用,影响房室分化、心管环化和心肌收缩等。在心脏发育过程中nppa和tbx20基因表达受到raldh2基因调控,可能参与RA信号缺乏导致心脏畸形的潜在分子机制。     

心脏室间隔起搏与右室心尖部起搏对心功能的影响

目的:探讨右心室间隔部(Right Ventricular Septum,RVS)起搏和右心室心尖部(Rightventricularape,RVA)起搏对心功能的影响,为临床提供参考.方法:采用前瞻性研究的方法,对我院自2008年8月-2011年8月收治的行起搏器治疗的72例患者随机均分为实验组和对照组,实验组采用RVS起搏,对照组采用RVA起搏,比较植入后15分钟和1年后测定两组间心室起搏参数差异及血流动力学参数左室射血分数(LVED、每搏量(sv)、心脏指数(CD、二尖瓣血流E峰和A峰最大充盈速度比值(E/A)差异.结果:植入后15分钟和1年后,实验组和对照组起搏参数起搏阈值、电极阻抗、心腔内R波幅度进行比较,差异无统计学意义(P＞0.05).植入后1年后,两组间的血流动力学参数比较,差异有统计学意义(P＜0.05).结论:RVS起搏优于RVA起搏,有望替代传统的右心室心尖部成为最佳的心室起搏部位.     

New concepts in pacemaker syndrome

After implantation of a permanent pacemaker, patients may experience severe symptoms of dyspnea, palpitations, malaise, and syncope resulting from pacemaker syndrome. Although pacemaker syndrome is most often ascribed to the loss of atrioventricular (A-V) synchrony, more recent data may also implicate left ventricular dysynchrony caused by right ventricular pacing. Previous studies have not shown reductions in mortality or stroke with rate-modulated dual-chamber (DDDR) pacing as compared to ventricular-based (VVI) pacing. The benefits in A-V sequential pacing with the DDDR mode are likely mitigated by the interventricular (V-V) dysynchrony imposed by the high percentage of ventricular pacing commonly seen in the DDDR mode. Programming DDDR pacemakers to encourage intrinsic A-V conduction and reduce right ventricular pacing will likely decrease heart failure and pacemaker syndrome. Studies are currently ongoing to address these questions.     

Hypertonicity-induced cation channels rescue cells from staurosporine-elicited apoptosis

Cell shrinkage is one of the earliest events during apoptosis. Cell shrinkage also occurs upon hypertonic stress, and previous work has shown that hypertonicity-induced cation channels (HICCs) underlie a highly efficient mechanism of recovery from cell shrinkage, called the regulatory volume increase (RVI), in many cell types. Here, the effects of HICC activation on staurosporine-induced apoptotic volume decrease (AVD) and apoptosis were studied in HeLa cells by means of electronic cell sizing and whole-cell patch-clamp recording. It was found that hypertonic stress reduces staurosporine-induced AVD and cell death (associated with caspase-3/7 activation and DNA fragmentation), and that this effect was actually due to activation of the HICC. On the other hand, staurosporine was found to significantly reduce osmotic HICC activation. It is concluded that AVD and RVI reflect two fundamentally distinct functional modes in terms of the activity and role of the HICC, in a shrunken cell. Our results also demonstrate, for the first time, the ability of the HICC to rescue cells from the process of programmed cell death.     

Inhibition of a Demand Pacemaker and Interference with Monitoring Equipment by Radio-frequency Transmissions

During the initial testing of Radio Leicester a swept-frequency technique for testing radio antennae was shown to affect demand pacemakers by inhibition of the pacing impulse and to interfere with physiological monitoring equipment. Adequate filtering of demand pacemakers is necessary to eliminate this interference. There is no evidence that such testing has any effect on the function of fixed-rate pacemakers. There is also a potential danger to implanted demand pacemakers by the use of similar polyscope generators used for servicing radio and television apparatus in industry.     

IKCa1 activity is required for cell shrinkage,phosphatidylserine translocation and death in T lymphocyte apoptosis

Apoptotic cell volume decrease (AVD) and exposure of phosphatidylserine (PtdSer) at the cell surface are early events in apoptosis. However, the ion channels responsible for AVD, and their relationship to PtdSer translocation and cell death are poorly understood. Real-time analysis of calcium-induced apoptosis in lymphocytes and thymocytes showed that AVD occurs rapidly, and precedes PtdSer translocation. Blockers of the K⁺ channel IKCa1 completely inhibited AVD. Blockade of IKCa1, and hence AVD, also completely prevented PtdSer translocation and cell death. Thus, IKCa1-mediated AVD is the earliest-defined essential step in calcium-induced apoptosis, required for both PtdSer translocation and cell death.     

Plasma membrane aquaporin activity can affect the rate of apoptosis but is inhibited after apoptotic volume decrease

Apoptosis is characterized by a conserved series of morphological events beginning with the apoptotic volume decrease (AVD). This study investigated a role for aquaporins (AQPs) during the AVD. Inhibition of AQPs blocked the AVD in ovarian granulosa cells undergoing growth factor withdrawal and blocked downstream apoptotic events such as cell shrinkage, changes in the mitochondrial membrane potential, DNA degradation, and caspase-3 activation. The effects of AQP inhibition on the AVD and DNA degradation were consistent in thymocytes and with two additional apoptotic signals, thapsigargin and C₆-ceramide. Overexpression of AQP-1 in Chinese hamster ovary (CHO-AQP-1) cells enhanced their rate of apoptosis. The AVD is driven by loss of K⁺ from the cell, and we hypothesize that after the AVD, AQPs become inactive, which halts further water loss and allows K⁺ concentrations to decrease to levels necessary for apoptotic enzyme activation. Swelling assays on granulosa cells, thymocytes, and CHO-AQP-1 cells revealed that indeed, the shrunken (apoptotic) subpopulation has very low water permeability compared with the normal-sized (nonapoptotic) subpopulation. In thymocytes, AQP-1 is present and was shown to colocalize with the plasma membrane receptor tumor necrosis factor receptor-1 (TNF-R1) both before and after the AVD, which suggests that this protein is not proteolytically cleaved and remains on the cell membrane. Overall, these data indicate that AQP-mediated water loss is important for the AVD and downstream apoptotic events, that the water permeability of the plasma membrane can control the rate of apoptosis, and that inactivation after the AVD may help create the low K⁺ concentration that is essential in apoptotic cells. Furthermore, inactivation of AQPs after the AVD does not appear to be through degradation or removal from the cell membrane. water movement; major intrinsic protein; channel; enzyme     

Maladaptive matrix remodeling and regional biomechanical dysfunction in a mouse model of aortic valve disease

Aortic valve disease (AVD) occurs in 2.5% of the general population and often requires surgical intervention. Aortic valve malformation (AVM) underlies the majority of cases, suggesting a developmental etiology. Elastin haploinsufficiency results in complex cardiovascular problems, and 20-45% of patients have AVM and/or AVD. Elastin insufficient (Eln+/-) mice demonstrate AVM and latent AVD due to abnormalities in the valve annulus region. The objective of this study was to examine extracellular matrix (ECM) remodeling and biomechanical properties in regional aortic valve tissue and determine the impact of early AVM on late AVD in the Eln+/- mouse model. Aortic valve ECM composition and remodeling from juvenile, adult, and aged stages were evaluated in Eln+/- mice using histology, ELISA, immunohistochemistry and gelatin zymography. Aortic valve tissue biomechanical properties were determined using micropipette aspiration. Cartilage-like nodules were demonstrated within the valve annulus region at all stages identifying a developmental abnormality preceding AVD. Interestingly, maladaptive ECM remodeling was observed in early AVM without AVD and worsened with late AVD, as evidenced by increased MMP-2 and MMP-9 expression and activity, as well as abnormalities in ADAMTS-mediated versican processing. Cleaved versican was increased in the valve annulus region of aged Eln+/- mice, and this abnormality correlated temporally with adverse alterations in valve tissue biomechanical properties and the manifestation of AVD. These findings identify maladaptive ECM remodeling in functional AVM as an early disease process with a progressive natural history, similar to that seen in human AVD, emphasizing the importance of the annulus region in pathogenesis. Combining molecular and engineering approaches provides complementary mechanistic insights that may be informative in the search for new therapeutic targets and durable valve bioprostheses.     

Reactive oxygen species are related to ionic fluxes and volume decrease in apoptotic cerebellar granule neurons: role of NOX enzymes

Reactive oxygen species (ROS) are produced early during apoptosis of cerebellar granule neurons induced by low potassium (K5) and staurosporine (Sts). In addition, K5 and Sts activate NADPH oxidases (NOX). Recently, we described that K5 and Sts induce apoptotic volume decrease (AVD) at a time when ROS generation and NOX activity occur. In the present study, we evaluated the relationship between ROS generation and ionic fluxes during AVD. Here, we showed that K5- and Sts-induced AVD was inhibited by antioxidants and that direct ROS production induced AVD. Moreover, NOX inhibitors eliminated AVD induced by both K5 and Sts. Sts, but not K5, failed to induce AVD in cerebellar granule neurons from NOX2 knockout mice. These findings suggest that K5- and Sts-induced AVD is largely mediated by ROS produced by NOX. On the other hand, we also found that the blockage of ionic fluxes involved in AVD inhibited both ROS generation and NOX activity. These findings suggest that ROS generation and NOX activity are involved in ionic fluxes activation, which in turn could maintain ROS generation by activating NOX, leading to a self-amplifying cycle.     

Regulatory volume increase (RVI) and apoptotic volume decrease (AVD) in U937 cells placed into hyperosmotic medium

Time course of changes in intracellular water, K+ and Na+ of U937 cells incubated in hyperosmolar medium with addition of 200 mM sucrose was studied. Ouabain-sensitive and ouabain-resistant Rb+ (K+) influxes were measured during regulatory cell volume increase (RVI) and apoptotic volume decrease (AVD). Microscopy of cells stained by Acrydine orange, Ethydium bromide, APOPercenrage Dye and polycaspase marker FLICA was performed. We found that initial osmotic cell shrinkage induced both RVI and AVD responses. RVI dominated at the early stage whereas AVD prevailed at the later stage. In view of the data obtained in U937 cells the current opinion that RVI "dysfunction" is a prerequisite for apoptosis and AVD (Subramanyam et al., 2010) should be revised. U937 cells are capable to trigger of apoptosis and AVD in spite of the unimpaired RVI response. It is concluded that AVD plays a significant role in preventing osmotic lysis of apoptotic cells rather than in the initiation of apoptosis.     

An unusual ‘bow tie’ image in pacemaker implantation

Upper venous system anatomic variations may cause difficulties during cardiac pacemaker implantation. Persistent left superior vena cava (PLSVC) and absent right superior vena cava could be an arrhythmogenic source of atrial arrhythmias and cardiac conduction disease. We represent dual-chamber pacemaker implantation in a patient with a very rare upper venous system anomaly, paroxysmal atrial fibrillation, sick sinus syndrome, that cause unusual fluoroscopic image.