关于心房扑动分类的建议

心房扑动 (简称房扑 )是临床常见的心律失常。其电生理机制认识比较清楚的是经过下腔静脉和三尖瓣环之间峡部的右房内的大折返。其中逆钟向折返的房扑称为典型房扑或Ⅰ型房扑 ;顺钟向折返的房扑称为不典型房扑或Ⅱ型房扑 ,这是对房扑最经典的分类。但是 ,随着房扑电生理机制研究的深入 ,新的房扑折返类型被发现 ,上述的分类方法已显滞后 ,由于目前许多类型房扑的电生理机制以及消融治疗方法仍不明确 ,房扑的分类仍没有统一的标准[1,2 ] ,使得临床中对各种房扑的名称趋于混乱 ,有必要重新进行分类。我们根据房扑心电图特点、电生理机制及其对…     

三条房室旁路并休眠旁路的心内电生理检查及导管射频消融治疗一例

3条房室旁路患者临床中非常少见 ,同时合并休眠旁路者更少。本文报道 1例 3条房室旁路并休眠旁路的心内电生理检查及导管射频消融治疗。　　病例资料　患者女性 ,2 0岁。阵发性心悸病史 6年。常规检查未发现器质性心脏病。窦性心律心电图示预激综合征 (图 1)。射频消融术中常规放置导线电极于冠状静脉窦、右心室心尖部以及高位右心房。程序刺激后诱发顺向性和逆向性房室折返性心动过速 ,以及短暂心房扑动和心房颤动伴旁路前传。消融导线电极经右股动脉置于二尖瓣环下 ,距冠状静脉窦口 1 5ｃｍ处标测窦性心律时ＡＶ最近 ,右心室刺激标测逆传…     

2016年欧洲心脏病学会癌症治疗与心血管毒性 立场声明解读

2016 年8 月,欧洲心脏病学会发布了肿瘤心脏病学领域首部用于指导临床实践的纲领性文件——《 2016 欧洲
心脏病学会癌症治疗与心血管毒性立场声明》。该声明对肿瘤治疗相关心肌功能不全与心力衰竭、冠状动脉疾病、
心脏瓣膜病、心律失常、高血压、血栓栓塞性疾病、周围血管病与卒中、肺动脉高压及心包并发症等病的发病机制、临
床评估与管理、预防缓解策略及长期随访流程进行了详细推荐。作者结合国内外现有文献,对声明的主要内容进行
解读。     

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

目的探讨房室结慢径区域消融对心房迷走神经调节功能及心房颤动易感性的影响。方法11条成年杂种犬,全麻下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管(Hallo导管),经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径路区域消融前后基础状态及迷走神经刺激下的窦性周长(SCL)及高位右心房(HRA)、低位右心房(LRA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的有效不应期(ERP)及心房易感窗口(VW)。结果①窦性周长的变化:消融前、后迷走神经刺激导致的SCL缩短值的差异无统计学意义[(107±19)比(108±8)次／min,P>0．05]。②有效不应期的变化:消融前、后迷走神经刺激导致的ERP缩短值在HRA分别为(69±37) ms、(55±34)ms,两者间差异无统计学意义(P>0．05);CSd分别为(55±30)ms及(42±32)ms,LRA分别为(66±24) ms及(19±21)ms,CSp分别为(46±24)及(7±18) mS,差异均有统计学意义(P值分别<0．05、0．01)。③心房易感窗口的变化:消融前后基础状态下各个部位刺激均较难诱发心房颤动(VW接近0)。消融前、后HRA迷走神经刺激诱发心房颤动能力的差异无统计学意义[(63±31) ms比(63±25) ms,P>0．05],CSd的VW有一定程度的降低[(35±37) ms比(57±28) ms,P=0．07],LRA及CSp的VW明显降低(LRA:(1±3)ms比(49±36) ms;CSp:(10±12) ms比(45±34)ms,P值均<0．05)。结论慢径区域消融未直接改变窦房结区域及高位右心房的迷走神经支配,部分削弱了冠状静脉窦远端的迷走神经功能。导致了低位右心房及冠状静脉窦口区域的去迷走神经效应。降低了低位右心房及冠状静脉窦区域早搏刺激诱发迷走神经介导房颤的易感性。     

大静脉肌袖电隔离治疗阵发性心房颤动延迟成功的探讨

目的　分析导管射频消融大静脉肌袖电隔离治疗阵发性心房颤动 (房颤 )早期复发与延迟成功发生率的关系 ,并探讨其可能的机制。方法　阵发性房颤患者在环状标测电极指导下行靶肌袖和 或全部大静脉肌袖的导管射频消融电隔离治疗 ,对于术后一周内经心电图和动态心电图证实的房颤复发病例 ,继续随访其房颤发作情况。结果　 131例患者共接受电隔离治疗 15 9次 ,随访 10 4例(79 3% ) ,失访 2 7例。平均随访 112± 37d时无房颤发作 5 9例 (5 6 7% ) ,房颤发作明显减少和持续时间明显缩短 7例 ,总有效率 6 3 5 %。平均随访 380± 2 2 6d时无房颤发作 81例 (77 8% ) ,房颤发作明显减少和持续时间明显缩短 4例 ,总有效率 80 8%。结论　阵发性房颤肌袖电隔离治疗后早期复发并不意味着房颤治疗的失败 ,部分病例 (17 3% )可以发生延迟成功。     

心室起搏依赖的心力衰竭患者应用希氏束起搏与传统起搏对心脏功能影响的对比研究

目的:探讨心室起搏依赖的心力衰竭患者应用希氏束起搏(HBP)的临床价值。方法:连续入选2017年6月至2018年6月于大连医科大学附属第一医院因心室起搏依赖(心室起搏比例高于40%)而植入永久起搏器且合并心力衰竭的患者132例。HBP成功者44例为HBP组,传统起搏组88例患者。比较两组患者治疗前后的QRS时限、NYHA心功能分级,超声心动图指标及起搏器参数的变化情况;根据基线左心室射血分数(LVEF)再将各组患者分为射血分数保留(HFpEF,LVEF≥40%)患者及射血分数降低(HFrEF,LVEF<40%)患者,再次评价两类患者中HBP和传统起搏的心功能的变化情况。结果:与术前比,HBP组患者术后(末次随访)QRS时限缩短、NYHA心功能分级改善、LVEF升高、左心室舒张末期内径(LVEDD)减小、二尖瓣反流(MR)程度减轻、左心房内径(LAD)缩小(P均<0.05);传统起搏组三尖瓣反流(TR)程度较术前加重(P<0.05),LVEF、LVEDD、MR程度、LAD均较术前无显著改善(P均>0.05)。132例患者中有HFrEF患者47例,其中HBP组20例,传统起搏组27例,HBP组HFrEF患者术后QRS时限缩短、NYHA心功能分级改善、LVEF升高、LVEDD减小、MR和TR程度均减轻、LAD缩小(P均<0.05);传统起搏组HFrEF患者QRS时限延长(P<0.05)。HFpEF患者共85例,其中HBP组24例。HBP组HFpEF患者术后NYHA心功能分级明显改善(P<0.05);而传统起搏组HFpEF患者的LVEF较术前下降、MR和TR程度均加重(P均<0.05)。结论:对于心室起搏依赖的心力衰竭患者,与传统起搏相比,HBP均能够改善患者心功能,这些临床益处在射血分数减低的患者中更为显著。     

右心室流入道室性心动过速的心电图特点及射频消融治疗

特发性室性心动过速 (室速 )常起源于右心室流出道及左心室间隔部 ,少见于左心室游离壁、左心室流出道[1] ;而起源于右心室流入道的室速则更少报道。在共 5 0例消融手术中遇到 5例起源于右心室流入道的室速 ,其中特发性室速 4例 ,另 1例为致心律失常性右心室心肌病 (ＡＲＶＣ)。本文就其心电图特点及射频消融治疗的体会进行总结。临床资料　 5例患者 ,男性 4例 ,女性 1例 ,年龄 2 2～ 38岁 ,均有阵发性室速病史 ,呈突发突止 ,发作间期无室性早搏 ,曾用多种抗心律失常药物治疗无效或效果不佳。超声心动图和Ｘ线检查 ,4例未发现有器质性心脏病…     

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.