双室同步起搏的临床应用及置入左室电极的初步体会

观察双室同步起搏治疗充血性心力衰竭 (CHF)的疗效 ,探讨左室电极置入的方法及注意事项。 10例患者均为原发性扩张型心肌病 (DCM)并CHF ,符合双室同步起搏治疗的指征。其中 8例置入Medtronic 2 187电极 ,1例置入Medtronic 2 188电极 ,1例置入右室主动固定电极。 9例左室电极置入成功 ,1例失败改行右室双部位起搏 ,术后患者左室舒张未径、左室射血分数及 6min步行距离均有改善 (术后 3个月与术前分别比较 :70 .8± 9.5vs 79.5± 12 .5mm ,0 .4 2± 0 .13vs 0 .2 5± 0 .10 ,384 .8± 4 5 .4vs 2 78.6± 34.5m ;P <0 .0 5或 0 .0 1)。借助电生理冠状静脉窦 (CS)标测电极、CS造影 (包括直接逆行CS造影和冠状动脉造影使CS间接显像 )对指导左室电极的置入有较大的价值。结论 :双室同步起搏治疗CHF疗效肯定 ,借助CS标测电极及CS造影可提高左室电极置入的成功率     

双室右房三心腔起搏在充血性心力衰竭治疗中的初步应用

目的　观察InSync80 4 0起搏器治疗扩张型心肌病 (DCM )伴充血性心力衰竭 (CHF)的疗效。方法　患者 ,男 7例 ,女 1例 ,年龄 4 8～ 75 (5 8 7± 10 2 )岁 ,均为扩张性心肌病伴充血性心衰 ,且有完全性左束支传导阻滞或左前分支传导阻滞 ,植入InSync80 4 0起搏器。左心室起搏通过冠状静脉窦植入Medtronic公司生产的 2 187电极 ,置于冠状静脉窦的分支静脉起搏左心室 ,左右心室电极和右房电极导线与InSync 80 4 0起搏器相连接。 结果　以InSync80 4 0起搏器起搏并辅以合适的房室间期 (AVD) ,患者心力衰竭的症状明显改善 ,NYHA心功能分级从Ⅲ -Ⅳ级提高到Ⅰ -Ⅱ级 ,超声心动图示心功能指标改善 ,核素检查示心室收缩较术前协调 ,起搏后心电图QRS时限缩短。结论　初步临床应用表明 ,以InSync80起搏器实行双心室同步起搏治疗充血性心力衰竭行之有效     

普通电极导线行右房左室或双心室起搏的初步临床观察

探讨普通电极导线置入心脏静脉起搏左室的可行性。选择 9例患者为研究对象 ,其中扩张型心肌病 3例、缺血性心脏病 3例、其他 3例 ,均伴不同程度的心力衰竭 ,心功能Ⅱ～Ⅳ级。所有患者都安置DDD起搏器。窦性心律伴房室阻滞 (AVB)或完全性左束支阻滞 (CLBBB)患者 ,行右房左室顺序起搏 ;房颤患者行双心室起搏。左心室起搏是将普通右心室导线 (MedtronicCapSureSP 4 0 2 3)通过冠状窦送入心脏静脉施行的。结果 :7例成功 ,2例失败。导线定位在左室后静脉 1例、后侧静脉 3例、侧静脉 3例。术中测左室起搏阈电压、阻抗和R波振幅分别是 0 .7± 0 .2V、6 2 3± 6 6Ω、10 .1± 6 .0mV。术后 2～ 18个月阈电压、阻抗分别是 0 .5± 0V、5 2 1± 5 1Ω。术后 1～ 2周平均心功能从2 .9级改善到 1.9级 ,平均心胸比值从 0 .6 1缩小到 0 .5 7,平均左室射血分数从 0 .39升至 0 .4 4。随访期未发现左室导线脱位 ,膈肌起搏等并发症。结论 :普通电极导线置入心脏静脉长期起搏左心室是可行的、牢靠的。     

右房左室起搏治疗慢性心力衰竭伴室内传导阻滞患者的初步临床观察

观察右房 左室起搏治疗慢性心力衰竭 (简称心衰 )的临床效果。选择 1 6例充血性心衰患者 (NYHA分级Ⅲ Ⅳ级 ) ,男 1 0例、女 6例 ,年龄 6 8.4± 6岁 ;均为窦性心律 ,合并有Ⅰ度房室阻滞 ,完全性左束支阻滞。按安置起搏器的模式分为右房 左室起搏治疗组 (LV组 ,n =6 ) ,右房双室起搏治疗组 (BiV组 ,n =1 0 )。左室起搏电极分别放置于心大静脉左室侧后分支 9例 ,心大静脉左室后分支 7例。观察起搏治疗前后左室心功能参数、6min步行距离、左室壁运动的同步性及体表心电图的变化。结果 :BiV组左室射血分数 (LVEF)由术前的 0 .2 3提高至 0 .31 (P <0 .0 0 1 ) ;在LV组LVEF由术前的 0 .2 4提高至 0 .33(P <0 .0 0 1 ) ;左室舒张末期容积指数在二组分别由术前的 1 4 9± 5 1ml/m2 和 1 5 3±5 3ml/m2 下降至 1 1 6± 38ml/m2 和 1 2 1± 4 1ml/m2 (P均 <0 .0 0 1 ) ;室间隔与左室后壁运动的延迟时间在二组分别由术前的 1 95± 94ms和 1 97± 89ms下降至 1 7± 6 0ms及 1 6± 5 6ms(P均 <0 .0 0 1 )。 6min步行距离则分别由术前的4 0 3± 5 3m和 4 0 1± 5 9m提高至 4 4 1± 6 2m和 4 4 2± 6 7m(P均 <0 .0 5 )。结论 :初步临床观察提示右房 左室起搏治疗与右房双室起搏治疗相比 ,同样可有效地改善慢性心衰?     

右心腔不同部位起搏的慢性血流动力学对比研究

比较右心耳 (RAA)、右室流出道 (RVOT)与右室心尖部 (RVA)起搏的慢性血流动力学效果 ,评价RVOT起搏的可行性。2 9例患者 ,9例RAA起搏、8例RVOT起搏、12例RVA起搏 ,分别在术前及术后 6 .11± 4 .0 1、5 .38± 2 .92、5 .5 0± 2 .88个月 ,用多普勒超声心动图观察右心腔不同部位起搏的慢性血流动力学参数 ,包括左室射血分数(LVEF)、左室内径缩短分数 (SF)、肺动脉瓣口峰值血流速度 (PV)、二尖瓣口E峰血流速度 (E)、A峰血流速度 (A)及比值 (E/A)。结果 :RAA起搏时 ,LVEF、SF分别下降为 4 .5 6 %± 3.71% ,3.33%± 2 .83% ,P <0 .0 5。RVOT起搏时 ,LVEF、SF、E/A分别下降为 6 .38%± 4 .6 9% ,4 .13%± 2 .75 % ,1.2 9± 0 .5 1,P <0 .0 1。RVA起搏时 ,LVEF、SF、PV、E、E/A分别下降为 1.4 2 %± 5 .32 % ,7.92 %± 3.96 % ,8.5 8± 11.33cm/s,8.17± 9.6 3cm/s,0 .2 7± 0 .2 9,P <0 .0 1或0 .0 5。A则上升为 7.91± 11.2 6cm/s(P <0 .0 5 )。RVOT起搏与RVA起搏相比LVEF、SF明显改善 (P均 <0 .0 5 ) ,且临床症状明显减轻 ;与右房起搏相比 ,E/A下降 (P <0 .0 5 ) ,其他指标在随访期内未显示出统计学意义上的差别。结论 :对于心功能较好的患者 ,右心腔不同部位起搏对慢性血流动力学均有一定程度的负面影响 ;R     

双心室起搏埋藏式心脏转复除颤器的安置

评价一次性置入双心室起搏埋藏式心律转复除颤器 (双腔ICD)的安全性和有效性。5例冠心病冠状动脉搭桥术后的患者 ,伴有严重的慢性充血性心力衰竭和恶性室性心律失常 ,置入双腔ICD。结果 :5例左室电极导管和双腔ICD均一次成功置入 ,左室电极放入冠状静脉的侧后枝 ,急性起搏阈值 0 .8± 0 .6V ,电阻 72 2± 12 8Ω ,R波振幅18.6± 5 .3mV ,电流 1.6± 0 .5mA ,而双心室起搏时其起搏电极参数均优于左室电极 ,除颤阈值≤ 14J。结论 :对伴严重慢性充血性心力衰竭和恶性室性心律失常的患者 ,置入双腔ICD是安全、易行的。     

植入性心脏起搏器更换时心室电极直接参数的变化

分析了本院 90年代以来更换起搏脉冲发生器时心室电极参数的直接测量结果。在 2 6例病人中 ,男 15例、女 11例 ,年龄 6 3 .9± 13.6 ( 19～ 90 )岁。Ⅲ度房室阻滞 14例、病窦综合征 12例。在更换手术中 ,应用起搏分析仪直接测量原心室起搏电极参数。结果 :至测量时原心室起搏电极在体内埋置时间为 114.2± 2 7.4( 5 8～ 179)个月。首次埋置时的起搏阈值为 0 .5 9± 0 .2 7V ,更换脉冲发生器时为 1.6 0± 0 .75V(P <0 .0 0 0 1) ,起搏阈值增加的幅度为198.1%± 141.1% ( 2 0 %～ 5 6 7% ) ,增加的绝对值为 1.0± 0 .7( 0 .1～ 3 .0 )V。更换脉冲发生器时 ,起搏电极阻抗 5 5 8.5± 136 .3Ω。更换起搏脉冲发生器后 ,继续使用原心室起搏电极 2 2例。术后随访 48.7± 30 .6 ( 6～ 96 )个月。 2例于更换术后 12 ,2 4个月 (即原心室起搏电极在体内埋置时间分别为 98,12 0个月 )分别出现起搏器感知功能不良。重新手术时发现 ,原心室电极起搏阈值或阻抗增高。其余病人起搏与感知功能均良好。结论 :植入性心室起搏电极使用约 10年后 ,大部分电极的直接测量参数仍在良好范围 ,可以考虑继续使用 ,但必须注意随访 ,定期复查     

右室双部位起搏治疗心力衰竭的临床观察

评价 15例患者经右室双部位起搏治疗慢性心力衰竭 (简称心衰 )的疗效。其中原发性扩张型心肌病心衰 13例、缺血性心肌病心衰 2例 ;心功能Ⅲ级 9例、Ⅳ级 6例。结果 :15例患者安置时右室心尖部起搏阈值 0 .5± 0 .3(0 .3～ 1.0 )V、R波振幅 15± 5 .98(6～ 2 4.6 )mV ,阻抗 6 13± 172 (32 0～ 90 0 )Ω。右室流出道起搏阈值 0 .7± 0 .2 6 (0 .3～1.3)V、R波振幅 13± 5 .5 5 (6 .5～ 2 3.6 )mV、阻抗 5 6 3± 194(30 0～ 90 0 )Ω ;双部位起搏阈值 1.45± 0 .45 (0 .9～ 1.7)V。双部位起搏心电图QRS波群时限比右室心尖部及右室流出道单部位起搏缩短了 40～ 90ms。超声心动图检查提示双部位起搏后二尖瓣返流面积平均减少 5 .6cm2 ,射血分数值提高 5 .2 %。经 6 .0± 1.5个月的随访 ,15例中除 2例因突发恶性室性心律失常猝死外 ,其余患者的心功能分别从Ⅲ、Ⅳ级改善到Ⅱ和Ⅲ级。右室双部位慢性起搏阈值1.85± 0 .5 6 (1.5～ 2 .5 )V。随访期间QRS波群时限平均下降 5 0ms。结论 :右室双部位起搏能有效的治疗心肌病患者的心衰。     

房室间期自动搜索功能起搏器对病窦综合征患者预后的影响

目的观察自动AV间期搜索功能双腔起搏器减少心室起搏的有效性及对心功能和快速房性心律失常的影响。方法 100例植入DDD/R起搏器的患者(有AV搜索功能50例,无AV搜索功能50例),术后1年内程控获取右室起搏百分比、高频心房事件、检查超声心动图及测试血浆心房利钠肽(ANP)值。结果有AV搜索功能组术后3,6,12个月右室起搏百分比明显小于无AV搜索功能组(18.7%±5.6%vs 82.4%±10.2%,19.8%±6.6%vs 77.3%±9.5%,18.4%±7.3%vs 79.2%±8.6%,P均<0.05)。有AV搜索功能组左室舒张末内径、左房内径、左室射血分数均明显改善(P均<0.05);ANP水平明显降低(203.10±28.20 pg/ml vs 298.80±31.50 pg/ml,P<0.05);高频心房事件也显著减少(18±9次vs 39±11次,P<0.05)。结论有AV搜索功能起搏器明显减少病窦综合征患者右室起搏比例,改善心功能,并减少高频心房事件。     

超声检查对肥厚型梗阻性心肌病起搏治疗血液动力学变化的探讨

用超声技术探讨起搏器对肥厚型梗阻性心肌病 (HCM)的作用机理。观察 4例HCM(左心导管和造影检查确诊 )患者的如下指标 :①起搏器置入前、后左室梗阻部位形态及运动变化情况 ;②不同起搏间期对左室心肌各部位收缩期运动顺序的影响 ;③观察自主心律与起搏心律对心功能的影响。结果 :①起搏后左室流出道动力性梗阻减轻 (76 .3± 5 2 .8vs 16 1.5± 47.4mmHg ,P <0 .0 5 )。但起搏后 ,肥厚的心肌收缩期梗阻左室流出道现象依然存在。②双腔起搏时 ,左室心肌激动顺序未见变化 ,但传导时限延长 (6 2 .5± 7.4vs 45 .5± 7.7ms,P <0 .0 5 )。③起搏后左室收缩、舒张诸项指标下降。结论 :起搏干扰心肌传导、激动和收缩的正常过程 ,使得其同步性劣于窦性心律时 ,由此可导致左室收缩压力以及狭窄处压力梯度的下降     

Dilated cardiomyopathy following right ventricular pacing for AV block in young patients: resolution after upgrading to biventricular pacing systems

Introduction: Cardiac resynchronization therapy (CRT) has been demonstrated to result in clinical improvement in older adult patients with dilated cardiomyopathy (DCM), specifically those with left bundle branch block and prolonged QRS duration. We sought to demonstrate the benefits of CRT on improvement in cardiac function and clinical outcome in young patients that developed congestive heart failure (CHF) and DCM following cardiac pacing for AV block.
Methods and Results: We reviewed the charts of six patients who developed CHF or low cardiac output symptoms and DCM following implantation of right ventricular (RV)-based pacing systems for AV block, and subsequently underwent CRT. Patients ranged in age from 6 months to 23.7 years (mean: 11.3 ± 3.6 years). AV block was congenital (3), post-surgery (2), and acquired (1). Pacing had been performed for 0.1–14.5 (7.6 ± 2.4) years prior to development of DCM. Two patients required listing for cardiac transplantation. Following CRT: (1) QRS duration shortened from 204 ± 15 to 138 ± 10 msec, P = 0.002, (2) left ventricular ejection fraction improved from 34 ± 6 to 60 ± 2%, P = 0.003, and (3) left ventricular end diastolic dimension shortened from 5.5 ± 0.8 to 4.3 ± 0.5 cm, P =0.03. All patients demonstrated clinical improvement and have been weaned from CHF medications and listing for cardiac transplantation.
Conclusions: CRT can benefit young patients that develop CHF and DCM following RV pacing for AV block. Upgrading to biventricular pacing systems should be considered early in the management of these patients prior to listing for cardiac transplantation.     

心室再同步化起搏的心电图表现及随访

目的探讨不同心室起搏部位体表十二导联心电图的变化及在双心室再同步起搏(CRT)随访中的应用。方法22例资料完整的充血性心力衰竭患者进行双心室再同步起搏治疗,其中21例经静脉置入左室导线,1例因冠状静脉窦畸形经胸左室外膜导线置入;右室导线均放置在心尖部。22例分别记录无起搏、右室起搏、左室起搏及双心室同步起搏四种不同状态下的十二导联心电图。结果22例术前心电图显示完全性左束支传导阻滞(CLBBB)16例,完全性心室内传导阻滞6例,行右室心尖部起搏时胸前导联(V1)均呈CLBBB型,肢体导联额面电轴左偏,Ⅰ导联呈r、R型占100%,左室起搏时胸前导联(V1)均呈右束支传导阻滞(CRBBB)型,额面电轴右偏,Ⅰ导联呈q、Q、QS型20例,占91%;双心室同步起搏后胸前导联(V1)呈CLBBB型13例,呈CRBBB型9例,额面电轴均右偏,Ⅰ导联呈q、Q、QS型占86.5%。结论不同部位心室起搏具有不同的心电图表现,双心室同步起搏具有特征性的心电图形态,CRT随访时通过对心电图形态和时限的观察有助于判断是否实现真正有效的双心室再同步起搏。     

双心室起搏的临床疗效观察

目的　探讨缺血性或扩张型心肌病合并充血性心力衰竭行永久性双心室起搏治疗的临床效果。方法　对 1 0例缺血性或扩张型心肌病合并难治性心力衰竭和左束支阻滞患者 ,常规植入右心室起搏导线的同时植入冠状静脉窦电极导线于左室侧静脉、心大或心中静脉 ,行双心室同步起搏 (其中 2例为四腔起搏 )。通过临床观察、超声心动图测定及 6分钟平地行走评定对心功能的影响。结果　在充血性心力衰竭合并左束支阻滞患者植入冠状静脉窦电极导线行双心室起搏 ,产生较窄 QRS波 ,临床心功能从 ～ 级提高至 ～ 级 ( NYHA) ,同时使二尖瓣返流减少 ,射血分数提高 ,左室舒张末期内径缩小 ,6分钟平地行走距离比术前明显提高。结论　双心室起搏对难治性心力衰竭可能有辅助治疗作用。     

Cardiac resynchronisation therapy versus dual site right ventricular pacing in a patient with permanent pacemaker and congestive heart failure.

A 46-year-old male patient who had long-term right ventricular (RV) pacing for symptomatic complete heart block, initially by an epicardial, later with an endocardial pacing lead at the RV apex, developed congestive heart failure (CHF) and chronic atrial fibrillation 7 years following the pacemaker implantation and was medically treated. During follow-up, his pacemaker was upgraded to a cardiac resynchronisation therapy (CRT) device, because of uncontrolled CHF symptoms, New York Heart Association (NYHA) functional class IV, while on drugs. The patient's symptomatic status improved to NYHA functional class II with CRT. After 17 months of CRT, the battery became depleted, because of the high capture threshold of the left ventricular lead. The patient was then given dual site RV pacing (RV outflow tract+RV apex) in place of CRT, which showed similar efficacy at 12 weeks follow-up.     

Assessment of heart failure and left ventricular systolic dysfunction after cardiac pacing in patients with preserved left ventricular systolic function

BACKGROUND: There is an accumulating data suggesting the deleterious effects of right ventricular pacing on left ventricular performance. Such pacing mimics left bundle branch block resulting in a prolonged QRS duration and causes ventricular asynchrony. AIMS: The purpose of this study is to assess heart failure and left ventricular systolic function after cardiac pacemaker implantation in patients with atrioventricular block and preserved systolic left ventricular function. Secondly, we sought to search for predictive factors of developing left ventricular dysfunction after pacing. METHODS: In this prospective study, we included patients who had been implanted for at least six months. They underwent medical history and examination, 12 leads electrocardiogram and echocardiography before pacemaker implantation and when attending to routine pacemaker follow up. RESULTS: Forty-three patients (22 men and 21 women, age 71+/-12 years) were included in this study. Twenty-nine patients had DDD pacing and 14 VVI pacing. The ventricular lead was implanted in the apex in all patients. After a median follow up of 18+/-11 months, 11 patients (25%) developed signs of congestive heart failure. NYHA was higher after implantation (1.64+/-0.7 versus 2.27+/-0.8, p>0.00001). Left ventricular ejection fraction decreased significantly during follow up (60+/-6% versus 51+/-13%, p=0.0002). Eleven (25%) patients developed left ventricular dysfunction. We compared patients who had left ventricular ejection fraction (LV EF) less or equal to 40% (group A) and patients having LV EF greater than 40% (group B) after implantation. Patients in group A had a paced QRS width significantly larger than group B (181+/-32 ms versus 151+/-26 ms, p=0.002), a significantly prolonged intra left ventricular electromechanical delay (115+/-59 ms versus 45+/-35 ms, p<0.0001) and interventricular delay (44+/-29 ms versus 27+/-18 ms, p=0.02). Age, sex, diabetes hypertension, pacing mode and percentage of ventricular pacing were similar in both groups. A paced QRS width of 180 ms had the best sensitivity and specificity for detecting left ventricular dysfunction: sensitivity=54% and specificity=93%, p=0.01, area under the curve=0.75. CONCLUSION: Patients with atrioventricular block and preserved left ventricular systolic function at baseline decrease significantly left ventricular ejection fraction after pacing. Induced ventricular asynchronism plays a major role in the deterioration of left ventricular function. Prolonged paced QRS width is a good predictor of left ventricular dysfunction after pacing. Larger prospective studies are needed to confirm these data.     

An electrocardiographic algorithm for determining the location of pacemaker electrode in patients with right bundle branch block configuration during permanent ventricular pacing

The expected morphology of right ventricular pacing is a left bundle branch block (LBBB) pattern. However, right bundle branch block (RBBB) can also be seen during permanent right ventricular pacing. The aim of this study was to develop an electrocardiographic algorithm to differentiate this benign condition from septal and free wall perforation with subsequent left ventricular pacing. Three hundred consecutive patients who had permanent ventricular or dual-chamber pacemaker implantation between 1999 and 2000 were screened and 25 patients (8.3%) who exhibited RBBB configuration were included in the study. Echocardiograms and chest radiographs were evaluated in order to identify the pacing lead location in this group. The authors formed a study group with their own 25 patients and 22 cases of RBBB with permanent pacemaker from previous publications (total 47 patients). Frontal axis, QRS morphology in lead V(1), and the precordial transition point, which is defined as the precordial lead where R wave amplitude is equal to S wave amplitude, were examined. Placement of precordial leads V(1) and V(2) 1 interspace lower than the standard location (Klein maneuver) eliminated the RBBB pattern in 12 patients. RBBB pattern with "true right ventricular pacing" was detected in 24 of the 25 patients, and in 11 of the 22 patients reported in the literature (total 35 patients). Right ventricular pacing was correctly identified in 34 of 35 patients with use of criteria including left superior axis deviation, RS or qR morphology in lead V(1), and precordial transition at lead V(3) with a high sensitivity and specificity. A simple surface electrocardiogram can accurately predict the lead location in patients having RBBB morphology with right ventricular pacing.     

Electrocardiographic Follow‐Up of Biventricular Pacemakers

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His‐Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow‐up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first‐degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.     

Safe right bundle branch block pattern during permanent right ventricular pacing

It is known that an electrocardiogram (ECG) after transvenous right ventricular (RV) pacing should yield left bundle branch block (LBBB) QRS patterns. When right bundle branch block (RBBB) pacing morphology appears in a patient with a permanent or temporary transvenous RV pacemaker, myocardial perforation or malposition of the pacing lead must be ruled out, even though the patient may be asymptomatic. We report a case of a 77-year-old man who underwent permanent transvenous VDD pacemaker implantation for symptomatic heart block. The postoperative ECG revealed a RBBB pacing configuration, but his chest X-ray and echocardiographic studies confirmed uncomplicated RV pacing. We review and discuss the literature concerning the differential diagnosis of such a safe RBBB ECG pattern.