肺癌合并静脉血栓栓塞症的临床特征及预后影响因素分析

目的:探讨肺癌合并静脉血栓栓塞症(venous thromboembolism,VTE)的临床特征、治疗模式、转归及影响因素.方法:选择2015年1月1日至2020年12月31日大连医科大学附属第一医院收治的肺癌患者5769例,筛选新发VTE患者,收集性别、年龄、吸烟史、临床分期、病理类型等临床资料,分析肺癌合并VTE...     

心房肌的复极与阵发性心房颤动发生机制的实验研究

目的心房肌的复极对阵发性心房颤动(简称房颤)的诱发及维持起着重要的作用.本研究使用单相动作电位技术(MAP)对在体犬左、右房肌的复极时间及房颤的诱发进行研究,以探讨心房肌对阵发性房颤发生和维持的潜在机制.     

上腔静脉隔离对迷走神经功能及心房颤动易感性的影响

目的 通过分析迷走神经调节的心房电生理指标(心房有效不应期及心房颤动易感窗口)的变化,间接揭示上腔静脉(SVC)隔离对犬的心房迷走神经功能及心房颤动(房颤)易感性的影响.方法 9条成年杂种犬,全身麻醉下行颈交感-迷走神经干剥离术.经右颈内静脉穿刺放置冠状静脉窦导管,经股静脉穿刺放置右心室导管(行临时右心室起搏)、环状标测导管(Lasso导管)及消融导管.静脉应用美托洛尔阻断交感神经活性.分别于SVC隔离前后在基础状态及迷走神经刺激时测量右心耳(RAA)、冠状静脉窦近端(CSp)和冠状静脉窦远端(CSd)的不应期(ERP)、心房易感窗口(VW)及窦性周长(SCL).结果 (1)窦性周长的变化SVC隔离前迷走神经刺激明显缩短SCL[(65.78±28.49)次/min vs(142.67±15.42)次/min,P《0.001],SVC隔离后基础状态及迷走神经刺激下SCL差异无统计学意义[(134.89±19.19)次/min vs(114.33±31.41)次/min,P》0.05].(2)有效不应期的变化SVC隔离前,迷走神经刺激下测得的心房ERP较基础状态下明显缩短[右心耳(RAA)分别为(51.11±18.33)ms vs(101.11±27.59)ms;CSd分别为(56.67±22.36)ms VS(98.89±14.53)ms;CSp分别为(48.89±25.22)ms vs(101.11±12.69)ms,P《0.001].SVC隔离后,迷走神经刺激所致的心房ERP缩短的能力明显下降(RAA分别为(94.40±16.70)ms vs(94.44±16.67)ms;CSd分别为(89±15)ms vs(96.7±18.0)ms;CSp分别为(93.3±18.7)ms vs(98.9±20.3)ms,P》0.05].(3)心房易感窗口的变化 SVC隔离前后基础状态下测得的VW无变化.SVC隔离后迷走神经刺激时测得的VW较隔离前明显降低[RAA分别为(6.67±11.18)ms vs(21.11±20.88)ms,CSd分别为(8.89±14.52)ms vs(16.66±23.97)ms,CSp分别为(2.22±6.67)ms vs(22.22±18.55)ms,P《0.05].结论 SVC隔离能导致迷走神经介导的窦房结抑制、心房不应期缩短能力及房颤易感窗口增加能力明显下降.提示SVC隔离可导致心房局部去神经反应,抑制迷走神经介导的房颤发生.     

心房颤动介导的心肌病

心房颤动介导的心肌病(atrial fibrillation mediated cardiomyopathy,AMC)用于描述房颤导致的可逆性心力衰竭,随着导管消融和起搏技术的进展,房颤合并心衰患者中约有50％ ～60％ 的患者可能是"房颤介导的心肌病",其发病机制目前尚未完全阐明,心房功能缺损、快速心室率等因素并不能...     

室性早搏后心率漂移对室性早搏危险性预测的临床分析

目的　对冠心病室性早搏患者及无器质性心脏病室性早搏患者心率漂移进行分析以揭示心率漂移的临床应用价值。方法　分析对 5 0例冠心病及 5 0例无器质性心脏病室性早搏患者的心率漂移进行分析 ,测定室性早搏后心率加速 ,RR加速 =(R1R2 +R2 R3+R3R4 ) / 3 ;室性早搏后心率减慢 ,RR减缓 =(R7R8+R8R9+R9R10 ) / 3;室性早搏前心率 ,RR =(R-1R-2 +R-2 R-3 +R-3R-4 ) / 3 ;心率漂移指标 :RR加速 -RR ,RR加速 -RR减缓 ,RR减缓 -RR。R1R2 、R2 R3、R3R4 为室性早搏后第 1至第 4次窦性心律 ,R7R8、R8R9、R9R10 为室性早搏后第 7至第 10个窦性心律 ,R-1R-2 、R-2 R-3 、R-3R-4 为室性早搏前第 1至第 4个窦性心律。结果　无器质性心脏病组RR、RR加速 、RR减缓 分别为 842± 6 7ms、72 3± 96ms、919± 89ms,冠心病组RR、RR加速 、RR减速 分别为 879± 83ms、80 7± 10 3ms、912± 12 1ms。非器质性心脏病组RR加速 与RR减速 及RR加速 与RR之间有显著性差异 (P <0 0 1) ,RR减速 与RR有显著差异 (P <0 0 5 )。冠心病组RR加速 与RR减速 之间有显著差异 (P <0 0 1) ,RR加速 与RR有显著性差异 (P <0 0 5 ) ,RR减速 与RR无显著性 (P >0 0 5 )。二组间RR加速 -RR减缓 分别为 183± 12ms及 10 2± 9ms(P <0 0 5 ) ,RR     

心房肌的复极与阵发性心房颤动发生机制的实验研究

目的　对在体犬左、右心房肌的复极时间进行研究 ,探讨阵发性心房颤动 (房颤 )发生与维持的潜在机制。方法　记录基础心律、非程序刺激及早搏刺激 (SR、S1 、S2 )时 1 4只犬左、右心房的单相动作电位 (MAP)和有效不应期 (ERP) ,测量每个动作电位的幅度和动作电位时程 [复极达90 %、80 %、5 0 %时的动作电位时程 (ms,APD90 、APD80 、APD50 ) ]。并在记录过程中同时观察房颤的诱发情况。结果　记录满意MAP信号 1 2例 ,共标测 2 6点 (右房 1 7点 ,左房 9点 ) ,MAP振幅平均(6 98± 1 76 )mV ,左心房APD90 和APD50 小于右心房 [(1 5 7 4± 4 3 5 0 )ms比 (1 70 9± 37 9)ms ,P <0 0 5 ;(88 4± 1 9 1 )ms比 (1 0 0 1± 2 1 2 )ms,P <0 0 5 )。其中左房刺激发作 38阵 ,明显多于右房 2 3阵 (P <0 0 5 )。由左房诱发房颤的早搏的偶联间期明显比在右房诱发的短 (P <0 0 5 )。起源于左房的房颤的早搏参数小于起源于右房的 (P <0 0 5 )。结论　左、右心房间具有MAP的异质性的复极特性 ,是诱发折返、发生和维持房颤的基质。     

房室结慢径消融对心房电生理性质的影响

Objective The ablation of the atrioventricular node slow pathway may reduce the inducibility of atrial fibrillation (AF) ,but the mechanisms remain unknown. We tried to investigate the impact of ablation on atria refractory period, and to elucidate the underlying mechanism. Methods Thirty-two patients with atrioventricular node reentrant tachycardia (AVNRT) were enrolled in the study. Atria effective refractory period (ERP) and vulnerable window (VW) at high right atrium (HRA),inferior right atrium (IRA),distal (CSd) and proximal CS (CSp) ,as well as sinus rate (SR) and effective refractory period of fast pathway (FERP) were measured before and after ablation. Results ( 1 ) After ablation, the ERP at HRA did not change:(214. 4 ± 35. 1 ) ms, (213.4 ± 37. 3) ms, P = 0. 6, on the other hand, the ERPs at following sites were significantly prolonged:CSp(218. 1 ±21.8)ms, (235.3 ± 23.6) ms,P ＜0. 0001 ;CSd(230. 9 ±21.0) ms, (244. 7 ±25. 1)ms,P＜0. 01;IRA(198.8 ±26.7)ms,(219.7 ±28. 7) ms,P ＜ 0.005,respectively. (2) The VW of HRA remained unchanged after ablation, while the VWs of CSp, CSd and IRA trended to decline despite no statistic significant. (3)SR showed a little increasing but without statistic significant after ablation (P = 0. 17 ).(4) ERP of fast pathway was significantly decreased after ablation: ( 391 ± 55 ) ms, ( 369 ± 78 ) ms, P ＜ 0. 01.Conclusions The decrease of ERPs at CS and IRA, as well as F-ERP after ablation may decline the inducibility of atrial fibrillation and indicates regional vagal denervation to the atrium.     

肺静脉电隔离对阵发性心房颤动患者P向量环的影响

目的探讨成功的肺静脉电隔离对心房除极的影响。方法记录接受环肺静脉电隔离术的18例阵发性心房颤动(PAF)患者术前及术后第1天窦性心律时的心向量图。测量P环的运行时间、P向量环在正交导联额面(F)、水平面(H)、左侧面(LS)的最大振幅及方向。同时记录P环从运行开始后每10ms的除极振幅。结果肺静脉隔离术后P环F最大振幅较术前降低(0.109±0.038mVvs0.128±0.040mV,P0.05)。P环运行时间,H及LS的最大振幅,F、H、LS的最大振幅方向,术前术后无差异(P0.05)。消融成功组(n=12)术后P环H最大振幅较术前降低(0.092±0.019mVvs0.122±0.030mV,P0.05),而术后复发组(n=6)则无明显变化。肺静脉隔离术后P环振幅降低发生在P环运行至40～80ms的部分,即P向量环的中部。结论PAF病人在肺静脉电隔离成功后P环最大振幅发生改变。     

心房肌复极的电整复性与阵发性心房颤动发生机制的实验研究

Objective Electrical restitution was believed to be a determinant responsible for the stability of heart rhythm. Although numerous studies focused on the role of action potential duration restitution (APDR) in the initiation and maintenance of ventricular fibrillation (VF), the relationship between atrial APDR and atrial fibrillation (AF) has not been fully understood. This study aims to investigate the characteristics of APDR of left atrium (LA) and right atrium (RA) in canines and the relevance to induction of AF. Methods Monophasic action potential (MAP) was recorded from LA and RA in 14 canines using the MAP recording-pacing combination catheter. APDR, plotted as action potential duration (APD) on the preceding diastolic interval (DI), was assessed by use of programmed stimulation with a single extrastimulus (S_1S_2) at LA and RA. Episodes of AF were recorded and analyzed. Results APD_(90) was significantly shorter in the LA than that in the RA [( 157.4 ± 43.5 ) ms vs. ( 170. 9 ± 37. 9)ms, P < 0. 05]. The mean slope of the APDR curve by S_1S_2 in the LA was significantly greater than that in the RA ( 1.3 ±0. 4 vs. 0. 9 ± 0. 3, P < 0. 05 ). The incidence of induced AF was significantly higher in the LA than in the RA (11/18 vs. 7/18, P < 0. 05). Conclusions The APDR and MAP characteristics are not uniform between atriums, which may be one of the important mechanisms responsible for the initiation of AF. Heterogeneity of APDR between LA and RA might create critical gradients or a dispersion of repolarization and subatrate for re-entrant arrhythmias and vulnerability to AF.     

抗菌药所致获得性QT间期延长综合征的研究现状

一些非心脏病药物能够延长心室复极时间(心电图为QT间期延长),即获得性QT间期延长综合征,后者可诱发致命性室性心律失常(如尖端扭转型室速),尤其在药物剂量过大或药物间的药代动力学发生相互干扰时出现.这些药物包括抗精神病药物、H1受体拮抗剂、抗菌药物等.近来一些研究[1～3]发现,抗菌药物也能导致QT间期延长综合征,现复习有关文献并综述如下: