The interrelationship between atrial fibrillation and atrial flutter

For a long time, it has been known that atrial fibrillation and atrial flutter have a close clinical interrelationship. Recent electrophysiological studies, especially mapping studies, have significantly advanced our understanding of this interrelationship. Regarding the relationship of atrial fibrillation with atrial flutter: Atrial fibrillation of variable duration precedes the onset of atrial flutter in almost all instances. During the atrial fibrillation, the functional components needed to complete the atrial flutter reentrant circuit, principally a line of block between the venae cavae, are formed. If this line of block does not form, classical atrial flutter does not develop. If this line of block shortens or disappears, classical atrial flutter disappears. In fact, it is fair to say that the major determinant of whether atrial fibrillation persists or classical atrial flutter develops is whether a line of block forms between the venae cavae. Regarding the relationship of atrial flutter with atrial fibrillation: Studies in experimental models and now in patients have demonstrated that a driver (a rapidly firing focus or a reentrant circuit of very short cycle length) can cause atrial fibrillation by producing fibrillatory conduction to the rest of the atria. When the driver is a stable reentrant circuit of very short cycle length, it is, in effect, a very fast form of atrial flutter. There probably is a spectrum of reentrant circuits of short cycle length, i.e., "atrial flutter," that depend, in part, on where the reentrant circuit is located. When the cycle length of the reentrant circuit is so short that it will only activate small portions of the atria in a 1:1 manner, the rest of the atria will be activated rapidly but irregularly, i.e., via fibrillatory conduction, resulting in atrial fibrillation. In short, there are probably several mechanisms of atrial fibrillation, one of which is due to a very rapid atrial flutter circuit causing fibrillatory conduction. In sum, atrial fibrillation and atrial flutter have an important interrelationship.     

房颤与房扑的射频消融治疗研究

目的 探讨房颤与房扑之间的相互关系，寻找房颤的射频治疗方法。方法 对40例阵发性房颤患者进行了电生理标测及射频消融。结果 40例中有6例患者发生房扑，行右房峡部消融，1例行Halo电极标测示峡部双向阻滞，随访12－30个月房颤消失或次数明显减少。结论 房颤与房扑为两种密切相关的心律失常，消融右房峡部可能对部分房颤患者起到治疗作用。     

心房颤动患者心房组织血管紧张素系统与心房纤维化的关系

目的 探讨心房颤动（房颤）患者血管紧张素系统基因转录和蛋白表达与心房纤维化的关系,研究心房纤维化在房颤维持和心房重构中的作用.方法 心外科手术病人53例,其中窦性心律者26例,房颤患者27例（房颤少于10年患者为房颤Ⅰ组,房颤超过10年患者为房颤Ⅱ组）.术前行超声心动图检查.手术中取右心房组织,Masson染色测定胶原容积分数（CVF）,分别通过逆转录-聚合酶链反应（RT-PCR）和蛋白印迹的方法测量血管紧张素Ⅱ受体、血管转化酶（ACE）mRNA和血管紧张素Ⅱ受体1型蛋白的表达量,用放射免疫的方法测定血管紧张素Ⅱ（AngⅡ）的水平.结果 同窦性心律组相比,房颤组心房扩大、CVF增高;房颤Ⅰ组心房血管紧张素Ⅱ受体1和2的mRNA水平差异无统计学意义,ACE mRNA升高,AngⅡ升高;房颤Ⅱ组心房血管紧张素Ⅱ受体1和2的mRNA有下降的趋势,未达统计学意义,ACE mRNA、血管紧张素Ⅱ受体1蛋白表达下降,有统计学意义.结论 血管紧张素系统在房颤患者的心房纤维化早期发展中发挥作用.     

糖尿病兔心房电机械功能受损与心房颤动的关系

目的 应用组织多普勒超声心动图(DTE)评价四氧嘧啶诱导的糖尿病兔心房电机械功能,同时观察心房病理、电生理改变及心房颤动(房颤)易感性的变化.方法 应用四氧嘧啶诱导成功糖尿病兔共8只,健康对照组8只,饲养8周,应用DTE测定心电图P波开始至心房各节段速度曲线上舒张晚期a'波开始的时间间期(Pastart)及心电图P波开始至DTE速度曲线上舒张晚期a＇波峰值处的时间间期( Papeak);建立Langendorff灌流的离体兔心脏模型,测量心房间传导时间(IACT)、心房各点有效不应期(AERP)、AERP的离散度(AERPD)、应用短阵快速刺激观察房颤诱发情况,应用天狼猩红染色评价左心房纤维化情况.结果 与对照组比较,糖尿病组兔左心房前后径明显增大[(6.8±0.6)mm对(8.3±0.6)mm,P＜0.01],室间隔增厚[(1.9±0.2)mm对(3.0±0.5) mm,P＜0.01];左心房侧壁Pastart及右心房Pastart延长[分别为(40.5±12.9) ms对(60.4±20.4) ms,P＜0.05;(59.8±20.1)ms对(83.0±11.0)ms,P＜0.05)];IACT延长[(37.6±8.9) ms对(27.7±2.1) ms,P＜0.01)],房颤诱发率升高(6/8对1/8,P＜0.05);病理检查提示糖尿病组左心房心肌间质明显纤维化.两组房间隔处Pastart,左心房后壁Pastart及Papeak均与IACT显著相关.结论 糖尿病兔心房电机械功能受损,与心房肌纤维化、心房间电传导延迟有关,可能是糖尿病发生房颤的机制之一.     

心房颤动与心房重构的最新进展

心房颤动（房颤,AF）是引起心血管发病和死亡的重要原因.房颤是常见的由一系列心脏疾病引起心房重构的终点事件,其本身也能引起心房重构从而促进心律失常的发展[1].随着人们对心房重构的机制及其在房颤进展中作用的逐渐认识,对离子通道调控机制和作用靶点的研究也有了较深入的发展.本文将重点综述这方面的进展.     

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.     

经导管线性消融术对左心房功能影响的研究

目的评价左心房线性消融术对心房颤动（房颤）患者左心房功能的影响。方法选择30例Carto系统标测指导下行左心房线性消融术的阵发性房颤患者，应用超声心动图测定其消融术前1～3d、术后3个月静息时窦性心律下左心房容积指标、二尖瓣口A波速度峰值（VA）及左心房射血力，分析消融术前后左心房功能的变化。结果消融术后反应左心房辅泵功能的指标左心房射血力、VA、左心房主动排空容积、左心房主动排空分数、左心房总排空分数显著下降，反应左心房管道功能的左心房管道容积增加，反应左心房储存功能的指标左心房总排空容积、左心房最大容积无明显变化。结论Carto系统标测下左心房线性消融术后左心房辅泵功能下降，管道功能增强，而储存功能无显著改变。     

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.     

Effects of Cilazapril on atrial electrical, structural and functional remodeling in atrial fibrillation dogs

Background and purpose

The effects of angiotensin-converting enzyme inhibitor on long-term atrial electrophysiologic and structural remodeling are still unclear. The purpose of this study is to investigate the effects of Cilazapril on atrial electrical, structural, and functional remodeling in atrial fibrillation (AF) dogs induced by chronic rapid atrial pacing.

Methods

Twenty dogs were randomly divided into sham-operated group (n = 6), control group (n = 7), and Cilazapril group (n = 7). One thin silicon plaque containing 4 pairs of electrodes was sutured to each atrium. A pacemaker was implanted in a subcutaneous pocket and attached to a screw-in epicardial lead in the right atrial appendage. The dogs in control group and Cilazapril group were paced at 400 beats per minute for 6 weeks. The dogs in Cilazapril group received Cilazapril (0.5 mg•kg⁻¹•d⁻¹) 1 week before rapid atrial pacing until pacing stop. Before and after 6-week rapid atrial pacing, atrial effective refractory period (AERP) at 8 sites, AERP dispersion, intraatrium conduction time, inducibility, and duration of AF were measured. Transthoracic and transesophageal echocardiographic examinations included left atrium (LA) maximal volume, LA minimal volume, LA ejection fraction, left atrial appendage (LAA) maximal volume, LAA minimal volume, LAA ejection fraction, LAA maximal forward flow velocity, and LAA minimal backward flow velocity were performed. Atrial collagen volume fraction was analyzed by Masson staining.

Results

After 6-week rapid atrial pacing, although there was no significant difference in AERP shortening and AERP rate adaptation reduction between the control group and the Cilazapril group, the inducibility and duration of AF were found to be dramatically lower in the Cilazapril group than those in the control group (AF inducibility, 65.7% vs 95.7%, P < .05; AF duration, 531.5 ± 301.2 vs 1432.2 ± 526.5 s, P < .01).The post-tachycardia intraatrium conduction times after 6 weeks with Cilazapril were significantly shorter than those in the control group. Cliazapril could partially prevent AERP dispersion increase induced by chronic rapid atrial pacing. Compared with the control group, the LA and LAA volumes were significantly smaller; LA ejection fraction, LAA ejection fraction, LAA maximal forward flow velocity, and LAA minimal backward flow velocity were dramatically higher in the Cilazapril group. The Cilazapril group had a significantly lower percentage of interstitial fibrosis than the control group.

Conclusions

Cilazapril can suppress structural and functional remodeling and prevent the induction and promotion of AF in chronic rapid atrial pacing dogs.     

伊布利特转复心房颤动和心房扑动的疗效观察

目的观察和比较伊布利特和普罗帕酮终止心房颤动(房颤)/心房扑动(房扑)的疗效及其不良反应。方法 268例发作持续时间<90 d的房颤/房扑患者,随机分组,分别静脉应用(1～2次,每次10 min推注)伊布利特(1.0 mg和1.0 mg)和普罗帕酮(70.0 mg和70.0 mg)。结果伊布利特转复房颤/房扑的成功率分别为67.6%(46/68)和92.4%(61/66),普罗帕酮转复房颤/房扑的成功率分别为32.5%(26/80)和29.6%(16/54)。伊布利特组平均转复时间(27±13)min,转复窦性心律时平均使用量为(1.5±0.4)mg。普罗帕酮组平均转复时间(39±7)min,转复窦性心律时平均使用量为(134.1±6.4)mg。房颤的转复率与左心房直径呈负相关,左心房直径<4.0 cm患者的转复率明显高了左心房直径≥4.0 cm患者的转复率;房扑持续时间可作为房扑终止的预测因子。扑动波周长延长是伊布利特终止房扑的主要特征。结论伊布利特作为一种Ⅲ类的抗心律失常药,在监测的条件下,能迅速、安全、有效地终止房颤/房扑。     

静脉地尔硫(卓)治疗老年人快速心室率房颤、房扑和室上速的临床观察

目的　观察静脉地尔硫艹卓 对老年人快速心室率的房颤、房扑及室上速的疗效与安全性。方法　 1 5例患者 (7例房颤、3例房扑、5例室上速 )静脉注射地尔硫艹卓 1 0～ 1 5mg,有反应者继以 1 0～ 1 5mg/ h浓度持续静点 6～ 1 2 h。结果　用药后心室率比用药前基础心率减少 >2 0 % ;转复为窦性心律或心室率 <1 0 0次 / min为治疗有反应 ,本组 1 5例患者 1 2例 (80 % )有反应 ;用药后心室率下降最大效应时间 1 1 min,心室率下降幅度 42± 1 6次 / min。结论　地尔硫艹卓 能安全地应用于快速心室率的房颤或房扑及室上速的老年人 ,并在大多数病人能迅速有效地达到心率的控制和中止室上速的发作 ,而且不会引起或加重心功能障碍。     

阵发性房颤患者房颤发作时心房电极植入的可行性

目的　探讨阵发性房颤患者在房颤发作时植入心房电极的方法和可靠性。方法　对 10例房颤发作时植入心房电极的患者与同期窦律下植入心房电极患者的植入时间、术中以及术后心房电极的感知、起搏功能进行对比随访观察。结果　阵发房颤患者恢复窦性心律后测定心房感知和起搏功能良好 ,房颤发作时所测得的房颤波振幅与窦性心律时所测心房波振幅有相关性 ,其手术时间和X线曝光时间与窦律下植入起搏器的患者无明显差异。结论　房颤发作时植入心房电极临床上是可行的     

Acute and long-term results of radiofrequency ablation of common atrial flutter and the influence of the right atrial isthmus ablation on the occurrence of atrial fibrillation.

AIMS: The purpose of this study was to evaluate the acute success rate and long-term efficacy of radiofrequency ablation of common type atrial flutter (AFL) by using a standardised anatomical approach in a large series of patients and to assess the influence of right atrial isthmus ablation on the occurrence of atrial fibrillation. There are no large scale prospective or retrospective multicentre studies for radiofrequency ablation of AFL. METHODS AND RESULTS: The study population consisted of 363 consecutive patients with AFL (mean age 58+/-16 years, 265 men) who underwent radiofrequency ablation at the inferior vena cava-tricuspid annulus (IVC-TA) isthmus using a standardised anatomic approach. Bidirectional isthmus block at the IVC-TA was achieved in 328 patients (90%). Following radiofrequency ablation, 343 patients (95%) were followed for a mean of 496+/-335 days. During the follow-up period, 310 patients (90%) remained free of AFL recurrences. Multivariate analysis identified five independent predictors of AFL recurrence: fluoroscopy time (p<0.001), atrial fibrillation after AFL ablation (p=0.01), lack of bidirectional block (p=0.02), reduced left ventricular function (p=0.035) and right atrial dimensions (p=0.046). Atrial fibrillation occurrence was significantly reduced after AFL ablation (112 in 343 patients, 33%) as compared to occurrence of atrial fibrillation before radiofrequency ablation (198 in 363 patients, 55%, p<0.001). CONCLUSIONS: The current anatomical ablation approach for AFL and criteria for evaluation of the IVC-TA isthmus block is associated with an acute success rate of 90% and a long-term recurrence rate of 10%. Radiofrequency ablation of common AFL results in a significant reduction in the occurrence of atrial fibrillation.     

长短周期现象与心房颤动和心房扑动

为了解心房颤动及心房扑动发生时的长短周期现象的临床意义,观察经动态心电图或监测心电图证实的心房颤动８例和心房扑动６例。结果显示：心房颤动或心房扑动发生前的长周期多见于房性期前收缩后代偿间歇及明显窦性心动过缓等心律失常;长短周期现象对心房颤动,心房扑动的启动作用可经心脏的程度刺激诱发和复制;６例患者经ＤＤＤ起搏治疗,陈发性心房颤动及心房扑动的发生率明显下降,部分病例还需服用抗心律失常药物。认为长短周     

非瓣膜病心房颤动对左心房大小的影响

目的　研究非瓣膜病心房颤动对左心房大小及左心室结构和功能的影响 ,探讨心房颤动与左心房扩大之间的因果关系。方法　选择 32 9例非瓣膜病心房颤动患者 ,根据心房颤动类型及心房颤动发作时间分组 ,比较各组间超声心动图参数。结果　心房颤动发作 1～ 3年组和 3年以上组左心房内径 ( L AD)均大于 1年以下组 ( P<0 .0 5 ,P<0 .0 1) ,而 3年以上组 L AD又大于 1～ 3年组 ( P<0 .0 5 ) ,3年以上组左心室舒张末期内径 ( L VED)大于 1年以下组 ( P<0 .0 5 ) ;持续性心房颤动组 L AD和 L VED均明显大于阵发性心房颤动组 ( P<0 .0 1) ;而持续性心房颤动患者心房颤动发作 3年以上组 L AD大于 1年以下组及 1～ 3年组 ( P<0 .0 1,P<0 .0 5 )。结论　心房颤动本身可引起左心房扩大 ,且左心房扩大常发生在心房颤动持续以后 ,因此转复心房颤动应尽早进行 ;心房颤动对左心室结构及功能也有一定影响 ,且持续性心房颤动的影响较大。     

Incidence and predictive factors of atrial fibrillation after ablation of typical atrial flutter

Although cavotricuspid isthmus radiofrequency catheter ablation is considered curative therapy for typical atrial flutter, many patients develop an atrial fibrillation after ablation. The purpose of our study was to determine the incidence and the predictive factors of post-ablation atrial fibrillation. One hundred and forty eight consecutive patients underwent cavotricuspid isthmus ablation for the treatment of typical atrial flutter between January 2004 and December 2005 in our electrophysiological department. Complete cavotricuspid isthmus block was successfully obtained in 96.6% of the patients. At the end of the electrophysiological study a sustained atrial fibrillation was inducible in 20 patients (13.5%). During an average follow-up of 21.3 ± 8.2 months, atrial fibrillation occurred in 27% of the patients. Univariate analysis identified four parameters correlated with post-ablation atrial fibrillation among the 21 parameters tested: the young age of the patients, a prior history of atrial fibrillation, an inducible atrial fibrillation, and a paroxysmal atrial flutter. Only inducible atrial fibrillation and paroxysmal atrial flutter were independent factors linked to atrial fibrillation after ablation. In our study the incidence of atrial fibrillation after cavotricuspid isthmus radiofrequency catheter ablation is 152 per 1,000 patient-years, i.e. 25 times higher than the incidence of atrial fibrillation in the general population of the same age. Twenty five percent of the patients who had neither prior history of atrial fibrillation nor structural heart disease suffered from atrial fibrillation during a mean follow-up of 21.3 ± 8.2 months. All these results suggest that atrial flutter and fibrillation could be manifestations of a more general electrophysiologic disease. They emphasize the need for all these patients to benefit from regular, long-term cardiological follow-up after cavotricuspid isthmus ablation because of the high incidence of atrial fibrillation. Treatment with antiarrhythmic and antithrombotic agents should also be adapted to these factors.     

老年高血压并存心房颤动患者左心房内径和血栓前状态研究

目的 探讨老年高血压并存心房颤动(房颤)患者左心房内径(LAD)的变化及其与血栓前状态各指标的相关性. 方法 高血压患者105例,其中65例并存房颤(房颤组),40例无房颤(非房颤组),30例健康体检无高血压和房颤为对照组.用M型心脏超声测定LAD,同时检测其纤维蛋白原(Fg)、D-二聚体(D-Dimer)、血浆假性血友病因子(wvF)及红细胞压积(HCT),并进行比较.再将房颤患者分为阵发性房颤组和持续性房颤组,比较其LAD、Fg、D-Dimer、vwF、HCT.然后以LAD为因变量,Fg、D-Dimer、vwF、HCT为白变量,进行直线相关分析. 结果 房颤组与对照组和非房颤组比较,LAD为(43.56±6.72)mm与(31.63±4.32)mm和(36.28±5.83)mm(均P＜0.05),Fg为(4.24±0.59)g/L与(2.80±0.46)g/L和(3.09±0.49) g/L(均P＜0.05),D-Dimer为(0.43+0.13) mg/L与(0.18±0.08) mg/L和(0.28±0.10) mg/L(均P＜0.05)；房颤组vwF、HCT分别为(290.44±29.02)％、0.46±0.07,与对照组(84.15±20.26)％、0.34±0.03比较,差异有统计学意义(均P＜0.05).非房颤组与对照组比较,LAD、D-Dimer差异有统计学意义(P＜0.05).持续房颤组与阵发房颤组比较,LAD、Fg、D-Dimer、vwF、HCT差异有统计学意义(均P＜0.05),LAD与Fg(r=0.683)、D-Dimer(r=0.735)、vwF(r=0.763)、HCT(r=0.759)呈正相关(均P＜0.01). 结论 LAD增大为房颤发生的危险因素,房颤患者存在血栓前状态,且LAD越大,血栓风险越大.     

Occurrence of atrial fibrillation after flutter ablation: the significance of intra-atrial conduction and atrial vulnerability

Atrial vulnerability and intra-atrial conduction delay are important substrates for paroxysmal atrial fibrillation (AFib); however, their significance is unknown in patients undergoing atrial flutter ablation. Antegrade (high right atrium to coronary sinus: HRA-CS) and retrograde (CS-HRA) intra-atrial conduction times and AFib inducibility were assessed in 61 patients undergoing ablation for type I atrial flutter. Twenty-three patients had structural heart disease and 18 AFib before the procedure. After 16 +/- 12 months of follow-up 17 patients experienced AFib, 5 of which progressed into chronic AFib. During the study, AFib was easily inducible in 14 patients, 7 of which developed AFib (P =.03). Patients with post- ablation AFib were older (59 +/- 11 vs. 44 +/- 15 years, P =.001), had longer intra-atrial conduction times before (98 +/- 17 ms vs. 68 +/- 20 ms, P <.001) and after ablation (91 +/- 19 ms vs. 73 +/- 21 ms, P =.01) than those without AFib. Discriminant analysis revealed that only age, previous AFib and inta-atrial conduction delay (>90 ms) were independent predictors of postablation AFib. Patients without a history of AFib and with normal intra-atrial conduction had a 3% risk of AFib, while patients with both factors had a 90% risk of AFib after ablation. Intra-atrial conduction delay is an important electrophysiological factor predicting atrial fibrillation after successful flutter ablation.     

心房超速递增刺激中止心房扑动

为探讨心房刺激中止心房扑动的方法及其效果,采用高于心房扑动频率心房超速起搏,S_1S_1递增刺激治疗心房扑动31例,其中心内右心房刺激11例,食管心房刺激20例.结果10例(32.3%)转为窦性心律,11 例(35.5%)诱发心房颤动后数s～3min内转为窦性心律,5例(16.1%)转为心房颤动后分别在20min、6h、1天、20天、1月后转为窦性心律,无效5例(16.1%),心内刺激与食管刺激效果差异无显著意义(P>0.05);转为心房颤动的16例,心室率由心房扑动时的132.6±28.8次/min变为心房颤动时的90.0±24.7次/min,心室率明显减慢(P<0.01),临床症状明显减轻,且无室性心律失常等并发症发生.提示心房超速递增刺激方法中止心房扑动有效、安全、简便,值得临床推广.