急性心肌缺血时肥厚左心室跨壁复极离散度及心律失常发生机制

目的:探讨急性心肌缺血过程中肥厚左心室跨壁复极离散度变化及与室性心律失常关系。方法:分别记录肥厚及正常对照心室肌标本在模拟缺血过程中、不同刺激周长下内外膜动作电位及跨壁复极离散度变化;对比室性心律失常发生率、分析机制。结果:①和对照组相比,肥厚组在缺血各个时段跨壁复极离散度均显著升高,且随缺血时间、刺激周长的延长逐步递增。②肥厚组在缺血过程中早后除极、延迟后除极发生率显著高于对照组,且多次形成跨壁折返性心律失常。对照组虽有延迟后除极,但未能形成跨壁折返。结论:肥厚心室跨壁复极离散度存在缺血时间、刺激周长的双重依赖;在此基础上早后除极、延迟后除极诱发跨壁折返是缺血肥厚心室心律失常的主要机制之一。     

心室跨壁复极离散度预测心脏再同步治疗除颤器术后快速室性心律失常的风险

目的：心脏再同步治疗除颤器（CRT-D）增加了心室复极离散度（TDR）,本研究旨在评价心肌跨壁复极离散度指标中的QTc间期,T波顶点（T p）T波终点（Te）之间的时限（TpTe）和TpTe /QTc是否与CRT-D患者需治疗的快速室性心律失常相关。方法：2011-01至2013-01连续选取160例于我院行CRT-D植入的患者,所选资料为术后即刻心电图,分析其V5导联的QTc间期,TpTe,TpTe/QTc值以评估其TDR,所有植入CRT-D患者均于我中心常规随访,随访时间为（20±10）个月。快速室性心律失常的发生均采自程控仪调取的CRT-D记录。结果：其中因持续性室性心动过速、心室颤动接受CRT-D治疗的患者为30例（治疗组,18.7%）,未治疗的患者为未治疗组（130例,81.3%）。治疗组的TpTe/QTc (0.24±0.05 vs 0.20±0.04,P<0.001)和 TpTe [(119±30) ms vs (95±20) ms,P<0.001]较未治疗组明显增加,但两组间QTc间期差异无统计学意义[（480±60）ms vs (470±70) ms,P=0.6]。QTc间期与CRT-D治疗的风险无相关性。TpTe/QTc ≥0.25预测CRT-D患者室性心律失常风险的敏感性和特异性分别为47%和91%,而TpTe≥120 ms预测CRT-D患者室性心律失常风险的敏感性和特异性分别为40%和95%。CRT-D术后患者生存曲线分析表明,TpTe/QTc和TpTe均能有效预测患者的预后情况（P<0.001）。结论：TpTe和TpTe/QTc 的增加显著增加再同步治疗除颤器患者术后需CRT-D治疗的风险。     

心脏再同步治疗对复极离散度和室性心律失常的影响

目的:探讨心脏再同步治疗(CRT)对复极离散度和室性心律失常的影响。方法:入选86例CRT植入患者,根据术后6个月左心室射血分数(LVEF)绝对值是否较基线水平提高≥10%,分为反应组(n=43)和无反应组(n=43)。比较两组患者CRT植入后不同时期QRS间期、校正的QT间期(QTc间期)、T波峰末间期(Tp Te间期)等复极离散度指标变化及室性心律失常事件情况。结果:反应组患者术后1年QRS间期和Tp Te间期较术前和术后24 h明显缩短(P均0.05),而无反应组各时期上述指标差异均无统计学意义(P0.05)。在术后1年中,反应组室性早搏(PVCs)和室性早搏连发(PVC runs)的发生次数,明显少于无反应组[lg PVCs:(1.78±0.77)vs(2.73±0.61);lg PVC runs:(0.64±0.48)vs(1.98±0.72),P0.05]。分别对CRT术后lg(PVCs)和lg(PVC runs)的多重线性回归分析发现,术后24 h的Tp Te间期是lg(PVCs)和lg(PVC runs)的独立预测因素(B=0.143,比值比=1.154,P=0.001;B=0.122,比值比=1.047,P=0.001)。结论:CRT心室逆重构可以减小复极离散度,降低患者室性心律失常事件发生风险,改善预后。术后当天的Tp Te间期时限对CRT术后室性心律失常事件有预测意义。     

跨室壁复极离散与恶性室性心律失常

目的探讨恶性室性心律失常病人的跨室壁复极离散度。方法恶性室性心律失常组11例,健康对照组13例,对两组的跨度壁复极离散度分别进行测量。结果恶性室性心律失常组病人的跨室壁复极离散度明显大于健康对照组(P<0.01),差异有统计学意义。结论跨室壁复极离散增大可能是发生恶性室性心律失常的预测指标之一。     

兔肥厚左心室跨壁复极离散度和室性心律失常发生机制

目的 探讨肥厚左心室跨壁复极离散度变化及室性心律失常发生机制.方法 制作压力超负荷兔模型,分别记录对照组、肥厚组心室肌内、外膜动作电位并同步记录跨室壁心电图,比较两组动作电位时限（APD90）、跨心室壁复极离散度（TDR）和室性心律失常发生率、尖端扭转性室性心动过速（Tdp）危险度评分.结果 （1）与对照组相比,肥厚组内、外膜APD90显著延长,以内膜层心肌更为明显;TDR显著增大（P＜0.01）;上述变化呈现显著慢频率依赖性;（2）肥厚组室性心律失常发生率、Tdp危险度评分明显高于对照组.结论 动作电位时限延长、跨心室壁复极离散度增大基础上的早期后除极和跨室壁折返激动是肥厚心室心律失常的主要机制.     

心脏再同步治疗对心肌复极离散度的影响

目的观察心室不同位点起搏时心电图上心肌复极标志的变化,了解以双心室起搏技术为核心的心脏再同步治疗（CRT）对心肌复极离散的影响。方法 入选接受CRT植入的患者在起搏器植入后1周内记录12导联心电图,分别将起搏器程控为无起搏、右心室内膜下起搏（RV—EndoP）、左心室外膜起搏（LV—EpiP）及双心室同步起搏（BivP）四种不同状态并记录心电图。阅读不同起搏位点时的QRS时限、QT问期及TP-E时限。QTc用Bazett公式[QTc=实测QT／（RR）1／2]进行矫正。结果基线QYc为（489．2±51．2）ms,而RV—EndoP、LV—EpiP起搏导致QR明显延长[RV-EndoP（537．3±45．7）ms,P〈0．05;LV—EpiP（592．4±60．2）ms,P〈0．001],而BivP起搏为（491．3±52．7）ms,P〉0．05;基线TP．F（113．8±15．7）ms,RV-EndoP、LV—EpiP均导致TP-E明显延长[RV．EndoP（124．8±24．7）ms,P〈0．05;LV．EpiP（133．3±37．8）ms,P〈0．005],BivP时TP-E时限为（109．9±17．1）ms,有轻度缩短,但差异没有统计学意义（P〉0．05）。结论左心室外膜起搏可明显延长心肌复极离散指标;双心室同步起搏可减少由单纯左心室外膜起搏引起的复极离散度的增大。     

高血压病左室肥厚患者的跨壁复极离散度

89例患者分为对照组,非左室肥厚组及左室肥厚组。测量三组心电图V5导联的QT间期和QTpeak,Tp-e。结果:与对照组及非左室肥厚组比较,左室肥厚组的Tp-e明显增大(P<0.01)。结论:左室肥厚显著增加跨壁复极离散度。     

卡维地洛瞬时效应对兔肥厚左心室跨壁复极离散度及心律失常影响

目的探讨血药浓度下卡维地洛瞬时效应对于兔肥厚左心室跨壁复极离散度及心律失常的影响。方法采用腹主动脉缩窄法制做左心室肥厚兔模型，术后持续予以卡维地洛1mg／kg，2次／d，共10周。高效液相色谱分析法测定稳定期血药浓度；对比台式液、血药浓度的卡维地洛台式液灌注下同一肥厚左室心肌组织块动作电位、跨壁复极离散度、QT间期及心律失常发生率。结果（1）稳定期血药浓度为0．1μmol／L。（2）该浓度的卡维地洛台式液灌注对肥厚大室心肌动作电位、跨壁复极离散度、QT间期及心律失常发生率无显著影响。结论常规剂量下，卡维地洛改善左室肥厚预后的作用与其瞬时效应无关。     

急性缺血对兔左心室跨壁复极离散度的影响

急性缺血是导致室性心律失常、心脏性猝死的主要原因之一。本研究以经冠状动脉灌注的兔左心室楔形心肌组织块为对象，着重探讨了急性无灌注缺血过程中兔左心室内外膜心肌动作电位、跨壁复极离散度（transmural dispersion of repolarization，TDR）演变规律及室性心律失常发生机制。     

缝隙连接与干细胞移植后心律失常

由于目前药物和消融治疗心律失常的有限性,使研究者欲开辟一种基于生物方法的非药物治疗手段.近年来,心脏疾病的细胞治疗越来越受到心脏病医牛的关注,尤其是干细胞治疗在缺血性心脏病的作用.然而,惟独十细胞对心律失常的治疗却处于"沉默"状态,这是因为干细胞治疗后的致心律失常作用所带来的危害.     

Electrocardiographic remodeling during cardiac resynchronization therapy

BACKGROUND: More information is required on the relationship between electrical and structural reverse remodeling in patients treated with cardiac resynchronization therapy. METHODS: QRS and JT intervals were investigated during different pacing modes before and 3 months after implantation of a device for biventricular (BiV) pacing in 20 patients with severe drug-refractory heart failure (with left ventricular ejection fraction < 40% and QRS > 120 ms); structural remodeling was evaluated by echocardiography. RESULTS: QRS interval was significantly shortened by BiV pacing both acutely (p=0.002) and at 3 months (p=0.007). No significant change was found in the JT interval. The extent of QRS shortening obtained by BiV pacing showed moderate correlations with the reduction of end-systolic and end-diastolic volumes (r=0.53, p=0.016 and r=0.45, p=0.045, respectively) as well as with increase of left ventricular ejection fraction (r=0.49, p=0.028) at 3 months. The widening of QRS observed during right ventricular (RV) pacing was greater after 3 months of BiV pacing (with respect to acute assessments), suggesting accentuation of pacing-induced electrical dyssynchrony after a period of pacing-induced resynchronization. CONCLUSION: The extent of QRS shortening induced by BiV pacing appears to correlate with the reverse structural remodeling (in terms of reduction in end-systolic volume). The acute changes and the remodeling process occurring at mid-term in the overall population of CRT-treated patients do not appear to involve the JT interval. A period of pacing-induced resynchronization appears to accentuate the potential for RV pacing-driven electrical dyssynchrony.     

Hemodynamic changes during cardiac resynchronization therapy

Cardiac resynchronization therapy (CRT) is a new method for the correction of inter- and/or intraventricular conduction delays of patients with heart failure. The long-term impact of CRT on central hemodynamics is not fully characterized. We performed complete right heart catheterization studies in 31 patients receiving a CRT device pre and 6 months after implantation. Most of the patients improved in their NYHA stage, their LVEF, and in parallel showed reduced right atrial (RA) pulmonary artery (PA) and pulmonary capillary wedge (PCW) pressures and pulmonary vascular resistance both at rest and at 25 watts. In addition, we found a reduction in heart rate accompanied by an increased mean arterial pressure both at rest and at 25 watts. Accordingly, brain natriuretic peptide levels (BNP) were lowered. It was concluded that, besides other well-known effects on ventricular coordination, central hemodynamics after 6 months were improved during CRT.     

心脏再同步治疗进展

心脏再同步治疗(CRT)是通过心脏同步起搏装置来治疗心衰的最新方法,大量循证医学证据CRT可以有效地提高部分收缩性心力衰竭患者的心功能,减少慢性心衰的病死率和再住院率。近年来,国内外已出台了CRT治疗的指南。但关于CRT的应用适应证、疗效评价和长期预后等方面目前仍存在着诸多争议。本文回顾分析了新近的CRT临床试验,并对CRT治疗适应证及目前存在的问题进行了讨论。     

系统性淀粉样变病累及心脏一例

患者男性,53岁.因胸闷、气喘7个月,水肿5个月,加重3个月于2007年12月14日收治入院.患者7个月前活动时出现胸闷和气喘,休息后可缓解,随后出现腹胀及纳差,在当地卫生院以"胃病"治疗,疗效差.     

心脏再同步化治疗的反应性对P波离散度及高频心房事件的影响

目的 观察心脏再同步化治疗（CRT）对心力衰竭(HF)患者P波离散度（Pd）和心房高频事件（AHRE）的影响。方法 选取2010年1月~2014年5月本院心内科收治的49例行CRT的HF患者,于术前、术后6个月和12个月行12导联心电图、动态心电图、超声心动图检查并定期随访,根据术后6个月NYHA心功能分级和超声心动图结果分为CRT有反应组和无反应组。结果 有反应组33例（67%）,无反应组16例（33%）,与术前相比较,术后6个月,有反应组左室舒张末期内径（LVEDD）显著缩小,左室射血分数（LVEF）显著提高,室性早搏（VPB ）显著减少（P<0.05）,左房最大内径（LAD）、Pd、房性早搏（APB）、AHRE差异未见统计学意义,术后12个月,有反应组除LVEDD显著缩小,LVEF显著升高,VPB显著减少外（P<0.05）, LAD、Pd显著减小、APB、AHRE显著减少（P<0.05）。无反应组术后6个月和12个月各参数与术前相比均未见统计学差异,有反应组术后12个月内总AHRE次数与术前Pd呈显著正相关（r=0.651,P=0.000）,而与术前LAD无显著相关性（r=0.169,P=0.060）。结论 CRT中远期效果可以改善心房重构和Pd、减少AHRE的发生,Pd是CRT后发生AHRE的强有力的预测因子。     

Improvement of P wave dispersion after cardiac resynchronization therapy for heart failure

Objective

The purpose of this study is to investigate the effect of cardiac resynchronization therapy (CRT) on P wave maximum duration (PWM) and P wave dispersion (PWD) in patients with advanced heart failure.

Methods

Forty-six patients (33 men; mean age, 60 ± 11 years) with CRT were enrolled in the present study. PWM and PWD were measured using 12-lead surface electrocardiography (ECG) at a paper speed of 50 mm/s and 20 mm/mV. Serial ECG, echocardiography, clinical assessment, and device interrogations were performed at baseline and 3 months after CRT.

Results

After 3 months of follow-up, PWM and PWD values were significantly decreased (129.6 ± 11.3 to 120.7 ± 10.7 milliseconds, P < .001; 42.6 ± 8.0 to 32.3 ± 10.1 milliseconds; P < .001, respectively). It showed a significant reduction in left atrial diameter (LAD) (46.5 ± 5.2 to 44.9 ± 5.6 mm, P = .021) and an improvement in left ventricular ejection fraction (LVEF) (29.0% ± 7.5% to 36.2% ± 8.0%, P < .001). The decrease of PWM and PWD was positively correlated with the reduction of LAD and negatively correlated with the improvement of LVEF. The reduction in atrial fibrillation burden was observed after 3 months of follow-up.

Conclusions

Cardiac resynchronization therapy decreases PWM and PWD along with an improvement of LVEF and a reduction of LAD. Further studies are needed to evaluate the clinical implications of decrease of PWD on prevention of atrial fibrillation.     

Pacing-induced increase in QT dispersion predicts sudden cardiac death following cardiac resynchronization therapy.

OBJECTIVES: This study was designed to determine whether cardiac resynchronization therapy (CRT) by means of biventricular pacing (BiVP) alters the QT interval (QT(c)) and QT dispersion (QTD), and whether such changes relate to the risk of developing major arrhythmic events (MAE). BACKGROUND: Prolonged QT(c) is associated with MAE. Left ventricular pacing and BiVP alter QT(c). METHODS: A total of 75 patients with drug-resistant heart failure (New York Heart Association functional class III/IV) and QRS duration > or =120 ms underwent CRT. The QT(c) and QTD were measured before and 48 days after BiVP. RESULTS: Over 807 days (range 93 to 1,543 days), 11 patients had a MAE. Compared to baseline, at 48 days after CRT, QTD increased in 47% of patients and QT(c) decreased in 53%. The QT(c) at follow-up was higher in MAE patients compared with no-MAE patients (35.9 +/- 14.2 ms vs. 0.52 +/- 6.0 ms; p = 0.0323). Similar differential responses for QTD were observed (46.4 +/- 13.5 ms in MAE vs. -5.1 +/- 4.1 ms in no MAE, p < 0.0001). The MAE occurred in 29% of patients exhibiting an increase in QTD and in 3% of those exhibiting a decrease (p = 0.0017). In multiple regression analyses, change in QTD from baseline (DeltaQTD) strongly predicted MAE, independent of DeltaQT(c), QRS duration, and left ventricular ejection fraction and end-diastolic volume (p < 0.001). Differences in survival curves were observed when patients were dichotomized according to whether QTD increased or decreased in relation to baseline values (p < 0.0001). CONCLUSIONS: The MAE in patients with BiVP are related to pacing-induced increases in QTD. Measures of ventricular repolarization at the time of pacemaker implantation may guide selection of patients for combined CRT and defibrillator therapy.     

心脏再同步治疗术中冠状静脉窦夹层破裂一例

患者女,70岁,因“胸闷气急1个月”入院.超声心动图示左心室射血分数（LVEF）0.18;心电图示完全性左束支阻滞,QRS时限140 ms.诊断：扩张性心肌病心功能Ⅳ级.入院第4天行心脏再同步治疗（CRT）,右心室电极导线植入成功后行序心室电极导线植入.经撕开鞘将冠状静脉凄标测电极导管送入冠状静脉窦,通过腔内电网及X线透视确认标测电极导管位于冠状静脉窦内,沿标测电极送入长鞘.