房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

多普勒超声心动图评估肺动脉压力的临床价值

目的:比较多普勒超声心动图(DE)和右心导管检查(RHC)估测肺动脉压力(PAP)值有无差异。方法:连续入选2006年1月1日至2017年11月1日,就诊于大连医科大学附属第一医院同时行RHC和DE的患者,根据是否存在心脏解剖畸形分为先天性心脏病(CHD)组和无分流组,排除14岁及存在右心室流出道梗阻和肺动脉瓣狭窄或其他复杂等畸形的患者。肺动脉高压(PAH)诊断标准参照2015年ESC/ERS肺动脉高压诊断与治疗指南。结果:研究共纳入347例患者,其中CHD组312例,无分流组35例。RHC确诊PAH患者269例(77. 5%),SPAP [50. 81(35,55)]mm Hg(1 mm Hg=0. 133k Pa);无PAH患者78例(22. 5%),SPAP [25. 58(24,29)]mm Hg。两组在年龄、体质量、心功能不全、红细胞分布宽度、BNP、右心室流出道宽度、右心室内径、左心房前后径、右心房前后径、右心房上下径及肺动脉内径等,差异均有统计学意义。年龄、体质量是患者发生PAH的影响因素,年龄大、体质量大的患者PAH发生风险增加(OR=1. 022,1. 028,P=0. 038,0. 046);缺损直径大小是CHD发生PAH的影响因素,缺损直径越大,发生PAH风险越高(OR=1. 063,P=0. 004)。在RHC确诊的的269例PAH患者中,发现RHC估测SPAP高于DE估测SPAP[50. 81(35,55) vs. 41. 19(22,53. 5) mm Hg,P0. 001],而无分流组中估测SPAP值,差异无统计学意义[69. 42(44. 5,87) vs. 70. 48(44. 5,93) mm Hg,P=0. 846];但二者估测的SPAP呈正相关(r=0. 598,P0. 001)。SPAP36 mm Hg时,DE确诊PAH灵敏性和特异性最高,分别为71. 7%和64. 3%。结论:应用DE估测的SPAP与RHC估测的SPAP值相关性较好,但二者仍存在一定差异,DE估测的SPAP低于RHC估测的SPAP; DE在评估无分流PAH患者SPAP准确性较高。     

先天性QT延长综合征合并阵发性三度房室传导阻滞一例

先天性QT延长综合征（LQTS）患者是心原性猝死的高危人群。LQTS合并房室传导阻滞（AVB）非常少见，而且死亡率高，半年死亡率在50％以上。本文报道1例LQTS合并阵发性三度AVB，在置入起搏器前后反复出现心原性晕厥。     

家族性电紊乱性心脏病未植入心律转复除颤器患者的长期随访研究

目的 研究家族性电紊乱性心脏病高危患者,未植入心律转复除颤器(ICD)的长期预后.方法 13例患者中11例长QT综合征(LQTS)、2例Brugada综合征,均有心脏性晕厥.男性4例,女性9例,平均年龄(44±19)岁.6例(46%)因心跳骤停住院治疗.4例LQTS植入起搏器,平均随访(7±4)年.结果 11例(85%)患者仍然发作晕厥,1例心脏骤停首次入院,5例(39%)心脏骤停再入院,2例LQTS死亡,其中1例(0.8%)猝死.结论 LQTS和Brugada综合征患者一旦出现晕厥,以后会反复发作,如果没有条件接受ICD治疗,其他的药物治疗、医生的密切监控随访、指导患者避免触发因素和针对家属的心肺复苏训练同样非常重要.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

Objective Atrioventricular node reentrant tachycardia (AVNRT) ablation may effect the vagal response,which is indicated by sinus tachycardia. On the other hand,atrial fibrillation (AF) ,which was found to be associated with vagal irmervation, often coexists with AVNRT. However,little is known about the im-pact of slow pathway ablation on local vagal innervation to atria. Methods In 11 dogs, bilateral cervical sympa-thovagal trunks were decentralized and metoprolol was given to block sympathetic effects. Linear lesion was per-formed from coronary sinus (CS) ostium to the middle area of Koch triangle. Atrial effective refractory period(ERP) ,vulnerability window (VW) of AF, and sinus rhythm cycle length (SCL) were measured at high fight atrium (HRA),low right atrium (LRA), distal (CSd) and proximal CS (CSp) at baseline with and without vagal stimulation before and after ablation. The histological study was also performed. Results (1) SCL during vagal stimulation remained unchanged before and after ablation(107±19)bpm vs (108±8) bpm (P > 0.05). (2) After ablation, ERP during vagal stimulation remained unchanged at HRA (55±34) ms vs (69 ±37) ms (P >0.05),and decreased slightly at CSd (42±32) ms vs (55±30) ms (P =0.08). However,at LRA and CSp,ERP was significantly decreased after ablation (19±21) ms vs (66±24) ms (P <0.001) ; and (7± 18) ms vs (46±24) ms (P < 0.001), respectively. (3) AF was difficult to be induced at baseline before and after ablation in all sites (VW close to 0). While during vagal stimulation, after ablation VW of AF significantly decreased at LRA (1±3) ms vs (49±36) ms (P < 0.005) and CSp (10±12) ms vs (45±34) ms (P < 0.05) ,decreased slightly at CSd after ablation (35±37) ms vs (57±28) ms (P =0.07) ,and remained un-changed at HRA (63±31) ms vs (63±25) ms (P > 0.05). (4) The altered architecture of individual gan-glia was histologically observed. Conclusions The decreased ERP shortening to vagal stimulation in CS and LRA induced by slow pathway ablation indicates that ablation in such area may result in the vagal dennervation in LRA and CS,thereby attenuating the susceptibility to vagal mediated AF. While unchanged SCL,ERP short-ening and VW to vagal stimulation in sinus node area and HRA indicate that slow pathway ablation did not change the vagal innervation to these sites.     

长QT13家系的临床表现和心电学特征研究

目的 探讨长QT13 （LQT13）家系临床表现、心电学特点和基因型之间的关系.方法 研究入选了大连医科大学附属第一医院心内科1个LQT13家系,4代人,共有家族成员49例.家族调查包括临床病史、体格检查、心电图、超声心动图.采集44例血样,根据基因检测结果确定基因诊断.进一步采集基因诊断阳性的患者和匹配的健康对照者数字化心电图和动态心电图资料,比较两组心电参数的改变.结果 家系研究示7例临床诊断为先天性长QT综合征（LQTS）.基因诊断9例阳性,包括7例临床确诊病例和2例疑似病例,女6例,男3例.基因突变为KIR3.4基因Gly387Arg突变.校正QT间期（QTc）：440～490 （454±22） ms.女性患者QT间期偏长,好发晕厥,悲伤易诱发晕厥,有时在夜间发作.QT间期450～460ms的患者没有或者只有1次晕厥发生.该家系患者的晕厥首发均在20岁以后,在20～50岁期间晕厥发作频繁,50岁以后几乎不再发作.2例植入起搏器,β受体阻滞剂治疗有效.与健康对照组相比,LQT13患者QT间期延长主要表现在Q波与T波波峰间期（QTp）的延长.T波波峰到T波终点之间的间期（TpTe）没有改变.T波形状的评分（MCS）研究发现,与健康对照组相比T波起始部分的面积增加,T波幅度没有改变.24h动态心电图心率变异性分析发现,LQT13患者低频成份和高频成份比值（LF/HF）比正常对照组降低.结论 KIR3.4基因Gly387Arg突变引起LQT13.该LQT13家系女性患者多见,首发晕厥发生在成年以后,QT间期轻度延长,主要表现在T波起始部分的延长.临床结果相对良性,没有植入型心律转复除颤器（ICD）,随访9年没有患者猝死.     

计算机模拟心脏电生理的研究进展

计算机模拟心脏电生理研究始于 6 0年代早期 ,近二十年发展迅速 ,1991年Ｍａｌｉｋ等[1] 检索了Ｍｅｄｌｉｎｅ中有关计算机模拟心脏方面的文章 ,其总数是过去二十年所有相关文章总和的三倍 ,比心血管病学研究总增长速度还快。计算机模拟心脏的研究主要分两大类 :电生理模拟和非电生理模拟。非电生理模拟是指心脏机械运动和血液动力学模拟。这里主要综述心电生理模拟的进展。1　心脏电生理模拟的分类　　心脏电生理模拟根据模拟的原理不同 ,大体上分三大类[2 ] :非传播性模型 ,双域模型和建立在惠更斯原理上的模型。非传播性模型把心脏电活…     

不应期离散与心肌电不稳定性关系的计算机模拟研究

目的建立有限因素的计算机模拟心肌模型,使用计算机模拟心肌探讨不应期离散与心电不稳定性之间的关系。方法在PC机上,采用VisualBasic编写应用程序,建立模拟心肌模型,模拟心肌由25×25个单元组成,各单元可以传导兴奋和恢复兴奋,在兴奋性没有完全恢复时,传导缓慢。根据电偶极子的原理,建立模拟心电图。采用颤动阈值(filrillationthreshold,FT)作为评价心电不稳定性的指标。改变不应期的持续时间和离散程度,测定心动周期(CL)从100TS开始到20TS,以10TS步长递减时的各个CL的颤动阈值,以及模拟心肌心电图的QT间期。结果不应期离散程度越大,FT值越低,出现自发性颤动的最短心动周期越长。不同原因的QT间期延长,颤动阈值并不总是降低。结论单纯不应期离散就可以导致折返性心律失常。不同原因的QT间期延长心电不稳定性的改变不同。