胺碘酮对心房颤动犬心房结构及基质金属蛋白酶-9表达的影响

目的 观察Ⅲ类抗心律失常药物乙胺碘呋酮(胺碘酮)对长期心房快速起搏诱发心房颤动(房颤)犬心房结构及基质金属蛋白酶-9(MMP-9)表达的影响,探寻胺碘酮对房颤犬心房结构重构的作用机制.方法 20只犬随机分为假手术组(n=6)、对照组(n=7)和胺碘酮组(n=7).对照组和胺碘酮组犬心房快速起搏6周(400次/min),建立房颤犬模型.胺碘酮组犬起搏后口服胺碘酮30 mg/(kg·d),直至起搏结束.超声评价各组犬起搏前后左心房、左心耳结构和功能;测定房颤诱发情况;Masson染色检测心房肌胶原容积分数(CVF);免疫组化法观察心房肌MMP-9蛋白表达情况.结果 胺碘酮能够有效防止心房快速起搏诱发房颤犬左心房、左心耳功能降低,使犬房颤诱发率和平均持续时间显著减少,降低房颤犬心房肌CVF值,有效抑制房颤犬心房肌MMP-9表达增加.结论 胺碘酮能够阻止长期心房快速起搏房颤犬心房结构的改变及心房纤维化,防止房颤犬心房结构重构,减少房颤发生.     

声学定量技术评价慢性心房颤动犬心房结构重构及卡托普利的保护作用

目的　用声学定量(AQ)技术评价慢性心房颤动(房颤)犬心房结构及功能改变,并监测卡托 普利的药物干预作用。方法　健康杂种犬26只,随机分为3组:起搏组(11只)及治疗组(9只)安置埋藏 式高频率心脏起搏器(400次/min),快速起搏犬右心耳8周;治疗组于起搏前3d至起搏8周,给予卡托普 利50mg口服,每日2次,于起搏前及起搏后1、4、8周,应用AQ技术监测心房面积和容量的变化。对照组 (6只)未安置起搏器,与起搏、治疗组同步行各项检查。结果　AQ监测发现起搏组于起搏1周后,左、右 心房面积显著增大,4、8周后左、右心房面积进一步增加,左、右心房容量从4周开始逐渐增加。治疗组起 搏1周后左、右心房面积及容量无明显变化,4周后有增大趋势,8周后左、右心房面积及容量轻度增大(与 起搏前比较,P<0.05),但明显小于同期起搏组(P<0.05)。结论　①心房快速起搏可致实验犬心房结 构重构,心房面积及容量扩大,卡托普利对心房结构重构有抑制作用。②AQ技术可有效监测心房结构重 构所致的心房面积及容量变化。     

共聚焦显微技术分析卡维地洛对人心房肌细胞内钙离子的影响

目的:研究卡维地洛对血管紧张素Ⅱ(AngⅡ)诱导的人心房肌细胞内钙超载的拮抗作用。方法:急性分离单个人心房肌细胞。实验分4组:正常对照组; AngⅡ组:加入终浓度为0.1μmol/L的AngⅡ;卡维地洛组:加入终浓度为1μmol/L的卡维地洛; AngⅡ+卡维地洛组:卡维地洛1μmol/L与AngⅡ0.1μmol/L同时加入。以Fluo 3/AM荧光指示剂负载,应用激光共聚焦显微镜技术,分别于加入干预药物后即刻与15 min检测[Ca2+]i变化。结果:对照组和卡维地洛组人心房肌细胞内荧光强度和荧光光密度值较低。AngⅡ加入后即刻,细胞内荧光光密度值开始增加,15 min后细胞内荧光强度和荧光光密度值显著增高(P<0.05)。而AngⅡ+卡维地洛组细胞内荧光光密度值显著低于AngⅡ组(P<0.05)。结论:AngⅡ可引起人心房肌细胞内Ca2+超载,卡维地洛能显著减轻AngⅡ诱导的人心房肌细胞内Ca2+超载。     

急性心房颤动犬缝隙连接蛋白40和43重构及胺碘酮的干预作用

目的 采用快速心房起搏致犬急性心房颤动(简称房颤)模型,观察心房肌缝隙连接蛋白40和43(Cx40、Cx43)含量的改变以及胺碘酮干预的效果.方法 18只成年杂种犬,随机等分为三组,即正常对照组、急性房颤组、胺碘酮组.快速心房起搏,对照组不起搏,胺碘酮组先静脉注射胺碘酮负荷量3 mg/kg,10～15 min内注入,后以维持量1.5 mg/kg静脉滴注进行干预,另两组给予等容量的生理盐水.连续刺激并且房颤8 h后,取右心耳组织,用Western blot 检测Cx40和Cx43的含量,用Lucifer Yellow划痕标记荧光传输技术在荧光显微镜上观察细胞缝隙连接通讯状态.结果 急性房颤组心房肌组织Cx40和Cx43含量较对照组降低(P均<0.05),胺碘酮组Cx40、Cx43含量较正常对照组低,差异有显著性(P均<0.05),较房颤组含量差异无显著性(P>0.05),胺碘酮可以改善急性房颤时细胞缝隙连接通讯的传导.结论 急性房颤犬缝隙连接蛋白40和43发生了结构重构,从而影响细胞间通讯,胺碘酮可以改善细胞间电信号传导,但不能改善缝隙连接结构重构.     

慢性乙型肝炎和肝硬化患者AngⅡ、Ang(1-7)及AngⅡ/Ang(1-7)比值的变化

目的研究慢性乙型肝炎和肝硬化患者肾素-血管紧张素系统(RAS)中血管紧张素Ⅱ(AngⅡ)、血管紧张素(1-7)[Ang(1-7)]及AngⅡ/Ang(1-7)比值的变化,探讨其在肝纤维化发病过程中的意义。方法收集20例慢性乙型肝炎患者、60例乙型肝炎肝硬化患者和20例健康对照者的一般临床资料及血浆标本,采用酶联免疫吸附法测定血浆中AngⅡ、Ang(1-7)的水平,分析AngⅡ、Ang(1-7)及AngⅡ/Ang(1-7)在各组之间的表达差异。结果肝硬化患者血浆AngⅡ、Ang(1-7)水平及AngⅡ/Ang(1-7)比值分别为(105.88±53.56)pg/ml,(77.95±27.43)pg/ml,1.34±0.48,均显著高于乙型肝炎组和对照组[(59.98±12.97)pg/ml、(21.53±18.27)pg/ml,(62.45±11.24)pg/ml、(27.06±12.76)pg/ml,0.97±0.16、0.72±0.39;均P<0.01];肝硬化患者Child-Pugh A级至C级AngⅡ、Ang(1-7)水平及AngⅡ/Ang(1-7)的比值逐渐升高,各组之间差异有统计学意义(P<0.05);AngⅡ/Ang(1-7)比值与Child-Pugh评分呈正相关(r=0.499,P<0.01)。结论随着肝纤维化或肝硬化患者的病情进展,AngⅡ/Ang(1-7)的比值逐渐增加,其水平对慢性肝病患者的病情评估具有指导意义。     

肾去神经术抗自发性高血压大鼠心肌胶原纤维增生的研究

目的通过研究肾去神经术(RDN)对自发性高血压大鼠(SHR)心肌组织血管紧张素Ⅱ(AngⅡ)表达的影响,验证RDN对SHR大鼠血压调节作用,探讨其抗心肌胶原纤维增生的作用及其可能机制。方法 30只约12周龄雄性SHR大鼠随机分成3组,分别为:手术组、假手术组、无手术对照组(阳性对照组),另取10只相同体重雄性WKY大鼠作为正常血压大鼠(阴性对照组)。术后10周处死实验动物,取心肌、肾脏组织,测定左心室质量分数(LVMI),酶联免疫吸附法(ELISA)测定肾脏匀浆组织去甲肾上腺素(NE)浓度及心肌匀浆组织AngⅡ浓度,病理切片HE染色观察心肌细胞形态,苦味酸天狼星红染色计算心肌胶原纤维含量。结果术后第2、4、6、8周收缩压及舒张压手术组均明显低于假手术组、无手术对照组(P<0.05),LVMI手术组[(2.48±0.12)mg/g]明显低于假手术组[(2.91±0.26)mg/g]、无手术对照组[(2.82±0.32)mg/g](P<0.05),肾脏NE含量及心肌匀浆液中AngⅡ含量手术组[NE:(80.26±7.42)ng/g;AngⅡ:(375.50±23.05)pg/g]明显低于假手术组[NE:(170.02±11.75)ng/g;AngⅡ:(421.52±36.84)pg/g]、无手术对照组[NE:(183.30±18.23)ng/g;AngⅡ:(419.07±43.87)pg/g](P<0.05),心肌胶原纤维手术组[1 631(888~3 121)]含量明显低于假手术组[5 961(3 539~13 456)]、无手术对照组[6 024(3 417~12 022)](P<0.05)。结论 RDN能明显降低SHR大鼠血压,抑制其心肌胶原纤维增生和左心室质量增加,此机制可能与抑制肾交感神经及降低心肌AngⅡ表达有关。     

地高辛对充血性心力衰竭患者血浆及淋巴细胞内血管紧张素Ⅱ的影响

目的探讨充血性心力衰竭(CHF)患者血浆及淋巴细胞内血管紧张素Ⅱ(AngⅡ)之间的关系及地高辛对其影响。方法25例慢性充血性心力衰竭患者,连续14天给予口服地高辛0.25 mg/d,15例健康对照组,采用放免法分别测定CHF患者服药前后及对照组血浆及淋巴细胞内AngⅡ的浓度。结果服用地高辛后血浆及淋巴细胞内AngⅡ含量明显降低[血浆:(223.75±77.28)ng/L vs(165.61±57.46)ng/L,淋巴细胞:(245.20±74.83)pg/106cellvs(189.33±85.97)pg/106cell,P均=0.000]。健康人淋巴细胞内AngⅡ的浓度与血浆含量不具有相关性(r=-0.419,P=0.120);CHF患者服用地高辛前血浆及淋巴细胞内AngⅡ浓度之间不具有相关性(r=0.041,P=0.850);CHF患者服用地高辛后血浆及淋巴细胞内AngⅡ浓度不具有相关性(r=0.058,P=0.784)。结论淋巴细胞内存在着不依赖于循环AngⅡ的局部AngⅡ。地高辛可降低血浆及淋巴细胞内AngⅡ浓度。     

AngⅡ对人心房肌细胞膜钙通道电流的影响及卡维地洛的拮抗作用

目的:观察AngⅡ对人心房肌细胞膜钙通道电流的影响及卡维地洛的拮抗作用,为应用卡维地洛治疗房性心律失常提供实验基础。方法:急性分离单个人心房肌细胞,采用全细胞膜片钳方法记录L-型钙电流(LCaL)。实验分4组:对照组,AngⅡ(0.1μmol/L)组,卡维地洛(1μmol/L)组,AngⅡ+卡维地洛组。结果:与对照组相比,0.1μmol/LAngⅡ使人心房肌细胞膜LCaL峰值电流密度明显增加(-12.74±1.65vs-5.78±0.82pA/pF,P<0.05)。1μmol/L卡维地洛对人心房肌细胞膜ICa-L无明显影响(-5.72±0.77pA/pF).但可拮抗AngⅡ的作用;AngⅡ+卡维地洛组的ICa-L峰值电流密度(-8.03±0.84pA/pF)与AngⅡ组相比有显著差异(P<0.05)。结论:AngⅡ对人心房肌细胞具有明显的电生理学作用,0.1μmol/LAngⅡ可促进人心房肌细胞膜ICaL.卡维地洛可拮抗AngⅡ对人心房肌细胞膜ICaL的作用。     

心力衰竭犬心房结构重构的实验研究

目的观察右室快速起搏建立心力衰竭犬模型的效果,探讨心房结构重构在心力衰竭与心房颤动形成过程中的作用机制。方法13只犬随机分为起搏组(n=7)和假手术组(n=6),于左、右心房各缝植4对电极,起搏电极缝植在右室心尖,连接实验用VOO型起搏器,快速心室起搏(220次/分)6周,建立心力衰竭犬模型,分别于起搏前、起搏6周后,应用经食管超声心动图测量左房收缩末容积;采用双平面Simpson法测量左室舒张期末和收缩期末容积,得出左室射血分数和心输出量,并应用光镜和电镜观察心房肌的超微结构。结果①假手术组术前和术后心脏各参数无明显变化。②起搏6周后,起搏组与假手术组比较,左房收缩末容积显著增大[(23.2±4.1)vs(13.5±1.9)cm3,P<0.01],左室舒张末期容积显著增大[(56.2±11.3)vs(33.7±9.6)cm3,P<0.01],左室收缩末期容积显著增大[(38.4±8.4)vs(14.5±8.6)cm3,P<0.01],射血分数显著降低[(31.4±10.2)vs(56.8±4.5)%,P<0.01],心输出量著降低[(1.2±0.5)vs(2.8±1.6)L/min,P<0.01]。③病理学结果显示起搏犬心房肌细胞变性、肌纤维溶解、线粒体肿胀以及间质胶原增生、水肿。结论心房结构重构是心力衰竭犬发生心房颤动的重要原因。     

心脏神经结丛消融联合低强度耳屏迷走神经刺激对犬房颤电生理特性的影响

目的 研究心脏神经节丛消融联合低强度耳屏迷走神经刺激对阵发性犬心房颤动(简称房颤)电生理特性的影响,探讨低强度耳屏迷走神经刺激对房颤消融术后的治疗价值.方法 21条健康成年比格犬随机分为3组:RAP组(500次/min快速心房起搏,n=7)、ABL组(心脏神经节消融+500次/min快速心房起搏,n=7)、LL-ST组...     

Capture of atrial fibrillation reduces the atrial defibrillation threshold

The effect of the atrial activity synchronization by single site right atrial pacing on atrial defibrillation threshold (ADFT) was investigated in patients with AF. Two series of randomized incremental cardioversion tests, with increasing energy levels from 0.5 to 10 J, were performed in 15 patients with recurrent episodes of idiopathic paroxysmal AF using two 7 Fr "single coil" catheters for internal cardioversion. After induction of sustained AF (> 10 minutes), shocks were delivered, preceded or not by 10 seconds of overdrive local atrial pacing, according to the randomization, using an external cardioverter defibrillator. A total of 187 shocks was delivered to the study population. ADFT was reduced when overdrive atrial stimulation preceded the cardioversion (3.6 +/- 1.6 vs 2.9 +/- 1.7 J, P = 0.02). Local atrial capture was considered on the basis of 1:1 phase locking between stimulus and atrial activation wave, and constant morphology of atrial wave criteria. Effective atrial capture was obtained in 8 of 15 patients. There was not significant difference in the mean of FF intervals of patients in which atrial capture was or was not stable (209 +/- 22 vs 208 +/- 28 ms). Patients were then considered according to the outcome of atrial pacing before direct current shock. A marked ADFTreduction was observed in patients with stable capture (3.8 +/- 1.7 vs 2.5 +/- 1.7 J, P = 0.0003), while no significant difference in ADFT was found when capture was not achieved (3.4 +/- 1.6 vs 3.6 +/- 1.5 J, P = NS). In conclusion, regularization of atrial electrical activity by atrial capture reduces the ADFT. A constant pacing entrainment seems to lower the energy required for electrical cardioversion by reducing the amount of fibrillating tissue.     

射频消融治疗心房颤动和心房扑动策略探讨

目的评价射频消融使肺静脉电解剖隔离和消除左房碎裂电位治疗心房颤动（简称房颤）的效果,进一步探讨与心房扑动（简称房扑）的关系。方法63例房颤患者分为两组,其中阵发性房颤32例,持续性房颤31例。在Ensite NavX三维标测系统下,建立左心房一肺静脉电解剖模型,分别对左、右肺静脉前庭大环状消融达完全左心房．肺静脉电解剖隔离,若房颤未终止或被诱发,再标测左心房内碎裂电位,消融碎裂电位;对22例合并典型房扑者行三尖瓣峡部消融。随访9个月观察影响手术复发的因素。结果所有患者均达左心房一肺静脉电解剖隔离。32例阵发性房颤患者中23例（71．9％）和31例持续性房颤患者8例（25．8％）经单纯肺静脉电隔离后房颤终止,不被诱发,两者相比有统计学意义（P〈0．01）;7例（21．8％）阵发性房颤和19例（61．3％）持续性房颤患者经联合消融左心房碎裂电位转复窦律,2例阵发性房颤和4例持续性房颤患者住院期间转复,术中总房颤即刻终止率两组相比较无统计学意义（P〉0．05）。阵发性房颤和持续性房颤患者消融成功率分别为84．4％和80．6％（P=0．697）,多元Logistic回归分析显示合并典型房扑是房颤术后复发的一个危险因素（P=0．007）。结论肺静脉电解剖隔离结合消除左心房碎裂电位是治疗房颤的一种有效策略,房颤和房扑的启动与维持可能存在一些共同机制。     

Role of high frequency atrial pacing for the termination of acute atrial fibrillation and atypical atrial flutter

BACKGROUND: The aim of this study was to assess the efficacy of high-frequency (HF) pacing from the right atrial appendage (RAA) or coronary sinus ostium (CS-Os) for the termination of acute atrial fibrillation (AF) and atypical atrial flutter (AAFL) during an electrophysiological (EP) study. METHODS: 128 episodes of acute fast atrial arrhythmias (FAAs; 93 AF and 35 AAFL) were analyzed in 110 patients. Patients were initially observed for 60s leading to spontaneous termination of 28 FAAs. The remaining 100 FAAs (70 AF) episodes were randomized to the following strategies: (A) pacing at RAA using up to 10 consecutive 20-Hz trains followed by the same stimulation protocol at CS-Os if RAA pacing failed, (B) pacing at CS-Os using the same stimulation protocol followed by HF pacing at RAA, or (C) observation up to 6 minutes ("no pacing"). RESULTS: The 20-Hz pacing at both RAA and CS-Os was associated with higher conversion of AAFL, as compared to strategy C (60% and 77% vs 11%; P < 0.05). Only HF pacing at CS-Os was superior to observation strategy for the conversion of AF (21% vs 4%; P < 0.05). CONCLUSIONS: The 20-Hz pacing protocol is superior to observation strategy for interruption of either acute AF or acute AAFL episodes; however, its efficacy is higher in AAFLs. These results can be helpful for the termination of acute atrial tachyarrhythmias during EPstudy and should be further evaluated in patients with implantable devices capable of antitachycardia pacing.     

The effect of the atrial pacing site on the total atrial activation time

The effect of dual site pacing for prevention of atrial fibrillation may be due to synchronization of right and left atrial activation. Little is known, however, about the effect of pacing from single right atrial sites on differences in interatrial conduction. Twenty-eight patients without structural heart disease were studied following radiofrequency catheter ablation of supraventricular arrhythmias. Pacing was performed using standard multipolar catheters from the presumed insertion site of Bachmann's bundle, the coronary sinus ostium, the high lateral right atrium, and the right atrial appendage (n = 8 patients). Bipolar recording was performed from the distal coronary sinus, the high and low lateral right atrium, and the posterolateral left atrium (n = 13 patients). The longest conduction time from each pacing to each recording site was considered the total atrial activation time for the respective pacing site. During high right atrial pacing, the total atrial activation time was determined by the conduction to the distal coronary sinus (118 +/- 18 ms), during coronary sinus ostium pacing by the conduction to the high right atrium (94 +/- 18 ms), and during Bachmann's bundle pacing by the conduction to the distal coronary sinus (74 +/- 18 ms). The total atrial activation time was significantly shorter during pacing from Bachmann's bundle, as compared to pacing from other right atrial sites. Thus, in normal atria, pacing from the insertion of Bachmann's bundle causes a shorter total atrial activation time and less interatrial conduction delay, as compared to pacing from other right atrial sites. These findings may have implications for alternative pacing sites for prevention of atrial fibrillation.     

Electrophysiological properties of the right atrial septum in patients with atrial tachyarrhythmias

Common-type atrial flutter (AFL) is a type of atrial tachyarrhythmia with counterclockwise rotation around the tricuspid annulus within the right atrium (RA). It was recently reported that the electrogram voltage reduction observed in the RA was involved in the development of AFL. However, the relationship between the low voltage areas and conduction velocity during AFL has not been fully described. In this study, patients with AFL (n = 17) and without AFL (n = 4) were examined using an electro-anatomical mapping system. The patients with AFL were divided into 2 groups; AFL group (n = 8) and coronary sinus ostium (CSO) group (n = 9). The AFL group was defined as exhibiting the maintenance of AFL and the CSO group sinus rhythm before the catheter ablation. The electrogram voltages of each area in the RA (septum, and posterior and lateral walls), conduction velocity during AFL and transverse and longitudinal conduction velocities were evaluated. In the septum, the mean electrogram voltage was significantly lower in the AFL and CSO groups than in the group without AFL. Moreover, the conduction velocity during AFL was significantly slower in the septum, and both the septal transverse and longitudinal conduction velocities were significantly slower in the AFL and CSO groups than in the group without AFL. In conclusion, these findings suggest that both the slower conduction velocities and lower voltage in the RA septum may be involved in the development of AFL. Thus, ablation of the RA septum may represent a therapeutic approach of AFL.     

Left atrial tachycardia after right atrial separation for chronic atrial fibrillation with atrial septal defects

A right atrial separation procedure was performed for the ablation of chronic atrial fibrillation in four cases, concomitant with the repair of the atrial septal defect. After the operation, chronic atrial fibrillation disappeared in three of them and left atrial tachycardia occurred in the other one. Left atrial tachycardia is an arrhythmia encountered after a right atrial separation procedure.     

不同心房部位起搏心房激动时间的变化

目的比较右心耳及房间隔起搏方式下心房激动时间的变化。方法双腔永久起搏器(DDD)安置术中,心房电极安置于右心耳42例,房间隔电极27例。术前、术后分别描计体表12导联心电图,测量右心耳及房间隔起搏前后最长P波时相(Pmax)及P波离散度(Pd)。结果右心耳起搏方式,Pmax及Pd术后较术前明显增加[Pmax:(138±23)msvs(127±16)ms,Pd:(19.4±9.0)msvs(13.5±7.3)ms];均P<0.05)。而房间隔起搏方式,Pmax及Pd术后较术前显著减少[Pmax:(122±12)msvs(133±17)ms,Pd:(11.1±6.6)msvs(15.5±8.0)ms,均P<0.05]。结论房间隔起搏方式相反于右心耳起搏方式,心房电活动更稳定。     

Clinical characteristics of focal atrial tachycardias arising from the atrial appendages during childhood

Background: Focal atrial tachycardias (ATs) arising from the atrial appendages (AAT) are uncommon in adults. On the other hand, we frequently encounter AATs during childhood. However, the topographic distribution and clinical characteristics of focal ATs during childhood have not yet been clearly revealed. The aim of this study was to investigate the clinical characteristics of AATs in childhood. Methods: The study population consisted of 16 consecutive pediatric patients with focal AT enrolled between March 1991 and June 2009. A retrospective analysis was performed. The patients with focal AT were divided into two groups: the AAT group and other AT (OAT) group, in which the foci arose from other atrial sites. Results: Fifty percent had AAT. The AAT patients consisted of more males (88% vs 25%; P < 0.05), were more often asymptomatic at the initial visit (75% vs 25%; P < 0.05), and more often presented with an incessant form of the AT (88% vs 25%; P < 0.05) than the OAT patients. Second‐degree atrioventricular block during slow ATs of <120 beats per minute were more often observed in the AAT patients (63% vs 13%; P < 0.05). The incidence of tachycardia‐mediated cardiomyopathy was 19% out of all our subjects and 38% of the AAT patients. Conclusions: The AATs are the major source of focal ATs in pediatric patients that are typically incessant. These characteristics probably explain why a much higher percentage of the patients are presented with TMC. (PACE 2011; 34:177–184)     

Clinical significance of the atrial fibrillation threshold in patients with paroxysmal atrial fibrillation

AF threshold and the other electrophysiological parameters were measured to quantify atrial vulnerability in patients with paroxysmal atrial fibrillation (PAF, n = 47), and those without AF (non-PAF, n = 25). Stimulations were delivered at the right atrial appendage with a basic cycle length of 500 ms. The PAF group had a significantly larger percentage of maximum atrial fragmentation (%MAF, non-PAF: mean +/- SD = 149 +/- 19%, PAF: 166 +/- 26%, P = 0.009), fragmented atrial activity zone (FAZ, non-PAF: median 0 ms, interquartile range 0-20 ms, PAF: 20 ms, 10-40 ms, P = 0.008). Atrial fibrillation threshold (AF threshold, non-PAF: median 11 mA, interquartile range 6-21 mA, PAF: 5 mA, 3-6 mA, P < 0.001) was smaller in the PAF group than in the non-PAF group. Sensitivity, specificity, and positive predictive value of electrophysiological parameters were as follows, respectively: %MAF (cut off at 150%, 78%, 52%, 76%), FAZ (cut off at 20 ms, 47%, 84%, 85%), AF threshold (cut off at 10 mA, 94%, 60%, 81%). There were no statistically significant differences between the non-PAF and PAF groups in the other parameters (effective refractory period, interatrial conduction time, maximum conduction delay, conduction delay zone, repetitive atrial firing zone, wavelength index), that were not specific for PAF. In conclusion, the AF threshold could be a useful indicator to evaluate atrial vulnerability in patients with AF.