右室流出道间隔部起搏与右室心尖部起搏对心室同步化的影响

目的:探讨右室流出道间隔部起搏(RVSP)与右室心尖部起搏(RVAP)对心室电、机械同步化影响的差异.方法:收集我院Ⅲ度房室传导阻滞患者共15例,均因心动过缓在入院后行临时右室心尖部起搏.术后24～48 h行右室流出道间隔部永久起搏.分别在两次术后观察心室起搏状态下心电图QRS时限,左右心室延迟时间(IVMD),室间隔与左心室后壁间的收缩延迟时间(SPWMD),QRS波起点距左心室12节段收缩速度峰值的时间标准差(Ts12SD).通过上述指标来评估RVSP与RVAP对心室电机械同步性影响的差异.结果:与RVAP相比较,RVSP组心电图QRs时限更短(P=0.007),心室收缩同步化指标IVMD,SPWMD,Ts12SD明显优于RVAP(P=0.000 9,P=0.000 5,P=0.000 4).结论:RVsP较RVAP更有利于保证心室电、机械同步化.     

右心室间隔部起搏对血流动力学的影响

目的 评价在房室顺序起搏治疗中,右心室间隔部起搏对血流动力学的影响.方法 20例植入双腔起搏器的患者,高度房室传导阻滞6例,完全性房室传导阻滞14例,按照心室电极的位置分为右心室心尖部起搏(RVA)组和右心室间隔部起搏(RVS)组.对2组患者术前、术后3个月随访时的QRS波形态和宽度、左心室射血分数(LVEF)、心室间机械运动延迟(IVMD)和血脑钠肽(BNP)水平进行比较.结果与术前相比,RVA组起搏心电图QRS时限增宽[(187.00±15.67)ms与(94.00±9.17)ms,t=15.98,P＜0.05],LVEF下降[(53.70±1.34)%与(58.60±1.65)%,t=7.30,P＜0.05],IVMD延长[(43.20±6.79)ms与(15.00±4.08)ms,t=7.75,P＜0.05],BNP升高[(89.70±8.30)ng/L与(40.00±4.73)ng/L,t=16.44,P＜0.05],而RVS组无明显变化(P均＞0.05);术后和RVA组相比,RVS组QRS时限缩短[(119.00±7.38)ms与(187.00±15.67)ms,t=12.42,P＜0.05],LVEF增加[(57.00±2.00)%与(53.70±1.34)%,t=4.09,P＜0.05],而IVMD缩短[(19.00±4.59)ms与(43.20±6.79)ms,t=7.94,P＜0.05],BNP降低[(44.加±9.18)ng/L与(89.70±8.30)ng/L,t=11.62,P＜0.05].结论 和传统的RVA起搏相比,RVS起搏尽可能地维持了双心室的正常激动顺序和双心室的同步性,对血流动力学的影响较小,RVS起搏比RVA起搏更接近生理性起搏.     

右室心尖部与右室流出道起搏近期效果比较

目的评价右心室流出道（RVOT）起搏和右心室心尖部（RVA）起搏对心脏同步性和心功能的影响。方法 41例病态窦房结综合征、高度及完全房室传导阻滞病人根据心室起搏电极植入部位的不同,分为RVOT起搏组（21例）和RVA起搏组（20例）。分别于术前和术后3、12个月通过超声心动图分别对病人左心室舒张末内径（LVEDD）,左心室收缩末内径（LVESD）、左心室射血分数（LVEF）、室间隔和左心室后壁之间的运动延迟（SP-WMD）、心室间机械延迟时间（IVMD）等指标进行观察随访。结果术后3、12个月时,RVOT起搏组的LVEDD、LVESDI、VMD和SPWMD均明显小于RVA起搏组,LVEF均明显高于RVA起搏组（t=2.14-12.61,P〈0.05）。结论 RVOT起搏较RVA起搏更有利于双心室电激动的同步性,且对心功能的不良影响较小。     

双腔起搏时Tei指数与常用优化房室延迟时间指标的对比研究

目的探讨Tei指数在双腔起搏器置入患者中对房室延迟(AVD)进行优化的价值。方法从首次安装双腔起搏器患者中选择12例,其中9例为病态窦房结综合征,3例为完全性房室传导阻滞。起搏器安装术后(7±3)个月对患者行超声心动图检查。本文以Tei指数优化AVD,与以左心室心输出量(LVCO)及左心室充盈时间(LVFT)常规优化的AVD进行比较,并对不同方法优化下的心功能参数进行比较。结果以LVCO和LVFT优化的AVD差异有统计学意义,AVD分别为(173.07±50.26)ms、(107.69±28.77)ms,P<0.01;Tei指数优化的AVD(157.69±57.17)ms介于以LVCO和LVFT优化的AVD之间;以Tei指数优化AVD时的LVCO与LVCO优化时的LVCO相比差异无统计学意义,LVCO分别为(3.41±0.47)L/min、(3.62±0.57)L/min,P>0.05;Tei指数优化AVD时的LVFT与LVFT优化时的LVFT相比差异亦无统计学意义,LVFT分别为(352.64±66.81)ms、(387.25±58.61)ms,P>0.05。结论Tei指数可以作为AVD优化的指标。     

右心室不同部位起搏对心功能的影响

目的研究右心室不同部位起搏对患者心功能的影响,探求最有利的永久性右心室起搏部位。方法 54例Ⅱ度Ⅱ型或Ⅲ度房室传导阻滞行永久性起搏器的患者,按起搏部位分为右心室心尖(RVA)组、右心室流出道(RVOT)组、右心室流入道(RVIT)组,分别观察三组术前及术后6个月QRS间期(QRSd)、左心室射血分数(LVEF)、每搏输出量(SV)、每分输出量(CO)、左心室收缩末内径(LVESD)、左心室舒张末内径(LVEDD)的差异,并比较三组间术后6个月上述参数的差异。结果与术前相比,三组起搏术后6个月QRSd均显著增加(P<0.01);RVA组起搏术后6个月LVEF、SV、CO均显著降低(P<0.05);RVOT组与RVIT组起搏术后6个月LVEF、SV、CO均无显著变化(P>0.05);三组起搏术后6个月LVESD、LVEDD均无显著变化(P>0.05)。三组间起搏后6个月QRSd有统计学差异,QRSd依次为RVA组>RVOT组>RVIT组(P<0.01);而三组间起搏后6个月LVEF、SV、CO、LVESD、LVEDD无统计学差异(P>0.05)。结论右心室流入道起搏QRSd最小,可能是理想的右心室起搏部位。     

TVI评价双腔起搏器术前、术后心室间运动同步性

目的 运用组织速度成像(tissue velocity imaging,TVI)技术评价双腔起搏器术前、术后心室间心肌运动同步性.方法 对比研究30例安置双腔起搏器术前、术后患者,获取标准心尖四腔、二腔及三腔切面,应用定量组织速度图(quantitative tissue velocity imaging,Q-TVI)技术描记左心室各室壁和右心室侧壁基底段、中段心肌以及室间隔心肌的组织多普勒速度曲线,测量每一取样点心肌运动曲线上自QRS波起始至收缩期峰值速度的时限(Ts)、舒张早期峰值速度的时限(Te).结果 双腔起搏器术前左心室收缩期和舒张期达峰时间较右心室延长(P＜0.05),双腔起搏器术后右心室收缩期和舒张期达峰时间较左心室无明显差异(P＞0.05).结论 安装起搏器术后较术前心室间心肌运动同步性有明显改善.     

DDD模式下右心室心尖部起搏与右心室流出道间隔部起搏的临床对比研究

目的 DDD模式下比较右心室心尖部（RVA）起搏与右心室流出道（RVOT）间隔部起搏对患者左心室重构及心功能的影响。方法回顾性分析2009年1月至2012年12月期间我院行永久起搏器（双腔DDD）植入治疗的患者219例,根据心室电极植入部位的不同分为A组（RVA起搏）、B组（RVOT起搏）,每组再根据患者术前左心室射血分数（LVEF）的不同分为两个亚组。调取患者12个月的随访资料,分析两组患者术后LVEF、左心房内径（LAD）、左心室舒张末期内径（LVEDD）及起搏治疗前后各项起搏参数、起搏QRS波群时限和术后并发症等。结果两组在手术成功率、术后并发症等方面的比较无显著差异。术后12个月,A组起搏阈值、电极阻抗较术中均有回落,LVEF较术前降低,LAD、LVEDD较术前增大,差异均有统计学意义（P〈0.05）;B组电极阻抗较术中有回落（P〈0.05）,起搏阈值、R波振幅与术中比较差异无统计学意义,LVEF、LAD、LVEDD与术前相比差异无统计学意义。B组的起搏QRS波群时限较A组显著缩短[（145.09±4.96）ms vs.（157.40±12.44）ms,P〈0.01]。对亚组进行分析发现：术前LVEF≥50%的患者,A、B两组仅LVEDD较术前有增大（P〈0.05）,LVEF和LAD与术前相比差异无统计学意义。术前LVEF〈50%的患者,A组患者的LVEF较术前降低,LAD、LVEDD较术前增大,差异均有统计学意义（P〈0.05）,而B组患者的LVEF、LAD、LVEDD与术前比较差异无统计学意义。结论运用主动固定电极行RVOT起搏在临床应用中是安全、可行的。经过12个月的起搏治疗,对术前心功能不全的患者,RVOT起搏能提供接近生理性的心室激动顺序,维持心室肌电-机械活动同步化,对患者心功能的损害小;对术前心功能正常的患者,虽然RVOT起搏提供了更为协调的心室收缩,但在保护患者左心室收缩功能及阻止左心室重构方面并未显示出优于RVA起搏的证据。     

双心室起搏与右心室起搏对充血性心力衰竭急性心功能的影响

目的最近研究提示心脏再同步治疗有效地改善了慢性心肌病心力衰竭患者心功能。本研究旨在探讨双心室和右心室起搏对心功能的相对影响。方法 15例慢性心力衰竭患者心功能Ⅲ级,左心室射血分数〈35%,QRS〉130ms和二尖瓣反流。安装心房-双心室再同步起搏器。彩色多普勒超声心动图观察心功能变化。结果急性双心室和右心室起搏并未影响左心室内径和短轴缩短率,也不影响左心室射血速度和排血量。左心室压力上升和下降峰速率无明显变化。等容收缩时间缩短（P〈0.05）,但不影响等容舒张时间。增加Z比例（P〈0.05）。缩短二尖瓣反流时间（P〈0.05）,对二尖瓣环和三尖瓣环运动幅度和峰速率无明显影响。双心室和右心室起搏之间无明显差别。结论双心室起搏改善了慢性心肌病心功能。双心室和右心室起搏无明显差别。双心室起搏是一种有前途的心脏再同步治疗方法。     

组织追踪显像技术对单腔、双腔起搏器置入患者左室收缩功能的评价

目的 探讨组织追踪显像技术(TTI)评价单腔及双腔起搏器术后左室收缩功能变化.方法 正常对照组40例,单腔起搏器组35例,双腔起搏器组40例.利用双平面Simpson法测量三组的左心室射血分数(LVEF);在TTI条件下,测量正常对照组的收缩期二尖瓣环位移(DS)及单腔、双腔起搏器组患者术前、术后1周的DS;在起搏器置入术中记录设定的心房心室电极的起搏阈值、阻抗及心室除极波的感知值.结果 与正常对照组相比,单腔起搏器组患者术后1周DS、LVEF明显减小(P＜0.05),双腔起搏器组患者术后1周DS、LVEF减少(P＜0.05).与术前相比,单腔起搏器组患者术后1周DS、LVEF显著下降(P＜0.05),而双腔起搏器组显著增加(P＜0.05).单腔与双腔起搏器患者术后比较,双腔起搏器患者术后1周DS、LVEF增加(P＜0.05).线性相关分析表明DS与LVEF的相关性较好(r=0.86,P＜0.01).结论 组织追踪显像技术对置入单腔及双腔起搏器患者左室收缩功能的评价有较高的应用价值.且双腔起搏模式对左室收缩功能的改善优于单腔起搏模式.     

右心室流入道起搏QRS波时限对心功能的影响

目的观察采用右心室流入道起搏治疗缓慢性心律失常时,QRS时限对心功能的影响及与心力衰竭的关系。方法随意选用44例病态窦房结综合征或Ⅲ度房室传导阻滞的患者,采用右心室流入道起搏治疗,将患者起搏时QRS时限133m s的分为A组(n=28);起搏时QRS时限≥133m s的分为B组(n=16),测量起搏器植入时、起搏3个月和6个月不同时期,QRS时限、血浆心钠肽(BNP)、心排血量(CO)、每搏输出量(SV)、射血分数(EF)和左室舒张末内径(LVDd)的变化。结果术后即刻测两组QRS时限、BNP值和心脏超声指标无显著性差异(P0.05)。术后3个月、6个月QRS时限、LVDd、BNP,B组明显高于A组,而EF、SV、CO,B组明显低于A组。结论右室流入道起搏部位QRS时限和心功能密切相关。QRS时限越宽,心功能纠正就越不明显或心衰进一步加重;反之,QRS时限越窄,心功能改善就越明显。     

室性早搏对左心室功能的影响

室性早搏是临床上最常见的心律失常,本文综述了室性早搏的形态、起源、负荷等特点对左心室功能的影响。室性早搏负荷大于20%,QRS时限>150 ms以及右心室起源的室性早搏更容易伴随或导致左心室功能下降。临床上对于频发室性早搏的及时治疗,能够起到改善心功能或预防心功能恶化的目的。导管射频消融治疗已成为特发性室性心律失常的最有效的治疗方法。     

室性心动过速和心室颤动治疗进展

室性心动过速（室速）和心室颤动（室颤）是心源性猝死最常见的原因。本文就器质性、特发性和离子通道病性室速/室颤的药物、器械、导管消融术及其他治疗等的最新进展进行了总结,以期能够达到规范临床诊疗的作用。     

超声心动图四维自动左心室容积测定技术在左心室室壁瘤成形术中的应用价值

目的 探讨四维自动左心室容积测定（4D auto LVQ）在室壁瘤左心室成形术中的应用价值。方法 采用4D auto LVQ技术评价7例广泛前壁心肌梗死合并心尖部室壁瘤患者左心室容积和功能,并与心脏MR测量心室容积及室壁瘤成形术后左心室收缩功能比较。结果 5例术前行心脏MR检查,5例行室壁瘤成形术。与二维超声心动图相比,4D auto LVQ测量室壁瘤患者左心室容积与心脏MR检查结果更接近。采用4D auto LVQ技术术前预测左心室收缩功能与术后实际左心室收缩功能接近。结论 4D auto LVQ技术可更精准、快捷地评价左心室容积和收缩功能,为制定室壁瘤成形手术方案提供客观资料。     

Effect of pacing-induced ventricular dyssynchrony on right ventricular function

Background: Asynchronous electrical activation induced by right ventricular (RV) pacing can cause several abnormalities in left ventricular (LV) function. However, the effect of ventricular pacing on RV function has not been well established. We evaluated RV function in patients undergoing long‐term RV pacing. Methods: Eighty‐five patients and 24 healthy controls were included. After pacemaker implantation, conventional echocardiography and strain imaging were used to analyze RV function. Strain imaging measurements included peak systolic strain and strain rate. LV function and ventricular dyssynchrony by tissue Doppler imaging (TDI) were assessed. Intra‐ and interobserver variabilities of TDI parameters were tested on 15 randomly selected cases. Results: All patients were in New York Heart Association functional class I or II and percentage of ventricular pacing was 96 ± 4%. RV apical induced interventricular dyssynchrony in 49 patients (60%). LV dyssynchrony was found in 51 patients (60%), when the parameter examined was the standard deviation of the time to peak myocardial systolic velocity of all 12 segments greater than 34 ms. Likewise, septal‐to‐lateral delay ≥65 ms was found in 31 patients (36%). All echocardiographic indexes of RV function were similar between patients and controls (strain: ?22.8 ± 5.8% vs ?22.1 ± 5.6%, P = 0.630; strain rate: ?1.47 ± 0.91 s^?1 vs ?1.42 ± 0.39 s^?1, P = 0.702). Intra‐ and interobserver variability for RV strain was 3.1% and 5.3%, and strain rate was 1.3% and 2.1%, respectively. Conclusions: In patients with standard pacing indications, RV apical pacing did not seem to affect RV systolic function, despite induction of electromechanical dyssynchrony. (PACE 2011; 34:155–162)     

Transseptal left ventricular endocardial pacing reduces dispersion of ventricular repolarization

Background: Cardiac resynchronization therapy (CRT) may be proarrhythmic in some patients. This may be due to the effect of left ventricular (LV) epicardial pacing on ventricular repolarization. The purpose of this study was to evaluate the effect of endocardial versus epicardial LV biventricular pacing on surface electrocardiogram (ECG) parameters that are known markers of arrhythmogenic repolarization. Methods: ECG markers of repolarization (QT dispersion, QTD; T peak to end, T_peak‐end; T_peak‐end dispersion, T_peak‐endD; QTc) were retrospectively measured before and after CRT in seven patients with transseptal LV endocardial leads (TS group), 28 matched patients with coronary sinus (CS) LV leads (CS group), and eight patients with surgical LV epicardial leads (SUR group). All ECGs were scanned and analyzed using digital callipers. Results: Compared to the CS group, the TS group CRT was associated with a significant postpacing reduction in QTD (?45.2 ± 35.6 vs ?4.3 ± 43.6 ms, P = 0.03) and T_peak‐end (?24.2 ± 22.1 vs 3.4 ± 26.7 ms, P = 0.02). There was a nonsignificant post‐CRT reduction in both T_peak‐endD (?11.3 ± 31.0 vs 2.4 ± 28.9 ms, P = 0.27) and QTc (?50.0 ± 46.4 vs 4.4 ± 70.2 ms, P = 0.06) in the TS versus the CS group. In contrast, there were no differences between the SUR and CS groups in terms of the effect of CRT on these repolarization parameters. Conclusions: CRT with (atrial transseptal) endocardial LV lead placement is associated with repolarization characteristics that are considered to be less arrhythmogenic than those generated by CS (epicardial) LV lead placement. Further work is needed to determine whether these changes translate to a reduction in proarrhythmia. (PACE 2011; 34:1258–1266)     

Sonographic measurement of lateral ventricular width in early ventricular dilation

Cerebral real-time ultrasound examinations from 35 high-risk premature newborn infants and 25 normal-term infants were reviewed for early signs of ventricular dilation. Measurements of the midbody lateral wall of the lateral ventricle to falx distance and ratio of this distance to the hemispheric width were obtained. Midbody lateral ventricular widths were also measured. Results indicate that displacement of the medial wall of the body of the lateral ventricle toward the midline is an earlier sign of ventricular dilation than is displacement of the lateral wall away from the midline.     

Epicardial ablation of ventricular tachycardia associated with isolated ventricular noncompaction

A 52-year-old man presented with sudden onset of palpitations and dizziness. Echocardiogram confirmed the diagnosis of isolated noncompaction of ventricular myocardium with moderated systolic dysfunction, and the electrocardiogram (ECG) revealed ventricular tachycardia (VT), of which the focus seemed to match an area of prominent left ventricular noncompaction on the 12-lead surface ECG. Through the activation mapping from the endo- and epicardium, simultaneously, a discrete potential preceding the QRS during VT was observed at the anterolateral epicardial wall. He subsequently underwent radiofrequency ablation, and VT was successfully eliminated.