碎裂QRS波在致心律失常性右心室心肌病诊断中的价值

Objective To evaluate diagnostic value of fragmented QRS complex (fQRS)in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Methods Forty-three patients [33 men, aged (40. 4 ± 13.9)years]meet the ISFC/ESC diagnostic criteria for ARVC were enrolled in this study. A standard twelve-lead electrocardiogram was obtained during the resting status. Characteristics of fQRS were detailedly studied by three doctors independently. A comparison of the prevalence among fQRS, epsilon wave and T wave inversion( TWI )in the right precordial leads exceeding V3 was done. Results Most fQRS could be found in the inferior leads (44. 3% ) and the right precordial leads (24. 2% ). Within the QRS complex, the prevalence of fQRS in the R wave was significantly higher than it in the S wave(58. 4% vs 32. 9% ,Z =4. 30,P ＜0. 01 ).fQRS could be found in a total of 31 of 43 cases( mean 4. 6 ± 1.7 ( range 2 to 9) per patient). The prevalence of fQRS was significantly higher than that of epsilon wave ( 73.8% vs 30. 2%, Z = 3.67, P ＜ 0. 01 ) and TWI (73.8% vs41.9% ,Z =2. 61 ,P＜0. 01 ). Conclusion fQRS was a common electrocardiographic abnormality,and most was found in the inferior and right precardial leads in patients with ARVC. It may be used as an important noninvasive preliminary screening electrocardiographic criteria.     

磁导航遥控射频导管消融治疗房室结折返性心动过速的初步体会

Objective To evaluate the safety and feasibility of remote radiofrequency catheter ablation of atrioventricular nodal reciprocating tachycardia (AVNRT) using the magnetic navigation system (MNS). Methods A total of 37 patients[female 29, mean age (44 ± 15 )years]with documented AVNRT were enrolled in this study from March 2007 to June 2009. A 4 mm tip magnetic mapping and ablation catheter ( Helios Ⅱ ,Stereotaxis, USA),which was remotely controlled by the MNS (Niobe Ⅱ , Stereotaxis, USA), was used for both mapping and ablation. Conventional slow pathway modification with focal ablation at the fight posterior septum was first performed in all patients. If it was failed, linear lesions at the base of Koch' s triangle was then done. Results After ablation, AVNRT was non-inducible in all 37 patients without any complication except one case experienced transient first degree AV block. Focal ablation was performed in 34 patients, and linear ablation strategy was used in the remaining three cases to achieve the end point. Among all the 37 patients, slow pathway ablation was achieved in 14, whereas slow pathway modification was reached in the remaining 23 cases.The mean procedural time, the RF deliveries, the duration of RF application were ( 120 ± 32) min, (2. 9 ± 1.6)times, ( 130 ± 33 )s,respectively. The total fluoroscopy time and the physician X-ray exposure time were(5.3 ±2. 7)min and(2.9 ± 1.1 ) min,respectively. There was no significant change of the AH interval,the HV interval,and the atrioventricular nodal conduction refractory period after ablation. Compared with the first 18 patients, the mean procedural time, the total fluoroscopy time and the X-ray fluoroscopy time during magnetic navigation were significantly decreased in the later 19 patients (P ＜0. 001 ). It indicated that the learning curve of remote catheter ablation using the MNS is short. Conclusion Remote catheter ablation using the MNS to cure AVNRT is safe and effective with short learning curve and decreasing X-ray exposure time for interventional physicians.     

起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律

目的 介绍起源于左侧希氏-浦肯野系统的特发性加速性室性自主心律,揭示其临床特征并探讨可能的电生理机制.方法 回顾分析4例特发性加速性室性自主心律患者的心电图形态特征、临床表现、治疗方法及预后.结果 4例患者,男性2例,平均年龄48(40～54)岁,均无器质性心脏病.室性自主心律均呈右束支阻滞型,其QRS时限0.11～0.13 s,符合左侧希氏-浦肯野系统起源,其中3例电轴右偏,1例电轴左偏.自主心律RR间期不规则,平均频率为87(55～110)次/min,与窦性心律交替出现.所有患者临床均表现为发作性心悸.1例患者室性自主心律在短期服用普罗帕酮后消失,另1例短期服用维拉帕米后消失,余2例未予以特殊处理后自然消退.平均随访4.5(2～8)年,临床无心律失常发作,亦无其他心血管事件发生.结论 起源于左侧希氏-浦肯野系统的加速性室性自主心律是左侧希氏-浦肯野系统特发性室性心律失常的一种表现形式,多数为自限性,临床呈良性经过.     

骨髓间充质干细胞移植对心肌梗死后心室肌细胞钾离子通道Ito Kv4.2的影响

目的 研究心肌梗死后移植骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMMSCs)对心室肌细胞钾离子通道Ito亚单位Kv4.2基因表达的影响方法 40只SD(Sprague-Dawley)大鼠随机分成4组(10只/组):假手术组、心肌梗死组、心肌梗死+干细胞组和心肌梗死+细胞培养基组.开胸结扎冠状动脉前降支建立心肌梗死模型,建模成功后,在梗死周围分别注入BMMSCs和细胞培养基,心肌梗死组仅建立心肌梗死模型,假手术组仅开胸子以前降支穿线但不结扎.2周后行心肌组织HE染色和荧光显微镜观察移植细胞,逆转录聚合酶链反应(RT-PCR)和Western blot分别检测钾离子通道Ito亚单位Kv4.2基因mRNA和蛋白水平.结果 (1)心肌组织免疫荧光检测发现,BMMSCs集中分布于梗死区和梗死心肌周围;(2)心肌梗死组和心肌梗死+细胞培养基组Kv4.2 mRNA量(0.39±0.02,0.41±0.04)和蛋白量(0.47±0.02,0.50±0.05)明显下降,与假手术组(0.76±0.05,0.74±0.06)相比差异有统计学意义(P＜0.01);心肌梗死+干细胞组Kv4.2 mRNA量和蛋白表达量(0.57±0.05,0.64±0.03)较心肌梗死组(0.39±0.02,0.47±0.02)明显升高(P＜0.01).结论 骨髓间充质干细胞移植后心肌梗死大鼠钾离子通道Ito亚单位Kv4.2基因表达上升,可能减少心律失常发生.     

N-乙酰半胱氨酸通过抑制活性氧-p38通路减轻缺氧复氧诱导的乳鼠心肌细胞凋亡

目的 探讨N-乙酰半胱氨酸(N-acetylcysteine,NAC)抑制缺氧复氧(hypoxia-reoxygenation,H/R)诱导的乳鼠心肌细胞凋亡的机制.方法 心肌细胞培养48 h后随机分为对照组、缺氧复氧组(H/R组)、缺氧复氧+NAC组(100 p.mol/L)(H/R+NAC组).H/R组心肌细胞先缺氧6 h,随后复氧72 h,H/R+NAC组在H/R组细胞培养液中加NAC(100 μmol/L).采用锥虫蓝检测心肌细胞活性.流式细胞仪与Annexin V测定细胞早期凋亡.TUNEL检测细胞晚期凋亡.活性氧绿色荧光显色试剂检测活性氧(reactive oxygen species,ROS)浓度.RT-PCR检测bcl2、bax基因mRNA水平.Western blot检测bel2、bax、p38与pp38基因蛋白水平.结果 H/R组有活性的细胞数量为74.9%,显著低于对照组(93.5%,P<0.01),H/R+NAC组有活性的细胞数为89.9%,显著高于H/R组(P<0.01).H/R组早期凋亡的心肌细胞数为25.2%,显著高于对照组(6.5%,P<0.01),H/R+NAC组早期凋亡的细胞数为11.1%,显著低于H/R组(P<0.01).H/R组晚期凋亡的心肌细胞数为33.5%,显著高于对照组(3.5%,P<0.01),H/R+NAC组晚期凋亡的细胞数为13.5%,显著低于H/R组(P<0.01).H/R组心肌细胞ROS产生显著高于对照组,H/R+NAC组心肌细胞ROS产生显著低于H/R组.H/R组pp38/p38条带密度比值(13.40)也显著高于对照组(3.89).H/R+NAC组pp38/p38条带密度比值(1.95)显著低于H/R组(13.4),P<0.01.H/R组bcl2 mRNA与蛋白水平显著低于对照组,bax mRNA与蛋白水平显著高于对照组.H/R+NAC组bcl2 mRNA与蛋白水平显著高于H/R组.H/R+NAC组bcl2/bax mRNA水平比值(1.79)显著高于H/R组(1.22),P<0.05,但仍低于对照组(1.85).H/R+NAC组bcl2/bax条带密度比值(0.71)显著高于H/R组(0.50),P<0.05,但仍低于对照组(2.53).结论 NAC通过抑制ROS-p38通路减轻缺氧复氧诱导的乳鼠心肌细胞凋亡,这一作用具有潜在的临床应用价值.     

心房颤动的碎裂电位消融

外科迷宫术治疗房颤的成功给电生理医师带来了曙光,但经过了多年的艰辛探索与不懈努力,经历了最初的困惑和迷茫后,在1998年由法国著名电生理学家Haissaguerre等[1]具有里程碑意义的开创性发现的基础上(肺静脉触发阵发性房颤),房颤的射频消融才真正拉开了序幕.自此,消融治疗房颤进入飞速发展的阶段.其治疗理念不断取得突破性的进展,治疗模式也渐趋成熟,从最初的点状消融,到节段性肺静脉隔离,以至主流术式之一的肺静脉前庭隔离;其术式渐趋稳定,成功率也越来越高.然而,2004年Nademanee等[2]另辟蹊径,提出针对房颤基质-碎裂电位(CFAEs)的射频消融术式.     

儿童脑性瘫痪综合治疗方法的探讨

目的 :探讨综合治疗小儿脑性瘫痪的疗效 ,旨在减轻脑瘫患儿的伤残程度。方法 :采用药物治疗、穴位注射、经络导平、功能锻炼、高压氧治疗。结果 :经综合治疗 ,患儿基本治愈率 2 7.9% ,显效率 5 1.5 % ,有效率 14 .7% ,无效率5 .9% ,总有效率 94.1%。结论 :早期诊断及多方面综合治疗 ,可明显减轻小儿脑性瘫痪的伤残程度 ,促进患儿正常发育。     

三维电解剖标测指导器质性心脏病室性心动过速导管射频消融的初步经验

器质性心脏病室性心动过速（室速）是一临床顽疾，也是导管射频消融治疗的难题。在上世纪九十年代，心肌梗死后室速和致心律失常性右室心肌病（ARVC）室速的成功标测与消融充分揭示了此类室速的电生理机制。目前认为，绝大多数器质性心脏病室速是瘢痕相关性的折返性心动过速，其缓慢传导区常位于瘢痕内部，入口和出口位于瘢痕边缘。     

心房颤动消融术后二尖瓣峡部房性心动过速的发生机制及消融治疗

目的探讨心房颤动(简称房颤)患者环肺静脉左房线性消融术后二尖瓣峡部房性心动过速(简称房速)的发生机制及其消融策略。方法122例房颤患者采用EnSite-NavX和环状电极行环肺静脉左房线性消融,术后32例复发房颤或房速,8例经EnSite-NavX激动标测及拖带标测证实存在二尖瓣峡部房速,在三维导航下于左下肺静脉口部下缘至二尖瓣环之间行线性消融,对不能成功阻断二尖瓣峡部传导者予以冠状静脉窦内消融。术中同时探查双侧肺静脉电位,如传导恢复予以再次隔离。结果8例中2例呈无休止性发作,6例为阵发性,可被程序刺激诱发。房速的周长217.5±20.6ms,其中顺钟向折返5例,逆钟向折返3例。二尖瓣峡部线性消融至完全性双向传导阻滞5例,3例心内膜途径失败者经冠状静脉窦内消融,其中1例获得成功。术后随访5.5±4.3个月,6例无房颤及房速发作,1例仍有阵发性房速发作。另1例术后房速呈无休止发作,予以胺碘酮及美托洛尔控制心室率治疗。结论环肺静脉线性消融术后发生的二尖瓣峡部房速与左房线性消融治疗房颤的致心律失常作用有关,其主要的机制是消融线相关的大折返性心动过速,阻断峡部传导可以治疗此类房速。     

左房线性消融治疗阵发性心房颤动对心率变异性的影响

目的通过观察左房线性消融术治疗阵发性心房颤动(简称房颤)术后心率变异性(HRV)的变化来评价其对自主神经系统的影响。方法对25例行射频消融术的阵发性房颤患者,术前及术后第3天行24h动态心电图检查,分别测定最大心率,最小心率,平均心率;时域指标:RR间期标准差(SDNN),RR间期平均值的标准差(SDANN),相邻RR间期差的均方根(RMMSD),相邻RR间期差值超过50ms的RR间期所占百分数(PNN50);频域指标:低频功率(LF),高频功率(HF),低频高频比值(LF/HF)。结果患者术前最大心率,最小心率,平均心率,SDNN,SDANN,RMSSD,PNN50,LF,HF,LF/HF分别为151±41次/分,47±5次/分,70±9次/分,126±26ms,111±24ms,27±7ms,6±5ms,98±66ms2,86±119ms2,2.4±3.5;术后各指标分别为136±37次/分,66±8次/分,84±9次/分,57±17ms,53±17ms,16±7ms,2±3ms,18±19ms2,16±19ms2,1.2±1.6;手术前后各指标相比,差异有显著性(P均<0.05)。结论左房线性消融术后HRV降低,此可能是射频消融治疗房颤的机制之一。