应用Amplatzer封堵器治疗室间隔缺损及对心脏传导系统影响的研究
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摘要
第一部分:犬室间隔缺损模型制备和封堵及对房室传导电生理影响研究
目的:采用改良后的主动脉大隐静脉近端吻合器打孔器成功地建立了膜部/干下型室间隔缺损(VSD)的犬模型并用国产Amp1atze VSD封堵器封堵VSD,通过心内电生理检查观察VSD制备和封堵前后房室传导的变化,其目的为:(1)建立犬VSD模型,有利于VSD的临床病理生理、血流动力学研究;(2)封堵室间隔缺损并探讨封堵对房室传导电生理影响,有利于了解并预防介入封堵并发症,为应用封堵器进行动物和临床介入治疗的研究进一步打下基础。
方法:(1)VSD制备和电生理检查:选用成年健康杂种犬8只,取左侧卧位,左侧胸垫高45度,并通过多功能超声观察心腔内解剖结构。开胸后暴露心脏,采用自主改良的直径不同的美国St.Jude主动脉大隐静脉近端吻合器打孔器,根据TTE定位,确定进针方向:垂直室间隔进针,送入打孔器至右室流出道。将打孔器垂直室间隔方向定在干下快速穿入左室,通过针尖倒刺确保勾出室间隔组织。通过心电监护可出现室性早搏,心脏听诊胸骨左缘闻及II-III级收缩期杂音,右室壁可扪及震颤,提示室间隔缺损,然后迅速退出打孔器。
术后即刻进行心脏表面行TTE检查,大血管短轴和胸骨旁长轴探查确定干下型/膜部VSD的存在,并测定其大小、分流方向和速度、压差和肺动脉压力各项指标。VSD制备前后测房室传导时间(AV间期)、房室传导文氏点和房室结有效不应期,观察VSD制作对犬房室传导系统产生影响。
(2)VSD封堵和电生理检查:选择腰部直径大于VSD最窄处2 mm国产Amp1atze VSD封堵器,在X透视和TTE引导下将留置导丝通过VSD至左室,沿导丝送入6～7 F输送,沿鞘将不对称VSD封堵器送到左室,首先释放左室伞,回撤鞘管使左室伞紧贴VSD左室面,再释放右室伞,TTE和左室造影确认无明显残余分流后,完全释放封堵器并撤出鞘管。封堵后即刻和一周再次复测房室传导时间(AV间期)、房室传导文氏点和房室结ERP,观察VSD封堵前后对犬房室传导系统产生影响。
结果:(1)手术结果:共有6只犬完成VSD制备和封堵手术, 6只犬VSD封堵完全,无残余分流,封堵器直径4.0～6.0 mm,平均4.8 mm。1例膜部VSD封堵后一直未苏醒,并出现三度房室传导阻滞(ⅢOAVB),心率缓慢,38次/分,术后2 h死亡。成活的5只术后随访1周后行TTE无残余分流,
(2)经胸超声检查:采用超声仪于VSD制备后即刻检查,1例干下型VSD,5例膜部VSD(图3),每只狗测3次,取平均值。VSD直径2.8～4.0 mm,平均3.4 mm;VSD处血流为左向右分流,测得最大流速1.6～4.2 m/s ,平均3.3 m/s;跨VSD处压差38～52 mmHg,平均46 mmHg;肺动脉收缩压25～32 mmHg,平均29 mmHg。
(3)电生理检查:VSD制作和封堵前后心内电生理检查结果:VSD制作后,复测房室传导时间(AV间期)、房室传导文氏点和房室结ERP无明显变化。但介入封堵后即刻出现ⅢOAVB 1例,并术后2 h死亡;5例存活封堵后平均AV间期延长,其中2例延长幅度超过60 ms(AV间期达150 ms以上);平均房室传导文氏点降低,房室结不应期变化无明显规律。术后一周检查,AV间期有所缩短,文氏点有所提高。
结论:(1)本研究主要是在经TTE引导下开胸心包穿刺方法,使用改良的主动脉大隐静脉近端吻合器打孔器成功建立犬干下型和膜部室间隔缺损模型。确保手术成功的要领如下:①对打孔器进行了改良,便于操作,减少并发症;②掌握狗的心脏解剖特点:通过体位调节及调整进针方向可较易获得干下型VSD或膜部VSD;③使用不同针部直径不同的打孔器可获得缺损口直接不同的室间隔缺损模型。
(2)通过室间隔打孔前后心内电生理检查发现:VSD模型建立过程中,只要应用器械适当,操作娴熟、准确、到位,解剖结构的了解,良好的麻醉,术中药物的使用,造成房室传导异常并发症的发生率很小,电生理检查各项指标无统计学变化。
(3)通过开胸心包穿刺能成功进行犬VSD的介入封堵,对今后封堵器的改良和临床介入封堵治疗研究提供实验基础。
(4)通过心内电生理检查观察VSD封堵前后房室传导的变化,发现VSD介入封堵后出现AV传导时间延长,甚至出现严重的房室传导阻滞,传导文氏点降低,说明VSD介入封堵手术及封堵器会对房室传导系统产生一定影响。所以在室间隔封堵操作过程中,如果使用器械不当,对解剖结构不了解,不能掌握VSD的影象和超声知识,动作粗暴,操作时间过长,极易误损伤房室传导系统。
(5)成功建立膜部/干下VSD模型并进行介入封堵和房室传导电生理研究,深入了解该类左向右分流的先天性心脏病的病理生理改变、研究临床血流动力学和发病机制的重要基础,对封堵器的改良和临床介入封堵治疗研究有重大意义。
第二部分:应用Amplatzer封堵器治疗室间隔缺损及对心脏传导系统的影响
目的:室间隔缺损(VSD)是一种常见的先天性心脏病,其中90%的VSD位于膜部及肌部,并以膜部为多,以往治疗方法主要是外科手术修补。先天性心脏病介入封堵治疗是近年来发展迅速的一种微创而有效的VSD治疗方法。从80年代后期,先后有多种装置应用于临床,取得一定效果,但由于装置其本身的种种缺陷和限制未能在临床推广,介入封堵引起心脏传导阻滞的并发症受到广泛关注。我们应用新型Amplatzer封堵器治疗膜周部及肌部室间隔缺损(VSD)的疗效,并通过心内电生理检查来观察介入封堵对心脏传导系统的影响的新内容,目的是深入探讨先天性心脏病的介入治疗临床效果和相关并发症,为此项新技术的发展提供充分的依据。
方法:(1)临床确诊的21例VSD患者,平均年龄8.7±5.4岁, 19例为膜周部VSD,2例为肌部VSD。术前心电图均为窦性心律。(2)封堵器和传送系统:新型的Amplatzer膜部VSD封堵器是由镍钛记忆合金丝编织而成的网状自膨胀非对称双盘状伞。特殊的传送系统由输送鞘(6～9 F)、扩张管、推送导管、推送螺杆、装载器组成。
(3)封堵方法:在X透视经胸和食道超声监测下,穿刺右侧股动、静脉。首先放入高右房和右室标测电极,进行电生理检查,测定房室传导时间(AV间期)和房室结不应期。随后进行心导管检查,测定各房室及主、肺动脉压力和血氧饱和度,计算Qp/Qs和肺血管阻力。进行左室及升主动脉造影,以确定VSD的位置及测量其大小、有无主动脉瓣返流等。建立股静脉(或右颈内静脉)—右室—VSD—左室-股动脉的导丝轨道。沿轨道经静脉途径送入输送鞘到左心室,经输送鞘把封堵器送至左室,在X线、食道或经胸超声的监视下放置Amplatzer VSD封堵器。封堵10 min后,重复行左室、升主动脉造影及超声检查,确认封堵器的位置、形态满意,无明显室间隔残余分流及主动脉瓣返流时,释放封堵器。
(3)术后即刻进行心内电生理复查,复测房室传导时间(AV间期)和房室结不应期。24 h复查超声心动图、胸部正侧位片、12导联心电图,并于术后2周、1个月、3个月、6个月时复查,观察封堵器位置、心脏功能及各瓣膜的结构;观察有无残余分流,有无即刻和迟发性房室传导异常。
结果:右心导管资料提示21例患者术前Qp/Qs比值为0.8～3.7(1.8±0.7),肺动脉平均压为11～24(15.4±4.6) mmHg。肺血管阻力0.5～2.3(1.4±0.4) wu/m2。19例膜周部VSD造影测量的缺损最窄处直径平均为2.0～8.3(4.0±1.9) mm ,11例合并膜部瘤的基底部直径平均为2.5～18(7.9±4.7) mm。二例肌部VSD缺损分别为3 mm和3.5 mm。
21例手术全部成功,共置入21枚封堵器,其中19枚为非对称Amplatzer膜部VSD封堵器,直径为6～14(7.8±2.7) mm ;2枚对称Amplatzer肌部VSD封堵器,直径分别为6 mm和8 mm。术后即刻超声及造影示即刻完全封堵18例,微量残余分流3例(14.3%),皆为膜周部VSD,微量残余分流均于术后24h复查超声时消失。术后即刻主动脉造影发现微量主动脉瓣返流l例,但无明显血液动力学改变。术中和术后随访没发现Ⅱ度以上的房室传导阻滞和束支传导阻滞。19例膜周部VSD封堵前、后即刻进行心内电生理检查,AV间期有不同程度的延长,其中有
3例术后即刻AV间期>200 ms,心电图P-R间期>200 ms,术后一周心电图检查2例P-R间期恢复正常(<200 ms)。封堵前后房室不应期无明显变化。二例肌部VSD封堵前、后即刻进行心内电生理检查AV间期和房室不应期无明显变化。结论:(1)AGA公司设计的这种新型膜部VSD封堵器具有:①体积小,对主动脉瓣的影响小,可应用于年龄和体重较小的患儿;②其输送鞘的特殊结构及与封堵器的特殊连接使封堵器定位更为精确,封堵器可多次回收及重置,操作更安全;③手术适应症广,疗效好。
(2)在手术中,我们体会到在封堵膜周部VSD时,根据缺损造影的结果选择封堵器的大小非常重要。如封堵器过大,可能影响主动脉瓣、三尖瓣和传导束,造成主动脉瓣关闭不全、右室流出道狭窄和传导阻滞;如封堵器过小,则可能造成堵闭不全而出现残余分流,甚至整个封堵器脱落在膜部瘤内或心室中,造成手术的失败。
(3)房室传导阻滞和束支传导阻滞是室间隔缺损封堵的并发症之一,通过封堵前后心内电生理检查发现封堵对房室传导会产生一定的影响。由于传导束靠近膜周缺损部的后下缘,封堵时易影响传导系统,造成房室传导时间延长,个别会产生房室传导阻滞和束支传导阻滞。造成传导阻滞的相关因素:①操作技术原因:输送鞘过大和递送不当;建立动-静脉导丝轨道时张力过大或过度牵拉,造成缺损口组织损伤而累及传导系统;②封堵器直径:封堵器选择过大,导致缺损边缘压力过高,直接压迫传导系统,或压迫导致缺损周围组织水肿,影响传导束,造成传导阻滞。为防止传导阻滞的发生,术前超声心动图详细了解VSD的结构和位置;术中左室造影精确测量缺损口大小,选择合适的封堵器;操作要轻柔和规范。术后心电监护48小时,观察2周以上。如果发生传导阻滞应静脉滴注糖皮质激素,必要时静脉滴注异丙基肾上腺素或安装临时起搏器。
应用新型Amplatzer膜部室间隔封堵器治疗膜周部和肌部VSD是安全、有效,作为一种新的介入诊疗技术有良好的应用前景。但中、远期疗效还需更多临床病例验证。对膜部VSD封堵器对传导系统的电生理影响需做更进一步研究。
Section A: Establishment and closure of ventricular septal defect and the effect of cardiac conductive system in dogs
Objective To research and understand the pathological and hemodynamic effect of ventricular septal defect (VSD), the experimental animal models of sub-arterial infundibular / membranous VSD were established with revised aortic cutter in dogs, To understand and evaluate the effect of the VSD occluding procedure on atrioventricular (AV) conductive system in dogs, we occluded the VSD with Amplatzer VSD occluder in the experimental animal models of VSD and observe atrioventricular conductive time (AV period), Wenckebach points of the atrioventricular conductive and atrioventricular nodal effective refractory period (ERP) before and after procedure by means of the cardiac catheter electrophysiologic examination.
Methods Thoracotomy was performed on eight dogs through right fourth costal region with left lateral decubitus padded 45 degree high after general anesthesia and intrabronchial intubation after transthoracic echocardiographic (TTE) examination , revised aortic cutter was put into right ventricle via an incision on right ventricular outflow, then vertically punctured through the septum by the help of TTE. VSDs were determined by the cardiac systolic murmur and TTE, then the aortic cutter was retreated out of the heart. The peak velocity and pressure of transseptal shunt was measured by TTE. The AV period, Wenckebach points of the atrioventricular conductive and ERP before and after VSD established procedure by the cardiac catheter electrophysiologic examination. All cases underwent an catheter closure using the new Amplatzer membranous VSD occluder. The 6-7 F sheath was placed to left ventricle through VSD. The VSD occluder was first released in the left ventricular side, pull back catheter a little then release right disc of device under the X-ray fluoroscopy and TTE guidance. The cardiac electrophysiologic examinations were performed before and after the closure procedure so as to observe the effect of atrioventricular conductive system.
Results Six dogs had successful acquisition of VSDs. One week later, Doppler echocardiography demonstrated defects varied from 2.8～4.0 mm, the mean value of 3.4 mm. The transseptal shunts with peak velocities ranged from1.6～4.2 m/s, the mean value of 3.3 m/s. Transseptal defect pressure was from 38～52 mmHg, the mean value of 46 mmHg. The pulmonary pressure was ranged from 25～32mmHg, the mean value of 29 mmHg. There were no obvious changes of echocardiographic paraments before and after the eatablishment of VSD. Six dogs had successful occlude of VSDs, of which one had a thee-degree A-V block and died 2 hours later, the others had a more prolonged the AV period and lower Wenckebach points after catheter closure than before (P<0.05), of which 2 cases had the AV period more than 150ms, the AV period and lower Wenckebach point in 5 cases had recovered a few within one week follow-up period. There were no obvious changes of atrioventricular nodal refractory period before and after catheter closure.
Conclusion Establishment and closure of ventricular septal defect with revised aortic cutter and Amplatzer VSD occluder were successful in dogs. Appropriate cutter and VSD device, familiar anatomy of heart, dexterous operation can ensure success and prevent complication. Adjusting direction and the choice of the cutter can get different types and diameters of VSD. The prolonged AV conductive time, even severe AV block, showed AV conductive system may be affected easily in the occlude of VSD, so it is necessary to monitor and operate carefully for preventing the AV and bundle branch block in and after operation. Successful Establishment and closure of ventricular septal defect have great significance to the development of VSD clinical intervention therapy.
Section B: Transcatheter closure of perimembranous and muscular ventricular septal defects using the new Amplatzer VSD occluder and the effect of cardiac conductive system
Objective Ventricular septal defects (VSD) is a common defect in congenital heart disease. About 70% of all VSDs are perimembranous/ membranous. The treatment of VSD need surgical repair before. The intervention therapy of congenital heart disease has developed rapidly. To evaluate the feasibi1ity, efficacy and complication of transcatheter closure of perimembranous and muscular VSD, we used the new Amplatzer membranous and muscular VSD occluder to occlude perimembranous and muscular VSD and observed the effect of membranous VSD occluding procedure on atrioventricular (AV) conductive system.
Methods Nineteen patients (12 males, 7 females) with perimembranous VSD and two patients (1 male, 1 female) with muscular VSD underwent an catheter closure using the new Amplatzer membranous and muscular VSD occluder. The new insymmetry Amplatzer membranous and symmetry muscular VSD occluder are made of nitinol wire with polyester mesh inside enhance clotting. The devices is available in sizes ranging from 4 to 20 mm. The device requires 6-9 Fr delivery sheath. All patients who were eligible for device closure by means of cardiac Doppler echocardiography routinely measure the parameters of hemodynamics and the angiography of left ventricle before catheter closure. Artery-venous track was set up under the X-ray fluoroscopy, transesophageal (TEE) or transthoracic echocardiography (TTE) guidance. Devices were first released in the left ventricular side, pull back catheter a little then release right disc of device. The echocardiography and the angiography of left ventricle and ascend Aorta were repeated 10 minters later. After identified the normal location and stability, no obvious resident shunt, the devices were release totally. Nineteen patients with perimembranous VSD underwent the cardiac electrophysiologic examination, including atrioventricular conductive time (AV interval) and atrioventricular nodal refractory period before and after catheter closure. All patients were followed up at 2 weeks,1 month,3 months and 6 months after the procedures.
Results The devices were deployed successfully in 21 patients.There was complete closure in 18 patients immediately,and tiny ( <2 mm ) residual shunt in 3 patients. The residual shunt all disappeared within 1 day. A-V interval was more prolonged after catheter closure than before in 19 patients with perimembranous VSD (P<0.01), of which 3 cases had the AV interval and P-R interval more than 200ms, the P-R interval in 2 cases had recovered normal within one week follow-up period. There were no obvious changes of atrioventricular nodal refractory time before and after catheter closure. There were no obvious changes of the AV interval and atrioventricular nodal refractory time before and after catheter closure in two patients with muscular VSD. There were no other severe complications in all 21 cases.
Conclusions Transcatheter closure of membranous and muscular VSD using the new Amplatzer membranous and muscular VSD occluder is safe and effective. The new Amplatzer membranous and muscular VSD occluder can be received back in operation and deployed again, The insymmetry structure of membranous VSD occluder has less effects on aortic valves. The AV conductive system may affected in the occlude of membranous VSD because AV conductive bundle near VSD closely, it is necessary to monitor and prevent the AV and bundle branch block. The operating technique,sizes of device and time of procedure all may be very important to prevent AV block and branch bundle.
目的:采用改良后的主动脉大隐静脉近端吻合器打孔器成功地建立了膜部/干下型室间隔缺损(VSD)的犬模型并用国产Amp1atze VSD封堵器封堵VSD,通过心内电生理检查观察VSD制备和封堵前后房室传导的变化,其目的为:(1)建立犬VSD模型,有利于VSD的临床病理生理、血流动力学研究;(2)封堵室间隔缺损并探讨封堵对房室传导电生理影响,有利于了解并预防介入封堵并发症,为应用封堵器进行动物和临床介入治疗的研究进一步打下基础。
方法:(1)VSD制备和电生理检查:选用成年健康杂种犬8只,取左侧卧位,左侧胸垫高45度,并通过多功能超声观察心腔内解剖结构。开胸后暴露心脏,采用自主改良的直径不同的美国St.Jude主动脉大隐静脉近端吻合器打孔器,根据TTE定位,确定进针方向:垂直室间隔进针,送入打孔器至右室流出道。将打孔器垂直室间隔方向定在干下快速穿入左室,通过针尖倒刺确保勾出室间隔组织。通过心电监护可出现室性早搏,心脏听诊胸骨左缘闻及II-III级收缩期杂音,右室壁可扪及震颤,提示室间隔缺损,然后迅速退出打孔器。
术后即刻进行心脏表面行TTE检查,大血管短轴和胸骨旁长轴探查确定干下型/膜部VSD的存在,并测定其大小、分流方向和速度、压差和肺动脉压力各项指标。VSD制备前后测房室传导时间(AV间期)、房室传导文氏点和房室结有效不应期,观察VSD制作对犬房室传导系统产生影响。
(2)VSD封堵和电生理检查:选择腰部直径大于VSD最窄处2 mm国产Amp1atze VSD封堵器,在X透视和TTE引导下将留置导丝通过VSD至左室,沿导丝送入6～7 F输送,沿鞘将不对称VSD封堵器送到左室,首先释放左室伞,回撤鞘管使左室伞紧贴VSD左室面,再释放右室伞,TTE和左室造影确认无明显残余分流后,完全释放封堵器并撤出鞘管。封堵后即刻和一周再次复测房室传导时间(AV间期)、房室传导文氏点和房室结ERP,观察VSD封堵前后对犬房室传导系统产生影响。
结果:(1)手术结果:共有6只犬完成VSD制备和封堵手术, 6只犬VSD封堵完全,无残余分流,封堵器直径4.0～6.0 mm,平均4.8 mm。1例膜部VSD封堵后一直未苏醒,并出现三度房室传导阻滞(ⅢOAVB),心率缓慢,38次/分,术后2 h死亡。成活的5只术后随访1周后行TTE无残余分流,
(2)经胸超声检查:采用超声仪于VSD制备后即刻检查,1例干下型VSD,5例膜部VSD(图3),每只狗测3次,取平均值。VSD直径2.8～4.0 mm,平均3.4 mm;VSD处血流为左向右分流,测得最大流速1.6～4.2 m/s ,平均3.3 m/s;跨VSD处压差38～52 mmHg,平均46 mmHg;肺动脉收缩压25～32 mmHg,平均29 mmHg。
(3)电生理检查:VSD制作和封堵前后心内电生理检查结果:VSD制作后,复测房室传导时间(AV间期)、房室传导文氏点和房室结ERP无明显变化。但介入封堵后即刻出现ⅢOAVB 1例,并术后2 h死亡;5例存活封堵后平均AV间期延长,其中2例延长幅度超过60 ms(AV间期达150 ms以上);平均房室传导文氏点降低,房室结不应期变化无明显规律。术后一周检查,AV间期有所缩短,文氏点有所提高。
结论:(1)本研究主要是在经TTE引导下开胸心包穿刺方法,使用改良的主动脉大隐静脉近端吻合器打孔器成功建立犬干下型和膜部室间隔缺损模型。确保手术成功的要领如下:①对打孔器进行了改良,便于操作,减少并发症;②掌握狗的心脏解剖特点:通过体位调节及调整进针方向可较易获得干下型VSD或膜部VSD;③使用不同针部直径不同的打孔器可获得缺损口直接不同的室间隔缺损模型。
(2)通过室间隔打孔前后心内电生理检查发现:VSD模型建立过程中,只要应用器械适当,操作娴熟、准确、到位,解剖结构的了解,良好的麻醉,术中药物的使用,造成房室传导异常并发症的发生率很小,电生理检查各项指标无统计学变化。
(3)通过开胸心包穿刺能成功进行犬VSD的介入封堵,对今后封堵器的改良和临床介入封堵治疗研究提供实验基础。
(4)通过心内电生理检查观察VSD封堵前后房室传导的变化,发现VSD介入封堵后出现AV传导时间延长,甚至出现严重的房室传导阻滞,传导文氏点降低,说明VSD介入封堵手术及封堵器会对房室传导系统产生一定影响。所以在室间隔封堵操作过程中,如果使用器械不当,对解剖结构不了解,不能掌握VSD的影象和超声知识,动作粗暴,操作时间过长,极易误损伤房室传导系统。
(5)成功建立膜部/干下VSD模型并进行介入封堵和房室传导电生理研究,深入了解该类左向右分流的先天性心脏病的病理生理改变、研究临床血流动力学和发病机制的重要基础,对封堵器的改良和临床介入封堵治疗研究有重大意义。
第二部分:应用Amplatzer封堵器治疗室间隔缺损及对心脏传导系统的影响
目的:室间隔缺损(VSD)是一种常见的先天性心脏病,其中90%的VSD位于膜部及肌部,并以膜部为多,以往治疗方法主要是外科手术修补。先天性心脏病介入封堵治疗是近年来发展迅速的一种微创而有效的VSD治疗方法。从80年代后期,先后有多种装置应用于临床,取得一定效果,但由于装置其本身的种种缺陷和限制未能在临床推广,介入封堵引起心脏传导阻滞的并发症受到广泛关注。我们应用新型Amplatzer封堵器治疗膜周部及肌部室间隔缺损(VSD)的疗效,并通过心内电生理检查来观察介入封堵对心脏传导系统的影响的新内容,目的是深入探讨先天性心脏病的介入治疗临床效果和相关并发症,为此项新技术的发展提供充分的依据。
方法:(1)临床确诊的21例VSD患者,平均年龄8.7±5.4岁, 19例为膜周部VSD,2例为肌部VSD。术前心电图均为窦性心律。(2)封堵器和传送系统:新型的Amplatzer膜部VSD封堵器是由镍钛记忆合金丝编织而成的网状自膨胀非对称双盘状伞。特殊的传送系统由输送鞘(6～9 F)、扩张管、推送导管、推送螺杆、装载器组成。
(3)封堵方法:在X透视经胸和食道超声监测下,穿刺右侧股动、静脉。首先放入高右房和右室标测电极,进行电生理检查,测定房室传导时间(AV间期)和房室结不应期。随后进行心导管检查,测定各房室及主、肺动脉压力和血氧饱和度,计算Qp/Qs和肺血管阻力。进行左室及升主动脉造影,以确定VSD的位置及测量其大小、有无主动脉瓣返流等。建立股静脉(或右颈内静脉)—右室—VSD—左室-股动脉的导丝轨道。沿轨道经静脉途径送入输送鞘到左心室,经输送鞘把封堵器送至左室,在X线、食道或经胸超声的监视下放置Amplatzer VSD封堵器。封堵10 min后,重复行左室、升主动脉造影及超声检查,确认封堵器的位置、形态满意,无明显室间隔残余分流及主动脉瓣返流时,释放封堵器。
(3)术后即刻进行心内电生理复查,复测房室传导时间(AV间期)和房室结不应期。24 h复查超声心动图、胸部正侧位片、12导联心电图,并于术后2周、1个月、3个月、6个月时复查,观察封堵器位置、心脏功能及各瓣膜的结构;观察有无残余分流,有无即刻和迟发性房室传导异常。
结果:右心导管资料提示21例患者术前Qp/Qs比值为0.8～3.7(1.8±0.7),肺动脉平均压为11～24(15.4±4.6) mmHg。肺血管阻力0.5～2.3(1.4±0.4) wu/m2。19例膜周部VSD造影测量的缺损最窄处直径平均为2.0～8.3(4.0±1.9) mm ,11例合并膜部瘤的基底部直径平均为2.5～18(7.9±4.7) mm。二例肌部VSD缺损分别为3 mm和3.5 mm。
21例手术全部成功,共置入21枚封堵器,其中19枚为非对称Amplatzer膜部VSD封堵器,直径为6～14(7.8±2.7) mm ;2枚对称Amplatzer肌部VSD封堵器,直径分别为6 mm和8 mm。术后即刻超声及造影示即刻完全封堵18例,微量残余分流3例(14.3%),皆为膜周部VSD,微量残余分流均于术后24h复查超声时消失。术后即刻主动脉造影发现微量主动脉瓣返流l例,但无明显血液动力学改变。术中和术后随访没发现Ⅱ度以上的房室传导阻滞和束支传导阻滞。19例膜周部VSD封堵前、后即刻进行心内电生理检查,AV间期有不同程度的延长,其中有
3例术后即刻AV间期>200 ms,心电图P-R间期>200 ms,术后一周心电图检查2例P-R间期恢复正常(<200 ms)。封堵前后房室不应期无明显变化。二例肌部VSD封堵前、后即刻进行心内电生理检查AV间期和房室不应期无明显变化。结论:(1)AGA公司设计的这种新型膜部VSD封堵器具有:①体积小,对主动脉瓣的影响小,可应用于年龄和体重较小的患儿;②其输送鞘的特殊结构及与封堵器的特殊连接使封堵器定位更为精确,封堵器可多次回收及重置,操作更安全;③手术适应症广,疗效好。
(2)在手术中,我们体会到在封堵膜周部VSD时,根据缺损造影的结果选择封堵器的大小非常重要。如封堵器过大,可能影响主动脉瓣、三尖瓣和传导束,造成主动脉瓣关闭不全、右室流出道狭窄和传导阻滞;如封堵器过小,则可能造成堵闭不全而出现残余分流,甚至整个封堵器脱落在膜部瘤内或心室中,造成手术的失败。
(3)房室传导阻滞和束支传导阻滞是室间隔缺损封堵的并发症之一,通过封堵前后心内电生理检查发现封堵对房室传导会产生一定的影响。由于传导束靠近膜周缺损部的后下缘,封堵时易影响传导系统,造成房室传导时间延长,个别会产生房室传导阻滞和束支传导阻滞。造成传导阻滞的相关因素:①操作技术原因:输送鞘过大和递送不当;建立动-静脉导丝轨道时张力过大或过度牵拉,造成缺损口组织损伤而累及传导系统;②封堵器直径:封堵器选择过大,导致缺损边缘压力过高,直接压迫传导系统,或压迫导致缺损周围组织水肿,影响传导束,造成传导阻滞。为防止传导阻滞的发生,术前超声心动图详细了解VSD的结构和位置;术中左室造影精确测量缺损口大小,选择合适的封堵器;操作要轻柔和规范。术后心电监护48小时,观察2周以上。如果发生传导阻滞应静脉滴注糖皮质激素,必要时静脉滴注异丙基肾上腺素或安装临时起搏器。
应用新型Amplatzer膜部室间隔封堵器治疗膜周部和肌部VSD是安全、有效,作为一种新的介入诊疗技术有良好的应用前景。但中、远期疗效还需更多临床病例验证。对膜部VSD封堵器对传导系统的电生理影响需做更进一步研究。
Section A: Establishment and closure of ventricular septal defect and the effect of cardiac conductive system in dogs
Objective To research and understand the pathological and hemodynamic effect of ventricular septal defect (VSD), the experimental animal models of sub-arterial infundibular / membranous VSD were established with revised aortic cutter in dogs, To understand and evaluate the effect of the VSD occluding procedure on atrioventricular (AV) conductive system in dogs, we occluded the VSD with Amplatzer VSD occluder in the experimental animal models of VSD and observe atrioventricular conductive time (AV period), Wenckebach points of the atrioventricular conductive and atrioventricular nodal effective refractory period (ERP) before and after procedure by means of the cardiac catheter electrophysiologic examination.
Methods Thoracotomy was performed on eight dogs through right fourth costal region with left lateral decubitus padded 45 degree high after general anesthesia and intrabronchial intubation after transthoracic echocardiographic (TTE) examination , revised aortic cutter was put into right ventricle via an incision on right ventricular outflow, then vertically punctured through the septum by the help of TTE. VSDs were determined by the cardiac systolic murmur and TTE, then the aortic cutter was retreated out of the heart. The peak velocity and pressure of transseptal shunt was measured by TTE. The AV period, Wenckebach points of the atrioventricular conductive and ERP before and after VSD established procedure by the cardiac catheter electrophysiologic examination. All cases underwent an catheter closure using the new Amplatzer membranous VSD occluder. The 6-7 F sheath was placed to left ventricle through VSD. The VSD occluder was first released in the left ventricular side, pull back catheter a little then release right disc of device under the X-ray fluoroscopy and TTE guidance. The cardiac electrophysiologic examinations were performed before and after the closure procedure so as to observe the effect of atrioventricular conductive system.
Results Six dogs had successful acquisition of VSDs. One week later, Doppler echocardiography demonstrated defects varied from 2.8～4.0 mm, the mean value of 3.4 mm. The transseptal shunts with peak velocities ranged from1.6～4.2 m/s, the mean value of 3.3 m/s. Transseptal defect pressure was from 38～52 mmHg, the mean value of 46 mmHg. The pulmonary pressure was ranged from 25～32mmHg, the mean value of 29 mmHg. There were no obvious changes of echocardiographic paraments before and after the eatablishment of VSD. Six dogs had successful occlude of VSDs, of which one had a thee-degree A-V block and died 2 hours later, the others had a more prolonged the AV period and lower Wenckebach points after catheter closure than before (P<0.05), of which 2 cases had the AV period more than 150ms, the AV period and lower Wenckebach point in 5 cases had recovered a few within one week follow-up period. There were no obvious changes of atrioventricular nodal refractory period before and after catheter closure.
Conclusion Establishment and closure of ventricular septal defect with revised aortic cutter and Amplatzer VSD occluder were successful in dogs. Appropriate cutter and VSD device, familiar anatomy of heart, dexterous operation can ensure success and prevent complication. Adjusting direction and the choice of the cutter can get different types and diameters of VSD. The prolonged AV conductive time, even severe AV block, showed AV conductive system may be affected easily in the occlude of VSD, so it is necessary to monitor and operate carefully for preventing the AV and bundle branch block in and after operation. Successful Establishment and closure of ventricular septal defect have great significance to the development of VSD clinical intervention therapy.
Section B: Transcatheter closure of perimembranous and muscular ventricular septal defects using the new Amplatzer VSD occluder and the effect of cardiac conductive system
Objective Ventricular septal defects (VSD) is a common defect in congenital heart disease. About 70% of all VSDs are perimembranous/ membranous. The treatment of VSD need surgical repair before. The intervention therapy of congenital heart disease has developed rapidly. To evaluate the feasibi1ity, efficacy and complication of transcatheter closure of perimembranous and muscular VSD, we used the new Amplatzer membranous and muscular VSD occluder to occlude perimembranous and muscular VSD and observed the effect of membranous VSD occluding procedure on atrioventricular (AV) conductive system.
Methods Nineteen patients (12 males, 7 females) with perimembranous VSD and two patients (1 male, 1 female) with muscular VSD underwent an catheter closure using the new Amplatzer membranous and muscular VSD occluder. The new insymmetry Amplatzer membranous and symmetry muscular VSD occluder are made of nitinol wire with polyester mesh inside enhance clotting. The devices is available in sizes ranging from 4 to 20 mm. The device requires 6-9 Fr delivery sheath. All patients who were eligible for device closure by means of cardiac Doppler echocardiography routinely measure the parameters of hemodynamics and the angiography of left ventricle before catheter closure. Artery-venous track was set up under the X-ray fluoroscopy, transesophageal (TEE) or transthoracic echocardiography (TTE) guidance. Devices were first released in the left ventricular side, pull back catheter a little then release right disc of device. The echocardiography and the angiography of left ventricle and ascend Aorta were repeated 10 minters later. After identified the normal location and stability, no obvious resident shunt, the devices were release totally. Nineteen patients with perimembranous VSD underwent the cardiac electrophysiologic examination, including atrioventricular conductive time (AV interval) and atrioventricular nodal refractory period before and after catheter closure. All patients were followed up at 2 weeks,1 month,3 months and 6 months after the procedures.
Results The devices were deployed successfully in 21 patients.There was complete closure in 18 patients immediately,and tiny ( <2 mm ) residual shunt in 3 patients. The residual shunt all disappeared within 1 day. A-V interval was more prolonged after catheter closure than before in 19 patients with perimembranous VSD (P<0.01), of which 3 cases had the AV interval and P-R interval more than 200ms, the P-R interval in 2 cases had recovered normal within one week follow-up period. There were no obvious changes of atrioventricular nodal refractory time before and after catheter closure. There were no obvious changes of the AV interval and atrioventricular nodal refractory time before and after catheter closure in two patients with muscular VSD. There were no other severe complications in all 21 cases.
Conclusions Transcatheter closure of membranous and muscular VSD using the new Amplatzer membranous and muscular VSD occluder is safe and effective. The new Amplatzer membranous and muscular VSD occluder can be received back in operation and deployed again, The insymmetry structure of membranous VSD occluder has less effects on aortic valves. The AV conductive system may affected in the occlude of membranous VSD because AV conductive bundle near VSD closely, it is necessary to monitor and prevent the AV and bundle branch block. The operating technique,sizes of device and time of procedure all may be very important to prevent AV block and branch bundle.
引文
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[1] Newman SJ, Bailey TL, Jones JL, et al. Multiple congenital anomalis in a calf [J]. J Vet Diagn Invest, 1999, 11(4): 368-371
[2] Tidholm A. Retrospective study of congenital heart defects in 151 dogs [J]. J Small Anim Pract, 1997, 38(3): 94-98
[3]刘瀚旻,罗春华,郭玉.外科手术制备先天性心脏病的动物模型的研究进展[J].中国实验动物学杂志,2002,1:57-60.
[4] Gu X, Han YM, Titus JL, et al. Transcatheter closure of membranous ventricular septal defects with a new nitinol prosthesis in a natural swine model [J]. Catheter Cardiovasc Interv, 2000, 50(4): 504-509.
[5]孙明,魏静义,赵林昌,等.心脏室间隔膜部及其与临近结构关系外科解剖学研究[J].南京医科大学学报,1995,1:90-92.
[6] Synhorst DP, Lauer RM, Doty DB, et al. Hemodynamic effects ofvasodilator agents in dogs with experimental ventricular septal defects [J]. Circulation, 1976, 54:472-477.
[7] Amin Z, GU X,Berry JM, et al. New device for closure of muscular ventricular septal defects in a canine model [J]. Circulation, 1999, 100(3): 320-328.
[8]刘瀚旻,魏新川,隋东虎,等.室间隔缺损动物模型的建立[J] .四川大学学报(医学版),2003,34(2):341-343.
[9] Zhang ZW, Zeng GH, Lin SG, et al. The development of a new perimenbranous ventricular septal defect occluder [J]. Zhonghua Xin Xue Guan Bing Za Zhi. 2005, 33(3): 228-31.
[10] Milo S, Ho SY, Wilkinson JL, et al. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg, 1980,79: 244-255
[11]秦永文,胡建强,赵仙先.自制镍钛合金室间隔缺损封堵器的生物相容性研究[J].第二军医大学学报,2001,22(11):1038-1040.
[1] Sideris EB,Walsh KP,Haddad JL, et al. Occlusion of congenital ventricular septal defects by the buttoned device.Heart,1997,77 (3) :276-279
[2] Kalrd GS,Verma PK,Dhall A, et a1.Transcatheter device closure of ventricular septal defects:immediate results and intermediate-termfo11ow-up.Am Heart J,1999,138(2 Pt l):339-344.
[3] Hijazi ZM,Hakim F,Haweleh AA, et a1.Catheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: initial clinical experience. Cathet Cardiovasc Interv,2002,56:508-515.
[4] Hijazi ZM. Device Closure of Ventricular Septal Defects. Catheterization and Cardiovascular Interventions. 2003,60:107-114.
[5]胡海波,蒋世良,徐仲英,等.应用新型Amplatzer封堵器治疗膜周部室间隔缺损的初步研究.中华心血管病杂志,2004,32(3):237-240
[6] Milo S, Ho SY, Wilkinson JL, et al. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg, 1980,79: 244-255
[7] Fukuda T, Nakamura Y, Iemura J, et al. Onset of complete atrioventricular block 15 years after ventricular septal defect surgery. Pediatr Cardiol, 2002,23: 80-83.
[8] Pedra CA, Pedra SR, Esteves CA, rt al. Transcatheter closure of perimembranous ventricular septal defects [J]. Expert Rev Cardiovasc Ther, 2004, 2 (2): 253-264
[9] Holzer R, de Giovanni J, Walsh KP, et al. Transcatheter closure of perimembranous ventricular septal defects using the Amplatzermembranous VSD occluder : immediate and midterm results of an international registry [J]. Catheter Cardiovasc Interv, 2006,68(4):620-627
[10] Yip WC, Zimmerman F, Hijazi ZM. Heart block and empirical therapy after Transcatheter closure of perimembranous ventricular septal defect [J]. Catheter Cardiovasc Interv, 2005,66(3):436-441
1) Hijazi ZM,Hakim F,Haweleh AA,et a1.Catheter。closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder:initial clinical experience [J].Catheter Cardiovasc Interv,2002,56:508—5l5.
2)李卫平,秦永文,王尔松,等.超声心动图在室间隔膜周部缺损经导管封堵术中筛选病例的作用[J].中华超声影响学杂志,2003,12(5):269-271
3) Thanopoulous EB,Walsh KP,Haddad JL,et al.Occlusion of congenital ventricular septal defects by the buttoned device [J].Heart,1997.77:276—279.
4) Bass JL, Kalra GS,Arora R,et a1.Initial human experience with the Amplatzer perimembranous ventricular septal occluder device [J].Catheter Cardiovasc Interv,2003,58:238—245、
5) Chessa M,Carminati M,Cao QL,et a1.Transcatheter closure of congenital and acquired muscular ventricular septal defect using the Amplatzer device [J].J Invasive Cardiol,2002,14:1066—1069.
6) Fraiss A.Piecaud JF,Avierinos JF, et a1.Transcatheter closure of traumatic ventricular septal defect:an alternative to surgical repair [J] ?Ann Thorac Surg,2002,74(2):582—585.
7) Arora R, Trehan V, Kumar A, et al. Transcatheter closure of congenital ventricular septal defects: experience with various devices [J]. J Interv Cardiol, 2003,16:83—91.
8) Kalra GS,Verma PK, Singh S,et a1.Transcatheter closure ventricular septal defect using detachable steel coil [J].Heart 1999,82:395—390.
9)左兆凯,候子龙,孙则刚,等.膜部室间隔缺损介入治疗的疗效观察[J].中国临床医学,2006,13(4):540-541
10)李亭亭,张宏艳.先天性心脏病室间隔缺损介入治疗的研究进展[J].国际儿科学杂志,2006,33(3):371-373
11)韩玲,张维君,戴汝平,等,导管介入性关闭膜部室间隔缺损术后并发症[J].中华心血管病杂志,1997,25:204—206.
12) Laussen PC,Hdnsen DD,Perry SB, et a1.Transcatheter closure of ventricular septal defects : hemodynamic instability and anesthetic management [J].Anesth Analg,1995, 80:1076一1082.
13) Kitagawa T,Durham LA 3rd,Mosca RS,et a1.Techniques and results in the management of multiple ventricular septal defects [J].J Thorac Cardiovasc Surg,1998,115:848—856.
14)马依彤,杨毅宁,汤宋鹏,等.应用Amplatzer偏心性封堵器介入治疗膜部室间隔缺损[J].中国介人心脏病学杂志,2003 ,37:60—62.
15) Kalra GS,Verma PK,Dhall A,et a1.Transcatheter closure ventricularseptal defects:immediate results and intermediate-term follow-up [J].Am Heart J, 1999,138:339—344.
16) Benton JP,Barker KS.Transcatheter closure ventricular septal defects:a nonsurgical approach to the care of the patient with acute ventricular septal rupture [J].Heart Lung,1992,21:356—364。
17) Nykanen DG,Perry SB,Keane JF,et a1.Transcatheter occlusion of ventricular septal defects:experience in 80 patients with congenital heart disease [J].Circulation,1993,88:2864—2866.
18) Tofeig M,Patel PG,Walsh KP.Transcatheter closure of mid-muscular ventricular septal defect with an Amplatzer VSD occluder device [J].Heart,1999,81:438—440.
[2] Tidholm A. Retrospective study of congenital heart defects in 151 dogs [J]. J Small Anim Pract, 1997, 38(3): 94-98
[3]刘瀚旻,罗春华,郭玉.外科手术制备先天性心脏病的动物模型的研究进展[J].中国实验动物学杂志,2002,1:57-60.
[4] Gu X, Han YM, Titus JL, et al. Transcatheter closure of membranous ventricular septal defects with a new nitinol prosthesis in a natural swine model [J]. Catheter Cardiovasc Interv, 2000, 50(4): 504-509.
[5] Sideris EB,Walsh KP,Haddad JL, et al. Occlusion of congenital ventricular septal defects by the buttoned device.Heart,1997,77:
[6] Kalrd GS,Verma PK,Dhall A, et a1.Transcatheter device closure of ventricular septal defects:immediate results and intermediate-term fo11ow-up.Am Heart J,1999,138(2 Pt l):339-344.
[7] Hijazi ZM,Hakim F,Haweleh AA, et a1.Catheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: initial clinical experience. Cathet Cardiovasc Interv,2002,56:508-515.
[8] Hijazi ZM. Device Closure of Ventricular Septal Defects. Catheterization and Cardiovascular Interventions. 2003,60:107-114.
[9]胡海波,蒋世良,徐仲英,等.应用新型Amplatzer封堵器治疗膜周部室间隔缺损的初步研究.中华心血管病杂志,2004, 32(3):237-240
[10] Milo S, Ho SY, Wilkinson JL, et al. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg, 1980, 79: 244-255
[11] Fukuda T, Nakamura Y, Iemura J, et al. Onset of complete atrioventricular block 15 years after ventricular septal defect surgery. Pediatr Cardiol, 2002, 23: 80-83.
[1] Newman SJ, Bailey TL, Jones JL, et al. Multiple congenital anomalis in a calf [J]. J Vet Diagn Invest, 1999, 11(4): 368-371
[2] Tidholm A. Retrospective study of congenital heart defects in 151 dogs [J]. J Small Anim Pract, 1997, 38(3): 94-98
[3]刘瀚旻,罗春华,郭玉.外科手术制备先天性心脏病的动物模型的研究进展[J].中国实验动物学杂志,2002,1:57-60.
[4] Gu X, Han YM, Titus JL, et al. Transcatheter closure of membranous ventricular septal defects with a new nitinol prosthesis in a natural swine model [J]. Catheter Cardiovasc Interv, 2000, 50(4): 504-509.
[5]孙明,魏静义,赵林昌,等.心脏室间隔膜部及其与临近结构关系外科解剖学研究[J].南京医科大学学报,1995,1:90-92.
[6] Synhorst DP, Lauer RM, Doty DB, et al. Hemodynamic effects ofvasodilator agents in dogs with experimental ventricular septal defects [J]. Circulation, 1976, 54:472-477.
[7] Amin Z, GU X,Berry JM, et al. New device for closure of muscular ventricular septal defects in a canine model [J]. Circulation, 1999, 100(3): 320-328.
[8]刘瀚旻,魏新川,隋东虎,等.室间隔缺损动物模型的建立[J] .四川大学学报(医学版),2003,34(2):341-343.
[9] Zhang ZW, Zeng GH, Lin SG, et al. The development of a new perimenbranous ventricular septal defect occluder [J]. Zhonghua Xin Xue Guan Bing Za Zhi. 2005, 33(3): 228-31.
[10] Milo S, Ho SY, Wilkinson JL, et al. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg, 1980,79: 244-255
[11]秦永文,胡建强,赵仙先.自制镍钛合金室间隔缺损封堵器的生物相容性研究[J].第二军医大学学报,2001,22(11):1038-1040.
[1] Sideris EB,Walsh KP,Haddad JL, et al. Occlusion of congenital ventricular septal defects by the buttoned device.Heart,1997,77 (3) :276-279
[2] Kalrd GS,Verma PK,Dhall A, et a1.Transcatheter device closure of ventricular septal defects:immediate results and intermediate-termfo11ow-up.Am Heart J,1999,138(2 Pt l):339-344.
[3] Hijazi ZM,Hakim F,Haweleh AA, et a1.Catheter closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder: initial clinical experience. Cathet Cardiovasc Interv,2002,56:508-515.
[4] Hijazi ZM. Device Closure of Ventricular Septal Defects. Catheterization and Cardiovascular Interventions. 2003,60:107-114.
[5]胡海波,蒋世良,徐仲英,等.应用新型Amplatzer封堵器治疗膜周部室间隔缺损的初步研究.中华心血管病杂志,2004,32(3):237-240
[6] Milo S, Ho SY, Wilkinson JL, et al. Surgical anatomy and atrioventricular conduction tissues of hearts with isolated ventricular septal defects. J Thorac Cardiovasc Surg, 1980,79: 244-255
[7] Fukuda T, Nakamura Y, Iemura J, et al. Onset of complete atrioventricular block 15 years after ventricular septal defect surgery. Pediatr Cardiol, 2002,23: 80-83.
[8] Pedra CA, Pedra SR, Esteves CA, rt al. Transcatheter closure of perimembranous ventricular septal defects [J]. Expert Rev Cardiovasc Ther, 2004, 2 (2): 253-264
[9] Holzer R, de Giovanni J, Walsh KP, et al. Transcatheter closure of perimembranous ventricular septal defects using the Amplatzermembranous VSD occluder : immediate and midterm results of an international registry [J]. Catheter Cardiovasc Interv, 2006,68(4):620-627
[10] Yip WC, Zimmerman F, Hijazi ZM. Heart block and empirical therapy after Transcatheter closure of perimembranous ventricular septal defect [J]. Catheter Cardiovasc Interv, 2005,66(3):436-441
1) Hijazi ZM,Hakim F,Haweleh AA,et a1.Catheter。closure of perimembranous ventricular septal defects using the new Amplatzer membranous VSD occluder:initial clinical experience [J].Catheter Cardiovasc Interv,2002,56:508—5l5.
2)李卫平,秦永文,王尔松,等.超声心动图在室间隔膜周部缺损经导管封堵术中筛选病例的作用[J].中华超声影响学杂志,2003,12(5):269-271
3) Thanopoulous EB,Walsh KP,Haddad JL,et al.Occlusion of congenital ventricular septal defects by the buttoned device [J].Heart,1997.77:276—279.
4) Bass JL, Kalra GS,Arora R,et a1.Initial human experience with the Amplatzer perimembranous ventricular septal occluder device [J].Catheter Cardiovasc Interv,2003,58:238—245、
5) Chessa M,Carminati M,Cao QL,et a1.Transcatheter closure of congenital and acquired muscular ventricular septal defect using the Amplatzer device [J].J Invasive Cardiol,2002,14:1066—1069.
6) Fraiss A.Piecaud JF,Avierinos JF, et a1.Transcatheter closure of traumatic ventricular septal defect:an alternative to surgical repair [J] ?Ann Thorac Surg,2002,74(2):582—585.
7) Arora R, Trehan V, Kumar A, et al. Transcatheter closure of congenital ventricular septal defects: experience with various devices [J]. J Interv Cardiol, 2003,16:83—91.
8) Kalra GS,Verma PK, Singh S,et a1.Transcatheter closure ventricular septal defect using detachable steel coil [J].Heart 1999,82:395—390.
9)左兆凯,候子龙,孙则刚,等.膜部室间隔缺损介入治疗的疗效观察[J].中国临床医学,2006,13(4):540-541
10)李亭亭,张宏艳.先天性心脏病室间隔缺损介入治疗的研究进展[J].国际儿科学杂志,2006,33(3):371-373
11)韩玲,张维君,戴汝平,等,导管介入性关闭膜部室间隔缺损术后并发症[J].中华心血管病杂志,1997,25:204—206.
12) Laussen PC,Hdnsen DD,Perry SB, et a1.Transcatheter closure of ventricular septal defects : hemodynamic instability and anesthetic management [J].Anesth Analg,1995, 80:1076一1082.
13) Kitagawa T,Durham LA 3rd,Mosca RS,et a1.Techniques and results in the management of multiple ventricular septal defects [J].J Thorac Cardiovasc Surg,1998,115:848—856.
14)马依彤,杨毅宁,汤宋鹏,等.应用Amplatzer偏心性封堵器介入治疗膜部室间隔缺损[J].中国介人心脏病学杂志,2003 ,37:60—62.
15) Kalra GS,Verma PK,Dhall A,et a1.Transcatheter closure ventricularseptal defects:immediate results and intermediate-term follow-up [J].Am Heart J, 1999,138:339—344.
16) Benton JP,Barker KS.Transcatheter closure ventricular septal defects:a nonsurgical approach to the care of the patient with acute ventricular septal rupture [J].Heart Lung,1992,21:356—364。
17) Nykanen DG,Perry SB,Keane JF,et a1.Transcatheter occlusion of ventricular septal defects:experience in 80 patients with congenital heart disease [J].Circulation,1993,88:2864—2866.
18) Tofeig M,Patel PG,Walsh KP.Transcatheter closure of mid-muscular ventricular septal defect with an Amplatzer VSD occluder device [J].Heart,1999,81:438—440.