心房颤动直流电复律前后左心房功能变化的超声心动图研究

目的评价体外直流电复律对心房颤动(房颤)患者复律后左心房大小和容量的影响以及左心房大小与功能的关系。方法随机选择房颤患者68例,按心脏复律的方式分为直流电复律组36例,药物复律组32例,应用超声心动图测定其左房内径和容积,计算左房主动、被动排空容积及左房射血力。分析左房内径和容积变化与左房收缩功能的关系。结果房颤时所有患者的左房扩大,而恢复窦性心律后直流电复律组和药物复律组的左房上下径显著降低(P<0.05或P<0.001)。直流电复律与药物复律组比较,左房最大和最小容积显著增大(P<0.001或P<0.01)。左房机械功能正常患者与25例左房机械功能异常患者比较有较强的左房射血力;左心房机械功能降低的患者左心房内径和容积分别与左心房射血力呈负相关(r=-0.73和-0.78,P<0.001),而且左心房主动排空分数降低,管道容积却增加。结论体外直流电复律后许多患者出现左心房功能降低,心房收缩功能延迟恢复与持续的左房扩大有关;而药物复律患者的左房射血力较强与恢复窦性心律后左房容积明显降低有关。     

速度向量成像技术评价心房颤动患者射频消融术后急性期左心房功能

目的 运用超声心动图速度向量成像(velocity vector imaging,ⅤⅥ)技术评价射频消融术后急性期对阵发性及持续性心房颤动患者左房功能的影响.方法 分别采集10例阵发性心房颤动患者术前术后、10例持续性心房颤动患者术后及对照组10例左房的容积及各壁的速度、应变及应变率,分别对比阵发性心房颤动患者术前术后、持续性心房颤动患者术后与对照组的左房功能.结果 射频消融术后急性期对阵发性心房颤动患者左房功能无损害,术后经体表标化的左房面积较对照组明显增大;持续性心房颤动患者左房的整体功能左房排空分数(LAEF)、左房的主动排空分数(LAaEF)及左房的扩展指数较对照组降低,左房房间隔及侧壁的收缩期应变减低,房间隔的收缩速度较对照组减低,差异有统计学意义(均P＜0.05).结论 ⅤⅥ显示射频消融术急性期对阵发性心房颤动患者左房功能无损害,持续性心房颤动患者左房功能减低.     

经导管线性消融术治疗阵发性房颤对左房近期功能的影响

目的应用超声心动图评价左房线性消融术治疗阵发性房颤对近期左房功能的影响。 方法28例因阵发性房颤行线性消融的患者，于术前和术后2～3个月行超声心动图检查。通过二维超声测量左房容积和排空能力，组织速度成像检测二尖瓣前瓣环舒张晚期峰值速度Va，应变率显像检测左房壁舒张晚期峰值应变率SRa，来观察左房储存功能、管道功能和辅泵功能的变化。 结果消融后左房收缩末容积和左房内径无明显改变；左房管道容积和舒张末容积增高；左房分数、左房射血力、二尖瓣血流VA、二尖瓣环Va显著降低；左房平均SRa和局部各壁SRa均显著降低，尤其以后壁和侧壁降低最明显。 结论线性消融术对近期左房局部和整体功能均存在一定程度的不利影响。     

老年人阵发性房颤对心功能的影响

目的:观察老年人阵发性房颤患者心脏功能的改变。方法:74例有阵发性房颤发作史的老年患者,将其分为阵发性房颤组(45例)及房颤复律组(29例),并与对照组(43例健康老人),采用十二导联心电图仪及彩色多普勒二维超声心动图仪,测定各组的左心房内径(LAD)、射血分数(LVEF)、每搏量、心输出量、心脏指数及窦性心律时的P波离散度(Pd)等指标并分别进行对比分析。结果:多普勒测得各组LAD、LVEF、每搏量、心脏指数、心输出量各指数比较为:阵发性房颤组与房颤复律组及对照组比差异显著性均为(P<0.05);房颤复律组与对照组比差异为不显著(P>0.05);房颤复律组E/A为0.68±0.17,与对照组比差异有非常显著性(P<0.01)。阵发性房颤患者的Pd及Pmax较对照组明显延长(P<0.01)。结论:老年人阵发性房颤患者有短时间左心功能改变,房颤复律后心功能明显改善,但仍存在不同程度舒张功能障碍,因此,应对老年阵发性房颤患者的复律持积极态度,这对维护患者心功能,改善预后有重要的临床意义。     

特发性持续性房颤射频导管消融术后血浆脑钠肽浓度与左房功能变化

目的观察分析特发性持续性房颤行房颤射频消融术后血浆脑钠肽(BNP)浓度及左房功能的变化。方法选取临床20例特发性持续性房颤患者,这些患者均行CARTO三维标测系统指导下的以环双肺静脉电隔离术为基础的导管消融术。分别于术前、术后1周、1个月、3个月随访观察血浆BNP浓度和心脏彩超。结果射频消融术后血浆BNP浓度、左房内径于术后1周、1个月、3个月减少,与术前相比差异有统计学意义(P0.05),这种变化持续至术后3个月;左房排空分数和左室射血分数于术后1周、1个月、3个月持续增加,差异有统计学意义(P0.05)。术后窦性心律维持组BNP平均浓度和左房平均内径小于房颤复发组,左房排空分数和左室射血分数大于房颤复发组,差异均有统计学意义(P0.05);直线回归分析表明,在术后随访过程中,BNP浓度变化与左房内径变化呈正相关(P0.05),与左房排空分数和左室射血分数变化呈负相关(P0.05)。结论以环双肺静脉电隔离术为基础的房颤射频消融术使特发性持续性房颤患者复律后,可使血浆BNP浓度减少,左房内径减少,左房排空分数和左室射血分数增加,左房功能改善。     

超声心动图对阵发性房颤患者左房顿抑及其影响因素的研究

目的探讨阵发性房颤患者复律后左房顿抑情况及其可能影响的因素。方法阵发性房颤组35例,持续性房颤组19例,对照组为同期体检健康者30例。超声心动图检测房颤患者复律当日、3 d、7 d、1个月的左房整体、局部收缩功能,并与对照组比较。房颤患者于复律当日检测血浆心钠素。结果阵发性房颤组复律当日和3 d时二尖瓣口血流频谱A峰最大流速(VA)、左房射血力(LAF)、肺静脉口血流频谱负向a波最大流速(PVa)、二尖瓣环舒张晚期负向a波速度峰值(MVa)及左房壁局部组织多普勒a波速度峰值(LAVa)均低于复律后7 d和1个月(P均0.05),复律当日、3 d、7 d上述指标阵发性房颤组均高于持续性房颤组(P均0.05)。多元回归分析显示阵发性房颤组房颤持续时间和血浆心钠素水平与复律当日LAF独立相关。结论阵发性房颤患者复律后存在左房顿抑,房颤持续时间和血浆心钠素水平是其独立危险因素。     

心房颤动与左心房大小的关系

作者对126例房颤病人进行超声心动图检查,旨在探讨房颤与左房大小的关系。126例房颤病人测值经统计学处理,各组均以1978年大连召开的超声诊断学术会议上通过的正常统一标准(下称正常值)。(1)风心病人阵发性房颤时左房内径41.5±3.90,持续性房颤时左心房53.0±11.6,以正常值为对照,左房内径均显著大于正常人(P<0.01)。(2)冠心病阵发性房颤者左心房内径35.3±9.3,持续性房颤者左房内径43.2±10.4,均显著大于正常人(P<0.01),(3)但冠心病持续性房颤病人与风心病人相比,左房内径显著小于后者,两者相差非常显著(P<0.01),冠心病阵发性房颤左房内径也小于风心病,两者相差显著(P< 0.05),(4)甲状腺功能亢进病人发生房颤时左房内径与正常人相比无显著差异(P>0.05),(5)特发性房颤病人左房内径与正常人相比也无显著差异(P>0.05),(6)扩张型心肌病房颤时左     

心脏彩超对房颤患者术后复发的预测价值

目的探讨心脏彩超对房颤患者术后复发的预测价值。方法选取2015年7月～2019年7月我院收治的心房颤动患者82例,术前对其进行心脏超声检查并依据术后3个月是否复发分为复发组33例和未复发组49例。对比两组心脏彩超参数导致患者术后复发的危险因素。结果 82例患者中33例患者复发,复发率40.24%;复发组LVESD、左房最大容积指数及左房最小容积指数较未复发组高,左房主动排空分数及左房总排空分数较未复发组低,差异有统计学意义(P<0.05);经多因素分析发现,左房主动排空分数与左房总排空分数是影响心房颤动患者术后的独立危险因素(P<0.05)。结论心脏彩超参数对于心房颤动患者术后复发预测具有一定参考价值,而左房主动排空分数与左房总排空分数是影响心房颤动患者术后的独立危险因素。     

运用左心房排空率评价高血压患者左心房功能的初步研究

目的 探讨左心房(左房)排空率(dV/dt)评价高血压患者左房功能的可行性及临床价值.方法 运用左房追踪技术(LA-tracking),分别获取31例健康志愿者(正常对照组)和21例高血压患者(病例组)的左房排空率曲线、左房容积曲线和长径曲线,测量左房排空率、左房容积和长径在左房充盈期、左室舒张早期及舒张晚期的峰值,分析左房充盈期的排空率峰值与左房最大容积的相关性.结果 与正常对照组比较,高血压组左室舒张早期的左房排空率峰值(dV/dt_E)明显降低,左室舒张晚期的左房排空率峰值(dV/dt_A)明显增大,差异具有统计学意义(P<0.05).左房充盈期的左房排空率峰值(dV/dt_S),左房容积(LAV)和长径(LAL)峰值在高血压组略高于对照组,但差异无统计学意义(P>0.05).两组dV/dtS与左房最大容积(LAV_S)均有良好的相关性(r_1=0.86,r_2=0.80).结论 左房排空率是从整体上定量评价左房功能的一种新参数.     

老年人房颤与NT-ProBNP、左房大小的关系及抗凝现状分析

目的观察老年人房颤与N-末端脑钠肽前体(NT-proBNP)及左房大小的关系,并分析其抗凝现状。方法对120例老年房颤患者的临床资料进行回顾性分析,包括初发、阵发、持续性、持久性、长期持续性房颤患者的NT-proBNP水平、左房内径和抗凝方法。结果 120例老年房颤患者中,初诊房颤占15.0%,阵发性房颤占30.0%,持续性房颤、持久性房颤、长期持续性房颤占55.0%。使用华法林抗凝治疗占41%,房颤发生脑栓塞占9.1%。持续性房颤、持久性房颤、长期持续性老年房颤的患者NT-proBNP明显高于阵发性、初诊房颤患者,其左房内径明显大于阵发性、初诊房颤患者的左房内径。抗凝治疗中华法林组栓塞事件发生率(2.08%)低于阿司匹林组(13.89%),而两组出血事件发生率无显著差异。结论持续性房颤、永久性房颤、长期持续性房颤在老年患者中占主导地位。房颤时间越长,左房内径越大,NT-proBNP也越高。华法林抗凝效果优于阿司匹林,且获益超过出血风险。     

Persistent Atrial Standstill with Atrial Inexcitability

Electrophysiologic studies including His bundle recording, atrial, and ventricular stimulation, were performed in three symptomatic patients with persistent atrial standstill of unknown etiology. The rhythm was junctional in two cases and ventricular in one. In two cases, evidence suggestive of associated impairment of the His bundle conduction system was found. The atria were inexcitable at multiple sites and no retrograde conduction to the right atrium could be elicited by ventricular pacing. Follow-up in the three cases, respectively for 48, 42 and 12 months after pacemaker implantation, revealed no return of spontaneous atrial electrical activity.     

Atrial Pressure and Experimental Atrial Fibrillation

SIDERIS, D.A., et al .: Atrial Pressure and Experimental Atrial Fibrillation . A possible profibrillatory effect on the atria of an elevated atrial pressure and the site of atrial stimulation was examined. In 15 anesthetized dogs, right or left atrial or biatrial pacing was applied at a high rate (300–600/min) for 5 seconds at double threshold intensity under a wide range of atrial pressures achieved by venous or arterial transfusion or bleeding. Induction of atrial fibrillation in 236 of 1,971 pacing runs was associated with a significantly higher (P < 0.001) atrial pressure (21.6 ± 12.2 mmHg, mean ± SD) than maintenance of sinus rhythm (16.8 ± 11.1 mmHg in 1,735 of 1,971 pacing runs). Stimulation of the right atrium resulted in atrial fibrillation more frequently than left atrial or biatrial stimulation, with biatrial stimulation less frequent than right or left atrial stimulation. The induction of atrial fibrillation was related to the atrial pressure and to the site of stimulation but not to the pacing rate or the prepacing heart rate. The prepacing heart rate, associated with failure to induce sustained atrial fibrillation, was higher than that associated with atrial fibrillation in 12 of 15 experiments (significantly in 6) and not significantly lower in 3 of 15. Atrial fibrillation lasting 1 minute or more was more frequently associated with simultaneous stimulation of both atria than of either atrium alone. Thus, an elevated atrial pressure may facilitate the induction of atrial fibrillation. The site of stimulation also plays an important role for both the induction and maintenance of atrial fibrillation in this model.     

Atrial Septal Versus Atrial Appendage Pacing:

HERMIDA, J.-S., et al. : Atrial Septal Versus Atrial Appendage Pacing: Feasibility and Effects on Atrial Conduction, Interatrial Synchronization, and Atrioventricular Sequence. Atrial septal (Se-P) and atrial appendage pacing (Ap-P) were compared in a randomized, controlled study to assess the feasibility, the reliability, and the effects of Se-P on atrial conduction, interatrial synchronization, and the AV sequence. The main baseline characteristics of the patients were comparable in both groups. There was no difference in feasibility or reliability between the two techniques. Compared to Ap-P   (n = 28)   , Se-P   (n = 28)   decreased the P wave duration, left atrial electromechanical delay (LAEMD), and interatrial interval (−1.6% vs   +28%, P < 0.001; −3%   vs   + 30%, P < 0.001; −130%   vs   + 78%, P < 0.001   ); it induced a smaller increase of the right AEMD, a slight reversal of the timing of the atrial systoles and a shortening of the PR interval (−13% vs   + 25%, P < 0.001   ) and of the interval separating atrial systoles from ventricular activation. Finally, the shortening of the PR interval was smaller during high Se-P versus low Se-P. Se-P avoids the undesirable prolongation of the atrial, interatrial, and AV conductions observed during Ap-P. In addition, Se-P creates a slight reversal of the timing of the atrial systoles and induces a shortening of PR interval, the extent of which could depend on the height of the pacing site on the septum. (PACE 2003; 26[Pt. I]:26–35)     

Familial Atrial Standstill with Coexistent Atrial Flutter

A child with familial atrial staudstill and a ventricular pacemaker had syncope due to atrial flutter that was treated bv His-bundle ablation. Bradycardia protection alone may be insufficient in patients with atrial standstill.     

Atrial and Ventricular Pressures in Atrial Flutter

The hemodynamic effects of atrial flutter (AF) are unknown. The purpose of the present study was to investigate the changes in atrial and ventricular pressures after induction of AF. In 23 patients with paroxysmal AF (age 59 ± 9 years), a hemodynamic study was performed both during sinus rhythm and after induction of the tachyarrhythmia. During AF, 13 patients showed a fixed 2:1 AV conduction and 10 patients showed variable conduction. Mean right and left atrial pressures increased (P < 0.001) and right and left ventricular end-diastolic pressures decreased (P < 0.001) after induction of AF. Roth the increase in mean atrial pressures and the decrease in ventricular end-diastolic pressures were present either in the patients with fixed 2:1 AV (heart rate: 133 ± 15 beats/min) or in those with variable conduction (heart rate 96 ± 15 beats/min), but were more marked in the former. AF produces an impairment of atrial function, as evidenced by the increase in mean atrial pressures and reduction in ventricular end-diastolic pressures in the absence of an elevated heart rate. The mechanisms responsible for the increase in mean atrial pressures are unknown; however, atrial contractions against closed AV valves seem to play an important role.     

Atrial Refractory Periods after Atrial Premature Beats in Patients with Paroxysmal Atrial Fibrillation

To study the effects of an atrial premature beat on atrial refractory periods, we investigated 11 patients (group A) who were the control group, 12 patients suffering from paroxysmal atrial fibrillation (group B), and 10 patients (group C) without arrhythmias but with cardiopathy or cardiomyopathy. At every eighth complex of a constant atrial electrostimulated rhythm a fixed premature extrastimulus was introduced, and effective and functional refractory periods (ERP and FRP) were measured in three different sites of the right atrium, before and after introduction of this extrastimulus. Average ERP and FRP shortened respectively in group A, from 220.28 ± 25.68 msec and 281.17 ± 28.15 msec before extrastimulation, to 190.58 ± 22.74 msec and 245.88 ± 19.86 msec after; in group B, from 219.44 ± 27.38 msec and 284 ± 30.06 msec to 191.66 ± 28.72 msec and 253.23 ± 34.01 msec; and in group C from 229.03 ± 29.65 msec and 289.67 ± 51.62 msec to 194.19 ± 24.6 msec and 237.74 ± 39.59 msec. The average dispersions of ERP and FRP in group A were, respectively: 41.81 ± 21.36 msec and 36.36 ± 18.04 msec before extrastimulation, 28.18 ± 18.14 msec and 35.45 ± 15.72 msec after. In group B: 26.66 ± 19.46 msec and 41.66 ± 16.96 msec versus 45.83 ± 23.91 msec and 45 ± 34.77 msec and in group C: 27 ±11.59 msec and 45 ± 29.15 msec versus 29 ± 18.52 and 27 ± 18.88. It is concluded that an atrial premature beat tends to shorten the dispersion of atrial refractory periods when patients are free of arrhythmias, and to lengthen them when paroxysmal atrial fibrillation are documented.     

Left Atrial Voltage during Atrial Fibrillation in Paroxysmal and Persistent Atrial Fibrillation Patients

Background: Left atrial (LA) endocardial voltage characteristics assessed during atrial fibrillation (AF) have not been previously compared in different AF types. This study was aimed at investigating the LA voltages and volumes in patients with paroxysmal and persistent AF. Methods: LA electroanatomic voltage maps acquired during AF were compared between consecutive patients without major structural heart disease undergoing first catheter ablation for paroxysmal AF (n = 100) or persistent AF (n = 100). The groups were comparable in baseline clinical characteristics. Results: Patients with persistent AF presented with lower median LA voltage (median 0.41, interquartile range [IQR] 0.31–0.51 mV versus median 0.99, IQR 0.47–1.56 mV; P < 0.001), and maximum LA voltage (4.07 ± 1.76 vs 6.42 ± 2.16 mV; P < 0.001). They also had a higher proportion of the LA points exhibiting voltage <0.2 mV (30 ± 20 vs 12 ± 11%; P < 0.001) and voltage 0.2–1.0 mV (55 ± 15 vs 42 ± 19%; P < 0.001). They further displayed higher LA volume/body surface area (75 ± 16 vs 58 ± 13 mL/m²; P < 0.001). In the multivariate regression model, both LA voltage (P < 10^?9) and LA volume (P < 10^?5) were significant determinants of AF type. Conclusion: Patients with persistent AF had significantly lower LA voltage compared with patients with paroxysmal AF even after adjustment for differences in indexed LA volume. LA voltage represents an independent covariate of clinical manifestation of AF. (PACE 2010; 541–548)     

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid-right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachman's bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120-ms cycle length was performed five times at each pacing site to evaluate the in-ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200-ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.     

Right Atrial Separation Procedure for Eliminating Chronic Atrial Fibrillation Associated with Atrial Septal Defect

Chronic atrial fibrillation (AF) had been documented in a patient with atrial septal defect for 7 years. A right atrial separation procedure was performed for ablation of chronic AF, concomitant with repair of the atrial septal defect, and followed by atrial electrophysiological mapping. A horizontal transectional incision extending to the borders of the atrial septum and the tricuspid annulus was made. Cryolesions of the atrial isthmus between the margin of the upper incision and the tricuspid valve annulus were created at -60†C for 2 minutes at a time. After the operation, the patient had restored normal sinus rhythm during a subsequent follow-up period of 48 months.