房室结慢径消融对心房电生理性质的影响

Objective The ablation of the atrioventricular node slow pathway may reduce the inducibility of atrial fibrillation (AF) ,but the mechanisms remain unknown. We tried to investigate the impact of ablation on atria refractory period, and to elucidate the underlying mechanism. Methods Thirty-two patients with atrioventricular node reentrant tachycardia (AVNRT) were enrolled in the study. Atria effective refractory period (ERP) and vulnerable window (VW) at high right atrium (HRA),inferior right atrium (IRA),distal (CSd) and proximal CS (CSp) ,as well as sinus rate (SR) and effective refractory period of fast pathway (FERP) were measured before and after ablation. Results ( 1 ) After ablation, the ERP at HRA did not change:(214. 4 ± 35. 1 ) ms, (213.4 ± 37. 3) ms, P = 0. 6, on the other hand, the ERPs at following sites were significantly prolonged:CSp(218. 1 ±21.8)ms, (235.3 ± 23.6) ms,P ＜0. 0001 ;CSd(230. 9 ±21.0) ms, (244. 7 ±25. 1)ms,P＜0. 01;IRA(198.8 ±26.7)ms,(219.7 ±28. 7) ms,P ＜ 0.005,respectively. (2) The VW of HRA remained unchanged after ablation, while the VWs of CSp, CSd and IRA trended to decline despite no statistic significant. (3)SR showed a little increasing but without statistic significant after ablation (P = 0. 17 ).(4) ERP of fast pathway was significantly decreased after ablation: ( 391 ± 55 ) ms, ( 369 ± 78 ) ms, P ＜ 0. 01.Conclusions The decrease of ERPs at CS and IRA, as well as F-ERP after ablation may decline the inducibility of atrial fibrillation and indicates regional vagal denervation to the atrium.     

心房肌复极的电整复性与阵发性心房颤动发生机制的实验研究

Objective Electrical restitution was believed to be a determinant responsible for the stability of heart rhythm. Although numerous studies focused on the role of action potential duration restitution (APDR) in the initiation and maintenance of ventricular fibrillation (VF), the relationship between atrial APDR and atrial fibrillation (AF) has not been fully understood. This study aims to investigate the characteristics of APDR of left atrium (LA) and right atrium (RA) in canines and the relevance to induction of AF. Methods Monophasic action potential (MAP) was recorded from LA and RA in 14 canines using the MAP recording-pacing combination catheter. APDR, plotted as action potential duration (APD) on the preceding diastolic interval (DI), was assessed by use of programmed stimulation with a single extrastimulus (S_1S_2) at LA and RA. Episodes of AF were recorded and analyzed. Results APD_(90) was significantly shorter in the LA than that in the RA [( 157.4 ± 43.5 ) ms vs. ( 170. 9 ± 37. 9)ms, P < 0. 05]. The mean slope of the APDR curve by S_1S_2 in the LA was significantly greater than that in the RA ( 1.3 ±0. 4 vs. 0. 9 ± 0. 3, P < 0. 05 ). The incidence of induced AF was significantly higher in the LA than in the RA (11/18 vs. 7/18, P < 0. 05). Conclusions The APDR and MAP characteristics are not uniform between atriums, which may be one of the important mechanisms responsible for the initiation of AF. Heterogeneity of APDR between LA and RA might create critical gradients or a dispersion of repolarization and subatrate for re-entrant arrhythmias and vulnerability to AF.     

房袖传导对期前刺激表现出递减传导一例(摘要)

目的：报告一例肌袖性房颤患者在电隔离上腔静脉过程中，房袖传导对期前刺激表现出递减传导。资料与方法：患者，女43岁，发作性心悸气短一年入院，心电图及动态心电图示：频发房早（呈“P ON T”样）；短阵房速。完善术前准备征得书面同意后，行常规电生理检查及射频消融术。于冠状窦口起搏，上腔静脉内记录。预设温度55度，能量30瓦，放电共240秒。结果：术中未能诱发房颤，但根据动态心电图特点，且上腔静脉内LASSO电极记录肌袖电位高大、明显，故先行隔离上腔静脉。LASSO电极在窦律下记录到肌袖电位位于心房电位之后，部分与心房电位融合，且LASSO1，10肌袖电位最提前。于冠状窦电极窦口起搏，行S1S2刺激，可见房袖呈递减传导，且肌袖组织较心房组织传导延迟程度严重。随S2提前，心房电位预肌袖电位之间距离间拉开，肌袖电位更加清晰明显。此外，肌袖电位最提前处（LASS01，10）传导延迟程度较其余电极轻，故随S2提前，各电极心房电位与肌袖电位间传导时间差异更明显，肌袖电位传导顺序更显著。于LASS0 1，10极附近放电共240秒，肌袖电位渐渐消失，于上腔静脉内起搏无上腔静脉－心房传导，即传出阻滞。成功隔离上腔静脉。结论：上腔静脉肌袖组织对期前刺激表现出递减传导，且较临近心房组织程度更严重，可使肌袖电位现实更清晰。同时，各电极心房与肌袖间传导时间差异随S2提前程度而加剧，一部分肌袖表现出传导上的“优越”，提示肌袖与心房间存在某种“传导通路”。     

阵发性心房颤动肌袖电隔离后复发病例的分析及再消融的体会(摘要)

目的 :结合 4例先后两次肺静脉电隔离成功治疗的阵发性心房颤动 (房颤 )患者 ,探讨导管射频消融肌袖电隔离治疗阵发性房颤后复发的机制 ,并对再次肌袖电隔离治疗的结果进行分析与评价。资料与方法 :对 4例进行肌袖电隔离治疗后复发的阵发性房颤患者 ,在Lasso标测导管指引下进行再次肌袖电隔离治疗。结果 :4例患者共对 14根靶静脉 (12根肺静脉和 2根腔静脉 )进行了射频消融治疗 ,较第一次消融的靶肺静脉数 (9根 )明显增多 ,隔离了除右下肺静脉外所有的肺静脉 ,其中 5根靶静脉恢复袖房传导 ,予以再次电隔离。电隔离一根靶静脉平均需进行 2 .9± 1.3次消融。术后平均随访 7.5± 5 .0 7(1-12 )个月 ,3例无房颤复发 ,1例发作次数明显减少。结论 :袖房传导的恢复及多异位灶起源可能是房颤复发的原因 ,对于阵发性房颤导管射频消融后复发病例 ,再次射频消融治疗是安全、有效的 ,有望彻底根治房颤     

导管射频消融经验性电隔离心脏静脉治疗阵发性心房颤动的疗效评价

目的研究导管射频消融经验性电隔离肺或上腔静脉治疗阵发性心房颤动(房颤)的疗效. 方法选择连续收治的行射频消融经验性电隔离心脏静脉的房颤患者58例,所有患者在术中均不能确定诱发房颤的靶静脉.男性39例,女性19例,年龄22～75(54±11)岁.     

阵发性心房颤动后心跳长间歇与窦房结恢复时间的关系及肺静脉隔离对其影响

目的 检测由于阵发性心房颤动反复发作导致心跳长间歇患者的窦房结恢复时间(SNRT),并分析肺静脉隔离对其影响. 方法 11例接受导管射频消融治疗的阵发性心房颤动患者,在4支肺静脉口外进行节段性肺静脉隔离,分析心跳长间歇与160次/min心房刺激测得的SNRT(SNRT160)及模拟心房颤动600次/min测得的SNRT(SNRT600)的关系及肺静脉隔离前后SNRT160及SNRT600的差异. 结果 11例患者均成功隔离所有肺静脉.12导联心电图或动态心电图提示与症状相关的心跳长间歇为(3464±918)ms.肺静脉隔离前测定的SNRT160为(1655±378)ms,SNRT600为(1682±419)ms;肺静脉隔离后测定的SNRT160为(1491±284)ms,SNRT600为(1518±218)ms.SNRT160及SNRT600肺静脉隔离前后比较差异无统计学意义.心跳长间歇与肺静脉隔离前后SNRT无相关性. 结论 阵发性心房颤动终止后发生的心跳长间歇与病态窦房结综合征所致的心跳长间歇的发生机制可能不尽相同.肺静脉隔离是治疗阵发性心房颤动诱发心跳长间歇安全有效的方法.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

心脏结节病致三度房室传导阻滞1例

正1病例资料患者,女,61岁,2015年12月以"活动后胸闷、气促3年余,再发加重1个月"为主诉入院。既往体健。患者3年前无明显诱因反复出现活动后胸闷、气促,不影响日常生活。1年前出现胸骨后及心前区胀痛,可放射至后背,伴心悸、乏力、多汗,持续半小时缓解。半年前胸闷、气促症状较前加重,轻微活动后即可出现,夜间不能平卧,伴咳嗽、咳白痰。入院后体检:双肺呼吸音粗,可闻及散在湿性