缬沙坦联合阿替洛尔治疗老年持续性心房颤动的临床疗效及对IL-6、AngⅡ、血管内皮功能的影响

目的探讨缬沙坦联合阿替洛尔治疗老年持续性心房颤动的临床疗效及对病人白细胞介素-6(IL-6)、血管紧张素Ⅱ(AngⅡ)、血管内皮功能(FMD)的影响。方法收集2015年1月-2017年1月在我院心内科治疗的心房颤动病人180例,随机分为缬沙坦组、阿替洛尔组和联合组,各60例。3组病人均接受抗心律失常、抗凝、降血脂等常规对症治疗,在此基础上分别给予缬沙坦、阿替洛尔、缬沙坦联合阿替洛尔治疗。比较3组治疗6个月后左心房内径(LA)、血清炎症因子(IL-6、AngⅡ)、FMD变化。结果治疗后,3组LA较治疗前均缩短(P 0.05),联合组缩短更明显,差异有统计学意义(P 0.01)。缬沙坦组和联合组血清IL-6、AngⅡ水平较治疗前明显下降,FMD较治疗前呈上升趋势,差异有统计学意义(P 0.05)。结论缬沙坦联合阿替洛尔治疗老年持续性心房颤动临床疗效肯定,可减缓左心房扩大,改善心房重构,降低炎症反应,有效改善FMD,预防血栓栓塞发生。     

培哚普利联合阿托伐他汀治疗对高血压合并阵发性心房颤动患者血清血管紧张素Ⅱ水平及房颤复发率的影响

目的探讨培哚普利联合阿托伐他汀治疗对高血压合并阵发性心房颤动(PAF)患者血清血管紧张素Ⅱ(AngⅡ)水平及1年内心房纤颤(房颤)复发率的影响。方法纳入2016年4月至2018年4月于四川省泸州市人民医院收治的高血压合并PAF住院患者92例,采用随机数字表法随机分为对照组和联合组,每组46例。对照组采用培哚普利治疗,联合组在对照组的基础上加用阿托伐他汀治疗,12周为1疗程。分别于治疗前、治疗12周后,采用免疫比浊法检测超敏C反应蛋白(hs-CRP);放射免疫法检测AngⅡ水平;ELISA法检测肿瘤坏死因子(TNF-α)水平;采用彩色多普勒超声检测左心室舒张期内径(LVDd)、左心室收缩期内径(LVDs)、左心房内径(LAD)和左心室射血分数(LVEF)。记录末次随访(治疗后12个月)时的收缩压、舒张压、LVDd、LVDs、LAD、LVEF和房颤复发率。结果治疗12周后,与对照组相比,联合组高血压合并PAF患者的收缩压、舒张压、LAD、LVDd、LVDs、血清hsCRP、TNF-α和AngⅡ水平均显著下降(P0.05),LVEF显著升高(P0.05);联合组的房颤复发率为17.39%,显著低于对照组的39.13%(P0.05)。结论培哚普利联合阿托伐他汀治疗可以降低高血压合并PAF患者的AngⅡ水平,改善血压和心功能,减少房颤复发率。     

血清超敏C反应蛋白、白介素6、肿瘤坏死因子α水平与持续性心房颤动并肺部感染患者左心房结构改变的关系研究

目的分析血清超敏C反应蛋白(hs-CRP)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平与持续性心房颤动并肺部感染患者左心房结构改变的关系。方法选取2014年6月—2015年6月成都市郫县中医医院内一科收治的持续性心房颤动患者150例作为房颤组,根据有无肺部感染分为肺部感染组54例,无肺部感染组96例;根据左心房内径(LAD)分为LAD40 mm组92例和LAD≤40 mm组58例。选取同期在本院门诊体检的窦性心律者50例作为对照组。比较对照组与观察组受试者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标〔LAD、左心房后壁背向散射积分(IBS)及背向散射积分周期变化值(CVIB)〕,比较肺部感染组与无肺部感染组患者血清hs-CRP、IL-6、TNF-α水平及左心房结构指标,比较LAD40 mm组与LAD≤40 mm组患者血清hs-CRP、IL-6、TNF-α水平。结果房颤组患者血清hs-CRP、IL-6、TNF-α水平及IBS高于对照组,LAD大于对照组,CVIB低于对照组(P0.05)。肺部感染组患者血清hs-CRP、IL-6、TNF-α水平高于无肺部感染组(P0.05);两组患者LAD、IBS、CVIB比较,差异无统计学意义(P0.05)。LAD40 mm组患者血清hs-CRP、IL-6、TNF-α水平高于LAD≤40 mm组(P0.05)。结论持续性心房颤动并肺部感染患者血清hs-CRP、IL-6、TNF-α水平升高,左心房增大并伴有心肌纤维化,hs-CRP、IL-6、TNF-α可能参与左心房结构改变过程。     

瑞舒伐他汀对慢性心力衰竭合并阵发性心房颤动的疗效观察

目的观察瑞舒伐他汀降脂之外对慢性心力衰竭合并阵发性心房颤动患者C反应蛋白(CRP)、白细胞介素6(IL-6)、脑钠尿肽(BNP)、左心室射血分数(LVEF)、左心房内径(LAD)、窦律维持及卒中的影响。方法 98例慢性心力衰竭合并阵发性心房颤动患者,在常规抗心衰治疗的基础上分为瑞舒伐他汀组(50例)和对照组(48例)。比较两组患者治疗前后、出院第1、12月CRP、IL-6、BNP、LVEF、LAD的变化,以及阵发性心房颤动再发、永久性心房颤动发生、心衰再住院及卒中发生的差别。结果与对照组比较,瑞舒伐他汀组在长期治疗后CRP、IL-6水平明显降低,LAD缩小,阵发性心房颤动再发、永久性心房颤动及卒中的发生均降低,LVEF、BNP及心衰再住院率两组之间差异无显著性。结论瑞舒伐他汀除降脂外,可降低慢性心力衰竭合并阵发性心房颤动患者的炎症水平,抑制心房重构,减少阵发性心房颤动的发作,但对左心室收缩功能无改善。     

老年不同类型房颤患者同型半胱氨酸及C反应蛋白水平的变化

目的观察不同类型老年房颤患者血浆同型半胱氨酸(Hcy)、C反应蛋白(CRP)水平,探讨其与房颤的关系。方法选择住院的老年房颤患者83例,其中30例阵发性房颤,28例持续性房颤,25例永久性房颤患者,窦性心律30例(对照组),分别检测患者血清中Hcy、CRP水平,同时应用超声心动图测定各组左心房内径(LAD),并对各指标作相关性分析。结果 1血清Hcy、CRP及LAD值永久性房颤、持续性房颤组、阵发性房颤组均高于对照组,永久性房颤组及持续性房颤组高于阵发性房颤组(均P0.05);2房颤患者LAD与Hcy、CRP呈正相关。结论炎症和氧化应激可能参与了左心房的电重构及结构重构,并促进了房颤的发生、发展。     

阿托伐他汀对慢性充血性心力衰竭合并阵发性心房颤动患者窦性心律维持及心功能的影响

目的 探讨阿托伐他汀对血脂正常的慢性充血性心力衰竭合并阵发性心房颤动患者窦性心律的维持作用及对心功能的影响.方法 将血脂正常的慢性充血性心力衰竭合并阵发性心房颤动的患者100例分成治疗组(n=57 例)和对照组(n=43 例),对照组在常规治疗基础上应用胺碘酮抗心房颤动治疗,治疗组再给予阿托伐他汀治疗,观察两组患者治疗6 个月的疗效.结果 治疗组的NYHA 分级以及LVEF 均显著改善,左心室收缩末期内径(LVESD)、左心房内径(LAD)以及左心室舒张末期内径(LVEDD)下降,IL-6、CRP 以及TNF-α低于对照组,差异均有显著统计学意义(均P＜0.01).治疗组复发病例、心房颤动复发率均低于对照组,差异均有统计学意义(均P＜0.05).结论 对血脂正常的慢性充血性心力衰竭合并阵发性心房颤动患者阿托伐他汀治疗,不仅可改善患者的心功能,还可降低患者阵发性心房颤动的复发率,可能与其抑制相关炎症反应有关.     

缬沙坦联合卡维地洛治疗对心力衰竭患者炎性因子及血管紧张素Ⅱ水平的影响

目的探讨缬沙坦对老年慢性心力衰竭患者血浆TNF-α、白细胞介素6(IL-6)和血管紧张素Ⅱ(AngⅡ)水平的影响。方法将95例老年慢性心力衰竭患者随机分为缬沙坦治疗组(对照组,48例)和缬沙坦联合卡维地洛组(联合治疗组,47例)。采用放射免疫法测定患者治疗前和治疗后3个月血浆TNF-α、IL-6和AngⅡ水平的变化。结果与治疗前比较,对照组、联合治疗组治疗3个月后血浆TNF-α、IL-6水平均有明显下降,差异有统计学意义(P<0.05);与对照组比较,联合治疗组TNF-α和IL-6下降更为显著,差异有统计学意义(P<0.05);两组AngⅡ水平在治疗前后差异无统计学意义(P>0.05)。结论单用缬沙坦或缬沙坦联合卡维地洛治疗慢性心力衰竭均能降低TNF-α、IL-6水平,心功能得到改善;缬沙坦联合卡维地洛治疗在降低TNF-α、IL-6水平和改善心功能方面优于单用缬沙坦。     

不同剂量阿托伐他汀对老年冠心病合并心房颤动患者炎症因子及预后的影响

目的:观察不同剂量阿托伐他汀对老年冠心病合并心房颤动(房颤)患者炎症因子及预后的影响,探讨阿托伐他汀抗房颤的可能机制。方法:将100例老年冠心病合并房颤患者随机分为2组,10mg阿托伐他汀组和20mg阿托伐他汀组,观察2组患者治疗前后血清炎症因子[高敏C反应蛋白(hs-CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]、左心房内径(LAD)及心房利尿钠肽(ANP)的变化,同时记录治疗6个月后2组患者窦性心律维持率及栓塞事件发生率。结果:治疗后,2组hs-CRP、IL-6、TNF-α、ANP水平及LAD内径均较治疗前降低(P0.05),且20mg阿托伐他汀组降低更明显(P0.05),同时20mg阿托伐他汀组较10mg阿托伐他汀组窦性心律维持率高,栓塞事件发生率低(P0.05)。结论:阿托伐他汀能降低老年冠心病合并房颤患者血清炎症因子水平,同时能降低ANP水平及LAD内径,提高窦性心律维持率、降低栓塞事件发生率,且呈剂量依赖性,这可能是阿托伐他汀发挥抗房颤作用的机制之一。     

缬沙坦对高血压合并持续性心房颤动患者左心房结构及左心室功能的影响

目的观察缬沙坦对高血压合并持续性心房颤动(房颤)患者在降压同时对其心率(HR)、血压(BP)、左心房结构及左心室功能的影响。方法对2004年1月至2005年6月哈尔滨医科大学第一临床医学院收治的高血压合并持续性房颤患者106例,在控制心室率、预防血栓治疗的基础上应用缬沙坦80mg/d,对照组用依那普利10mg/d。3个月、6个月后对照观察其对心率、血压、左心房结构及左心室功能的影响。缬沙坦组54例,依那普利组52例。结果分别观察3个月、6个月后两组血压、心率均控制理想,两组间差异无显著性意义(P>0.05)。左心房直径缬沙坦组治疗前平均(50±7)mm,3个月后为(46±4)mm,6个月后为(40±3)mm,与治疗前相比差异有显著性意义。依那普利组3个月、6个月后左心房也有缩小,但差异不显著。治疗组治疗前NY分级Ⅱ、Ⅲ级占64%,治疗后3个月、6个月分别下降至33%、15%。而依那普利组也有明显下降,3个月、6个月分别下降至45%、25%,下降程度不如缬沙坦组明显。结论长期应用缬沙坦(3个月以上)可以显著改善左心房结构、左心室功能和持续性房颤患者的长期预后。     

辛伐他汀对高血压并发阵发性心房颤动的作用及机制

目的:研究辛伐他汀对高血压并发阵发性心房颤动(房颤)患者房颤再发率和持续性房颤发生率的影响以及其对血高敏C反应蛋白(hsCRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)以及肾素、血管紧张素Ⅱ(AngⅡ)的水平的影响.方法:将87例高血压并发阵发性房颤患者随机分为2组:辛伐他汀组45例,常规治疗的同时,予口服辛伐他汀20 mg/d;对照组42例,仅给予常规治疗.追踪24个月,观察2组治疗1年后阵发性房颤再发率和持续性房颤的发生率,并检测治疗前及治疗1年后hsCRP、IL-6、TNF-α、肾素、AngⅡ的表达水平.结果:辛伐他汀组房颤再次发作7例(15.6%),明显低于对照组(14例,33.4%);辛伐他汀组转为持续性房颤2例(4.5%),亦明显低于对照组(5例,11.9%);差异均有统计学意义(P<0.05).辛伐他汀组治疗后血清hsCRP、IL-6、TNF-α、肾素、AngⅡ的水平,与对照组比较均下降,差异有统计学意义(P<0.05).所有再发房颤患者的血清hsCRP、IL-6、TNF-α、肾素、AngⅡ水平均比未再发房颤患者的明显升高,差异有统计学意义(P<0.01).结论:高血压并发阵发性房颤的患者应用辛伐他汀治疗,能够降低阵发性房颤的再发率,减少持续性房颤的发生率,而且降低血清hsCRP、IL-6、TNF-α、肾素、AngⅡ的水平,后者可能与房颤再发相关,提示炎症反应及肾素-血管紧张素-醛固酮系统的激活具有促进心房颤动的发生和持续的作用.     

心房颤动患者心房纤维化研究进展

心房颤动的发生和维持与心房重构有关。心房纤维化是心房颤动患者心房结构重构最突出的表现,目前被认为是发生心房颤动的结构基础,是心房颤动发生、维持的一个重要因素。现综述心房颤动患者心房纤维化及其发生机制。通过对心房颤动患者心房纤维化结构改变及肾素-血管紧张素系统、转化生长因子、基质金属蛋白酶等在心房纤维化的发生和心房颤动发生、维持中的作用等的全面阐述,,探讨了心房颤动患者心房纤维化的研究进展。防治心房颤动新的策略取决于对心房纤维化机制更好的理解。     

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.     

Atrial Tachycardias Following Atrial Fibrillation Ablation

One of the most important proarrhythmic complications after left atrial (LA) ablation is regular atrial tachycardia (AT) or flutter. Those tachycardias that occur after atrial fibrillation (AF) ablation can cause even more severe symptoms than those from the original arrhythmia prior to the index ablation procedure since they are often incessant and associated with rapid ventricular response. Depending on the method and extent of LA ablation and on the electrophysiological properties of underlying LA substrate, the reported incidence of late ATs is variable. To establish the exact mechanism of these tachycardias can be difficult and controversial but correlates with the ablation technique and in the vast majority of cases the mechanism is reentry related to gaps in prior ablation lines. When tachycardias occur, conservative therapy usually is not effective, radiofrequency ablation procedure is mostly successful, but can be challenging, and requires a complex approach.     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

心房颤动致心房重构分子机制研究进展

心房颤动是临床上一种常见的心律失常,心房颤动致心房重构是近年来研究发现的一个重要的电生理现象。心房颤动本身能够导致心房电生理、功能和结构的改变。本文综述了心房颤动致心房快速的电生理变化和缓慢的蛋白质表达及其分子改变机制。通过对心房电生理重构、离子重构和蛋白质重构和超微结构及其功能变化等不同方面的全面阐述,探讨了心房重构的分子机制研究进展。防治心房颤动新的策略将取决于心房重构机制更好的理解。     

Atrial Fibrillation: The Role of Atrial Defibrillation

Dual defibrillator implantation represents an emerging option to treat patients with drug refractory atrial fibrillation. Atrial antitachycardia pacing and cardioversion have been demonstrated to be highly effective in treating spontaneous tachyarrhythmias and may reduce atrial fibrillation burden by preventing atrial remodeling. Device implantation has been associated to improved quality of life and reduced hospitalization rate. Patient selection and tailored device programming are critical as regard to clinical outcome. Individual psychological profile analysis as well as underlying heart disease and atrial fibrillation clinical patterns represent the main drivers for the right strategy. Controlled studies are needed in order to define the subset of patients who can benefit more from device implantation.     

Right Atrial Thrombi and Depressed Right Atrial Appendage Function After Cardioversion of Atrial Fibrillation

BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.     

胸腔静脉在心房颤动发生机制中的作用

心房颤动是临床上常见的心律失常。肺静脉、上腔静脉、Marshall静脉等在心房颤动发生中扮演重要角色,现就胸腔静脉的组织学、电生理特征及其与心房颤动关系进行综述。