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1.
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.  相似文献   

2.
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.  相似文献   

3.
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。  相似文献   

4.
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.  相似文献   

5.
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。  相似文献   

6.
阵发性房颤患者房颤发作时心房电极植入的可行性   总被引:1,自引:0,他引:1  
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  相似文献   

7.
非瓣膜病心房颤动对左心房大小的影响   总被引:6,自引:0,他引:6  
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。  相似文献   

8.
目的 观察快速起搏猪右心房制备持续性心房颤动(AF)的效果,探讨白藜芦醇(RES)干预对持续性AF猪的心房结构重构的影响.方法 18只小家猪(雌雄不拘)按完全随机设计的分组方法(采用动物编号和随机分组表)分为起搏组(ATP组)、假手术组(Sham组)和RES干预组各6只,采用Seldinger血管穿刺技术送入双极电极至右心房并连接实验用起搏器(AOO),ATP组和RES干预组的右心房快速起搏(500次/min)2周,制备持续性AF实验模型.3组猪分别于起搏前和起搏2周后进行电生理和经胸壁超声心动图检查,以检测AF的持续时间、左右心房大小及左心房收缩末面积.RES干预组猪于起搏前1周开始服用RES(2.5 mg·kg-1·d-1).起搏2周后取各组猪的左右心房组织标本,观察心房组织形态学和间质纤维化的改变,用免疫组织化学分析软件计算胶原容积分数(CVF)来反映间质纤维化程度.结果 (1)起搏2周后,ATP组AF的发生率较RES干预组明显升高(100%比66.7%,x2=10,P<0.01)、持续时间延长[(26.41±9.89)min比(9.56±1.36) min,F=10.7,P=0.01].(2)起搏2周后,ATP组和RES干预组猪的左右心房明显比起搏前增大;但RES干预组的左心房收缩末面积明显低于ATP组[(599.2±8.7) mm2比(744.3±29.9) mm2,F=130.61,P<0.01].(3)RES干预组左右心房组织CVF明显低于ATP组(56%±6%比73%±7%;59%±6%比75%±7%,均为P<0.01).结论 快速起搏猪右心房可成功制备持续性AF模型;RES干预可以明显抑制快速起搏右心房诱发的持续性AF猪的心房结构重构,减少AF的发生.  相似文献   

9.
目的:探讨心房晚电位预测阵发性心房颤动的价值。方法:以P波触发体表信号平均心电图记录技术测试55例老年人(正常组),35例有单发房性早搏者(房早组)及50例阵发性心房颤动患者(房颤组)的心房晚电位(包括滤波后P波时限,P波终末20 ms、30 ms、40 ms的电压均方根值)并进行比较分析。结果:滤波后P波时限:较之正常组与房早组,房颤组的显著延长(P<0.01),正常组与房早组无显著差异(P>0.05)。P波终末20 ms电压均方根值:正常组为(5.89±2.07)μV,房早组为(5.03±2.04)μV,房颤组为(3.96±1.80)μV,较之正常组与房早组,房颤组的显著降低(P<0.01,P<0.05),正常组与房早组无显著差异(P>0.05);P波终末30 ms电压均方根值:较之正常组、房早组,房颤组的显著降低(P<0.01.P<0.05).房早组亦较正常组显著降低(P<0.05)。结论:P波触发体表信号平均心电图记录心房晚电位可作为预测阵发性心房颤动的一个快速、无创性指标。  相似文献   

10.
心房超速递增刺激中止心房扑动   总被引:2,自引:0,他引:2  
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.  相似文献   

11.
AIMS: This study evaluates a simple echocardiographic rhythm independent expression of left atrial (LA) function, 'the left atrial function index' (LAFI). BACKGROUND: Quantitation of LA function is challenging and often established parameters including peak A are limited to sinus rhythm (SR). We hypothesized that atrial function could be characterized independent of rhythm by combining analogues of LA volume, reservoir function and LV stroke volume. METHODS: Seventy-two patients with chronic atrial fibrillation (CAF) were followed for six months post cardioversion (CV). Thirty-seven age matched healthy subjects were controls. The LAFI = LAEF x LVOT-VTI/LAESVI (LAEF = LA emptying fraction, LAESVI = maximal LA volume indexed to BSA, LVOT-VTI = outflow tract velocity time integral). RESULTS: The LAFI pre-CV in the CAF group was depressed vs controls (0.10 +/- 0.05 vs 0.54 +/- 0.17; P = 0.0001). Post-CV, LAFI was lower in persistent AF than in those restored to SR (AF vs SR: 0.08 +/- 0.03 vs 0.15 +/- 0.08; P = 0.0001), improved progressively in SR and was unchanged when AF persisted. CONCLUSION: The LAFI, a simple, rhythm independent expression of atrial function, appears sensitive to differences between individuals in AF and those restored to SR and justifies clinical and investigative applications.  相似文献   

12.
目的 评价典型心房扑动(房扑)对心房颤动(房颤)导管消融复发的影响.方法 120例药物治疗无效的阵发性房颤患者在三维电解剖标测系统和肺静脉环状标测电极导管联合指导下行环肺静脉电隔离.其中17例(14.2%)合并典型房扑(房扑组,其余作为对照组),行三尖瓣环峡部消融,三尖瓣环峡部消融终点为三尖瓣环峡部双向阻滞.房颤复发定义为导管消融3个月后发生房性快速心律失常.结果 房扑组房颤病程(9.8±10.7)年,长于对照组(5.9±6.3)年,差异有统计学意义(P=0.036).房扑组与对照组相比,年龄、性别、合并器质性心脏病、左心房直径、左心室射血分数差异无统计学意义.随访91~401(237±79)d,房扑组房颤复发率为47.1%,对照组房颤复发率为12.6%,两组间差异有统计学意义(P=0.001).经校正年龄、房颤病程、合并器质性心脏病、左心房直径等因素,Cox多因素分析发现消融术前合并房扑是房颤复发的独立危险因素(危险比3.52,95%可信区间1.32~9.34,P=0.012).结论 典型房扑可能增加房颤导管消融术后房颤的复发,房颤导管消融前应对患者是否合并典型房扑进行认真评价.  相似文献   

13.
14.
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.  相似文献   

15.
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.  相似文献   

16.
目的:采用人工心脏起搏的方法制备家兔急性心房颤动模型,分别探讨胺碘酮与氯沙坦对心房颤动导致心房重构的不同干预效果.方法:40只家兔随机分为0.9%氯化钠溶液组(对照组)、胺碘酮组、氯沙坦组、合用组,分别灌胃给药1周,以600次/min的频率起搏心房8 h,并分别于起搏前、起搏后0.5、1、2、4、6、8 h及停止起搏后10、20、30 min重复测定心房有效不应期(AERP).结果:①经过8 h快速起搏后对照组AERP200(100.63±7.5)ms和AERP150(95.01±6.2)ms均较起搏前明显缩短(均P<0.01),AERP200较AERP150缩短更为明显(P<0.05),胺碘酮组、氯沙坦组及合用组快速起搏前后AERP无显著变化.②停止快速起搏后,对照组AERP逐渐恢复,AERP200和AERP150在10 min内基本恢复至起搏前的95.78%和96.76%,30 min内基本恢复至起搏前的99.07%和99.39%.结论:短期快速心房起搏可致心房电重构;胺碘酮和氯沙坦可以逆转心房电重构.  相似文献   

17.
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.  相似文献   

18.

Background

There is evidence suggesting that growth differentiation factor 15 (GDF‐15) appears to be associated with stroke in patients with atrial fibrillation (AF). AF‐related thromboembolic stroke is predominantly attributed to the thrombus from the left atrium (LA) or left atrial appendage (LAA).

Hypothesis

GDF‐15 is related to LA/LAA thrombus in nonvalvular AF (NVAF) patients.

Methods

A total of 894 patients with NVAF without anticoagulation therapy were included in this study. All patients routinely underwent transesophageal echocardiography for detection of LA/LAA thrombus. GDF‐15 was measured by enzyme‐linked immunosorbent assay. Logistic regression models were used to test for association.

Results

LA/LAA thrombus was detected by transesophageal echocardiography in 69 (7.72%) patients with AF. The GDF‐15 levels in the patients with LA/LAA thrombus were significantly higher than those without LA/LAA thrombus (log10 GDF‐15: 2.989 ± 0.023 ng/L vs 2.831 ± 0.007 ng/L; P < 0.001). Logistic regression analysis showed that GDF‐15 was an independent risk factor for LA/LAA thrombus (odds ratio [per quarter]: 1.799, 95% confidence interval: 1.381‐2.344, P < 0.001) after adjusting for potential clinical risk factors. The optimal cutoff point for GDF‐15 predicting LA/LAA thrombus was 809.9 ng/L (sensitivity, 75.3%; specificity, 61.5%), determined by ROC curve. The area under the curve was 0.709 (95% confidence interval: 0.644‐0.770, P < 0.001).

Conclusions

Elevated GDF‐15 indicated a significantly increased risk for LA/LAA thrombus in NVAF patients. Thus, GDF‐15 might be a potentially useful adjunct in discriminating LA/LAA thrombus in NVAF patients.  相似文献   

19.
伊布利特转复心房颤动和心房扑动的疗效观察   总被引:2,自引:0,他引:2  
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。  相似文献   

20.
Twelve-lead electrocardiograms revealed no atrial activity and a wide QRS escape rhythm at 38 beats/min in a 20-year-old man who presented with syncope. Doppler echocardiography documented the absence of A wave both in the tricuspid and mitral valve flow. The only mechanical activity was documented at the left atrial appendage. An electrophysiologic study demonstrated electrical inactivity in the right atrium and an atrial tachycardia in the left atrium. Atrial pacing with maximum output did not capture the atria. Our case represents an advanced stage of partial atrial standstill, with a mechanical and electrical atrial activity confined only to the left trial appendage. The patient remained asymptomatic after receiving a VVIR pacemaker and anticoagulation therapy.  相似文献   

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