迷走神经活动对心房电重构的影响

目的 研究迷走神经干预对心房电重构的影响.方法 24只杂种犬随机分为3组,为排除交感神经对心房电重构的影响,3组犬均应用美托洛尔阻断交感神经效应.A组10只犬快速心房起搏过程中无迷走神经干预,B组8只犬应用阿托品阻断迷走神经效应,C组6只犬在快速心房起搏过程中同时进行迷走神经刺激.在右心房(RA)、冠状静脉窦(CS)和右心室(RV)放置多极导管.通过RA电极导管进行600次/min心房起搏30 min构建急性心房电重构模型.在右心房快速起搏前后测量基础状态(无迷走神经刺激)和迷走神经刺激下的心房有效不应期(AERP)和心房颤动(房颤)易感窗口(VW).结果 A组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).B组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前无明显变化(P＞0.05).C组犬右心房快速起搏后基础状态下及迷走神经刺激时的AERP较起搏前明显缩短(P＜0.05).A组及C组右心房快速起搏后AERP缩短值明显大于B组(P＜0.05),但A组及C组AERP缩短值差异无统计学意义(P＞0.05).迷走神经刺激下,B组犬在右心房快速起搏前后均较难诱发房颤(VW接近0),A组及C组犬右心房快速起搏后较起搏前容易诱发房颤(P＜0.05).结论 短期右心房快速起搏导致的心房电重构过程中伴随着迷走神经兴奋性增强.迷走神经兴奋性增强及迷走神经刺激加重心房电重构,导致房颤易感性增加.迷走神经阻滞能减轻心房电重构,降低房颤易感性.     

心脏再同步治疗术后新发心房颤动与窦性心律的对比分析

目的 分析心脏再同步治疗（CRT）术后1年内慢性心力衰竭（CHF）患者出现新发心房颤动（房颤）与保持窦性心律的疗效对比情况.方法 接受CRT治疗CHF患者54例,所有患者术前均无房颤病史,于术前和术后6、12个月进行程控随访及临床、超声心动图检查.结果 1年随访结束时,54例患者中有12例（22.2%）出现新发房颤,其余42例保持窦性心律.窦性心律组术后临床及超声心动图指标均较术前明显改善（P＜0.001）.新发房颤组术后心功能、左心室射血分数（LVEF）、左心室舒张末内径也较术前有明显改善（P＜0.05）,但左心房内径及二尖瓣反流无明显变化.两组间比较,左心房内径在窦性心律组较新发房颤组有明显缩小的趋势（P=0.057）.亚组分析,阵发性房颤患者术后心功能、LVEF较术前改善（P＜0.05）,而持续性房颤患者术后各指标较术前均无明显变化.CRT术后新发房颤危险因素经Logistic回归显示为术前二尖瓣反流程度（P=0.046,OR=3.729）和新发房颤发生前的心房起搏比例（P=0.010,OR=1.050）.结论 CRT术后新发房颤与二尖瓣反流程度加重和心房起搏比例增高明显相关.新发阵发性房颤一般不影响CRT疗效,新发持续性房颤CRT术后疗效较差.     

最小化心室起搏减少病态窦房结综合征患者心房颤动的发生

目的 探讨最小化心室起搏对病态窦房结综合征(病窦综合征)患者心房颤动(房颤)发生的影响.方法 入选2003年4月至2008年4月因病窦综合征植入DDD起搏器的患者112例,随机、单盲分为最小化心室起搏组56例(A组),和传统双心腔起搏组56例(B组),分别于3、6个月进行随访,以后每年1次,每次随访内容包括病史询问、起搏器程控、超声心动图.主要观察指标为房颤发生率,次要观察指标为超声心动图(包括左心房内径、左心室舒张末内径和左心室射血分数)和因心力衰竭再入院情况.结果 平均随访时间为(33.7±17.1)个月,与B组相比,A组的心室起搏平均比例显著减少(10.1%vs92.3%,P＜0.001),但两组的心房起搏平均比例相近(73.6%vs72.8%,P=0.98).B组累计房颤发生率明显低于A组(RR=0.65,95%可信区间0.59～0.93,P=0.015).与植入前相比,A组各阶段超声心动图变化差异无统计学意义;而B组左心房内径逐渐增大.术后2年起,B组左心房内径与植入前相比,或与同期的A组相比,差异有统计学意义.结论 右心室心尖部起搏使病窦综合征患者房颤发生率增加,左心房内径增大.因此,对房室传导正常的病窦综合征患者,建议最小化心室起搏,鼓励心室自身传导.     

心房颤动患者经导管射频消融术后不同时期左心房结构及功能的动态变化

目的:观察射频消融术对阵发性和持续性心房颤动(房颤)患者左心房结构和功能不同时期的影响。方法:临床诊断房颤的79名患者作为研究对象(阵发性房颤组65例、持续性房颤组14例),随访1年,行超声心动图检查监测左心房最大面积(左心房左右径×上下径)、左心房最大容积(LAVmax)、左心房最小容积(LAVmin)、左心房P容积(LAVp)等左心房结构指标,并通过左心房被动射血分数(LAPEF),左心房主动射血分数(LAAEF),左心房排空容积等指标探讨左心房功能的变化。体检非房颤人群22例作为对照组。全部数据采用SPSS17.0软件包进行统计学分析。结果:①消融术前检测显示:房颤组左心房最大面积、LAVmax、LAVmin均高于正常对照组(P0.05);并且持续性房颤组左心房增大更显著(P0.05)。房颤组LAAEF低于正常对照组(P0.05),其中持续性房颤组下降更明显(P0.05)。LAPEF及左心房排空容积各组间差异无统计学意义。②两组房颤患者术后左心房最大面积、LAVmax较术前均有变小(P0.05),但两者出现变化的时间点不同,阵发性房颤组在术后1年明显变小(P0.05),持续房颤组在术后近期就出现明显变小(P0.05)。两组LAAEF、LAPEF、排空容积等较术前均无显著性变化。③持续性房颤组左心房最大面积术后近期、中期变化率大于阵发性房颤组(P0.05),但至术后1年变化率两者差异无统计学意义。结论:经导管射频消融术能缩小房颤患者增大的左房结构,近、中期在持续性房颤患者更加显著;经导管射频消融术本身对左心房功能无明显影响。     

具有多种抗心房颤动模式起搏器的临床应用

目的评价心房程序起搏预防和治疗阵发性房颤的效果.方法对15例阵发性房颤患者置入Selection 900E(AF2.0)型起搏器,调查分析术前2个月和术后2个月及4个月阵发性房颤事件各指标. 结果患者术后2个月及4个月较术前2个月在有症状阵发性房颤事件数有明显地降低(34.2±18.01,19.73±7.79对66.30±26.06);术后4个月较术后2个月有症状阵发性房颤事件数、阵发性房颤事件总数、房颤总持续时间、房颤负荷均降低(P＜0.05),而心房起搏比率无明显改变.结论生理性心房程序起搏减少阵发性房颤事件的发生,降低房颤负荷,并可以明显减少临床抗心律失常药物使用的种类和剂量.     

氯沙坦对阵发性心房颤动患者血清脑钠素及血管紧张素Ⅱ水平的干预作用

目的:探讨阵发性心房颤动(房颤)患者脑钠素(BNP)、血管紧张素Ⅱ(AngⅡ)的变化及氯沙坦的治疗价值。方法:入选患者分为阵发性房颤组(房颤组)40例,窦性心律组(对照组)40例。房颤组按治疗方法的不同又分为2亚组,A亚组服用胺碘酮及氯沙坦,B亚组单纯服用胺碘酮;对照组患者行原发病治疗。分别检测房颤组和对照组治疗前及房颤组的A、B亚组治疗后24个月的血浆肾素(PRA)、AngⅡ、BNP水平及平均左心房内径(LAD),进行对照分析。结果:①房颤组BNP、PRA、AngⅡ水平及LAD较对照组增加(P<0.05);②房颤组血BNP水平与LAD、AngⅡ浓度明显相关(r分别为0.362,0.294,P<0.05)。③房颤组治疗后A亚组较B亚组BNP水平降低(P<0.05),PRA、AngⅡ水平升高(P<0.05)。④氯沙坦干预能提高窦律维持率(P<0.05),可降低47%的房颤复发危险(RR=0.45,95%CI0.260~0.749,P<0.05)。结论:阵发性房颤患者BNP水平的升高可能与心房重构有关,氯沙坦可通过干预房颤的心房重构降低BNP水平并降低阵发性房颤的复发。     

具有多种抗心房颤动模式起搏器的临床应用

目的:评价心房程序起搏预防和治疗阵发性房颤的效果。方法:对15例阵发性房颤患者置入Selection 900E(AF2.0)型起搏器,调查分析术前2个月和术后2个月及4个月阵发性房颤事件各指标。 结果:患者术后2个月及4个月较术前2个月在有症状阵发性房颤事件数有明显地降低(34.2±18.01,19.73±7.79对66.30±26.06);术后4个月较术后2个月有症状阵发性房颤事件数、阵发性房颤事件总数、房颤总持续时间、房颤负荷均降低(P<0.05),而心房起搏比率无明显改变。 结论:生理性心房程序起搏减少阵发性房颤事件的发生,降低房颤负荷,并可以明显减少临床抗心律失常药物使用的种类和剂量。     

心房起搏治疗阵发性心房颤动的临床观察

近年来大量资料证实心房起搏有明显的抗房性心律失常作用 ,本研究对一组接受心房起搏治疗的缓慢型心律失常合并阵发性心房颤动 (房颤 )患者进行了回顾性分析。1.资料与方法 :选择 1993年 2月～ 2 0 0 0年 7月 ,对合并有阵发性房颤患者 38例植入永久性心房起搏装置 ,年龄 38～ 78(6 0± 17)岁。其中 33例为病窦综合征 (病窦 ) ,5例为高度房室传导阻滞。阵发性房颤指术前记录至少 1次房颤发作者。 5例病窦合并阵发性房颤患者 ,由于经济原因 ,行单纯右心房起搏 (ＡＡＩ) ;3例合并房间传导阻滞的患者 ,选择ＤＤＤ起搏器 ,行双心房 右心室三腔起…     

美托洛尔联合螺内酯及美托洛尔联合缬沙坦治疗孤立性阵发性心房颤动的疗效观察

目的该项研究旨在明确美托洛尔联合螺内酯或联合缬沙坦治疗孤立性阵发性心房颤动是否能有效抑制心房电重构及结构、功能重构。方法随机分成四组,美托洛尔组(A组)、美托洛尔+螺内酯组(B组)、美托洛尔+缬沙坦组(C组)、对照组(D组)。服药1年后比较各组进展为持续性心房颤动的发生率,同一组患者治疗前后及治疗一年后不同组间左心房整体射血分数(LAEFtotal)、左心房被动射血分数(LAEFpassive)、左心房主动射血分数(LAEFactive)、左心房最大容积指数(LAVI)、心房颤动发作频率、心房颤动持续时间是否存在显著差异。结果 A组、B组及C组1年后进展为持续性心房颤动的发生率低于D组(P0.05),A组、B组、C组间无统计学差异(P0.05)。各干预组服药1年后较服药前A组LAEFtotal、LAEFpassive、LAEFactive、LAVI无明显变化(P0.05),心房颤动发作频率、心房颤动持续时间较前降低(P0.05)。B组及C组LAEFtotal、LAEFpassive、LAEFactive明显升高(P0.05),LAVI、心房颤动发作频率、心房颤动持续时间明显降低(P0.05)。治疗1年后,A组、B组和C组各指标均低于D组(P0.05),B组与C组优于A组(P0.05)。结论美托洛尔联合螺内酯或联合缬沙坦治疗孤立性阵发性心房颤动可有效控制心房颤动反复发作,缩短心房颤动持续时间,能有效抑制左心房结构及功能重构,可延缓阵发性心房颤动进展为持续性心房颤动。     

醛固酮及心房间质重构与心房颤动关系的实验研究

目的 探讨醛固酮(Aid)及心房间质蕈构与心房颤动(房颤)发生发展的关系.方法 18只犬随机分为对照组(普通喂食)、培哚普利组(培哚普利1 mg·1kg-1·d-1)、螺内酯组(螺内酯10mg·kg-1·d-1).均置入起搏器并持续起搏8周.动态检测左心房的形态功能和血浆Ald水平,记录停止起搏后维持房颤的例数及持续的时间,处死动物后检测心房组织Ald水平及心房肌纤维化的情况.结果 起搏前三组间血浆Ald水平差异无统计学意义(P>0.05),而起搏4周及8周后培哚普利组、螺内酯绢明显低于对照组(P<0.05);对照组起搏后4周及8周显著高于起搏前(P<0.05),而培哚普利组、螺内酯组起搏前后差异无统计学意义(P>0.05).起搏4周及8周后,对照组左心房左右径、上下径、收缩末期容积和舒张末期容积较起搏前明显增大,而左房射血分数(LAEF)较起搏前显著降低(P<0.05);与对照组相比,培哚普利组、螺内酯组起搏后上述指标均明显减小,而LAEF显著增大(P<0.05).与对照组相比,培哚普利组、螺内酯组停止起搏后维持房颤犬明显减少,平均持续时间也明显短于对照组,而培哚普利组、螺内酯组之间差异无统计学意义.对照组左右心房肌胶原体积分数值明显高于培哚普利组、螺内酯组(P<0.05),而培哚普利组、螺内酯组之间差异无统计学意义(P>0.05).结论 在房颤发生发展中,血浆及心房肌Ald水平升高,心房肌纤维化加重,左房内径及容积会逐渐增大而收缩功能降低;螺内酯和培哚普利可抑制Ald水平升高及心房肌纤维化加重、改善心房结构及功能的变化、减少房颤的发生率及持续时间,且二者效果相似.     

左室不同起搏部位对心脏再同步化治疗短期疗效的影响

目的探讨左室不同起搏部位对心脏再同步化治疗(CRT/D)患者术后短期(1周及6个月)疗效的影响。方法入选成功行CRT/D手术,且相关观察数据完整患者共36例。分析术中左室电极植入情况,左室起搏部位根据左室电极末端左前斜45度时的投影结合其相应心脏静脉的部位确定,分为靠近间隔部组(A组)和游离壁组(B组)。比较两组患者术后1周常规心脏超声变化,随访6个月CRT/D临床应答及并发症情况。结果术后1周,两组的左室射血分数均较术前明显提高;与A组相比,B组对心脏功能的改善更为明显,左房内径、左室收缩末期容积、二尖瓣返流情况仅在B组有所改善。术后随访6个月,35例有应答,B组中1例无应答,两组术后6个月无应答和并发症的发生率均无明显差别。结论 CRT/D治疗慢性心力衰竭在短期内即可使患者获益。左室电极位于游离壁可以更好的改善心脏功能,逆转心室重构。     

短时快速激动对肥厚心肌电生理特性的影响及其与室性心律失常的关系

观察短时快速激动对肥厚心肌电生理特性的影响并探讨其与室性心律失常 (VA)发生的关系。以部分结扎腹主动脉方法制作心肌肥厚模型。阻滞自主神经后 ,在心外膜右室流出道 (RVOT)、右室心尖部 (RVA)、左室流出道(LVOT)及左室心尖部 (LVA)四个部位以 2 2 0 ,2 4 0 ,2 6 0次 /分的频率刺激测定各部位的单相动作电位时限 (MAPD)及有效不应期 (ERP)。然后于 1∶1房室传导下 ,随机进入普通右房电刺激组 (2 2 0次 /分 )和快速右房电刺激组 (2 6 0次 /分 ) ,持续 30min后 ,重复上述测定过程。记录心室后除极的发生次数。最后诱发心室颤动 (VF) ,记录诱发率和VF持续时间。结果 :心肌肥厚组快速激动后除RVA外 ,其他各部位的ERP值均显著延长 (2 2 0 ,2 4 0 ,2 6 0次 /分频率刺激下的前后ERP值 (ms)为 :RVOT 15 1± 18vs181± 2 1,14 5± 17vs173± 14 ,14 0± 15vs 16 7± 14 ;RVA 16 1± 17vs 171± 19,15 5± 16vs 16 6± 19,15 2± 17vs 16 2± 18;LVOT 16 5± 2 7vs192± 2 0 ,16 1± 2 5vs187± 2 1,15 4± 17vs178± 15 ;LVA 170±15vs191± 15 ,16 5± 15vs189± 11,15 9± 13vs 182± 11)。而对照组在快速激动后的ERP延长并不显著。心肌肥厚组和对照组在普通刺激下 ,ERP均无明显延长。各组在刺激前后的MAPD?     

右心室流出道起搏与常规心尖部起搏的对比研究

目的 评价右心室流出道间隔部起搏临床应用的有效性及安全性.方法 将所入选患者按右心室起搏电极置入部位随机分为被动固定导线心尖部(常规组)和螺旋电极起搏右心室流出道间隔部(非常规组),比较两组患者在术中及术后起搏参数变化及不良反应情况.结果 非常规组在术中测试起搏阈值及电流明显高于常规组,但术后1个月差异无统计学意义;术中阻抗及R波振幅二者无明显差异.非常规组起搏时QRS时限较常规组明显要窄,但差异无统计学意义.无患者发生不良反应.结论 选择性部位起搏的临床应用安全、有效.     

Future easy and physiological cardiac pacing

The right atrial appendage (RAA) and right ventricular apex (RVA) have been widely considered as conventional sites for typical dual-chamber atrio-ventricular cardiac (DDD) pacing. Unfortunately conventional RAA pacing seems not to be able to prevent atrial fibrillation in DDD pacing for tachycardia-bradycardia syndrome, and the presence of a left bundle branch type of activation induced by RVA pacing can have negative effects. A new technology with active screw-in leads permits a more physiological atrial and right ventricular pacing. In this review, we highlight the positive effects of pacing of these new and easily selected sites. The septal atrial lead permits a shorter and more homogeneous atrial activation, allowing better prevention of paroxysmal atrial fibrillation. The para-Hisian pacing can be achieved in a simpler and more reliable way with respect to biventricular pacing and direct Hisian pacing. We await larger trials to consider this "easy and physiological pacing" as a first approach in patients who need a high frequency of pacing.     

Prevention of recurrent atrial fibrillation with chronic dual-site right atrial pacing

Objectives. We investigated 1) the feasibility, safety and efficacy of multisite right atrial pacing for prevention of atrial fibrillation (AF); and 2) the ability of atrial pacing in single- and dual-site modes to increase arrhythmia-free intervals in patients with drug-refractory AF.Background. We recently developed and applied a novel technique of dual-site right atrial pacing in an unselected group of consecutive patients with AF requiring demand pacing. A prospective crossover study design was used to evaluate single- and dual-site right atrial pacing modes.Methods. The frequency of AF during the 3 months before pacemaker implantation was analyzed. Consecutive consenting patients underwent insertion of two atrial leads and one ventricular lead with a DDDR pulse generator. Patients were placed in a dual-site pacing mode for the first 3 months and subsequently mode switched to single site pacing for 3 months. Mode switching was repeated at 6-month intervals thereafter.Results. Atrial pacing resulted in a marked decline in AF recurrences (p < 0.001). During dual-site pacing with an optimal drug regimen, there was no AF recurrence in any patient compared with five recurrences in 12 patients during single-site pacing (p = 0.03). The mean (±SD) arrhythmia-free interval before pacing (14 ± 14 days) was prolonged with dual- (89 ± 7 days, p < 0.0001) and single-site pacing (76 ± 27 days, p < 0.0001). Symptomatic AF episodes showed a declining trend during dual- and single-site pacing compared with those during the preimplantation period (p = 0.10). Mean antiarrhythmic drug use for all classes declined from 4 ± 1.9 drugs before implantation to 1.5 ± 0.5 (p < 0.01) drugs after implantation. Twelve (80%) of 15 patients remained in atrial paced rhythm at 13 ± 3 months.Conclusions. We conclude that multisite right atrial pacing is feasible, effective and safe for long-term application. Atrial pacing significantly prolongs arrhythmia-free intervals in patients with drug-refractory paroxysmal AF. Dual-site right atrial pacing may offer additional benefits and should be considered either as the primary mode or in patients unresponsive to single-site pacing.     

Pacemaker prevention therapies for the control of drug-refractory paroxysmal atrial fibrillation.

AIMS: Atrial septal pacing has been shown to prevent paroxysmal atrial fibrillation (PAF) refractory to drugs in patients without inappropriate bradycardia. This study assesses the effects of atrial septal pacing using new pacing algorithms designed to prevent the initiation or maintenance of PAF. METHODS AND RESULTS: Eleven Medtronic AT500 and 6 Guidant Pulsar Max pacemakers were implanted. The incremental benefit of prevention pacing therapies was compared with DDDR pacing by analysis of pacemaker-stored electrograms, ambulatory electrocardiography, symptoms and quality of life questionnaires. RESULTS: Atrial septal pacing reduced AF burden by >50% in 13/17 patients (76.5%). Activation of a combined pacing algorithm (atrial pacing preference; atrial rate stabilization; and post mode-switch overdrive pacing) in patients with AT500 pacemakers produced a marginal reduction in AF burden (mean %AF 0.61 ON, 0.73 OFF, P=0.53 ns). Conversely in the Pulsar Max group when atrial pacing preference was activated, AF burden was slightly increased (mean %AF 5.84 ON, 3.73 OFF,P =0.13). Symptoms improved with atrial septal pacing but did not change when prevention algorithms were activated. CONCLUSION: Atrial septal pacing resulted in a marked improvement in AF burden and symptoms. Activation of specific prevention pacing algorithms provided more continuous atrial pacing but had limited and heterogeneous effects on AF burden.     

Comparison of atrial contribution to cardiac hemodynamics in patients with normal and severely compromised cardiac function

The importance of atrial contribution to cardiac function in patients with congestive heart failure is controversial. Ten patients with severe congestive failure (Group A) and 10 patients with normal ventricular function (Group B) were studied during atrial and ventricular pacing. Left ventricular ejection fraction, baseline pulmonary capillary wedge pressure, and baseline cardiac index were different between Group A and Group B patients: 22 +/- 10 vs. 65 +/- 11 (p less than 0.01); 21 +/- 5 vs. 8 +/- 4, (p less than 0.01); and 2.8 +/- 0.5 vs. 3.5 +/- 1.0 (p = 0.05). Compared with atrial pacing, cardiac index decreased from 2.8 +/- 0.6 to 2.2 +/- 0.5 (p less than 0.01) in Group A and from 3.6 +/- 0.7 to 2.9 +/- 0.5 (p less than 0.01) in Group B, during ventricular pacing. Pulmonary capillary wedge pressure increased by similar amounts in both groups during ventricular pacing. The change in cardiac index, % change in cardiac index, and change in pulmonary capillary wedge pressure from atrial to ventricular pacing, were not different between Group A and Group B patients. By logistic regression analysis, no association was found between the % change in cardiac index and the following variables: left ventricular ejection fraction, left ventricular end-diastolic volume, baseline pulmonary capillary wedge pressure, change in pulmonary capillary wedge pressure, and baseline cardiac index. The atrial contribution to resting steady-state cardiac function is similar between patients with severe congestive failure and those with preserved ventricular function.     

Right ventricular apical lead position is associated with prolonged signal-averaged P-wave duration

Aim

The study aimed to determine if right ventricular apical pacing is associated with adverse change in atrial substrate compared with right ventricular septal pacing.

Methods

Patients with septal leads and dual-chamber devices with more than 3 months of follow-up and 70% or higher cumulative percentage of ventricular pacing were compared with a matched group of apically implanted leads with a cumulative percentage ventricular pacing of 70% or higher. Device parameters were recorded, and high-resolution recordings were obtained for signal-averaged P-wave (SAPW) analysis. Previously obtained SAPW recordings taken from 49 healthy patients and 73 patients with paroxysmal atrial fibrillation were used as negative and positive controls, respectively.

Results

Ten patients with septal leads (mean age, 71.9 ± 12.1 years; mean months implanted, 10.5 ± 3.2 months) and 9 patients with apical leads (mean age, 71.9 ± 5.7 years; mean months implanted, 11.4 ± 6.4 months) were enrolled. The SAPW duration was longer in the apical cohort compared with the septal cohort (144.8 ± 6.9 and 133.0 ± 5.5 milliseconds, respectively; P = .001), whereas there was no significant difference between septal and normal cohorts (133.0 ± 5.5 and 129.3 ± 7.1 milliseconds, respectively; P = .08).

Conclusions

Apical pacing is associated with prolonged P-wave duration relative to septal pacing and controls: this may manifest as increased risk of atrial tachycardias and presents a potentially novel benefit of septal pacing.     

房室传导正常的病窦综合征患者心房或心室起搏的长期随访

评价长期心房或心室起搏对病窦综合征 (SSS)患者心功能及房性心律失常的影响 ,对 1 1 8例SSS伴房室传导正常的患者 (AAI组 56例、VVI组 62例 )进行随访。随访 40 .8± 2 .3个月 ,VVI组 62例中 1 9例NYHA分级增加 ,而AAI组 56例中 4例NYHA分级增加 (P <0 .0 5)。左室射血分数VVI组明显下降 (从 0 .491± 0 .0 4 1至 0 .451± 0 .0 4 3 ,P <0 .0 5) ,而AAI组则增加 (从 0 .482± 0 .0 75增至 0 .535± 0 .0 59,P <0 .0 5)。左房内径VVI组明显增加 (从 33± 6增至 40± 6mm ,P <0 .0 5) ,AAI组从 34± 7增至 36± 6(P >0 .0 5)。房性心律失常发生率VVI组明显增加 (从 35 .5 %增至 45 .2 % ,P <0 .0 5) ,AAI组减少 (从 2 6 .8%降至 0 % ,P <0 .0 1 )。结论 :心房起搏对SSS患者是一安全、可靠的起搏方式 ,可减少房性心律失常的发作 ,有助于患者心功能的改善