VVI起搏室房逆传诱发的心律失常

人工心脏起搏器植入患者的心电图由患者的自主心律与起搏心律共同构成，自主心律时发生的各种心律失常也可在植入起搏器后发生。植入起搏器后，起搏器以“按需”方式工作的单腔或双腔起搏器产生的心律，都将与逸搏或逸搏心律相似。也就是说起搏心律类似室性逸搏及逸搏心律伴室房传导所诱发的心律失常也可在起搏心律中发生。     

起搏心律伴逆传文氏现象及室性反复搏动

一女性患者 ,80岁。 6年前安置了VVI起搏器 ,现因头晕行动态心电图检查发现起搏心律伴逆传文氏现象及室性反复搏动。提示在安置起搏器前 ,心内电生理检查发现有室房逆传 ,无论有无形成反复心律 ,不宜安置VVI起搏器 ,避免发生起搏器综合征     

VVI起搏心律伴室房逆传致起搏器综合症一例

患者，女性，62岁，因“窦性停搏”于99年7月1日植入intermedics VVI起搏器。术后检测起搏器的起搏及感知功能良好，起搏频率70次／分，出院一周后患者出现头晕、胸痛症状，并逐渐加重，患者的亲属则认为她太娇气，患者本人也未来医院检查，随后患者头晕症状继续加重，以致于一人不能外出，并出现气短、下肢浮肿等心衰症状。患者胸痛严重时，自行在附近的私人诊所静滴抗生素，未来医院就诊，     

VVI起搏器室房逆传的心电图特征及其临床意义

人工心脏起搏器植入患者的心电图由患者的自主心律起搏心律共同构成,自主心律时发生的各种心律失常也可在植入起搏器后发生。植入VVI起搏器后,起搏器以“按需”方式工作的单腔起搏器产生的心律类似逸搏及逸搏心律,逸搏及逸搏心律伴室房传导所诱发的心律失常也．可在起搏心律中发生。本文通过VVI起搏室房传导的31例心电图分析,从而来探讨VVI起搏器室房逆传的心电图特征及产生机制,并所涉及的临床意义。     

人工起搏室房逆传夺获心房

1概念 人工心室起搏时（例如VVI起搏模式）,起搏激动沿室房传导途径逆传并夺获心房,形成逆行P波（P^-波）。     

VVI心室起搏逆传心房致房性融合波1例

患者男,75岁。因“胸痛3h”于9月30日入院,入院诊断主动脉夹层动脉瘤。入院心电图示：心房率63次/min,心室率36／min,显示三度房室传导阻滞,室性逸搏心律。一月后行VVI起搏,心电图示：图Ⅱa、Ⅱb为心电图Ⅱ导联的连续记录(见图1),VVI起搏心律,P-P间期0．68s,心房率88次／min,R-R间期1．12s,心室率(起搏)54次/min,呈     

完全性房室阻滞VVI起搏后逆传P波与窦性P波相互干扰一例

1临床资料及起搏心电图分析患者男性，64岁，因活动后胸闷、胞癌发作4年，头昏、黑半年，1周内昏倒6次入院。入院心电图（ECG）示Ⅲ度房室阻滞（AVB），室性自主心律，QRS波群增宽呈左束支阻滞（LBBB）形，心室率45bpm。静脉注射阿托品无效。临床诊断：冠心病，劳力型心绞痛，Ⅲ度AVB（结下阻滞），心源性晕厥。入院次日植入Siemens2040k起搏器，随访1年起搏功能正常。多次ECG示：部分起搏的QRS波群后有逆传P（P）波，其出现与窦性P波至起搏QRS波群之间距有关。为证实其相互关系，同步描记Ⅱ导联及食管导联ECG（见附图）。图示…     

起搏术后心房颤动的影响因素及心房颤动与心钠素的关系

目的观察心脏起搏术后发生心房颤动(简称房颤)的影响因素及房颤与血心钠素(ANP)的关系。方法选择安装心脏起搏器的患者103例进行随访,分析房颤与年龄、起搏方式、心律失常类型、左房内径(LAD)、左室射血分数(LVEF)和血ANP的关系。结果①65岁以下患者房颤发生率低于65岁以上组(P<0.05)。②VVI组房颤发生率高于DDD组(P<0.05)。③慢快综合征组房颤发生率较缓慢型病窦综合征和房室传导阻滞组高(P<0.05)。④VVI房颤组术后LAD增大、LVEF下降(P<0.05),VVI房颤组术后与DDD组比较有差异(P<0.05)。⑤VVI房颤组和VVI窦性心律组ANP浓度较DDD组高(P<0.05);各组不同心功能级别(NYHA)之间ANP浓度随着心功能级别的加重而升高。结论长期心脏起搏术后房颤的发生可能与年龄大、VVI起搏、病窦综合征(慢快型)、LAD增大、LVEF降低及ANP浓度升高相关。     

室房逆传的再探讨

目的 探讨在体房室结无室房逆传或逆传功能明显低于房室顺传的机制。方法 对128例心脏介入性诊疗术患者，分别作心房、心室刺激，观察经房室结顺传及室房逆传的电生理特征。结果 除21例三度房室传导阻滞外，107例房室顺传文氏点大于150次／min；有经房室结室房逆传者12例（11．2％），其中室房逆传文氏点10例小于130次／min，2例为130次／min。95例（88．8％）及21例三度房室传导阻滞者均无室房逆传。结论 绝大多数在体房室结固有逆传功能明显低于房室顺传，或呈单向传导。房室旁道和／或房室结逆传快径路是室房逆传良好的主要原因及形成阵发性室上性心动过速等病症的根本机制。     

脑钠肽与心房颤动关系的研究进展

脑钠肽是心肌细胞分泌的一种循环激素,目前脑钠肽在心血管领域的诊断和治疗价值已成为人们关注的热点。充血性心力衰竭诊断、治疗、预后,急性冠脉综合征患者的危险分层,都与血脑钠肽水平升高有着密切的关系。血浆脑钠肽浓度与心房颤动的关系也受到越来越多的重视,脑钠肽在心房颤动预测,相关治疗,预后判断中有重要的临床应用价值。近两年来相关研究进展较快,现将有关报道综述如下。     

血浆脑利钠肽与房颤病人复律和复发的临床研究

目的研究阵发性或持续性房颤(Af)病人转复窦性心律时,血浆脑利钠肽(BNP)水平及其临床意义。方法选取62例心功能(1~3)级病人,采用放免法测定房颤及窦性心律时病人血浆中BNP的浓度,观察两组BNP水平、房颤发作次数。结果病人房颤发生时BNP浓度为(88.36±22.32)pg/mL,比复律后窦性心律时(57.48±20.32)pg/mL明显增高(P<0.05),高BNP水平病人组房颤发生次数较低BNP水平病人多。多因素分析显示血浆BNP水平与Af持续时间是转律后窦性心律维持的独立影响因子。结论血BNP浓度增高是发生心房颤动的预告因子,高水平的BNP更容易复发房颤,血浆BNP水平低或Af持续时间短者转律后窦性心律较易维持。     

Mortality and Incidence of Atrial Fibrillation in Paced Patients

Mortality and AF Incidence in Paced Patients. This review presents and discusses available data from randomized controlled trials on the prognosis of pacemaker patients, especially the incidences of atrial fibrillation (AF) and death, the impact of pacing mode selection, and the impact of AF on prognosis. The incidence of AF is several times higher in paced patients than in the nonpaced population. The annual incidences of AF and chronic AF are at least 5% and 3%, respectively, after pacemaker implantation. Mean lifetime cumulative incidences of AF and chronic AF can be estimated at approximately 30% to 40% and 20%, respectively. The most important predictors of AF are brady‐tachy syndrome, sick sinus syndrome, and selection of VVI(R) pacing mode. The expected lifespan in paced patients is shorter than in the age‐matched nonpaced population. One of the factors decreasing lifespan in paced patients most likely is the high incidence and prevalence of AF. In patients with sick sinus syndrome, VVI pacing significantly increases AF and mortality compared with AAI pacing. In a mixed population of patients with bradycardia, DDD(R) pacing causes AF less often than does VVI(R) pacing. Survival does not differ between these pacing modes within the first 3.5 years after pacemaker implantation. At the present time, AAI(R) should be the preferred pacing mode in patients with sick sinus syndrome, and DDD(R) should be used for other patients without chronic AF for prevention of AF. It is not clear whether prevention of AF will improve survival of paced patients.     

B型利钠肽与孤立性心房颤动

目的:探讨B型利钠肽(BNP)与孤立性心房颤动(AF)的血栓事件发生、复律及再发之间的关系。方法:103例孤立性AF患者行食道超声(经食道超声心动图)、头颅计算机断层摄影术或磁共振(CT／MRI)检查及血BNP测定。探讨BNP在AF血栓事件及其相关因素中的作用。根据血栓事件将患者分为有血栓事件组(n=15)和无血栓事件组(n=88)。对于有复律指征的患者,根据AF复律及再发情况分为复律不成功患者(复律失败或随访期内再发,n=16)和复律成功患者(复律成功并随访期内维持窦性心律,n=7),分别进行对比研究。结果:服药后无血栓事件组BNP降低幅度优于血栓事件组,有显著性显异(P<0．05)。复律成功患者较复律不成功患者BNP水平低[(60±32)ng／L比(178±70)ng／L,P<0．05]、病程短[(3．0±1．9)个月比(7．6±2．5)个月,P< 0．05]和左心房内径小[(42．3±3．4)mm比(48．6±5．1)mm,P<0．05],均有显著性差异。多因素Logistic回归分析: BNP是预测孤立性AF血栓事件的独立因素(P<0．05);BNP、左心房内径和AF病程是预测AF复律及再发的独立因素(P均<0．05)。结论:BNP可作为预测孤立性AF血栓事件和AF复律与再发的临床指标。     

氨基末端B型利钠肽前体与心房颤动的研究进展

目前氨基末端B型利钠肽前体正广泛应用于临床试验和心血管研究中,近年的研究显示心房颤动与氨基末端B型利钠肽前体水平升高有关。现主要就近年来关于氨基末端B型利钠肽前体作为危险因子和预测因素在心房颤动治疗方面的研究进展进行综述。     

Different Patterns of Angiotensin II and Atrial Natriuretic Peptide Secretion in a Sheep Model of Atrial Fibrillation

INTRODUCTION: It is well established that rapid atrial rates, as in atrial fibrillation (AF), cause atrial electrical and structural remodeling leading to the maintenance of AF. The role of neurohumoral changes in this pathophysiologic vicious circle remains unclear. METHODS AND RESULTS: We followed the concentrations of angiotensin II (AT II) and atrial natriuretic peptide (ANP) in a sheep model of AF. The sheep were atrially paced at 600 beats/min for 15 weeks. Electrophysiologic study was performed at regular intervals, and venous blood samples were taken. There was a slow increase in the vulnerability for AF. The cumulative incidence of sustained AF was 80% after 15 weeks of pacing. This increased vulnerability for AF was accompanied by atrial electrical remodeling and an increase in atrial pressure. AT II increased rapidly and stayed elevated: 17+/-4 pg/mL at baseline, and 40+/-11 and 39+/-7 pg/mL after 1 and 12 weeks of pacing, respectively. ANP rose more progressively: 35+/-7 pg/mL at baseline, and 72+/-17, 95+/-10, and 106+/-23 pg/mL after 1, 3, and 12 weeks, respectively. ANP levels correlated with atrial pressure and inducibility of AF. There was no relation between these parameters and AT II levels. CONCLUSION: AT II and ANP increased significantly in this animal model of AF. Elevation of AT II occurs early and seems to be dependent on rapid atrial rate rather than the presence of AF. ANP increased more progressively. It paralleled the inducibility of AF and atrial stretch. Both neurohumoral pathways may form a potential therapeutic target for treatment of patients with AF.     

心脏起搏对血浆脑利钠肽影响的临床研究

研究DDD与VVI起搏方式对血浆脑利钠肽 (BNP)水平的影响及其临床意义。 4 7例安装了起搏器心功能II级以上患者 ,分为DDD起搏组与VVI起搏组 ,术前测血浆BNP值及行心脏彩色多普勒超声检查 ,术后 4～ 6月内随访血浆BNP、心脏彩色多普勒超声检查。比较两组患者BNP差别、心脏射血分数 (EF)差异。结果 :DDD起搏组BNP水平较VVI组为低 (5 7.2 3± 19.19pg/mlvs 88.35± 2 3.11pg/ml,P <0 .0 5 ) ;EF值在DDD起搏组较VVI组为高 (0 .5 6± 0 .0 8vs 0 .4 5± 0 .16 ,P <0 .0 5 )。两组患者的BNP与LVEF均呈显著负性相关 (P <0 .0 5 )。结论 :DDD起搏与VVI起搏方式相比血浆BNP水平较低 ,对慢性心功能不全患者的心脏功能影响较小。     

Gene Expression of the Natriuretic Peptide System in Atrial Tissue of Patients with Paroxysmal and Persistent Atrial Fibrillation

INTRODUCTION: Circulating cardiac natriuretic peptides play an important role in maintaining volume homeostasis, especially during conditions affecting hemodynamics. During atrial fibrillation (AF), levels of plasma atrial natriuretic peptide (ANP) becomes elevated. The aim of this study was to gather information about gene expression of the natriuretic peptide system on the atrial level in patients with AF. METHODS AND RESULTS: Right atrial appendages of 36 patients with either paroxysmal or persistent AF were compared with 36 case matched controls in sinus rhythm for mRNA expression of pro- atrial natriuretic peptide (pro-ANP), pro-brain natriuretic peptide (pro-BNP), and their natriuretic peptide receptor type-A (NPR-A). We investigated patients without (n = 36) and with (n = 36) valvular disease. Persistent AF was associated with higher mRNA expression of pro-BNP (+66%, P = 0.04, in patients without valvular disease, and +69%, P < 0.01, in patients with valvular disease) and lower mRNA expression of NPR-A (-58%, P = 0.02, in patients without valvular disease, and -62 %, P < 0.01, in patients with valvular disease). The mRNA content of pro-ANP was only increased in patients with valvular disease (+12%, P = 0.03). No changes were observed in patients with paroxysmal AF. CONCLUSION: This study demonstrates that persistent, but not paroxysmal, AF induces alterations in gene expression of pro-BNP and NPR-A on the atrial level. Although AF generally is associated with an increase of plasma ANP level, a change in mRNA content of pro-ANP is only observed in the presence of concomitant valvular disease and is of minor magnitude.