心脏再同步化治疗慢性心力衰竭的疗效评价及无效原因分析

目的 评价心脏再同步化治疗(CRT)对慢性心力衰竭患者的临床和超声心动图疗效,总结CRT无效的原因.方法 研究施行CRT的患者53例,男37例,女16例,年龄41～82岁.患者术前均采用血流多普勒和组织多普勒的方法进行收缩不同步的评价,术前和术后6个月进行美国纽约心脏病学会(NYHA)心功能分级评价、心电图和超声心动图检查.临床有效者定义为术后6个月NYHA心功能分级改善1级以上的患者.超声心动图有效者定义为术后6个月左室收缩末容积缩小＞15%或左室射血分数绝对值增加＞5%的患者.结果 CRT术后6个月时,7例患者死亡,46例患者存活.其中NYHA心功能分级至少改善1级者40例,临床有效率为75.5%;超声心动图有效者37例(69.8%).术后6个月:左心室缩小;左室射血分数由(27.4±6.7)%增加到(40.4±10.0)%,P＜0.01;左心房内径缩小;二尖瓣反流减少;肺动脉收缩压由(49.6±13.6)mm Hg(1 mm Hg=0.133 kPa)降低为(38.7±14.5)mm Hg.窦性心律组(42例)的超声有效率显著高于心房颤动组(11例).在窦性心律患者中,与CRT无效组(10例)相比,有效组(32例)起搏前的QRS较宽(P＜0.05),肺动脉收缩压较低(P＜0.05),左室射血前时间较长(P＜0.05);起搏前两组间腔室大小、LVEF、二尖瓣反流面积和组织多普勒的各个收缩不同步参数的差异无统计学意义.结论 CRT能改善心力衰竭患者的左室收缩功能和左室重构,减少二尖瓣反流,降低肺动脉收缩压.窦性心律组的CRT疗效优于心房颤动组.在非缺血性心肌病和左束支传导阻滞患者占多数的研究中,QRS宽度、左室射血前时间和肺动脉收缩压可能预测CRT的疗效.     

心脏再同步化治疗起搏参数优化对心脏同步性及心功能的影响

目的 应用组织多普勒研究心脏再同步化治疗(CRT)术后A-V、V-V间期优化对心脏同步性能及心功能的影响,探索A-V、V-V间期优化在增强CRT临床疗效中的作用.方法 32例慢性心力衰竭患者接受CRT治疗,于术后7天、3个月、6个月进行A-V、V-V间期优化,观察心脏同步性和心功能变化.采用彩色超声诊断仪进行图像采集及下线分析.结果 经观察,术后7天、3个月、6个月的A-V间期需行优化的例数分别为28例、10例、6例,V-V间期需行优化的例数分别为29例、6例、5例.与CRT术前相比:CRT治疗术后未优化时的左室12节段组织速度达峰时间标准差明显改善[(68.8±26.4)ms与(41.6±23.1)ms,P＜0.01],左室射血分数增加[(28±4)%与(31±3)%,P＜0.05],主动脉瓣前向血流速度时间积分增加[(13.6±3.1)cm与(15.5±4.3)cm,P＜0.05],舒张早期跨二尖瓣血流峰速和舒张早期心肌组织运动峰速的比值下降(13.1±5.3与9.3±4.3,P＜0.05),左室舒张充盈时间延长[(313.2±93.6)ms与(368.6±97.1)ms,P＜0.05].与术后未优化时相比:术后7天优化心脏同步性指标进一步改善(P＜0.05),心功能指标无明显改变;术后3个月、6个月优化与术后7天优化相比,心脏同步性指标无明显改变,P＞0.05;术后6个月优化的左室射血分数增加,左室舒张充盈时间延长,P＜0.01.结论 CRT术后7天,A-V、V-V间期优化治疗改善心脏同步指标;术后6个月优化进一步改善心功能.     

心脏再同步化治疗慢性心力衰竭伴持续性心房颤动的疗效

目的评价心脏再同步化治疗(CRT)慢性心力衰竭(简称心衰)合并持续性心房颤动(简称房颤)患者的临床疗效。方法选择慢性心衰患者53例,其中42例窦性心律患者及11例房颤患者接受双心室起搏治疗,术后3个月进行随访,观察患者的心功能分级,6 min步行距离,超声心动图测定各房室腔内径大小、左室射血分数(LVEF)、二尖瓣返流以及速度向量成像超声评价同步性参数的变化。结果 53例三腔起搏器置入术均取得成功。与术前相比,术后3个月房颤CRT患者心功能分级(2.30±0.47级vs 3.0±0.02级)、左房内径(44.9±3.8 mm vs52.2±4.2 mm,P<0.05),LVEF(0.43±0.02 vs 0.32±0.03)及二尖瓣返流(1.5±0.2 vs 3.18±1.75,P<0.01)均有明显改善,速度向量成像超声结果显示,室内不同步较术前有明显改善。窦性心律患者术后各项心功能及不同步指标较术前亦有明显改善,与房颤CRT患者比较差异无显著性。结论对于慢性心衰合并持续性房颤患者,CRT与窦性心律一样可以改善心功能。     

老年心力衰竭患者心脏再同步化治疗术后心脏电学重构与机械重构

目的探讨心脏再同步化治疗(CRT)术后老年心力衰竭(心衰)患者心脏的电学重构和机械重构效应。方法入选因心衰而住院行CRT的70例老年患者,对其术前、术后1、6个月分别进行电学重构指标和机械重构指标检测并随访。结果 70例老年心衰患者均成功完成CRT。与术前比较,术后1、6个月起搏QRS间期明显缩短[(127.23±14.25)ms和(133.37±9.43)ms vs(149.86±13.35)ms,P<0.01];LVEF明显升高,左心房前后径、左心室舒张末内径、左心室收缩末容积、肺动脉压力、室间机械延迟、左心室间隔与后壁运动延迟明显降低(P<0.05,P<0.01)。CRT后6个月有效率达69%。结论 CRT置入术后能够在一定程度上逆转心室间的电学传导、逆转老年心衰患者的左心室机械重构,使老年心衰患者的心脏功能得以改善。     

心脏再同步化治疗对慢性心力衰竭的临床疗效

目的：观察心脏再同步化治疗（cardiac resynchronization therapy,CRT）对慢性心力衰竭（chronic heart failure,CHF）的临床疗效。方法选择2010年12月至2013年12月于我院成功植入C RT的慢性心力衰竭患者36例。在治疗前和治疗后6个月,分别对患者进行NYHA分级及6 min步行试验的评价,应用心脏超声评价患者左室射血分数（LVEF）、左室质量指数（LVMI）、左室舒张末期容量指数（LVEDVI）、左室收缩末期容量指数（LVESVI）等左室功能指数,对治疗前及治疗后6个月上述指标行t 检验,分析其差异性。结果治疗6个月时,患者 LVEF、LVMI、LVEDVI、LVESVI较治疗前有明显改善,且差异有统计学意义（P均＜0．05）;患者NYHA心脏功能分级及6 min步行试验较治疗前有明显改善,且差异有统计学意义（P均＜0．05）。结论 CRT-D明显改善慢性心衰的心功能,提高患者生活质量及运动耐量。     

比索洛尔和卡维地洛治疗慢性心力衰竭的临床疗效观察

目的研究比索洛尔和卡维地洛治疗慢性心力衰竭的临床疗效及安全性。方法选择125例慢性心力衰竭患者,按心功能分级(NYHA)Ⅱ~Ⅳ级,经超声心动图证实左心室射血分数≤40%,将患者随机分配到比索洛尔组(62例)或卡维地洛组(63例),均治疗30周。每次随访评估心功能,记录主要心脏不良事件。结果两组左心室射血分数明显改善,比索洛尔组提高11%,卡维地洛组提高12%,左心室射血分数改善程度组内比较均有显著性意义(P<0.01)。心力衰竭症状两组均较前改善,心功能分级比索洛尔组和卡维地洛组心功能Ⅲ级治疗后减少至5例(8.1%)和6例(9.5%),两组治疗前后组内比较有显著性意义(P<0.01)。比索洛尔组和卡维地洛组主要心脏不良事件发生率分别为32.3%和34.9%,组间比较无显著性意义(P>0.05)。结论慢性心力衰竭患者应用比索洛尔和卡维地洛一样安全有效,比索洛尔可以达到与卡维地洛靶剂量长期治疗相同的疗效。     

心脏再同步化治疗心衰的手术操作和疗效回顾

目的:探讨和总结心脏再同步化治疗(CRT)器治疗心衰的疗效。方法:21例心功能Ⅲ～Ⅳ级的心力衰竭患者,符合左室射血分数(LVEF)35%、心电图QRS波宽度≥160ms、左室舒张末期内径60mm的CRT建议标准。评价手术时间、X线曝光时间和术前后的单次最远行走距离、6min步行距离、NYHA心功能分级。结果:经左侧(n=20)和右侧锁骨下静脉(n=1)CRT的手术时间分别为(143.3±30.8)min和235min,而X线曝光时间分别为(19.7±15.5)min和75min;CRT术后单次最远行走距离显著增加[(921.7±253.8)m:(675.8±172.1)m,P0.01],6min步行距离术后较术前显著增加[(409.8±43.6)m:(292.5±55.6)m,P0.01],而NYHA心功能IV级者所占的百分率术后比术前显著减少(23.8%:85.7%,P0.01)。结论:对左室射血分数35%、心电图QRS波宽度≥160ms、左室舒张末期内径60mm的心衰患者,行CRT可显著改善6min步行距离和NYHA心功能分级。     

超声心动图预测心脏再同步化治疗反应的进展

心室收缩机械不同步是心脏再同步化治疗的重要前提,而目前评价室壁机械运动同步性的方法有很多,其中以超声心动图的应用较为广泛。本文主要介绍不同超声心动图参数在评价慢性心力衰竭患者左心室收缩同步性方面的作用,以进一步探讨超声心动图对心脏再同步化治疗反应的预测价值。     

心脏再同步治疗房室间期的优化

目的评价房室（AV）间期动态优化的心脏再同步治疗对慢性心力衰竭的疗效。方法63例因心力衰竭接受心脏再同步治疗的患者分别于植入起搏器术后1周、6个月及12个月在超声指导下行AV间期优化。定义最佳AV间期为超声心动图指标E、A峰最大分离并无切尾。同时分别行超声心动图及心电图、6分钟步行距离试验（6MHW）、明尼苏达HF患者生活质量问卷评分（QOL）。结果本组最佳优化AV间期在90～140（110.45±19.47）ms。CRT植入后1周同植入前比较,左室射血分数（LVEF,22.07%±6.77%比18.53%±4.83%）和左心室舒张期充盈时间（LVFT,293.27±24.79ms比272.35±56.00ms）明显提高,QRS波宽度变窄（129.40±6.65ms比138.25±28.00ms）,P均〈0.05,差异有统计学意义。跟优化前比,AV间期动态优化后的6个月和12个月LVEF值由22.07%±6.77%增加至32.24%±10.34%及36.86%±9.29%;6min步行距离（6MHW）由术前268.70±22.25m增加至327.12±15.24m及347.62±15.04m;QRS时限无明显变化;左心室舒张末期直径（LVEDD）由71．43±7．12mm降至65．88±9．85mm和57．06±6．54mm;生活质量问卷评分（QOL）由72．14±6．24降低至61．68±12．28和55．15±11．02;NHYA心功能分级由3．12±0．55减至1．68±0．67和1．82±0．43。结论动态优化AV间期可以提高心脏再同步治疗对慢性心力衰竭的短期、中期、远期疗效。     

心脏再同步化治疗心力衰竭合并持续性心房颤动的疗效

目的评估心脏再同步化治疗(CRT)对心力衰竭(简称心衰)合并持续性心房颤动(简称房颤)患者的疗效。方法 12例慢性心衰的持续性房颤患者,心室率本身是慢的或经过药物治疗严格控制心室率,成功植入CRTD并打开心室感知反应及房颤传导反应功能。比较CRT-D植入术前和植入术后1年患者的总体幸福感量表(GWB)及心脏病症状评分(CSS),6 min步行试验,心功能分级以及超声心动图指标:左房内径(LAD)、左室舒张末期内径(LVDD),左室射血分数(LVEF),二尖瓣返流面积(MRA),心室间机械运动延迟(IVMD),左室12节段达峰时间标准差(12-Ts-SD)和左室12节段达峰时间最大差值(12-TP-MAX-D)。结果①12例随访1年内均无因心功能恶化再次入院,无死亡。②双室有效起搏比率达到93%±5%。③有3例在CRT-D植入后自行转复为窦性心律。④CRT-D植入后1年GWB、CSS,6 min步行试验,心功能分级较植入前均有明显改善[(70.25±16.61)vs(54.62±15.27),(16.67±5.23)vs(9.28±4.52),(320±65.24)m vs(214±43.74)m,2.43 vs 3.30,P均0.05];CRT-D植入后1年,LAD缩小,LVEF升高,MRA减少[(40.2±10.6)mm vs(47.5±12.3)mm,(0.40±0.07)vs(0.28±0.05),(3.8±1.6)cm2vs(5.6±2.3)cm2,P均0.05];IVMD、12-Ts-SD和12-TP-MAX-D得到改善[(35.4±17.8)ms vs(48.1±12.3)ms,(31.5±10.7)ms vs(44.5±15.2)ms,(100.6±22.9)ms vs(127.5±42.7)ms,P均0.05]。结论慢心室率或经过药物治疗严格控制心室率的持续性房颤合并心衰患者能从CRT-D治疗中获益。     

心脏再同步化治疗顽固性心力衰竭合并心房颤动

目的总结心脏再同步化治疗(CRT)合并心房颤动(房颤)的心力衰竭(心衰)的疗效,分析这类患者CRT反应的可能原因。方法 2003年3月至2007年3月接受CRT合并房颤的难治性心衰患者5例,4例为扩张型心肌病,1例为缺血性心肌病,NYHA心功能Ⅲ～Ⅳ级。4例经冠状窦途径成功置入左室电极,1例冠状窦途径失败后行右室双部位起搏(流出道间隔部和心尖部)。结果术后平均随访(12±13)个月,所有患者术后临床症状均有不同程度的改善,NYHA分级提高0+～2级;生活质量和活动耐力均有改善。平均双室起搏比例(90±9)%,其中第2、4、5例术后频发室性早搏,平均双室起搏比例偏低(77%～83%)。第2例加用胺碘酮后比例由83%升至95%,NYHA分级提高2级。5例患者先后于术后1～33个月死亡,直接死亡原因为室性心律失常者2例,心衰恶化者3例。结论 CRT同样可以使合并持续性房颤的难治性心衰患者受益,可以提高生活质量、活动耐力。保证完全的双室起搏是合并房颤的心衰患者对CRT反应的关键因素之一。合并房颤的难治性心衰患者可能更需要在严重心衰早期积极地选择CRT。部分合并房颤的难治性心衰患者,在行CRT同时应考虑植入除颤器。     

Relationship between device-detected subclinical atrial fibrillation and heart failure in patients with cardiac resynchronization therapy defibrillator

BackgroundAtrial fibrillation (AF) is a leading preventable cause of heart failure (HF) for which early detection and treatment is critical. Subclinical‐AF is likely to go untreated in the routine care of patients with cardiac resynchronization therapy defibrillator (CRT‐D).HypothesisThe hypothesis of our study is that subclinical‐AF is associated with HF hospitalization and increasing an inappropriate therapy.MethodsWe investigated 153 patients with an ejection fraction less than 35%. We divided into three groups, subclinical‐AF (n = 30), clinical‐AF (n = 45) and no‐AF (n = 78). We compared the baseline characteristics, HF hospitalization, and device therapy among three groups. The follow‐up period was 50 months after classification of the groups.ResultsThe average age was 66 ± 15 years and the average ejection fraction was 26 ± 8%. Inappropriate therapy and biventricular pacing were significantly different between subclinical‐AF and other groups (inappropriate therapy: subclinical‐AF 13% vs clinical‐AF 8.9% vs no‐AF 7.7%: P = .04, biventricular pacing: subclinical‐AF 81% vs clinical‐AF 85% vs no‐AF 94%, P = .001). Using Kaplan‐Meier method, subclinical‐AF group had a significantly higher HF hospitalization rate as compared with other groups. (subclinical‐AF 70% vs clinical‐AF 49% vs no‐AF 38%, log‐rank: P = .03). In multivariable analysis, subclinical‐AF was a predictor of HF hospitalization.ConclusionsSubclinical‐AF after CRT‐D implantation was associated with a significantly increased risk of HF hospitalization. The loss of the biventricular pacing and increasing an inappropriate therapy might affect the risk of HF hospitalization.     

Longstanding atrial fibrillation causes depletion of atrial natriuretic peptide in patients with advanced congestive heart failure

BACKGROUND: Congestive heart failure (CHF) is characterized by neurohormonal activation, including increased plasma concentrations of atrial natriuretic peptide (ANP) and N-terminal ANP (N-ANP). Onset of atrial fibrillation (AF) further increases these peptides, but it may be hypothesized that concentrations decrease during longstanding AF due to inherent atrial degeneration. AIM: We sought to investigate the relation between neurohormonal activation in patients with CHF and the duration of concomitant AF. METHODS: The study group comprised 60 patients (age 70 +/- 8 years) with advanced CHF due to left ventricular systolic dysfunction (left ventricular ejection fraction (LVEF) < 0.35) and chronic AF (duration 21 (1-340) months). Plasma neurohormone concentrations were measured, and multiple regression analysis was performed to identify their clinical predictors. RESULTS: Median plasma neurohormone concentrations were: ANP 113 pmol/l, N-ANP 1187 pmol/l, norepinephrine 496 pg/ml, renin 127 micro units/l, aldosterone 128 pg/ml and endothelin 8.1 pg/ml. Norepinephrine, renin, aldosterone and endothelin were not significantly related to the duration of AF. In contrast, ANP decreased along with the duration of AF (P = 0.03), while the same trend was observed for N-ANP (P = 0.10). However, for these peptides a first order interaction with LVEF was present, which was not observed in the other neurohormones. In patients with LVEF > 0.25 ANP and N-ANP increased along with the duration of AF, whereas in patients with LVEF < or = 0.25 an inverse relation between ANP (P = 0.02) and N-ANP (P = 0.04) and the duration of AF was present, longer-standing AF being associated with lower concentrations. CONCLUSION: In patients with advanced CHF with low LVEF plasma ANP and N-ANP concentrations decrease during longstanding AF. This finding agrees with the concept that longstanding AF leads to impaired ability of the atria to produce these neurohormones due to inherent degenerative changes.     

Anti-thrombotic strategies for patients with atrial fibrillation and heart failure

Atrial fibrillation occurs commonly in the setting of congestive heart failure and, in fact can cause left ventricular dysfunction due to a rapid ventricular response over time, termed tachycardia-mediated cardiomyopathy. The combination of atrial fibrillation and congestive heart failure leads to a high risk of stroke for the patient and appropriate antithrombotic therapy can minimize this incidence of stroke. Stroke risk can be markedly reduced by treatment with warfarin and complications of anticoagulation minimized by close attention to maintaining the INR between 2.0 and 3.0.     

胺碘酮治疗心衰并发房颤的有效性和安全性研究

评价胺碘酮对心衰并发房颤患者心室率的影响，转复窦性心律的可能性，以及治疗的安全性。采用随机、单盲、安慰剂对照方法，运用２４ ｈ 动态心电图监测心率。结果:①胺碘酮对心衰并发房颤患者的转复律为２３．５３％ ，高于对照组（３．３３％ ），Ｐ＜ ０．０１。②治疗２ 周后试验组１２ 导联心电图所得平均心室率、Ｈｏｌｔｅｒ监测下２４ ｈ 最大心室率、平均心室率明显下降（Ｐ＜ ０．０１），最小心室率无影响（Ｐ＞ ０．０５）。③两组间左室射血分数（ＬＶＥＦ）无差异（Ｐ＞ ０．０５），均无尖端扭转性室性心动过速发生，试验组ＱＴｃ延长，但改为维持量后ＱＴｃ恢复正常。结论:胺碘酮能使一部分心衰并发房颤患者复律，并且无论复律与否，均能减慢心室率，而不影响心功能的改善，严重副反应较少发生     

Lack of prevention of heart failure by serial electrical cardioversion in patients with persistent atrial fibrillation

OBJECTIVE—To investigate the occurrence of heart failure complications, and to identify variables that predict heart failure in patients with (recurrent) persistent atrial fibrillation, treated aggressively with serial electrical cardioversion and antiarrhythmic drugs to maintain sinus rhythm.DESIGN—Non-randomised controlled trial; cohort; case series; mean (SD) follow up duration 3.4 (1.6) years.SETTING—Tertiary care centre.SUBJECTS—Consecutive sampling of 342 patients with persistent atrial fibrillation (defined as > 24 hours duration) considered eligible for electrical cardioversion.INTERVENTIONS—Serial electrical cardioversions and serial antiarrhythmic drug treatment, after identification and treatment of underlying cardiovascular disease.MAIN OUTCOME MEASURES—heart failure complications: development or progression of heart failure requiring the institution or addition of drug treatment, hospital admission, or death from heart failure.RESULTS—Development or progression of heart failure occurred in 38 patients (11%), and 22 patients (6%) died from heart failure. These complications were related to the presence of coronary artery disease (p < 0.001, risk ratio 3.2, 95% confidence interval (CI) 1.6 to 6.5), rheumatic heart disease (p < 0.001, risk ratio 5.0, 95% CI 2.4 to 10.2), cardiomyopathy (p < 0.001, risk ratio 5.0, 95% CI 2.0 to 12.4), atrial fibrillation for < 3 months (p = 0.04, risk ratio 2.0, 95% CI 1.0 to 3.7), and poor exercise tolerance (New York Heart Association class III at inclusion, p < 0.001, risk ratio 3.5, 95% CI 1.9 to 6.7). No heart failure complications were observed in patients with lone atrial fibrillation.CONCLUSIONS—Aggressive serial electrical cardioversion does not prevent heart failure complications in patients with persistent atrial fibrillation. These complications are predominantly observed in patients with more severe underlying cardiovascular disease. Randomised comparison with rate control treatment is needed to define the optimal treatment for persistent atrial fibrillation in relation to heart failure.