心脏迷走神经与心房颤动关系的研究进展

自从Coumel等[1]提出了在心脏结构正常的患者中,心房颤动(房颤)可能是由迷走神经兴奋引起后,迷走神经在房颤触发和维持中的作用已成为大家研究的热点。心脏的迷走神经系统是由迷走神经干、迷走神经丛和迷走神经节后神经元组成。心脏表面神经节丛由大量神经节和神经纤维束彼此交     

射频消融第三脂肪垫对犬心房电生理参数及心房颤动诱发的影响

目的研究射频消融第三脂肪垫对犬心房电生理参数及心房颤动(房颤)诱发的影响。方法观察12只杂种犬在不同起搏周长下,消融第三脂肪垫前后心房不同部位有效不应期(AERP)、AERP离散度、AERP频率适应性,房颤诱发率及其诱发窗口的变化。结果与消融前相比,消融后心率变化差异无统计学意义(P>0.05)。随着起搏周长变短,AERP明显缩短,且差异具有统计学意义(均为P<0.05)。消融术后高位左心房、低位左心房、左心耳部位AERP明显缩短,高位右心房、低位右心房、右心耳部位AERP明显延长(均为P<0.05)。AERP离散度差异无统计学意义(P>0.05)。消融后不同测量部位的房颤诱发率均降低及房颤诱发窗口增宽。结论消融第三脂肪垫达到部分去迷走神经化,使左心房AERP缩短,同时使房颤诱发率降低及房颤诱发窗口增宽。     

心外膜脂肪垫网络迷走神经干对窦房结和房室结功能的影响

目的 探讨心外膜窦房结脂肪垫(SAN-FP)和房室结脂肪垫(AVN-FP)网络迷走神经干调控心脏活动的主控区.方法 杂种犬18只,分为A组和B组,以不同电压分别刺激左右迷走神经干、SAN-FP和AVN-FP,测定窦性心率(SR)和AH间期,A组先消融SAN-FP,在刺激迷走神经干的情况下测定SR和AH间期,再联合消融SAN-FP和AVN-FP,B组则先消融AVN-FP,再联合消融AVN-FP和SAN-FP.结果 ①右侧迷走神经干刺激产生的迷走效应强于左侧(SR减慢75％对41％),SAN-FP刺激引起SR减慢的最大幅度为13％;②优先消融SAN-FP后刺激迷走引起SR减慢的效应显著减弱,AH间期显著延长,联合消融后刺激迷走对SR的影响与消融前差异无统计学意义,但AH间期较消融前和单独消融时均显著延长;③优先消融AVN-FP刺激迷走引起SR减慢效应较消融前差异无统计学意义,AH间期较消融前明显延长,联合消融后刺激迷走对SR和AH间期的影响较单独消融时差异无统计学意义.结论 迷走神经干刺激的迷走效应右侧大于左侧,右侧迷走神经干主要通过AVN-FP调控窦房结功能.心外膜脂肪垫是迷走神经干调控窦房结和房室结功能的重要环节,AVN-FP是主控区,SAN-FP为辅助区.     

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

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性,慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬,全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管）,经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min,P〉0．05],提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms,P〉0．05],CSd分别为[（55±30）ms对（42±32）ms,P=0．08],IRA分别为[（66±24）ms对（19±21）ms,P〈0．001],CSp分别为[（46±24）ms对（7±18）ms,P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响,对CSd区域的迷走神经调节功能有一定的影响,而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后,HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms,P〉0．05],CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms,P     

消融心房脂肪垫治疗心房颤动的研究现状

近年研究表明,迷走神经过度兴奋与一部分心房颤动的发生密切相关。由于支配心房的迷走神经丛主要分布于心房外膜的脂肪垫中,因此,以心房去迷走神经化为终点的脂肪垫消融成为一项新的心房颤动治疗措施。初步研究的结果显示,该术式治疗心房颤动确实有效,但同时也存在若干弊端。现就消融心房脂肪垫治疗心房颤动的现状作一综述。     

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.     

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.     

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.     

Long-term evaluation of atrial fibrillation ablation guided by noninducibility

BACKGROUND: Pulmonary vein (PV) isolation and linear lesions are effective in eliminating paroxysmal atrial fibrillation (AF), but linear lesions probably are not required in all patients. Noninducibility of AF has been shown to be associated with freedom from arrhythmia in 87% of patients. OBJECTIVES: The purpose of this study was to prospectively evaluate the role of noninducibility in guiding a stepwise approach tailored to the patient. METHODS: In 74 patients (age 53 +/- 8 years) with paroxysmal AF, PV isolation was performed during induced or spontaneous AF. If AF was inducible after PV isolation, one to two additional linear lesions were placed at the mitral isthmus and/or left atrial roof, with the endpoint of noninducibility of AF or atrial flutter. Inducibility (AF/atrial flutter, lasting > or = 10 minutes) was assessed using burst pacing at an output of 20 mA down to refractoriness from the coronary sinus and both atrial appendages. RESULTS: In 42 patients (57%), PV isolation restored sinus rhythm and rendered AF noninducible. In the 32 patients with persistent or inducible AF after PV isolation, a single linear lesion achieved noninducibility in 20, whereas two linear lesions were required in 12 and resulted in conversion to sinus rhythm and noninducibility in 10. Using this stepwise approach, a total of 69 patients (93%) were rendered noninducible. During follow-up of 18 +/- 4 months, 67 patients (91%) were free from arrhythmia without antiarrhythmic drugs. Repeat procedures were performed in 23 patients: repeat ablation was required to consolidate prior targets in 15 patients (20%), and "new" linear lesions, which were not predicted by inducibility during the index procedure, were required in 8 (11%). CONCLUSION: Noninducibility can be used as an endpoint for determining the subset of patients with paroxysmal AF who require additional linear lesions after PV isolation. This tailored approach is effective in 91% of patients while preventing delivery of unnecessary linear lesions.     

病态窦房结综合征合并阵发性心房颤动的射频消融治疗

目的探讨病态窦房结综合征患者合并阵发性房颤的射频消融治疗效果。方法 7例病态窦房结综合征合并阵发性房颤患者,术前动态心电图诊断为病态窦房结综合征,24小时内有数次停搏及多次阵发房颤发作,其中有5例患者停搏均发生在房颤终止时,2例停搏与房颤发作无明显关联。接受环肺静脉前庭电隔离术。术后动态心电图随访。结果该7例患者,有2例房颤复发,1例再次接受手术并成功,1例拒绝再次手术。动态心电图提示有4例(考虑为快慢综合征)心动过缓明显好转,2例(考虑为慢快综合征)房颤发作明显减少但是心动过缓无改善,接受心脏永久起搏器置入治疗。此7例患者术前与术后1个月最大心率、最小心率、平均心率比较,最小心率、平均心率术后较术前增加,最大心率术后较术前无明显变化。结论快慢型病态窦房结综合征合并阵发性房颤患者对房颤射频消融治疗效果较好,大部分患者术后心动过缓明显改善,而不需要置入心脏永久起搏器。     

伊布利特在持续性心房颤动射频消融术中转律的疗效特点

目的 评价伊布利特在持续性心房颤动(房颤)射频消融术中应用的有效性及影响因素.方法 入选接受射频消融手术的持续性房颤患者18例,男性16例,女性2例,平均年龄(56.3±14.0)岁,体质量(81.22±8.93) kg,合并原发性高血压3例、肥厚型心肌病2例.所有患者术中经环肺静脉电隔离、线性消融、碎裂电位消融后房颤未终止,或者转为心房扑动,给予伊布利特l mg、10min内静脉注射,观察开始给药后30 min内的转复率及4h内的不良反应.根据用药后是否成功转律分为转律组与非转律组.结果 (1)18例患者用药后30 min内成功转律11例,转复律为61.11％,平均转律时间为(13.80 +7.64) min,转复剂量为(0.94±0.13)mg.1例患者用药后15 min时出现窦性停搏16 s,后恢复稳定窦性心律,术后观察4h无不良反应,另1例患者用药后出现窦性心动过缓,持续约lh后恢复正常心率,期间无低血压等血流动力学改变.余16例患者术中及术后4h内无室性心动过速及低血压等不良反应.(2)使用伊布利特后30 min的AA间期(0.51±0.08)s,明显长于用药前的AA间期(0.39±0.21)s,P＜0.01;用药后30 min的QTc(0.51±0.08)s,明显长于用药前QTc(0.39±0.21)s,P＜0.01.(3)两组临床资料差异无统计学意义.转律组患者左房瘢痕区比例(5.12±3.83)％,明显小于非转律组左房瘢痕区比例(12.40±11.03)％,P＜0.01.(4)左心房内径＜40mm患者的转复率(75.00％)与内径≥40 mm患者的转复率(50.00％)差异无统计学意义(P＞0.05).结论 静脉注射伊布利特在持续性房颤射频消融术中应用疗效迅速,对消融后心房扑动转复率更高.转律的成功率与术中标测瘢痕区面积所占比例相关.     

胸腔镜辅助微创与导管射频消融治疗持续性心房颤动的对比研究

目的 回顾性研究胸腔镜辅助微创与导管射频消融治疗持续性心房颤动(房颤)的临床疗效.方法 对北京安贞医院172例持续性房颤患者进行射频消融,83例行胸腔镜辅助微创射频消融(微创组),另89例行环同侧肺静脉左心房线性消融(导管组).其中男116例,女56例;年龄32～80(56±12)岁.房颤病史平均(72 ±68)个月....     

心房颤动导管消融：更上一层楼

十余年来,心房颤动（房颤）导管消融已经从一项探索中的技术发展为广泛应用的房颤治疗方法,其进展日新月异.目前,房颤导管消融的技术更成熟,风险效益比更明确,普及更广泛,已然进入了快速发展的成熟时期.     

外源性与内源性自主神经刺激对心房颤动诱发性的影响

目的探讨心脏外源性与内源性自主神经刺激对心房颤动(房颤)诱发性的影响。方法16只成年犬静脉麻醉后,分离右颈迷走神经干(VST);再行右侧开胸手术,暴露靠近右上肺静脉的心脏脂肪垫(内含心脏自主神经丛,即GP),将1根电极导管固定贴靠于右上肺静脉,使其头端电极贴靠右上肺静脉与左房交界处,进行程序期前刺激,采用2倍、4倍、10倍阈值的刺激强度进行基础程序期前刺激(control),并测量相应的心房不应期(ARP)及房颤诱发窗宽(WOV);再分别加用VST刺激或GP刺激,测量在相应刺激条件下程序期前刺激所获得的ARP及WOV。结果平均基础心率(HR)为153±22次/min,VST刺激下HR为79±44次/min,GP刺激下HR为87±99次/min(后二者比较,P>0·05)。最短的ARP在control状态下为101±20ms、VST刺激下为90±17ms、GP刺激下为91±13ms,VST刺激下及GP刺激下均较control明显缩短(P<0·05),VST刺激下与GP刺激下的差异无统计学意义(P>0·05)。三者的累计WOV分别为control22±34ms、VST刺激下44±45ms、GP刺激下99±75ms,三者间每两者的差异均有统计学意义(P<0·05)。结论在降低心率相近的情况下,电刺激心脏内源性自主神经丛与电刺激心脏外源性自主神经引起的不应期缩短相近,但前者更容易诱发房颤。     

递进式个体化心房基质消融治疗心房颤动

目的 以肺静脉电学隔离为终点的心房颤动（房颤）消融术式的疗效难以令人满意。本研究旨在探索规范化的递进式个体化心房基质改良消融术治疗房颤的方法。方法 124例患者（男性96例,女性28例）,年龄27-76（53．6±8．7）岁。其中92例为阵发性房颤,32例为持续性／永久性房颤。若无自发房颤则在心房进行持续递增的快速刺激（频率200—600次／min）诱发房颤。均在非接触式标测观察房颤时心房激动情况,将最常激动部位做为房颤基质进行改良消融,并根据消融后重复等电位标测的结果作出递进式调整,直至房颤被终止不再被诱发。结果 在既不隔离肺静脉也不寻求碎裂电位的情况下,87．1％（108／124）的房颤消融转复为窦性心律,其余被转为非典型心房扑动（房扑）或房性心动过速（房速）。可将消融灶分为3种类型,其中以7字形的A型线性消融最关键,71．6％的阵发性房颤可被A型消融终止且不再被诱发,而68．8％的持续性／永久性房颤则需通过B型消融终止。随访（21．6±5．3）个月,90．3％（112／124）的患者不服药亦无房颤发生。其余9．7％（12／124）的患者有顽固性非典型房扑／房速,其中仅1．6％（2／124）的患者伴有阵发性房颤。结论 递进式的心房基质消融术可以将房颤有效地转复为窦性心律,并有满意的远期疗效。此种术式简单易行有望在NavX和Carto标测下复制。