心脏自主神经消融治疗缓慢性心律失常

心脏迷走神经张力病理性增高,可导致窦房结功能异常、房室传导阻滞,引起缓慢性心律失常。此类患者多有心悸、乏力、头晕、晕厥等症状,严重者可致猝死,过去常需采用起搏器治疗。近年来有报道采用心脏去神经消融的方法治疗上述疾病,取得了良好效果,为迷走神经张力增高导致的缓慢性心律失常的治疗提供了新的途径。     

心脏神经消融治疗缓慢性心律失常

自主神经功能的障碍常引起心原性晕厥、功能性房室阻滞和窦房结功能障碍.巴西的Pachon M等人尝试用射频消融技术祛除窦房结和房室结的迷走神经支配而治疗这类疾病.     

心脏自主神经消融治疗缓慢性心律失常研究进展

缓慢性心律失常是各种原因引起的长RR间期,其中部分由心血管反射因素触发而引起功能性心动过缓或传导延缓、中断,严重者可引起晕厥,后者又称之为心脏抑制型血管迷走性晕厥（VVS）。心脏自主神经节（GP）消融在近二十年中发展迅速,并已被证明是治疗VVS及相关心动过缓的有效方法。影响GP消融成功率的因素包括：具体的消融部位、GP定位、手术技术、消融终点评估以及其他干预措施的整合。文章就GP消融治疗VVS及心动过缓的最新进展做一综述。     

心脏神经消融术对神经反射性缓慢性心律失常的治疗价值

目的:回顾性分析心脏神经消融术在治疗神经反射性缓慢性心律失常的有效性和安全性。方法:入选2017年12月至2020年1月在中国医学科学院阜外医院心律失常中心行心脏神经消融术治疗的39例神经反射性缓慢性心律失常的患者。术前22例诊断为间歇性高度房室传导阻滞,7例诊断为窦性停搏,6例诊断为窦性心动过缓,3例患者同时有高度房...     

射频消融治疗快速心律失常房室结损伤的预防

目的 总结经验教训,提高射频消融的安全性。方法 回顾分析了10例射频消融并发房室结损伤的病例,提出其预防及处理方法。结果 400例射频消融术中并发房室结损伤10例（占2.5%）,其中发生Ⅲ度房室传导阻滞（AVB）需要安装永久起搏器2例（占0.50%),一过性Ⅲ度AVB、一过性Ⅱ度Ⅰ型AVB和和一过性Ⅰ度AVB共8例（占2.00%)。结论 射频消融并发房室结的损伤与操作的经验有关,严格操作规程,纯熟掌握操作技术和影响学知识,严密监测消融中心电图变化,及时正确处理,可以使损伤减少到最低限度。     

房室结双径路与心律失常

近年来经外科手术标测和经导管射频消融术选择性消融慢径路或快径路治疗房室结内折返性心动过速(AVNRT),进一步证实房室结双径路不仅是功能性的,且有解剖学基础.双径路与阵发性室上性心动过速(PSVT)和房室传导中的一些特殊现象正日益引起临床关注,现作简述如下.一、房室结双径路与室上性心动过速1.双径路与房室结内折返性心动过速     

房室结消融联合心脏起搏器植入治疗难治性房性心律失常的体会

相当一部分药物疗效不佳或不能耐受药物副作用或不愿意长期服用药物的房颤患者需要进行房室结消融联合心脏起搏器治疗[1～7]。近年来,导管消融术已成为相当一部分房颤的一线治疗措施[8～11,12]。文本报道1例药物难治性房性心律失常病例诊治经历并文献复习。临床资料患者女,53岁,自1980年开始出现突发性心悸,伴胸闷、喘气和出汗,无黑矇、晕厥、胸痛等,曾在     

伊布利特对犬心脏窦房结和房室结的作用

目的观察伊布利特对犬心脏窦房结、房室结的影响。方法 18只成年健康雄性杂种犬,麻醉后气管插管,开胸并缝合电极,伊布利特按0.10 mg/kg静脉推注给药(10 min缓推,给药30 min后按照0.01 mg/min静脉滴注维持),观察给药前后心率、窦房结和房室结功能的变化。结果伊布利特对心率有明显的抑制作用,作用的高峰时间在给药后20～30 min,2 h后心率基本恢复到用药前的水平;1只犬在给药后出现长达5 s的窦性停搏;试验中,1只犬在给药后5 min出现房室结2:1下传,给药后20 min该现象自行消失。结论伊布利特可明显减慢窦性心率,对窦房结的自律性有一定的抑制作用,对房室结的功能也有一定的抑制作用。     

心脏结周消融治疗缓慢心律失常

目的 探讨心脏结周消融治疗缓慢心律失常的可行性和安全性 方法 选择症状严重,拟行起搏器治疗的功能性心动过缓患者,在影像解剖和心内电图神经电位指引下行导管射频消融.结果 10例患者,男性8例,女性2例,1例有器质性心脏病,6例房室阻滞,4例窦房结功能障碍.在窦房结和房室结周围均记录到神经电位,放电10～15 s神经电位消失.消融中先出现迷走神经激惹效应,之后窦房结和房室结功能改善.9例术中心动过缓消失,1例失败.随访2～12个月,2例复发,余症状消失,无并发症.结论 心脏结周消融治疗迷走介导的缓慢心律失常安全可行.     

自主神经节丛消融对窦房结及房室结功能的急性期影响

目的探讨神经节丛(GP)消融对窦房结(SAN)及房室结(AVN)功能的影响。方法 7条犬开胸并在左、右心房及肺静脉缝置多极电极导管以备记录及刺激,对左侧及右侧GP分别进行消融,消融前后分别测定静息心率、SAN及AVN功能,SAN功能包括测定6个不同水平起搏周长(380,350,330,300,280及250 ms)时SAN恢复时间(SNRT)以及校正的SNRT(cSNRT);AVN功能包括AH间期(H is束电图记录的房室结传导时间)、递增起搏时出现文氏房室传导阻滞时起搏周长、出现2∶1房室传导阻滞时起搏周长、右房短阵超速起搏诱发心房颤动(简称房颤)时的平均心室率。结果 GP消融后窦性心率无显著改变,长起搏周长时SNRT及cSNRT无显著变化,而短起搏周长时则显著减少(P0.05)。各起搏周长下AH间期、出现文氏房室传导阻滞及2∶1房室传导阻滞时的起搏周长、房颤时平均心室率在GP消融前后均无显著变化。结论 GP消融在较短起搏周长情况下增强了SAN功能,但对AVN功能无明显影响,可能与GP消融时同时破坏了副交感及交感神经成分有关。     

选择性消融窦房结与房室结周围神经治疗阵发性心动过缓

目的探讨选择性消融窦房结与房室结周围神经,治疗缓慢性心律失常的方法与初步效果。方法选择症状严重,拟行起搏器治疗的阵发性心动过缓者,在X线与64排螺旋CT心脏解剖影像指导下,以手工或磁导航遥控操作,标测窦性心律心房激动顺序,围绕并避开心房最早激动位点和His束区域,记录心内电图神经组织电位,温控射频消融,观察消融反应,随访治疗效果。结果13例患者,男9例,女4例,年龄36.46±9.51(14～51)岁。1例有器质性心脏病,高度房室传导阻滞7例,病窦综合征4例,病窦综合征合并高度房室传导阻滞1例,窦性心动过缓1例,6例黑矇或晕厥。在窦房结和房室结周围均记录到神经组织电位,放电10～15s神经组织电位消失。消融中先出现迷走激惹效应,之后窦房结和房室结功能改善。12例术中心动过缓消失,1例失败。随访13±5.89(3～20)个月,2例复发,余症状消失,无并发症。结论选择性消融窦房结与房室结周围神经治疗迷走介导的缓慢心律失常,可行、安全、有效。     

Identification and characterization of atrioventricular parasympathetic innervation in humans

INTRODUCTION: We hypothesized that in humans there is an epicardial fat pad from which parasympathetic ganglia supply the AV node. We also hypothesized that the parasympathetic nerves innervating the AV node also innervate the right atrium, and the greatest density of innervation is near the AV nodal fat pad. METHODS AND RESULTS: An epicardial fat pad near the junction of the left atrium and right inferior pulmonary vein was identified during cardiac surgery in seven patients. A ring electrode was used to stimulate this fat pad intraoperatively during sinus rhythm to produce transient complete heart block. Subsequently, temporary epicardial wire electrodes were sutured in pairs on this epicardial fat pad, the high right atrium, and the right ventricle by direct visualization during coronary artery bypass surgery in seven patients. Experiments were performed in the electrophysiology laboratory 1 to 5 days after surgery. Programmed atrial stimulation was performed via an endocardial electrode catheter advanced to the right atrium. The catheter tip electrode was moved in 1-cm concentric zones around the epicardial wires by fluoroscopic guidance. Atrial refractoriness at each catheter site was determined in the presence and absence of parasympathetic nerve stimulation (via the epicardial wires). In all seven patients, an AV nodal fat pad was identified. Fat pad stimulation during and after surgery caused complete heart block but no change in sinus rate. Fat pad stimulation decreased the right atrial effective refractory period at 1 cm (280 +/- 42 msec to 242 +/- 39 msec) and 2 cm (235 +/- 21 msec to 201 +/- 11 msec) from the fat pad (P = 0.04, compared with baseline). No significant change in atrial refractoriness occurred at distances >2 cm. The response to stimulation decreased as the distance from the fat pad increased. CONCLUSION: For the first time in humans, an epicardial fat pad was identified from which parasympathetic nerve fibers selectively innervate the AV node but not the sinoatrial node. Nerves in this fat pad also innervate the surrounding right atrium.     

Selective parasympathetic denervation following posteroseptal ablation for either atrioventricular nodal reentrant tachycardia or accessory pathways

Baroreflex gain and coronary sinus norepinephrine and epinephrine levels were measured before and immediately after radiofrequency ablation in the posteroseptal region in 9 patients with atrioventricular nodal reentrant tachycardia or posteroseptal accessory pathways. Arterial baroreflex gain was significantly reduced after radiofrequency ablation (p = 0.046), whereas coronary sinus epinephrine and norepinephrine levels did not change significantly compared with preablation levels.     

Radiofrequency ablation of left-sided atrioventricular accessory tract to treat supraventricular tachycardia]

Eleven procedures of radiofrequency catheter ablation of left-sided atrioventricular accessory tract were performed in 10 patients with atrioventricular reentry tachycardia aged 13-57 (32.7 +/- 13.2) years old. 10 patients, 9 with overt preexcitation syndrome and 1 with concealed bypath tract, had paroxysmal supraventricular tachycardia refractory to drugs for 1-31 (7.8 +/- 9.8) years. The ablation was succeeded in 9 cases (90%). The accurate localization of the accessory tract and the operating skill of ablation electrode were the key factors of success in ablation and reducing exposure to x-ray.     

Functional characterization of atrial electrograms in sinus rhythm delineates sites of parasympathetic innervation in patients with paroxysmal atrial fibrillation.

OBJECTIVES: This study sought to characterize left atrial (LA) sinus rhythm electrogram (EGM) patterns and their relationship to parasympathetic responses during atrial fibrillation (AF) ablation. BACKGROUND: The mechanistic basis of fractionated LA EGMs in patients with paroxysmal AF is not well understood. METHODS: We analyzed 1,662 LA ablation sites from 30 patients who underwent catheter ablation for paroxysmal AF. Pre-ablation EGM characteristics (number of deflections, amplitude, and duration) were measured in sinus rhythm. Parasympathetic responses during radiofrequency application (increase of atrial-His interval by > or =10 ms or decrease of sinus rate by > or =20%) were assessed at all sites. We also prospectively studied the effect of adenosine, a pharmacological agent mimicking acetylcholine signaling in myocytes, on LA EGMs. Finally, we performed mathematical simulations of atrial tissue to delineate possible mechanisms of fractionated EGMs in sinus rhythm. RESULTS: A specific pattern of pre-ablation sinus rhythm EGM (deflections > or =4, amplitude > or =0.7 mV, and duration > or =40 ms) was strongly associated with parasympathetic responses (sensitivity 72%, specificity 91%). The sites associated with these responses were found to be located mainly in the posterior wall of the LA. Adenosine administration and mathematical simulation of the effect of acetylcholine were able to reproduce a similar EGM pattern. CONCLUSIONS: Parasympathetic activation during AF ablation is associated with the presence of pre-ablation high-amplitude fractionated EGMs in sinus rhythm. Local acetylcholine release could potentially explain this phenomenon.     

Influence of intravenous clonidine on normal and pathological sinus and atrioventricular nodes and carotid sinus sensitivity

A number of clinical observations have suggested that clonidine may be responsible for dizziness and even syncope. The aim of this study was to assess the effects of this drug on normal and pathological sinus and AV nodes and on carotid sinus sensitivity. 19 patients were investigated (average age: 73 years). 14 patients complained of dizziness or syncope, including 3 patients with spontaneous sinus node dysfunction. 5 patients were asymptomatic; 3 were investigated for severe sinus bradycardia (1 on clonidine); 1 patient had sinoatrial block and 1 patient underwent pre-operative assessment for intraventricular block. The sinus node was studied using Mandel's method at 100, 120 and 150/min; the AV node was studied by the extrastimulus method with fixed atrial cycle of 600 ms. The following parameters were measured: Wenckebach point, AH interval in spontaneous and paced cycle length of 600 ms, effective refractory periods. Carotid sinus sensitivity was tested by right and left carotid sinus massage. These parameters were measured under basal conditions and 15 and 30 minutes after IV injection of 0.150 mg of clonidine. Two groups of patients were identified from the results under basal conditions: group 1:11 patients with corrected post-stimulation pauses less than 525 ms, and group 2:8 patients with at least one corrected post-stimulation pause of over 525 ms. Clonidine influenced the post-stimulation pauses significantly in both groups. However, the number of pathological pauses increased much more in group 2 than in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)     

中位法射频消蚀慢径路治疗房室结折返性心动过速

导管射频消蚀术（ＲＦＣＡ）治疗房室结折返性心动过速４３例，采用＂中位法＂选择性阻断慢径路，该技术的关键是：①在Ｘ线右前斜位３０度下，将消蚀电极置于冠状窦口和希氏束连线的中点附近；②消蚀电极双极记录到小Ａ大Ｖ波；③放电时有交界性心律（包括快交界律、慢交界律、交界性早搏）；④以间断放电和时间递增的方法控制消蚀过程；⑤消蚀终点为放电总累积时间达６０～９０秒，重复电生理检查证实慢径阻断或心动过速不能诱发。经１～３个部位的消蚀彻底阻断慢道３６例，遗留慢径传导７例（有心房回波２例）。除１例术后第二天发生一过性Ⅲ°ＡＶＢ，二周恢复正常外，余无并发症发生，随访３～２４个月（平均１４±６），停用任何抗心律失常药，无心动过速发作。消蚀成功率１００％。认为“中位法”是消蚀房室结慢径路治疗房室结折返性心动过速的安全、简便和有效的方法，部分病例保留慢传导并不增加复发率。