经食管心房起搏对功能性左束支阻滞的研究

目的研究V1导联左束支阻滞QRS波形的早期表现,以及左束支阻滞从不完全性到完全性在V1导联QRS波形的演变规律及影响功能性左束支阻滞显现的因素。方法100例经食管心房程序刺激显现的具有直接显示性左束支文氏阻滞特征的功能性左束支阻滞病人与100例无功能性束支阻滞的正常者作对比研究。结果①功能性左束支阻滞的检出率为6.73%;②V1导联左束支阻滞的早期QRS波形的表现为SV1增深;③左束支阻滞从不完全性到完全性在V1导联QRS波形的演变规律为正常rS→深S波的rS→窄QS→宽QS;④功能性左束支阻滞的房室交界区功能不应期略短于左束支有效不应期,而房室交界区相对不应期、功能不应期则显著短于对照组(P<0.01)。结论V1导联左束支阻滞的早期QRS波形的表现为SV1增深,左束支阻滞从不完全性到完全性在V1导联QRS波形的演变规律为正常rS—深S波的rS—窄QS—宽QS。     

真性左束支阻滞(107)

完全性左束支诊断的传统标准包括:QRS波时限≥0.12s;V5、V6导联R波宽大伴切迹;V1导联QRS波呈QS形或rS形;并有继发性ST-T改变。2011年Strauss提出真性左束支阻滞的新概念及标准。[心电图诊断标准]Strauss在传统左束支阻滞的诊断标准上提出3点补充意见:①V1、V2导联的QRS     

左右束支非等速非同步传导阻滞1例

患者,男,73岁.因水肿10 d加重伴咳嗽气促3 d入院,临床诊断为冠心病、心律失常、心功能3～4级、2型糖尿病、肺部感染.图1为人院常规同步12导联心电图检查:窦性心律,心率88次/min,P-P相对固定;P-R间期呈3:2文氏变化:140 ms/180 ms/脱落.QRS波群间期增宽0.12 s呈3:2周期性变化:P-R 140 ms时,V1联呈R型,Ⅰ导联S波粗钝为完全性右束支传导阻滞;P-R 200 ms时,V1导联呈QS型,Ⅰ导联R波完全性左束支传导阻滞;之后QRS波群脱落.周而复始构成3:2房室文氏传导伴QRS波群完全性右束支/左束支传导交替阻滞.心电图诊断:窦性心律,完全性左、右束支非等速非同步传导阻滞.     

思考与分析

V_3导联心电图窦 P 和 QRS 均规则出现,频率各为80次/min 和50次/分,P 与 R 无固定关系,但均各自按其固有频率发放激动,房率快于室率,故可确诊Ⅲ°房室传导阻滞。QRS 形态有3种:(1)R_1呈 rS 型,S 波宽大,ORS 时限达0.12s,为完全性左束支传导阻滞型,R_4形态同R_1。但 QRS 时限<0.12s,为不完全性左束支阻滞。(2)R_(2、5)呈 Rs,s 波略粗钝,为不完全性右束支传导阻滞型。(3)R_(3.6)呈 R 型,R 顶端错折,QRS 时限达0.1 2s,为完全性右束支传导阻滞。这3种形态的 QRS 波按一定的顺序周而复始规律性出现,故考虑逸搏发生于阻滞区以下的房室交界区,并在前向传导中伴有左右束支不同步、不等速的传导阻滞。R_1激动沿右束支下     

经食管心房起搏研究功能性右束支阻滞

经食管心房起搏检出１０１例功能性右束支阻滞。右束支阻滞的早期表现为ＳＶ１变浅，右束支阻滞由不完全性到完全性在Ｖ１导联演变规律为ｒＳ－ｒｓ－ｒＲ或ｒＳ－ｒｓ－ｒｓｒ‘－ｒｓＲ’。功能性右束支阻滞组的房室交接区功能不应各短于右束支有效不应期，而心房有效不应期不应期与房室交接区有效不应期则显著短于对照组。     

左束支传导阻滞的分度标准

1)一度阻滞:①轻度:不完全性左束支阻滞前改变或早期的不完全性左束支传导阻滞。②中度:不完全性左束支传导阻滞。③重度:QRS时间可以更加延长的“完全性”左束支阻滞,或伴有左分支阻滞的左束支传导阻滞。 2)二度阻滞:①Ⅰ型(文氏型):左束支传导阻滞的QRS时间渐长至完全性,即由正常渐长至≥0.12S,且呈周期性改变。②Ⅱ型(莫氏型):完全性左束支阻滞的传导比例为2:1或其他比例,如4:3、3:2等。     

Mahaim氏预激综合征掩盖心肌梗死图形1例

患者男,81岁。临床诊断:陈旧性下壁心肌梗死,预激综合征。心电图特征:图1A为窦性心律,心率88次/min,P R间期180ms,QRS时间150ms。Ⅱ、Ⅲ、aVF、V2、V3导联呈QS型,V1导联呈qR型,V4V6导联呈qrS型,q波时间>40ms,深度>其R波的四分之一,为完全性右束支阻滞合并下壁、广泛前壁心肌梗死。图1B为窦性心律,心率75次/min,P R间期180ms,QRS波上升支起始粗钝,为“预激”波,V1V3导联呈rS型,V46导联呈Rs型,Ⅱ、aVF导联呈Rs型,Ⅲ导联呈Qr型,为Mahaim氏预激,心肌梗死图形几乎被完全掩盖。心电图诊断图1A:①窦性心律;②完全性右束支阻滞(RBBB…     

房室结折返性心动过速合并束支阻滞时心内电图特征

探讨房室结折返性心动过速 (AVNR)合并束支阻滞时心内电图特征及其机制。 6 0例AVNRT患者 ,男 2 3例、女 37例 ,年龄 39± 11岁。将病例分为 3组 :Ⅰ组合并左束支组滞 (CLBBB) ;Ⅱ组合并右束支阻滞 (CRBBB) ;Ⅲ组无束支阻滞。心内电生理测定心动过速的频率 (HR)、冠状窦口A波至V波的距离 (AVcs)、His束处A波到V波的距离 (AVH)。三组心动过速的心率分别为 171± 2 3,16 6± 19,170± 17次 /分 ,三组之间差异无显著性 (P >0 .0 5 ) ;Ⅰ组与Ⅱ、Ⅲ组AVcs、AVH 比较 ,差异有显著性 ( 81± 12msvs 46± 11ms,49± 9ms;5 6± 13msvs 5 1± 10ms、5 0± 10ms,P均 <0 .0 5 ) ;Ⅱ组与Ⅲ组之间AVcs、AVH 差异无显著性。结论 :AVNRT合并束支阻滞时心动过速的心率无明显变化 ;当合并CLBBB时 ,His束到心室的传导时间延长 ,导致冠状窦与His束处的A、V间距延长 ;合并CRBBB时无上述现象发生。     

左侧旁道伴左束支阻滞1例

患者女、42岁，因反复发作心悸10余年入院，常规心电图（图1A）有典型δ波，V1导联呈RS形态，R〈S，QRS时限110ms，PJ间期220ms，诊为B型预激综合征，拟行经导管射频消融。常规电生理检查示心房超速刺激诱发左束支阻滞型宽QRS波心动过速，心房激动顺序呈偏心性，诊断为左侧旁道引起的房室折返性心动过速。有效消融过程中（图1C），δ波消失，而V1导联QRS波群变成完全性左束支阻滞形，     

双径路及交替性左右束支阻滞2例

例1患者女、70岁,因反复晕厥入院。门诊行24h动态心电图检查V1导联连续记录(图1A)示:窦性心律,心率83bpm。下传心室QRS波呈左、右束支阻滞型,且不固定比例交替。同时PR间期亦呈长短交替,长短PR间期差>0.06s,其中右束支阻滞型QRS波前PR间期长,约0.16s,左束支阻滞型QRS波前PR间期短,约0.08s,两者形成十分固定的"匹配"关系。患者的24h动态心电图记录还出现较长时间的完全性右束支阻滞及完全性左束支阻滞,其前也分别呈现固定的长短两种PR间期(图略),上述情况可以排除室性期前收缩,考虑为房室结双径路,快径路经左束支下传心室,慢径路经右     

房室结慢径消融后心动过速复发机制

目的 探讨慢径消融后房室结折返性心动过速(AVNRT)复发机制.方法 对56例(男23例,女33例)平均年龄45.23±15.21岁的AVNRT患者进行射频消融前后电生理数据比较.结果 56例中6例复发(复发组).复发组与非复发组术后房室结快径前传有效不应期(ERP-FP)均缩短,复发组由308.33±41.67ms缩短为222.85±55.89ms(P<0.01).非复发组由343.68±62.28ms缩短为287.60±47.94ms(P<0.01).复发组术后ERP-FP缩短更明显,与非复发组比较有显著性差异(P<0.01).结论 射频消融后ERP-FP过度缩短可能使AVNRT复发.     

人工心房调搏S_1-S_2/(S_1-S_1)~1/2的临床意义

心室肌相对不应期可用人工心房调搏法产生Ashman现象时的S_1-S_2间期来表示,但产生Ashman现象时的S_1-S_2时程受其前的S_1-S_2长短影响。笔者用S_1-S_2/(S_1-S_1)~(1/2)作为心室肌相对不应期校正公式,对A(病人)组72例及B(正常对照)组100例的心房调搏,结果进行对照分析两组S_1-S_2(x±s)分别为536±76ms及530±62ms(P>0.05),而用S_1-S_2/(S_1-S_2)~(1/2)计算结果S_1-S_2(x±s)分别为685±65ms;518±66ms(P<0.01)。提示:S_1-S_2/(S_1-S_2)~(1/2)可作为心室肌相对不应期校正公式,而且当其大于或等于640ms时提示心肌相对不应期延长。     

早期口服卡维地洛对兔陈旧性心肌梗死边缘带不应期和钠电流的影响

研究卡维地洛(Car)对陈旧性心肌梗死(OMI)心室梗死边缘带有效不应期(ERP)及钠电流(INa)的影响。家兔按体重随机分为3组,OMI组:开胸结扎冠状动脉左回旋支;Car组:手术同OMI组,并于手术前开始服用Car0.33mg·kg1·d1;假手术(Sham)组:开胸,但不结扎冠状动脉,各组动物均喂养3月。整体心脏Langendorff灌流下记录边缘带的ERP。应用双酶法分离左心室梗死边缘带(IBZ)的心肌细胞。利用膜片钳记录在电压钳模式的INa。结果:OMI组ERP较Sham组显著延长(216.9±4.6msvs160.0±3.8ms,P<0.01),Car组ERP为179.2±9.7ms,较OMI组明显缩短。OMI组IBZ存活心肌细胞的INa的密度较Sham组显著性降低,动力学研究显示,INa半失活电压曲线V1/2移向更负,其恢复时间常数值延长,从而导致INa恢复减慢;而Car组心肌细胞的INa的密度较OMI组明显增大,P<0.05,INa稳态失活曲线和恢复曲线与Sham组无显著差异。结论:卡维地洛可以抑制OMI后心室肌ERP延长,并使INa密度增大。此可能是该药减少OMI后心律失常的发生,降低病死率的机制之一。     

Functional bundle branch block: Discordant response of right and left bundle branches to changes in heart rate

Faster heart rates shorten refractoriness more in some tissues than in others. This study investigates whether faster heart rates shorten relative refractoriness more in the right than left bundle branch in humans. Premature atrial stimulation at 2 or more basic cycle lengths was performed in 314 patients with no evidence of atrioventricular conduction system disease. In 10 patients, both functional right and left bundle branch block (BBB) developed with premature atrial stimulation. Functional right BBB occurred at the longer basic cycle length, and functional left BBB at the shorter cycle length in 8 patients. In 2 patients functional right and functional left BBB were present at the same cycle length, but functional left BBB occurred at a shorter premature atrial coupling interval. For all patients, the mean functional right bundle branch relative refractoriness was 438 ms at a basic cycle length of 847 ms, and functional left bundle branch relative refractoriness was 357 ms at a cycle length of 622 ms (p <0.01). The HV interval was 45 ± 15 ms at control and increased with functional left BBB to 77 ± 19 ms (p <0.01), but not with functional right BBB. Thus, relative refractoriness of the right and left bundle branches are rate-dependent and discordant. At longer cycle lengths, relative refractoriness of the right bundle branch is greater than that of the left bundle branch, and at shorter cycle lengths relative refractoriness of the left bundle branch is greater than that of the right bundle branch. The relative refractory period curves “cross over” and can explain the presence of both functional right and left BBB in the same patient.     

切割前房结通路对家兔房室结电生理特性的影响

为进一步了解房室结整体电生理特性以及消融治疗房室结折返性心动过速的机制，选择性切割无房室结双径现象离体家兔心的前房结通路（Ｋｃｈ三角前区）观察其对房室结电生理参数的影响。与切割前相比，切割后ＡＨ间期、房室结功能不应期、房室结前传文氏周长、室房逆传文氏周长及ＶＡ间期延长（分别为４５．６４±８．６８ｍｓｖｓ３８．２３±６．１３ｍｓ，１６６．３４±１５．３３ｍｓｖｓ１４４．４８±１０．８６ｍｓ，１６３．３７±１７．２２ｍｓｖｓ１３８．３６±１２．４３ｍｓ，２０２．６０±４１．５０ｍｓｖｓ１６８．５０±２０．３０ｍｓ，６８．６０±１．６０ｍｓｖｓ５４．５０±７．１０ｍｓ，Ｐ均＜０．０５）。提示毁损房室交界区特定部位可以影响房室结整体电生理特性。     

经食管电生理检查中的交替文氏现象

在５６１例经食管电生理检查中，检出各类交替文氏现象（ＡＷ）８１例，共１３７例次，占１４．４％，其中Ａ型、Ｂ型、ＡＢ混合型、三层房室ＡＷ分别为４４，６０，１８，６例次，分别占３２．１％、４３．８％、１３．１％、４．４％；房室结双径路间、束支、房室旁束的ＡＷ分别为５，２，２例次，分别占３．６％、１．５％、１．５％。将７９例ＡＷ者（Ａ组）与８０例无ＡＷ者（Ｂ组）的电生理资料进行比较，显示：①窦性心率（ＳＲ），Ａ组较Ｂ组慢（７２±１４．２ｂｐｍｖｓ７８±１２．６ｂｐｍ，Ｐ＜０．００１）。②房室相对不应期（ＡＶＲＲＰ）、房室功能不应期（ＡＶＦＲＰ）、房室有效不应期（ＡＶＥＲＰ），Ａ组分别为６０９．０±１１９．４，４９６．６±９６．０，３６０．０±８８．０ｍｓ，与Ｂ组（５４６．０±６８．９，４２９．３±６１．５，３０７．０±５１．３ｍｓ）比较差异有高度显著性，Ｐ均＜０．００１。③心房有效不应期（ＡＥＲＰ），Ａ组与Ｂ组比较无显著差异（２６５．０±４２．３ｍｓｖｓ２６５．０±３７．３ｍｓ，Ｐ＞０．０５）。④随Ｓ１Ｓ１刺激间距缩短，Ａ组的房室传导顺序为：１１→文氏型→２１→交替文氏型→３１或心房Ｐ波脱漏；Ｂ组的房室传导顺序则?     

Feasibility,safety and outcomes of left bundle branch pacing in octogenarians

ObjectivesLeft bundle branch pacing (LBBP) provides physiological pacing at low and stable threshold. The safety and efficacy of LBBP in elderly population is unknown. Our study was designed to assess the safety, efficacy and electrophysiological parameters of LBBP in octogenarian (≥80 years) population.ResultsLBBP was successful in 10 out of 11 patients. Mean age 82.1 ± 2.5 yrs. Follow up duration 7.7 months(range4–10). Indication for pacing included atrioventricular (AV) block 5 patients, Left bundle branch block (LBBB) with low ejection fraction (EF) 4 patients, sinus node dysfunction in 1. QRS duration reduced from 145.9 ± 27.7ms to 107.1 ± 9.5ms (p value0.00001) LV ejection fraction increased from 47.6% to 58.4% after LBBP (p value0.017). Pacing threshold was 0.58 ± 0.22 V and sensed R wave 17.35 ± 6.5 mV and it remained stable during follow up. LBBB with low EF patients also showed similar reduction in QRS duration along with improvement in LVEF.ConclusionLBBP is a safe and effective strategy (91% acute success) of physiological pacing in elderly patients. LBBP also provided effective resynchronization therapy in our small group of elderly patients. The pacing parameters remained stable over a period of 10 months follow up.     

Narrow QRS Tachycardia with Ventriculoatrial Dissociation Mediated by a Left Fasciculoventricular Fiber

A 30-year-old man presented with narrow QRS tachycardia. The intracardiac electrocardiogram showed an atrial-HIS (AH) interval of 75 msec and a HIS-ventricular (HV) interval of 44 msec during baseline. Atrial incremental pacing revealed HV shortening, with apparent incomplete right bundle branch block (RBBB) morphology without QRS complex axis deviation. The induced tachycardia exhibited several QRS morphologies: a narrow QRS, complete RBBB and complete left bundle branch block (LBBB) morphology. Spontaneous conversion of the QRS pattern from wide to narrow was observed. The cycle length of the tachycardia was significantly shortened (from 316 to 272 ms) from LBBB morphology to narrow QRS complex. The atrial activation was dissociated from the ventricular activation during all tachycardias. Each QRS complex during tachycardia was preceded by a HIS deflection and HV interval was 35 ms, which was shorter than that of sinus rhythm. HIS deflection was earlier than right bundle potential during all kinds of tachycardia. This tachycardia is most likely mediated by a left fasciculoventricular fiber which connects the HIS bundle below the atrioventricular node to the myocardial tissue of the left ventricle. The HIS-Purkinje system is used as an antegrade conduction limb and the fasciculoventricular fiber as a retrograde limb in the tachycardia circuit.     

利用组织多普勒评价左束支阻滞患者心室内不同步

利用组织多普勒测量不同步指数评价左束支阻滞 (LBBB)患者心室内不同步 ,对 15例LBBB患者 (LBBB组 )和 15例正常人 (对照组 )左心室各壁基底、中间、心尖段 ,获取组织多普勒速度曲线 ,分别测量QRS波起点到S波起点的时间 (Q Sb) ,计算心室内同步性指数 (TSI)和各室壁壁内的同步性指数 (RSI)。结果 :LBBB组患者各壁Q Sb延长 ,以室间隔、前壁、下后壁显著 ;TSI和左室室间隔的RSI较对照组明显增高 (分别为 30 .86± 9.78msvs 14 .81± 6 .89ms;2 7.13± 16 .82msvs 12 .19± 10 .70ms ,P均 <0 .0 1)。结论 :LBBB时左室激动顺序异常 ,左室各壁各节段出现不同程度的收缩延迟 ,心室内不同步明显 ;同一室壁内的不同步 ,以室间隔最显著。     

Differentiation between left bundle branch block and left ventricular hypertrophy: Implications for cardiac resynchronization therapy

Recent clinical trials have demonstrated that cardiac resynchronization therapy (CRT) reduces heart failure hospitalizations and mortality in patients with complete left bundle branch block (LBBB), but potentially not those with right bundle branch block or nonspecific LV conduction delay, such as that due to LV hypertrophy (LVH). Furthermore, endocardial mapping and simulation studies have suggested that one-third of patients diagnosed with LBBB by conventional electrocardiographic criteria are misdiagnosed, and these patients likely have a combination of LVH, LV chamber dilatation and delayed initiation of LV activation (incomplete LBBB). Increase in LV size due to hypertrophy/dilatation and slowed intramyocardial conduction velocity prolong QRS duration in patients with LVH, which can frequently go above the QRS duration threshold of 120 ms conventionally used to diagnose LBBB. New strict criteria for diagnosing complete LBBB have been proposed that utilize longer QRS duration thresholds (130 ms in women and 140 ms in men) and require the presence of mid-QRS notching/slurring in at least 2 of the leads I, aVL, V1, V2, V5 or V6. The emergence of CRT has led to an increased need to differentiate complete LBBB from LVH and other types of intraventricular conduction delay, which should be further studied.