阵发性心房颤动患者上腔静脉肌袖与心房的电学连接特征

总结 16例阵发性心房颤动患者上腔静脉 (SVC)肌袖的电生理标测和导管射频消融电隔离的结果 ,评价SVC肌袖和心房电连接的类型和特点。在环状标测电极指导下 ,对 16根SVC肌袖进行电位的记录、分析以及开口部的点或段的消融电隔离治疗。根据窦性心律和心房起搏下的肌袖内环形电极标测的袖电位激动顺序 ,即电突破点的数目和位置 ,以及有效放电对袖电位及其电突破点的影响 ,总结和分析袖房之间的电连接类型和特点。结果 :共标测和电隔离SVC肌袖 16根。其中呈单束状电连接 8根 (5 0 % ) ,双束状电连接 7根 (43.7% ) ,多束状电连接 1根 (6 .3% )。 16根SVC平均每根电连接束为 1.6± 0 .6根 ,共消融 2 .1± 0 .6个节段和部位 ,每个部位进行了2 .3± 0 .7次的放电。所有病例均达到完全电隔离的标准。结论 :SVC袖房之间电连接的类型多为单束状和双束状 ,在袖房连接处行点或节段性消融即可达到完全袖房电隔离的结果。     

阵发性心房颤动患者肺静脉与心房电连接特征的临床研究

目的 总结阵发性心房颤动(房颤)患者肺静脉的电生理标测和导管射频消融电隔离的结果，评估中国人肺静脉与心房的电连接类型和特点。方法 顽固性阵发性房颤患者43例，在环状标测电极指导下行肺静脉电位(PVP)记录和分析，并对能标测到PVP的肺静脉进行开口部的点或段的消融电隔离治疗。根据窦性心律和心房起搏下的肺静脉内环形标测电报导管标测到的PVP的激动顺序，以及有效放电对PVP的影响，分析和总结肺静脉与心房之间的电连接特点。结果 共标调和域电隔离肺静脉100根，其中呈单束状电连接35根(35％)，双束状电连接48根(48％)，多束状电连接11根(11％)，环状电连接3根，无电连接3根。结论 根据环状电报标测到的PVP激动顺序和对放电的反应，提示肺静脉与心房之间电连接的类型多为单束状和双束状(83％)，说明对于大多数肺静脉不必进行环状消融，而只需在肺静脉与心房连接处进行点状或节段性消融即可达到完全电隔离的效果。     

普通型心房扑动的新现象

普通型心房扑动 (AFL)的完整折返环路以及界嵴 (CT)和AFL的关系仍不太清楚 ,笔者应用电解剖 (CARTO)标测系统执行两项研究。Ⅰ :对 12例持续AFL的病人实施右房CARTO标测及多部位拖带。于三尖瓣环 (TA)周围测量传导速度。双电位 (DP)位于右房后下壁 ,相当于解剖上的界嵴 ,从下腔静脉 (IVC)与心房肌的连接处向上、稍前延伸 ,其长度为 40 .9± 7.9mm。所有病人的DP间期从上至下逐渐增加。在 9例逆向AFL病人中 ,右心耳后基底部的后方一狭长心肌位于折返环内 ,结果来自右心耳基底前、后方的两个心房激动波融合于右房下游离壁。在另 3例病人中 (1例顺钟向、2例逆钟向 )右心耳基底部后方未发现位于折返环内 ,迫使折返环仅绕三尖瓣与右心耳基底部前方之间的心肌兴奋右房下游离壁。在AFL的折返环中 ,没有固定的缓慢传导区 ,大部分病人的缓慢传导区位于间隔部和侧壁。Ⅱ :对 7例普通型AFL及 6例非AFL病人 ,在冠状窦起搏下 ,标测右房后壁。通过在右房重建中出现DP确认CT。以 6 0 0 ,30 0ms周长以及静脉注射氟卡胺 (1mg/kg)后以 6 0 0ms周长起搏冠状窦 ,分别测量CT上、中、下部位的刺激信号至双电位中第一及第二个心房激动波的传导时间 (SD1及SD2 )和此部位的电位间期 (DPI)。在AFL病例中 ,与以 6 0 0ms周长起搏冠状     

探索不用Halo电极射频消融治疗典型心房扑动的方法

目的探讨不用Halo电极消融典型心房扑动(AF)的方法和右心房峡部传导时间间期的意义。方法对9例AF患者进行了心脏电生理检查和射频消融。将普通标测电极分别放置高位右房(A点)、低位右房(B点)、希氏束(C点)、冠状窦(CS34为D点),标测AF发作时右房激动顺序,起搏时和消融后测量右心房峡部传导时间间期(BD、DB)。结果不用Halo电极成功消融9例AF病例。消融后于冠状窦口处起搏时起搏信号至右房下侧壁的时间间期(DB=140.7ms±66.1ms)和右房下侧壁起搏时起搏信号至冠状窦口CS34的时间间期(BD=123.2ms±42.1ms)均较消融前(DB=66.0ms±12.5ms,BD=62.5ms±13.0ms)明显延长,P<0.01。结论不用Halo电极能成功消融典型AF,该方法简便、费用低;右心房峡部传导时间间期的定量测定可作为判断峡部完全性双向传导阻滞的方法之一。     

探索不用Halo电极射频消融治疗典型心房扑动的方法

目的探讨不用Halo电极消融典型心房扑动(AF)的方法和右心房峡部传导时间间期的意义.方法对9例AF患者进行了心脏电生理检查和射频消融.将普通标测电极分别放置高位右房(A点)、低位右房(B点)、希氏束(C点)、冠状窦(CS34为D点),标测AF发作时右房激动顺序,起搏时和消融后测量右心房峡部传导时间间期(BD、DB). 结果不用Halo电极成功消融9例AF病例.消融后于冠状窦口处起搏时起搏信号至右房下侧壁的时间间期(DB=140.7ms±66.1ms)和右房下侧壁起搏时起搏信号至冠状窦口CS34的时间间期(BD=123.2ms±42.1ms)均较消融前(DB=66.0ms±12.5ms,BD=62.5ms±13.0ms)明显延长,P＜0.01. 结论不用Halo电极能成功消融典型AF,该方法简便、费用低;右心房峡部传导时间间期的定量测定可作为判断峡部完全性双向传导阻滞的方法之一.     

左房快速起搏对肺静脉口及心房肌电重构的影响

目的探讨左房快速起搏对肺静脉口、左右心耳电重构的影响。方法运用快速起搏左心耳的方法建立心房颤动(AF)模型,在起搏前及起搏后的第1,3,5,7d对左、右心耳;左上、左下肺静脉口;右上、右下肺静脉口的有效不应期(ERP)、ERP频率适应性、ERP离散度及心房间的传导时间进行测定。采用S1S2程序刺激,基础起搏周长(PCL)分别为400,300,200ms,S2为200ms,以5ms的步长递减。程序刺激结合Burst刺激对上述心房部位进行AF的诱发,记录AF的发生率。在第8天关闭起搏器,采用上述相同方法对起搏停止后即刻;2,4,6,24h的上述各部位的ERP进行测定。结果起搏1d后各个基础起搏周长下各部位的ERP明显缩短,ERP频率适应性降低,ERP离散度增大(P<0.05),而心房间传导时间无明显变化(P>0.05);起搏终止后各部位的ERP逐渐延长,但起搏终止后6hERP与快速起搏前相比仍有明显缩短(P<0.05);24h后ERP基本恢复到起搏前水平,两者相比无明显差异(p>0.05);随着起搏时间的延长各部位AF的诱发率逐渐增高(P<0.05)。结论快速心房起搏不仅引起心房肌电重构,亦引起肺静脉电重构。     

地尔硫卓对心房有效不应期和单相动作电位重构的干预研究

为研究地尔硫卓对快速心房起搏诱发的心房肌急性电重构的影响 ,将 4 0例无器质性心脏病的室上性心动过速患者射频消融成功后 30min随机分为两组 ,地尔硫卓组 15例 ,对照组 2 5例 ;地尔硫卓组给予药物干预 ,对照组以生理盐水替代 ,应用双极记录及单相动作电位记录法检测基础状态下、药物负荷量后 (即快速心房起搏前 )及4 0 0ms周长心房起搏后右心耳、高位右房、低位右房和His束周围等部位有效不应期 (ERP)和右房单相动作电位复极 90 %的时程 (MAPD90 )。结果 :对照组快速心房起搏后心房各部位ERP和右房MAPD90 较刺激前有明显缩短 ,地尔硫卓组心房快速起搏前后各部位ERP和右房MAPD90 无明显改变。结论 :快速心房起搏可使无器质性心脏病和心房颤动病史的患者心房ERP和MAPD90 明显缩短 ,地尔硫卓可阻止快速心房起搏诱发的心房ERP和MAPD90 的缩短 ,提示细胞内钙超载可能是心房ERP和单相动作电位重构的重要原因之一。     

增龄对健康犬心房、肺静脉电生理特性的影响

目的 :探讨犬肺静脉 （PV）、心房电生理特性随年龄变化特点。方法 :健康杂种犬 15只按年龄分成 3个阶段组 :老、中、幼龄组 ,每组 5只。经锁骨下、股静脉穿刺和房间隔穿刺放置导管 ,采用刺激诱发心房纤颤 （AF） ,标测肺静脉PV、上腔静脉 （SVC）、左、右心房电位 ,测量各自有效不应期 （ERP）、功能不应期 （FRP） ,传导时间。结果 :3组AF诱发率分别为幼龄组 0 %、中龄组 2 0 %、老龄组 10 0 % ;起源于PV的AF占 83.3% ,其它为 16 .7% ;ERP :老龄犬PV的ERP显著短于幼龄组 ,为 132± 38msvs2 34± 5 1ms（P <0 .0 1） ,老龄组的PV的ERP显著短于心房的ERP ,为 132± 38msvs2 0 0± 34ms（P <0 .0 5 ） ;老龄犬组SVC的ERP显著短于幼龄组 （P <0 .0 5 ）。老、中、幼 3组PV起搏部位发生递减性传导百分率分别为 89%、33%、31% ,传导时间延长分别为 92± 5 5ms、2 7± 31ms、2 2± 38ms,老龄组与后两者比较均有非常显著差异 （P <0 .0 1）。结论 :PV电生理特点随年龄变化 ,电重构集中发生在老龄阶段 ,主要表现为不应期显著缩短和递减性传导 ,可能是PV致AF的主要原因。     

典型心房扑动下腔静脉-三尖瓣环峡部电传导特性

目的比较典型心房扑动(房扑)与无房扑患者，下腔静脉-三尖瓣(TV—IVC)峡部的电传导特性。方法 12例同期来本院作射频消融的患者，A组6倒为频繁发作的典型房扑，B组6例为无房扑史的室上性心动过速(室上速)。观寨右房下侧壁(H1-2)和冠状窦口(CS9-10)以周期为600，500，400，300ms起搏时以及房扑和室上速时，TV—IVC峡部传导时间变化。基本刺激周期500ms时，分别测定峡部内、外侧局部心房不应期。结果 ①H1-2起搏时，A组蛱部传导时间较B组平均延长20.3%±11.6%(3.9％～28．9%，但P＞0．05)。CS9-10起搏时，A组峡部传导时间较B组传导时间平均延长27.1％±10.5%（12．5％～35.8％．但P>0．05)。②房扑时峡部传导时间133±6．6ms。室上速峡部传导时间61．1±12．7ms．两组(P<0．05)。③A、B组峡部局部心房有效不应期(ERP)差异无显著性。结论下腔静脉-三尖瓣峡部是折返环的一部分。但窦性心律时蛱部无显著传导延迟。房扑功能慢传导区不一定局限于该部位。     

环孢素A对持续心房起搏犬心房电生理特性的影响

目的观察钙调神经磷酸酶抑制剂环孢素A(CsA)对慢性心房起搏犬电生理特性的影响。方法健康杂种犬18只,随机分为假手术组(Sham组,只手术不起搏)、快速起搏组(ATP组,植入固律型单腔起搏器,400次/分持续起搏8周)、CsA组(快速起搏基础上喂食环孢素A10mg.kg-1.d-18周),每组6只。实验前后进行电生理检测。记录并比较各组右房有效不应期(ERP)、传导速度(CV)、折返波长(WL)、心房颤动(简称房颤)负荷、频率自适应性等反映心房电生理特性的指标。结果快速起搏8周后ATP、CsA两组右房ERP值均较各组术前及假手术组明显缩短(P<0.05),但缩短程度CsA组显著小于ATP组(BCL300ms时,P<0.05)。两组频率自适应性,CV、房颤诱发率和持续时间无差异。结论环孢素A能够一定程度上抑制快速起搏导致的心房ERP的缩短,但并不因此改变房颤的诱发与维持。     

腔静脉作为研究大静脉电隔离作用模型的实验研究

研究腔静脉的电生理特性和组织学特点看其是否可作为研究肺静脉电隔离作用的简便易行的模型。选择1 0只杂种犬为研究对象 ,记录犬腔静脉的电活动 ,在距腔静脉 心房交界处 2cm和 1cm的部位行电生理检查 ;检查后分别取腔静脉 心房交界处、距交界处 2cm和 1cm的组织行组织学检查。结果 :①犬上腔静脉内均可记录到A波 ,在距上腔静脉 心房交界处 2cm部位起搏能夺获心房 ;只有 2 0 %的下腔静脉在距下腔静脉 心房交界处 1cm可记录到A波 ,起搏能夺获心房。②组织学检查显示腔静脉近心端的中膜层主要由心肌纤维所构成 ,形成环行结构 ,心肌纤维在上腔静脉的延伸约 2～ 3cm ,在下腔静脉则为 1cm左右 ,然后逐渐减少消失。结论 :腔静脉内能记录到A波 ,起搏能夺获心房 ,组织学结构类似肺静脉的心肌袖结构。所以 ,腔静脉可作为研究肺静脉电隔离作用的模型 ,尤其是上腔静脉     

Electrical connection between the right atrium and the superior vena cava,and the extent of myocardial sleeve in a patient with atrial fibrillation originating from the superior vena cava

We describe a case in which the superior vena cava (SVC) was electrically isolated by an application of radiofrequency energy to a point with electrical connection between the right atrium and the SVC in a patient with atrial fibrillation (AF) originating from the SVC. The connection was located in the posteroseptal region between the right atrium and the myocardial sleeve extending into the SVC. Local AF occurred after radiofrequency ablation and rapid activities were recorded all around the SVC, whereas the atrium was still in sinus rhythm. It is suggested that focal AF in the SVC contributes not only to the initiation but also to the maintenance of AF, and the myocardial sleeve extends into the SVC through a connection point to cover the entire internal lumen.     

心房颤动上腔静脉节段性电隔离方法及安全性评估

目的:分析心房颤动(房颤)上腔静脉节段性电隔离的具体手术方法,并评估其安全性.方法:入选2017年11月至2018年9月期间我院阵发性房颤患者50例,患者常规进行肺静脉隔离后,继续行上腔静脉隔离.消融前进行上腔静脉造影,显示上腔静脉与右心房解剖关系,并在CARTO系统运用PentaRay电极导管进行上腔静脉及右心房三维...     

Treatment of tachycardic atrial fibrillation by catheter-assisted electrical stimulation of the cardiac parasympathetic nervous system

Treatment of tachycardic atrial fibrillation (AF) is difficult in patients with congestive heart failure because many drugs which exert negative dromotropic effects (beta-blockers, calcium channel antagonists) may depress ventricular contractility and/or decrease arterial blood pressure. We have identified 2 intravascular sites in the superior (SVC) and inferior vena cava (IVC) where parasympathetic nerves, which innervate the atrioventricular node, can be stimulated electrically. In 8 dogs, a 7-F catheter with an expandable electrode basket at its tip was non-fluoroscopically positioned in the SVC and in the proximal IVC (time for positioning: 3-5 minutes). High-frequency electrical parasympathetic stimulation (PS) with 20 Hz at an impulse duration of 0.1 ms was performed during pacing induced AF. RESULTS: With increasing stimulus strength, a graded ventricular rate slowing was observed during PS in the SVC and IVC (P < 0.01, ANOVA). The negative dromotropic effect started instantaneously after onset of PS and ceased immediately after termination of PS. During ventricular pacing at a constant rate, no decrease of the arterial blood pressure was observed during PS. PS in the IVC yielded significantly lower stimulation thresholds than in the SVC. CONCLUSIONS: Transvenous parasympathetic stimulation for ventricular rate control during AF can easily be achieved in the SVC and IVC in dogs. This procedure may provide a foundation for investigating the usefulness of PS in humans. If the results translate to patients, PS may be very beneficial in the treatment of AF in patients with congestive heart failure.     

Effects of verapamil on superior vena cava electrical remodeling induced by short-term pacing from right atrium and superior vena cava in human

BackgroundAlthough the superior vena cava (SVC) may be involved in the triggering or maintenance of atrial fibrillation (AF), the electrophysiological properties of SVC in human are ill-defined.MethodsThe baseline effective refractory periods (ERPs) of high right atrium (HRA), SVC and the conduction time (CT) between HRA and SVC were measured at pacing cycle lengths (PCL) of 600 and 400 ms respectively in 20 patients (12 females, age 46 ± 13 years) with paroxysmal supraventricular tachycardia. Immediately after acute electrical remodeling (ER) induced by constant HRA or SVC pacing at PCL of 400 ms for 5 min, ERPs of HRA, SVC and the CT between HRA and SVC were determined. After verapamil was administered, the same protocols for determining ERPs of HRA, SVC and the CT between HRA and SVC were repeated.ResultsThe baseline ERP of SVC was significantly longer than that of HRA. The CT from SVC to HRA was significantly longer than that from HRA to SVC. After acute ER, both the ERPs of HRA and SVC were significantly shortened. However, no significant changes of the CT between HRA and SVC could be demonstrated. After verapamil infusion, significant shortening of the ERP of HRA and SVC still occurred following acute ER and the ERP of SVC was still longer than that of HRA.ConclusionsIn human, ER can occur both in HRA and SVC after a short and moderately rapid heart rate pacing either from HRA or SVC. Verapamil cannot prevent such ER from occurring.     

丹参酮ⅡA磺酸钠对家兔快速心房起搏时心房动作电位及有效不应期的影响

研究丹参酮ⅡA磺酸钠(TSN)对家兔短期快速心房起搏时在体心房单相动作电位(AMAP)及心房有效不应期(AERP)的影响,探讨其防治心房颤动的可能机制。家兔24只,随机分为对照组与TSN组各12只。将电极经颈内静脉置入右房记录AMAP,观察基础状态下、给药后0.5h及以600次/分心房快速起搏后0.5,8hAMAP及其频率适应性的变化。结果:与起搏前相比对照组在S1S1200ms刺激时测量的AERP(AERP200)在起搏后0.5h缩短21.2ms,起搏后8h缩短21.6ms(P<0.05),且心房肌的频率适应性丧失。TSN在基础状态下对AMAPA、AMAPD无明显影响,但使AERP200由105.9±3.8ms延长至114.7±7.2ms(P<0.05)。起搏后TSN组维持原有的心房肌频率适应性。结论:快速心房起搏使心房肌的频率适应性丧失而致电重构,TSN能减轻短期快速心房起搏所致电重构。     

Prevalence of typical atrial flutter with reentry circuit posterior to the superior vena cava: use of entrainment at the atrial roof.

AIMS: Upper turn-around of the reentry circuit in typical atrial flutter (AF) is classically described to be located in front of the superior vena cava (SVC), but circuits posterior to the SVC as well as lower loop reentry (LLR) involving only the lower part of the right atrium have been described. However, true prevalence of such AF circuits remains unknown. METHODS AND RESULTS: Fifty consecutive patients (46 men, 68 +/- 9 years old) undergoing radiofrequency (RF) ablation of typical counter-clockwise AF were prospectively investigated. Prior to RF deliverance, AF was entrained by pacing 10 ms shorter than the AF cycle length (AFCL). Post-pacing interval (PPI) at the cavotricuspid isthmus (CTI) and at the atrial roof (AR)-between SVC and the high tricuspid annulus-were determined. AR was considered to be part of the AF circuit when local PPI-AFCL was < or =20 or 30 ms or, in case of long PPI at the CTI isthmus, if difference between AR-PPI and CT-PPI was < or =10 ms. In 47 patients, CTI-PPI-AFCL was < or =30 ms (94%). Among them, AR-PPI-AFCL was >30 ms in 12 cases (25%). In the remaining three patients, AR-PPI-AFCL did not exceed CTI-PPI-AFCL by more than 10 ms. In 42 patients, CTI-PPI-AFCL was < or =20 ms (84%). Among them, AR-PPI-AFCL was >20 ms in 16 cases (39%). In the remaining eight patients, AR-PPI-AFCL was more than 10 ms longer than CTI-PPI-AFCL in only one instance. Taken together, AR PPI was >20 or >30 ms longer than AFCL or >10 ms longer than CTI PPI when prolonged in 17 (34%) and 12 patients (24%), respectively. CONCLUSION: In around a quarter to one-third of patients referred for RF ablation of typical AF, the atrial roof is not part of the circuit, thus they may present a 'posterior' variant of the typical counter-clockwise AF reentry circuit.     

快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

Inhomogeneity in the appearance of electrical remodeling during chronic rapid atrial pacing: evaluation of the dispersion of atrial effective refractoriness

In the present study, the long-term process of progression of electrical remodeling at various atrial sites, which is not well understood, was compared while monitoring continuously the electrophysiologic parameters at multirecording sites in canine atria during continuous atrial burst pacing. A rapid pacing device was implanted in 5 dogs, and continuous atrial burst pacing (400 beats/min) was delivered at the right atrial appendage (RAA). Four pairs of epicardial wire electrodes were sutured on (1) the RAA, (2) Bachmann's bundle (BB), (3) the right atrium close to the inferior vena cava (IVC), and (4) the left atrium (LA). The distal ends of those wires were exteriorized posteriorly and used for pacing and recording. The atrial effective refractory period (AERP), AERP dispersion (AERPd), atrial conduction time (CT) and inducibility of atrial fibrillation (AF) were evaluated during burst pacing for 14 days and during the subsequent 7 days' recovery. The AERP at the LA pacing site was shorter than that at the other sites on day 0. The AERP shortening was greater in the RAA and LA sites than in the BB and IVC sites. The AERPd increased during pacing and reached the maximum level on day 3, and then decreased during the recovery phase. Prolongation of CT tended to be longer between the RAAand IVC sites than that between the other sites. The incidence of AF induction became higher in accordance with the time course of the rapid pacing phase. There was another peak of AF induction on days 7-10. In a canine chronic rapid atrial stimulation model, the progression of electrical remodeling (ie, the shortening of the AERP and the prolongation of the CT) was not homogeneous in both atria, the AERPd showed a temporal increase between days 3 and 7 and matched the increase in AF inducibility at the LA pacing site, the increase in the AERPd was mainly caused by more rapid AERP shortening at the RAA or LA sites, and the LA site always showed a shorter AERP than the other atrial sites in the control state and during the rapid pacing phase, whereas AF inducibility was higher at the LA site than the other sites.