血清标志物半乳糖凝集素-3与心房颤动射频消融术后复发的相关性分析

目的:该研究旨在揭示血清标志物半乳糖凝集素-3(Gal-3)在心房颤动患者中的表达情况,并探讨基础血清Gal-3水平预测心房颤动射频消融术后复发率的价值。方法:连续入选就诊于北京安贞医院因非瓣膜性心房颤动行心房颤动射频消融术的患者共152例,其中阵发性心房颤动组110例(72.4%),持续性心房颤动组42例(27.6%)。入院后手术前经深静脉采集血液样本冻存,应用酶联免疫吸附试验法(ELISA)测定基础血清Gal-3水平,同时采集基线临床、实验室资料,建立样本库。对心房颤动射频消融术后患者进行前瞻性临床随访,判断射频消融术后复发情况并记录。结果:基础血清Gal-3水平在阵发性/持续性心房颤动中差异无统计学意义[7.11(9.06, 41.60)vs. 8.88(3.14, 53.12)μg/L,P=0.582]。随访时间为(340.9±145.8)d,心房颤动复发共42例(27.8%),其中持续性心房颤动组13例(31.0%),阵发性心房颤动组29例(26.6%)。心房颤动复发组血清Gal-3水平高于维持窦律者[38.52(3.65, 220.73)vs. 4.00(0.22, 13.69)μg/L,P=0.001]。多因素回归分析显示,血清Gal-3是心房颤动射频消融术后复发的危险因素(OR=1.009,95%CI:1.005～1.014,P0.001)。结论:心房颤动复发组血清Gal-3水平高于维持窦律者,可作为预测心房颤动射频消融术后复发的危险因素,帮助临床医生筛选更适合接受心房颤动射频消融手术的患者并使其从手术中获益。     

心率变异性与P波离散度与射频消融术后阵发性心房颤动复发的关系

目的探究与分析心率变异性与P波离散度与射频消融术治疗阵发性心房颤动后复发的关系。方法选择我院收治的60例给予射频消融术治疗阵发性心房颤动复发患者,按照复发的时间分为早期复发组(n=32)与晚期复发组(n=28),对比两组手术前后心率变异性与P波离散度指标。结果早期复发组术后与早期复发组术前相比连续24小时窦性RR间期标准差(SDNN)降低、相邻R-R间期差的均方根(r MSSD)降低、高频功率(HF)降低、低频功率(LF)降低、LF/HF降低,差异有统计学意义(P0.05)。早期复发组与早期未复发组相比24小时记录中所有连续5分钟RR间期平均值的标准差(SDANN)、rMSSD、HF、LF及最大P波时程(Pmax)较高,LF/HF较低,差异具有统计学意义(P0.05)。晚期治愈组与晚期复发组相比手术后LF/HF较高、Pmax及Pd较低,差异具有统计学意义(P0.05)。结论 Pmax对接受射频消融术的阵发性心房颤动患者术后早期与晚期复发均具有预测能力,P波离散度指标用于判断射频消融术治疗阵发性心房颤动晚期复发具有一定的预测价值。     

不同剂量的瑞舒伐他汀对心房颤动患者心房纤维化程度的影响

目的探讨不同剂量的瑞舒伐他汀对行导管射频消融术的心房颤动(房颤)患者心房纤维化程度的影响。方法连续纳入150例CARTO指导的首次行导管射频消融术的房颤患者,术中在窦性心律下对左心房进行高密度电压标测,左心房低电压面积比反映心房纤维化程度,术后采用随机数字表法将患者分为3组,分别给予常规处理和不同剂量的瑞舒伐他汀:对照组,小剂量组(10 mg/d)和中剂量组(20mg/d),随访期为3月;采用酶联免疫吸附法(ELISA)测定血清趋化素(chemerin)和半乳糖凝集素-3(Gal-3)水平;chemerin和Gal-3水平与心房纤维化程度的相关性用Pearson相关分析。结果治疗前,3组患者的左心房低电压面积比、chemerin和Gal-3水平比较差异无统计学意义(P0.05);相关性分析显示,血清chemerin(r=0.732,P0.01)和Gal-3(r=0.837,P0.01)水平与心房纤维化程度呈正相关;术后3月,3组患者的chemerin和Gal-3水平较术前均降低,差异有统计学意义(P0.05);与对照组相比,不同剂量瑞舒伐他汀均能降低chemerin和Gal-3水平,而中剂量组降低的更明显[(101.2±20.7)ng/ml vs.(135.3±19.2)ng/ml,(2.2±1.1)ng/ml vs.(4.8±1.3)ng/ml],差异有统计学意义(P0.05)。结论瑞舒伐他汀可降低血清chemerin和Gal-3水平,推测其可以减轻心房纤维化程度,且呈剂量依赖性。     

右心房大小预测阵发性心房颤动合并左心房增大导管射频消融术后的复发

目的:左心房大小可以预测心房颤动(房颤)导管射频消融术后的复发。本研究旨在探讨右心房大小是否可以预测房颤射频消融术后复发。方法:纳入2009-01-2011-12在北京安贞医院行导管射频消融术的阵发性房颤患者共196例。阵发性房颤的消融策略为双侧环肺静脉隔离(PVI)。术后以常规心电图和动态心电图随访患者心律失常复发情况。运用回归分析方法甄别与心律失常复发相关的危险因素并检测其预测效力。结果:术后随访(25.3±18.1)个月,共有111例消融术后复发。右心房横径(RAD)和左心房内径(LAD,r=0.285,P0.001),左心室射血分数(r=-0.241,P=0.001)和左心室舒张末期内径(r=0.239,P=0.001)有关。多因素Cox回归分析显示RAD可以独立预测房颤合并LAD增大患者术后复发(HR 1.044,95%CI1.007~1.082,P=0.021)。其中RAD的截断值为35.5 mm时的预测敏感性为85.4%,特异性为29.2%。KaplanMeier分析两组的窦性心律维持率有显著性差别(Log Rank P=0.034)。结论:右心房增大可以独立预测阵发性房颤合并左心房增大患者的房颤术后远期复发。推测双心房参与房颤的发生与维持。     

心房总传导时间与阵发性心房颤动射频消融术后复发的关系

目的探讨心房总传导时间(TACT)与阵发性心房颤动(简称房颤)导管射频消融术(RFCA)后复发的关系。方法入选2012~2014年行RFCA的阵发性房颤患者116例,TACT测定即在术前基础心律为窦性心律时,脉冲多普勒采样容积放在二尖瓣环上的左房侧壁,从体表心电图Ⅱ导联P波的起始时间至组织多普勒追踪A’波波峰的时间(PA-TDI)间期,测定3个心动周期,取其平均值,术后3个月空白期后评定治疗效果并随访6个月。根据随访结果将患者分成复发组和未复发组。结果随访结束,116例患者中29例(25%)患者复发,复发组TACT较未复发组长[(144±23)ms vs(124±20)ms,P0.001)],多因素分析发现TACT是预测阵发性房颤RFCA术后复发的独立因素(OR=1.045,95%CI 1.021~1.073,P0.001)。结论 TACT可用于预测阵发性房颤射频消融术后复发。     

单核细胞与高密度脂蛋白胆固醇比值对射频消融术后晚期心房颤动复发的预测价值

目的探讨单核细胞/HDL-C比值(MHR)对老年阵发性心房颤动(房颤)患者射频消融术后晚期复发的预测价值。方法纳入江苏省苏北人民医院行导管射频消融术的老年阵发性房颤患者82例,根据消融术3个月后房颤是否复发分为复发组31例和未复发组51例,收集入选患者术前临床资料,采用logistic回归分析术后复发的影响因素。结果老年阵发性房颤行射频消融术患者术后晚期复发率为37.8%,复发组房颤病程、单核细胞、MHR及左心房内径明显高于未复发组,HDL-C明显低于未复发组,差异有统计学意义(P0.05,P0.01)。logistic回归分析显示,校正相关因素后,左心房内径和MHR是阵发性房颤射频消融术后晚期复发的独立危险因素(OR=1.280,95%CI:1.079～1.518,P=0.005;OR=1.482,95%CI:1.153～1.906,P=0.002)。ROC曲线分析显示,MHR预测阵发性房颤射频消融术后晚期复发的曲线下面积为0.76(95%CI:0.650～0.870,P=0.000)。结论 MHR是老年阵发性房颤患者射频消融术后晚期复发的独立预测因素。     

预防心房纤维化对心房颤动患者射频导管消融术后复发的影响

目的探讨心房纤维化的药物预防对心房颤动(房颤)患者射频导管消融术后复发的影响。方法选取2017年6月-2018年3月于武汉大学人民医院行首次射频导管消融术的非瓣膜性房颤患者112例。收集患者临床资料并进行随访,记录患者术后预防心房纤维化的药物类型和剂量,根据随访1年的结果将患者分为术后复发组(n=19)和未复发组(n=83)。比较两组患者一般资料、实验室检查和服用药物的差异,采用SPSS 22数据分析判断心房纤维化的药物预防对房颤患者射频导管消融术后复发的影响。结果房颤患者消融术后复发组与未复发组的性别、年龄、房颤类型、高血压、糖尿病、冠心病等疾病、hs-CRP、e GFR、SCr、UA的差异无统计学意义(P> 0. 05),复发组的房颤初发年龄、房颤病史及NT-pro BNP水平明显高于未复发组(P <0. 05)。药物预防心房纤维化可减少房颤患者射频导管消融术后的1年复发率(P=0. 015),较长的房颤病史是房颤术后复发的独立危险因素。结论房颤患者射频导管消融术后复发率与房颤初发年龄、房颤病史和NT-proBNP水平相关,药物预防心房纤维化可降低房颤患者射频导管消融术后的1年复发率。     

碎裂QRS波预测肥厚型心肌病合并心房颤动患者射频消融术后心律失常复发的探讨

目的:探讨碎裂QRS波(f QRS)与肥厚型心肌病(HCM)合并心房颤动患者导管消融术后的复发是否有关。方法:纳入在北京安贞医院行导管消融术的HCM合并心房颤动患者共91例(阵发/持续性心房颤动:60/31)。消融策略包括:阵发性心房颤动患者行双侧肺静脉隔离(PVI);持续性心房颤动患者行PVI加左心房顶、二尖瓣峡部和三尖瓣峡部线性消融。术前评估基线心电图,fQRS定义为常规12导联心电图中至少2个连续导联的QRS波存在≥2个R波或者R波的波顶或S波的波谷出现顿挫波。术后定期随访,复发定义为导管消融术后心电图或动态心电图记录的任何类型的30s的房性快速性心律失常。结果 68.1%(62/91)患者fQRS阳性。fQRS最常见于下壁导联(75.8%)。平均随访18个月,窦性心律维持率为54.2%(59/91),74.6%(44/59)复发发生在1年以内。fQRS阳性组复发率高于fQRS阴性组(79.0%vs.34.5%,P0.001)。多因素Cox回归分析表明,fQRS是术后快速房性心律失常复发的危险因素(HR=3.243,95%CI:1.147~9.167,P=0.026)。结论:fQRS是HCM合并心房颤动患者导管消融术后房性心律失常复发的预测因子,可用于预测该类患者心房颤动射频术后转归。     

P波离散度与阵发性心房颤动患者射频消融术后复发关系的Meta分析

目的系统评价P波离散度(Pd)与阵发性心房颤动(PAF)患者射频消融术后复发的关系。方法计算机检索PubMed、EMbase、万方、维普、中国知网数据库中关于Pd与PAF患者射频消融术后复发关系的病例对照研究。依据纳入标准筛选文献后,采用Revman5.2软件进行Meta分析。结果最终纳入7篇文献,中文4篇,英文3篇。经漏斗图检验,可能存在发表偏倚。Meta分析结果显示:复发组术前Pd值显著高于治愈组(MD=10.37,95%CI:4.71～16.03),差异有统计学意义(Z=3.59,P=0.0003)。结论术前Pd高的PAF患者射频消融术后易复发,Pd可作为心房颤动复发的预测指标之一。     

肥厚型心肌病合并心房颤动患者射频消融术后心律失常复发心电指标的预测

目的:探讨心电指标f QRS与QTc联合是否能更好预测肥厚型心肌病(HCM)合并心房颤动患者导管消融术后的复发。方法:纳入在北京安贞医院行导管消融术的HCM合并心房颤动患者共120例(阵发/持续性心房颤动72/48)。消融策略包括:阵发性心房颤动患者行双侧肺静脉隔离(PVI);持续性心房颤动患者行PVI加左心房顶、二尖瓣峡部和三尖瓣峡部线性消融。术前评估基线心电图,f QRS定义为常规12导联心电图中至少两个连续导联的QRS波存在≥2个R波或者R波的波顶或S波的波谷出现顿挫波。采用Bazett公式校正QT间期。术后定期随访,复发定义为导管消融术后心电图或动态心电图记录的任何类型的>30 s的房性快速性心律失常。结果:59.2%(71/120)患者f QRR阳性。f QRS最常见于下壁导联(81.7%)。QTc间期(443.90±38.59)ms。平均随访13.4个月,窦性心律维持率为42.5%。多因素Cox回归分析表明,f QRS阳性(HR=1.922,95%CI:1.151~3.210,P=0.012)和QTc>448 ms(HR=1.982,95%CI 1.155~3.402,P=0.013)分别是术后复发的危险因素。f QRS和QTc联合能更好预测心房颤动术后复发。结论:f QRS和QTc延长是HCM合并心房颤动患者导管消融术后复发的独立预测因素。f QRS和QTc联合可用于预测该类患者心房颤动射频术后转归。     

心房颤动与心房扑动的关系

心房颤动(atrial fibrillation，AF)是临床上最常见的持续性的心律失常。AF患者往往有心房扑动(atrial flutter，AFL)发作，而AFL患者也常伴有AF^[1-3]。在使用抗心律失常药物治疗过程中，AF可能变为AFL^[4-5]，或AFL蜕变为AF^[6-9]。这些现象提示二者在发生和维持机制上可能存在一些共性和相互关联。     

Treatment of atrial flutter and rapid atrial tachycardia with transesophageal atrial pacing

Eight patients with atrial flutter (AF) and rapid atrial tachycardia (AT) (5 common AF, 1 uncommon AF and 2 AT) were treated with transesophageal atrial pacing (TEAP). In 5 patients no antiarrhythmic agent was used during this study, and in 3 patients procainamide was administrated intravenously. Conversion to sinus rhythm was successfully achieved in 7 patients (5 common AF and 2 AT). Two patients were converted to sinus rhythm immediately after pacing, and transient atrial fibrillation was induced before conversion to sinus rhythm in 5 patients. TEAP failed to terminate the arrhythmia in 1 patient with uncommon AF. Administration of procainamide reduced the atrial rate in 2 common AF and 1 AT, which were successfully converted to sinus rhythm by TEAP, but induced a rapid ventricular response in 2 patients, one of whom also developed hypotension before conversion. No significant complication due to TEAP was observed in this study. In conclusion, TEAP is a noninvasive method with fewer complications and has nearly the same high efficacy for converting AF and rapid AT to sinus rhythm as DC cardioversion or transvenous atrial pacing.     

心房颤动患者心房组织血管紧张素系统与心房纤维化的关系

目的 探讨心房颤动（房颤）患者血管紧张素系统基因转录和蛋白表达与心房纤维化的关系,研究心房纤维化在房颤维持和心房重构中的作用.方法 心外科手术病人53例,其中窦性心律者26例,房颤患者27例（房颤少于10年患者为房颤Ⅰ组,房颤超过10年患者为房颤Ⅱ组）.术前行超声心动图检查.手术中取右心房组织,Masson染色测定胶原容积分数（CVF）,分别通过逆转录-聚合酶链反应（RT-PCR）和蛋白印迹的方法测量血管紧张素Ⅱ受体、血管转化酶（ACE）mRNA和血管紧张素Ⅱ受体1型蛋白的表达量,用放射免疫的方法测定血管紧张素Ⅱ（AngⅡ）的水平.结果 同窦性心律组相比,房颤组心房扩大、CVF增高;房颤Ⅰ组心房血管紧张素Ⅱ受体1和2的mRNA水平差异无统计学意义,ACE mRNA升高,AngⅡ升高;房颤Ⅱ组心房血管紧张素Ⅱ受体1和2的mRNA有下降的趋势,未达统计学意义,ACE mRNA、血管紧张素Ⅱ受体1蛋白表达下降,有统计学意义.结论 血管紧张素系统在房颤患者的心房纤维化早期发展中发挥作用.     

Prognostic differences between atrial fibrillation and atrial flutter

This report presents the outcome of a cohort of 94 patients with atrial fibrillation from the Canadian Registry of Atrial Fibrillation, in which we paid particular attention to the probability of stroke and death. We also evaluated warfarin use over time and compared left atrial dimensions in patients with atrial flutter with those with atrial fibrillation.     

Supraventricular tachyarrhythmias: atrial flutter and atrial fibrillation

Symptoms range from mild palpitations to overt cardiac failure and cardiogenic shock, depending on the ventricular rate and the patient's underlying cardiac status. Drug therapy is the mainstay treatment. In atrial fibrillation, digoxin is used to control the ventricular response and therefore improve cardiac function. Verapamil may also be used for this purpose.     

The interrelationship between atrial fibrillation and atrial flutter

For a long time, it has been known that atrial fibrillation and atrial flutter have a close clinical interrelationship. Recent electrophysiological studies, especially mapping studies, have significantly advanced our understanding of this interrelationship. Regarding the relationship of atrial fibrillation with atrial flutter: Atrial fibrillation of variable duration precedes the onset of atrial flutter in almost all instances. During the atrial fibrillation, the functional components needed to complete the atrial flutter reentrant circuit, principally a line of block between the venae cavae, are formed. If this line of block does not form, classical atrial flutter does not develop. If this line of block shortens or disappears, classical atrial flutter disappears. In fact, it is fair to say that the major determinant of whether atrial fibrillation persists or classical atrial flutter develops is whether a line of block forms between the venae cavae. Regarding the relationship of atrial flutter with atrial fibrillation: Studies in experimental models and now in patients have demonstrated that a driver (a rapidly firing focus or a reentrant circuit of very short cycle length) can cause atrial fibrillation by producing fibrillatory conduction to the rest of the atria. When the driver is a stable reentrant circuit of very short cycle length, it is, in effect, a very fast form of atrial flutter. There probably is a spectrum of reentrant circuits of short cycle length, i.e., "atrial flutter," that depend, in part, on where the reentrant circuit is located. When the cycle length of the reentrant circuit is so short that it will only activate small portions of the atria in a 1:1 manner, the rest of the atria will be activated rapidly but irregularly, i.e., via fibrillatory conduction, resulting in atrial fibrillation. In short, there are probably several mechanisms of atrial fibrillation, one of which is due to a very rapid atrial flutter circuit causing fibrillatory conduction. In sum, atrial fibrillation and atrial flutter have an important interrelationship.