经食管心脏电生理检查误诊房室折返性心动过速的不典型房室结折返性心动过速的特点及分析

目的探讨食管电生理检查中被误诊为房室折返性心动过速的不典型的慢快型房室结折返性心动过速的特点。方法回顾性分析5例误诊为房室折返性心动过速患者的食管电生理及心内电生理资料。结果 5例患者在食管电生理检查S1S2程控期前刺激中,均未观察到S2-R间期有跳跃性延长,心动过速的R-P-EB间期70ms;逆行P-波在V1导联直立,下壁导联倒置;食管电生理诊断为左后间隔隐匿性旁道参与的房室折返性心动过速。心内电生理诊断为慢快型房室结折返性心动过速,并成功消融慢径路。结论部分R-P-EB间期70ms的不典型慢快型房室结折返性心动过速食管电生理特点与后间隔隐匿性旁道参与的房室折返性心动过速类似,必要时需心内电生理检查加以明确。     

房室双旁道的食管心脏电生理特征

目的：探讨房室双旁道食管心脏电生理检查的特征性改变。方法：对14例经射频导管消融术证实的房室双旁道的食管心脏电生理检查作回顾性分析。结果：10例房室双旁道的电生理特征为：（1）心房起搏时显示两种不同的预激图形和／或特殊类型室性融合波群，经食管心房起搏有利于显现左侧旁道。（2）诱发出两种逆向型房室折返性心动过速，由两条旁道形成折返环路。（3）顺向型房室折返性心动过速时，出现两种不同的R－P^-间期和P^-波或房性融合波。（4）排除房室结双径路后，逆向型房室折返性心过速的频率快于顺向型房室折返性心动过速。（5）预激旁道的部位与顺向型房室折返性心动过速时P^-波提示的部位不同。（6）双旁道隐匿性传导是造成其中一条旁道丧失传导功能的重要因素之一。另4例未能表现出上述电生理特征，其中右侧隐性旁道合并左侧隐匿性旁道1例，右侧隐匿性双旁道1例，左侧隐匿性双旁道2例。结论：食管心脏电生理检查能够确诊大部分的房室双旁道，采用多导联同步记录及在房室折返性心动过速时仔细分析电生理表现有助于揭示房室双旁道。     

左右房室旁道交替性逆传参与房室折返性心动过速射频消融成功一例

患者男性,28岁,因发作性心悸5~6年入院。心内电生理检查发现右侧His束旁道及左侧游离壁隐匿性旁道交替性逆传参与顺向型房室折返性心动过速,其VV(RR)间期330~350ms,并且QRS波形态一致。导管消融成功阻断旁道传导,随访9个月心动过速无复发。结论:左右旁道交替性逆传参与同次房室折返性心动过速发作,临床相对少见,应注意识别。     

差异性传导对房室及房室结折返性心动过速心内电图的影响

目的 分析差异性传导对室上性心动过速心内电图产生影响的机制,探讨解决问题的方法。方法 选择室上性心动过速病人357例,其中房室折返性心动过速出现差异性传导26/187例,房室结折返性心动过速出现差异性传导6/170例,观察出现差异性传导时心内电图的影响。结果 房室结折返性心动过速出现差异性传导时,心动过速的频率和心内电图无改变。右侧旁道介导的房室折返性心动过速出现右束支差传导心电图类似于慢一快型房室结折返性心动过速,同时伴心率下降。出现左束支差传时,心电图类似于慢一慢型房室结折返性心运过速或房速,心率不变,左侧旁道介导的房室折返性心动过速出现差传时,心内激动顺序不变,出现左束支差传时心率下降,右束支差传时心率不变。结果 差异性传导对房室结折返性心动过速及左侧旁道介导的房室折返性心动过速心内电图无影响。但对右侧旁道介导的房室折返性心动过速心内电图有较大的影响,旁道的电生理特性结合电生理检查有助于鉴别诊断。     

快频率依赖性室房逆传左侧隐匿性房室旁道参与的心动过速及射频导管消融

目的探讨快频率依赖性室房逆传特性左侧隐匿性房室旁道的电生理特点及射频消融。方法对8例心电图显示窄QRS波群心动过速的患者行电生理检查,分析房室、室房传导情况、心动过速特点、旁道定位,并行射频消融。结果8例患者均证实存在快频率依赖性室房逆传特性左侧隐匿性旁道,在较慢频率起搏右心室时旁道逆传发生阻滞,而以中等频率起搏时表现为间断旁道逆传,较快频率起搏时才表现为旁道1：1传导且均诱发了房室折返性心动过速,于快频率心室刺激下标测消融靶点,消融均获成功。结论左侧隐匿性房室旁道有时可发生快频率依赖性室房逆传现象,并伴发房室折返性心动过速,在射频消融中需注意分辨,以免漏诊。     

依赖异丙肾上腺素逆传的房室折返性心动过速

目的：探讨4例依赖异丙肾上腺素逆传的房室折返性心动过速的发作情况及电生理特点。方法：对4例射频导管消融前常规电生理检查未能诱发出阵发性定性心动过速及A－H间期跳跃，亦未见旁道逆传者，静脉滴注异丙肾上腺素、右心室刺激时发现左侧旁道逆传，并均诱发出正向型房室折返性心运过速；停止注射后，左侧旁道逆传功能消失，亦不能诱发出房室折返性心动过速。结果：静脉滴注异丙肾上腺素，右心室起搏下用逆行法于二尖瓣环心室侧消融，4例均获成功；术后静脉滴注异丙肾上腺素下再行右心室起搏，未见旁道逆传现象。结论：部分隐匿性旁道构成的房室折返性心动过速发作依赖异丙肾上腺素，射频导管消融在静脉滴注异丙肾上腺素及右心室起搏下进行。     

左室游离壁隐匿性慢旁道伴房室结三径路导致无休止心动过速一例

患者男性,62岁,诊断为左侧游离壁隐匿性慢传导旁道伴房室结三径路(慢快型)。患者的房室交界区在340~240ms的范围内存在2条慢径,慢径虽不参与该心动过速折返环的组成。但是每次房室折返性心动过速只能由心房程序刺激S2跳跃后激动沿房室结慢径前传诱发。     

隐匿性慢旁道的电生理特性及其参与的心律失常

通过电生理研究证实1例隐匿性慢旁道。该旁道与正道共同形成室房双径路文氏现象及房室折返性心动过速,并成功地进行了射频消融治疗。对隐匿性慢旁道的多种电生理表现及诊断进行讨论。     

右侧游离壁双旁道并两种窄QRS波房室折返性心动过速射频消融一例

患者男性,38岁,术前诊断B型预激综合征并顺向型房室折返性心动过速(O-AVRT),射频消融阻断右侧游离壁显性旁道后,发作另外一种频率较慢的窄QRS波心动过速,呈无休止性,电生理特性和射频消融证实右侧游离壁尚存一条隐匿性慢旁道并房室折返性心动过速。     

双旁道合并逆向型房室折返性心动过速一例

预激性心动过速是指各种心动过速时,旁路或作为折返环的前传支,或作为与该心律房室之间的传导通路,它比逆向型心动过速的含义更为广泛。逆向型房室折返性心动过速,在预激环形运动性心动过速中十分少见,预激患者心动过速中自发性逆向型心动过速的发生率约为5%~10%。本例患者经腔内心电生理证实存在右侧游离壁旁道和右后间隔旁道,当预激性心动过速发生时,由于存在双旁道,其折返环路更为复杂,尽管体表心电图诊断为逆向型房室折返性心动过速,但从电生理角度,不能排除从一条旁路前传,从另一旁路逆传的可能性,也不能排除前传旁道仅仅作为无辜旁道,本身并不是折返环的一部分的可能。     

Fatigue Phenomenon in Accessory Pathways

Fatigue Phenomenon in APs. Fatigue phenomenon is transient failure of conduction following a period of repetitive excitation. Fatigue in iiccessory pathways is uncommon, and its electrophysiologic characteristics and clinical implications are unknown. Among the 215 patients who underwent electrophysiology studies from July 1992 to December 1993, 4 (2%) were found to exhibit fatigue over accessory pathways. The accessory pathway was posteroseptal in three patients and right free wall in one patient. The mean anterograde effective refractory period of the accessory pathway was 295 ± 26 msec (range 270 to 330, basic drive cycle length 600 msec). Three patients had neither retrograde accessory pathway conduction nor inducible tachycardia even with infusion of isoprotereno). The fatigue phenomenon was observed after both atrial and ventricular stimulation in three patients and only after ventricular stimulation in one patient. Fatigue was dependent on duration more than rate of stimulation. We conclude that pathways exhibiting fatigue have a low margin of safety for conduction and are unlikely to be clinically problematic.     

The no-flow phenomenon during diagnostic coronary angiography

OBJECTIVES: Slow flow of dye in epicardial coronary arteries is not an infrequent finding in patients during routine coronary angiography. The extreme form of this phenomenon, namely, no flow or Thrombolysis in Myocardial Infarction (TIMI) 0-1, is very uncommon with life-threatening consequences. We consider the present report as the first one, to our knowledge, that describes this angiographic entity and how prompt recognition and adequate management prevent certain death in this population. DESIGN, SETTING, AND PATIENTS: Retrospective review of the cardiac catheterization laboratory database at our medical center. Out of 5700 cardiac catheterizations performed by the authors during the past 5 years, 10 cases (0.17%) were identified as having no flow or very slow flow during their routine diagnostic coronary angiogram. CASE ANALYSIS: The no-flow phenomenon occurred during the first coronary injection in the left coronary system. We specifically emphasize that none of these cases was a consequence of inadvertent air injection, vasospasm, or coronary dissection. In 80% of our cases, flow was completely absent (TIMI 0), and in two cases (20%) it was very slow and never filling the distal vessel (TIMI 1). Despite immediate recognition and prompt maneuvers and treatment with intracoronary vasodilator administration, 60% of these patients progressed to full cardiopulmonary arrest with all of them having extended cardiopulmonary resuscitation (CPR) and pharmacological treatment. Only one patient required intra-aortic balloon pump (IABP) support and temporary pacemaker. All patients recovered completely with no clinical consequences. Characteristics of patients with this complication are described, and several possible etiologies are analyzed. CONCLUSIONS: Definite conclusions for the reason of the no-flow phenomenon are not possible at present, despite multiple different theories that could explain it. What is important from the clinical standpoint is that, although rare, it is a potentially life-threatening condition during diagnostic coronary angiography that should be recognized and aggressively treated. We consider the present report as the first one, to our knowledge, that describes this angiographic entity, and how prompt recognition and adequate management prevents certain death in this population.     

An analysis of the mechanism by which cetiedil inhibits the gardos phenomenon

Energy depletion in the human erythrocyte causes a rise in intracellular calcium. This in turn accelerates the transmembrane movement of potassium and chloride, resulting in cell dehydration. This process, known as the Gardos phenomenon, is inhibited by cetiedil. The present study examines the mechanism by which cetiedil inhibits the Gardos phenomenon. The ability of cetiedil to retard the initial step in the Gardos phenomenon, a rise in intracellular calcium, was first tested. Cetiedil did not prevent calcium accumulation. Cetiedil's ability to inhibit anion movement was next evaluated, as cetiedil could appear to be blocking K movement when in fact it was preventing the movement of its accompanying anion. No inhibitory effect on anion movement was seen. Since cetiedil prevented neither calcium accumulation nor anion movement, it must inhibit the Gardos phenomenon by preventing the opening of the K-specific gate in the erythrocyte membrane. The fact that cetiedil's effect on the Gardos phenomenon could not be removed with repeated cell washing indicates that this effect is irreversible.     

经食管电生理检查中的裂隙现象

在165例食管电生理检查中发现39例患者存在心脏传导系统多部位的裂隙现象共46例次(占24%),其中7例同时发生在2个部位.根据发生部位的不同试将其分成6型,探讨其发生部位及产生机理.     

预激综合征的蝉联现象

为探讨预激综合征患者旁道蝉联现象发生的机制和临床意义,经食管电生理检查,观察到18例显性预激综合征患者旁道的蝉联现象,并分别测定旁道有效不应期和房室结的下传有效不应期。结果显示:旁道有效不应期均长于房室结下传有效不应期(分别为388.89±57.34ms和299.44±27.38ms,P<0.01)。提示:(1)旁道有效不应期长于房室结下传有效不应期是旁道蝉联现象的先决条件;(2)正常房室结的1:1传导亦是产生旁道下传蝉联现象的条件之一;(3)蝉联现象可用于解释临床上间歇性预激综合征的显现。     

益钙宁治疗高钙血症的疗效观察

用鳗降钙素类似物－益钙宁治疗１０例次７例患者高钙血症。经７天观察，血钙在４小时及２４小时均显著降低，但４８小时回升到近治疗前水平，出现“脱逸”现象，随后几天血钙波动在较高水平。     

赛庚啶对糖尿病黎明现象的作用

作者观察了40例糖尿病患者1a.m.及7a.m.血糖、生长激素及皮质醇的变化,对18例患者采用赛庚啶治疗,探讨了赛庚啶对糖尿病患者黎明现象的作用。结果表明:糖尿病患者7a.m.血糖、生长激素及皮质醇高于1a.m.。赛庚啶可使7a.m.血糖、生长激素及皮质醇降低。提示糖尿病清晨血糖升高与生长激素、皮质醇水平升高有关,服用赛庚啶可防治糖尿病黎明现象。     

Ⅱ型糖尿病患者的黎明现象探讨

本文对10例NIDDM进行了黎明现象测试,受试者于午夜至6:00～6:30a.m.保持睡眠状态,0:30～8:00a.m.每30分钟采血一次,作FBG、血浆INS、GH(自0a.m.开始采血)、F、E、NE及血清TT_3测定。结果示FBG于4:00a.m.后开始上升,于7:00a.m.达最高值;INS于0～5:00a.m.逐渐下降,且与增高的血糖浓度无相关。0a.m.时的GH高峰值与增高的血糖浓度成正相关。F(3:00a.m.后)、NE、E(4:00a.m.后)分泌浓度均呈有意义的增高,但与增高的血糖浓度均无相关。     

非胰岛素依赖型糖尿病患者黎明现象的观察

本文对10例NIDDM患者的黎明现象进行了观察。受试者在常规饮食和口服降糖药的情况下,于0:00～8:00时每小时抽血一次,测定BG、F、GH、GG和INS,并于0:00、3:00、5:00、8:00时分别采血测定ACTH。如按凌晨BG上升至少大于1mmol/L作为黎明现象的判定标准,则本组出现这种现象的频率为6/10。本观察结果提示,在常规治疗的NIDDM患者中,黎明现象也常见到。胰岛素作用缺乏和对抗激素F升高,可能在黎明现象的发生机理中起作用。     

动态心电图显示房室结双径路及有关特殊心电现象

为探讨房室结双径路(DAVNP)在动态心电图直接显示的条件、主要诊断线索及与之有关的特殊心电现象,对 7例在动态心电图直接显示DAVNP的心电图特征和有关特殊心电现象进行了回顾性分析。结果: 7例患者的动态心电图均出现PR间期跳跃性的改变,并有蝉联现象及不典型文氏现象发生,呈DAVNP特征。结论:动态心电图中PR间期的跳跃性改变提示DAVNP的存在,为临床诊治提供更多的依据。