ATP试验诊断房室结双径路的临床意义

阵发性室上性心动过速是临床常见的快速性心律失常之一,房室结双径路参与折返所致者约占阵发性室上性心动过速的50%[1],房室结双径路的诊断多以食道心房调搏和(或)有创性心内电生理检查而确诊.然而,此两种诊断方法都给患者带来不同程度的痛苦.     

食管心电图结合12导联同步心电图在折返性室上性心动过速诊断中的应用

目的:探讨食管心电图结合12导联同步心电图在折返性室上性心动过速诊断中的作用。方法:75例有心悸史的患者记录心动过速时12导联同步心电图,食管心电图以及心内电生理检查结果。结果:在食管心电图合并12导联心电图中RP′≤70ms的患者,诊断为房室结折返性心动过速,经心内电生理检查证实特异性为100%,敏感性为97.33%。70ms140ms的患者,诊断为房室折返性心动过速伴右侧旁路,经心内电生理检查证实特异性为100%,敏感性为100%。结论:测量折返性室上性心动过速食管心电图和12导联同步心电图的RP′间期,可以鉴别房室结折返性心动过速和房室折返性心动过速,并预测旁路定位。     

经食道心房调搏诊治室上性心动过速

目的 探讨经食道心房调搏诊治室上性心动过速及其安全性。方法 回顾性分析41例经食道调搏诊治的室上性心动过速患者的临床资料。结果 诱发出室上性心动过速37例，其中提示房室旁路12例(其中经房室结下传型房室折返性心动过速11例，经旁路下传合并房颤1例)，房室结双径路26例(其中诱发房室结折返性心动过速24例，房室结双径路现象2例)，左房性心动过速并心房分离1例，未见异常2例。SS刺激法终止正在发作或诱发的M36例，其中23例一次转律成功。进行药物筛选16例，4例能被胺碘酮终止发作，8例为心律平所终止，异搏定终止2例。3例电极通过鼻腔困难，改经口腔顺利进行。出现明显恶心并呕吐9例，食道烧灼感5例，出现食道痉挛l例。结论 经食道调搏诊治室上性心动过速快捷、准确、安全，特别适合不具备心内电生理检查及射频消融条件的基层医院。     

ATP试验诊断房室给双径路的临床意义

阵发性室上性心动过速是临床常见的快速性心律失常之一,房室结双径路参与折返所致者约占阵发性室上性心动过速的50％,房室结双径路的诊断多以食道心房调搏和(或)有创性心内电生理检查而确诊。然而,此两种诊断方法都给患者带来不同程度的痛苦。为探讨无创且不给患者增加痛苦或减少检查时的不适感,我们探讨了在窦性心率下静推三磷酸腺苷(adenosine triphosphale,ATP)诊断房室结双径路的意义。1 对象和方法1.1 对象 有反复发作的室上性阵发性心动过速发作史,有或无发作时的心电图记录,行食道心房调搏检查,管深34～37cm,阈值19～25V,S_1S_2刺激,S_1频率比自身心率快10％,S_2从舒张     

房室结双径路消融中特殊电生理现象分析与处理

目的 :分析房室结折返性心动过速 (AVNRT)慢径路消融中特殊电生理现象及处理体会。方法 :慢径路消融前常规行心内电生理检查。结果 :有特殊电生理现象者 8例 ,其中 3例患者AVNRT开始时表现为房室 2 :1传导 ,阻滞点在希氏束以上部位 ;3例患者房室结功能曲线呈连续性 ;1例为慢 -慢型AVNRT ;1例心内电生理检查未能诱发出AVNRT。所有患者慢径消融均成功。结论 :术前应行详细的心内电生理检查和仔细鉴别 ,其消融方法与典型AVNRT相同     

房室结三径路食管心房调搏诱发房室结折近性心动过速

房室结三径路伴房室结折返性心动过速(AVNRT)的临床报道不多见。如果每条经路都能双向传导,理论上三径路者可有6种类型的AV-—RT,而实际发生的大多为慢快型。本文分析15例房室结三径路,食管心房调搏诱发AVNRT的机制及电生理特点。 1 资料和方法 对象为10余年来因心悸及快速心律失常而行食管电生理检查诊断为房室结三径路者,检查前停用各种抗心律失常药5个半衰期以上。按常规食管电生理检查方法进行,如果S_1S_2或S_1S_2S_3法不能显示三径路或诱发AVNRT,则给阿托品2mg静注后再重复以上检查。     

射频消融术后迟发性房室传导阻滞1例分析

对射频消融术后迟发性房室传导阻滞1例分析如下。1病历摘要男,41岁。因反复心悸1 a余入院。常规心电图检查示阵发性室上性心动过速伴功能性右束支传导阻滞,每次发作均用异搏定5 mg缓慢静脉推注,可迅速转为窦性心律。此次入院体检:一般情况好,无阳性体征。心内电生理检查示房室结双径路,并诱发房室结折返性心动过速(AVNRT)(慢-快型)。     

射频消融治疗房室结折返性心动过速11例

射频消融术(RFCA)是1991年国内用于治疗快速心律失常的介入性技术。自1993年3月～1994年5月,我们采用RFCA对11例房室结双径路(AVNDP)患者进行了房室结改良术,现对其疗效的观察报告如下。 1 资料与方法 1.1 临床资料 11例中,男8例,女3例;年龄36～62岁,平均50.4岁。心动过速史1～18年,平均9.5±6.2年。多数病例长期服用心得安、心律平、异搏定等药物不能预防发作。发作时多伴有头晕、黑朦、心悸等症状,术前经食道电生理检查或心内电生理检查,均证实为AVNDP,并诱发出房室结折返性心动过速(AVNRT)。 1.2 方法     

房室结双径路消融中特殊电生理现象分析与处理

目的：分析房室结折返性心动过速（AVNRT）慢径路消融中特殊电生理现象及处理体会。方法：慢径路消融前常规行心内电生理检查。结果：有特殊电生理现象者8例，其中3例患者AVNRT开始时表现为房室2：1传导，阻滞点在希氏束以上部位；3例患者房室结功能曲线呈连续性；1例为慢-慢型AVNRT；1例心内电生理检查未能诱发出AVNRT。所有患者慢径消融均成功，结论：术前应行详细的心内电生理检查和仔细鉴别，其消融方法与典型AVNRT相同。     

起源于冠状静脉窦口的右侧旁路合并房室结双径路的诊断与鉴别

目的探讨复杂多径路心动过速时的应用拖带和程序S2刺激进行诊断和鉴别分析。 方法回顾性分析1例间歇性预激波患者频发室上性心动过速,经心脏电生理检查行右心室拖带刺激和心室程序S2刺激,测量最后一跳刺激信号到自身心房波间期减去心动过速下心室到心房的间期(SA-VA)和起搏后间期(PPI)－心动过速周长(TCC),并行常规射频导管消融术治疗。 结果术中心室分级刺激S1S1：350 ms诱发右侧旁路参与的房室折返性心动过速,TCL为372 ms, PPI为395 ms,继续行心房S1S2：500/310 ms刺激,"跳跃"诱发同前一样的室房波不融合心动过速。再次行心房S1S1：280 ms刺激,可反复诱发慢快型房室结折返性心动过速。在旁路参与的心动过速下给予心室程序S2刺激,测量PPI为385.1 ms, TCL为360.1 ms,PPI－TCL≤20 ms,证实为右侧旁路参与的房室折返性心动过速,同时存在慢快型房室结折返性行心动过速,给予常规射频导管消融成功径路和旁路。术后随访12个月未有心动过速发作。 结论通过右心室心室拖带刺激,以及测量SA-VA间期和PPI-TCL间期可以用来鉴别典型房室结折返性心动过速与间隔房室旁路。     

Paroxysmal tachycardia in children and teenagers with normal sinus rhythm and without heart disease

The purpose of this study was to evaluate the value of esophageal programmed stimulation in children and teenagers with normal sinus rhythm ECG and normal noninvasive studies, having palpitations and syncope, and no documented tachycardias. Paroxysmal tachycardias are frequent in children and are often related to accessory connection. These tachycardias are sometimes difficult to prove. Transesophageal atrial pacing was performed at rest and during infusion of isoproterenol in 31 children or adolescents aged 9-19 years (16 +/- 3 years) with normal sinus rhythm ECG and suspected or documented episodes of paroxysmal tachycardia. Sustained tachycardia was induced in 27 patients, at rest in 13 patients, and after isoproterenol in 14 remaining patients. Atrioventricular nodal reentrant tachycardia was found as the main cause of paroxysmal tachycardia (22 cases). Six patients were followed by a vagal reaction and dizziness. These patients had spontaneous tachycardia with syncope. In three other patients, atrial fibrillation was also induced. Concealed accessory pathway reentrant tachycardia was identified in three patients. In two patients, a regular wide tachycardia with right bundle branch block morphology was induced; the diagnosis of verapamil-sensitive ventricular tachycardia was made in a second study by intracardiac study. In conclusion, atrioventricular nodal reentrant tachycardia was found as the main cause of symptoms in children with normal sinus rhythm ECG. Syncope is frequently associated and provoked by a vagal reaction. This diagnosis could be underestimated in adolescents frequently considered as hysterical because noninvasive studies are negative.     

经导管射频消融治疗阵发性室上性心动过速1106例临床分析

目的探讨经导管射频消融治疗阵发性室上性心动过速的效果及安全性。方法2003年7月至2011年1月在厦门市心脏中心行心内电生理检查及射频消融术治疗的心动过速患者1106例,分析各型心动过速的构成比,评价术中成功率及其相关因素,长期随访观察复发率及并发症发生率。结果共纳入阵发性室上性心动过速患者1106例,男女比例为1：1,其中房室旁道型心动过速588例,房室结折返型心动过速477例,房性心动过速41例。术中即刻消融成功1087例（98．3％,1087／1106）,复发43例（3．9％,43／1106）,其中房室结折返型心动过速复发7例（1．5％,7／477）;房室旁道复发33例（5．6％,33／588）,左侧旁道复发16例（3．9％,16／302）,右侧旁道17例（9．1％,17／186）;房性心动过速复发3例（8．1％,3／41）。并发症发生率为1．5％（17／1106）,主要为气胸6例,血气胸1例,肺栓塞1例,左颈皮下气肿1例,术中一过性Ⅲ度房室传导阻滞2例,术中I度房室传导阻滞3例,术后持续性Ⅲ度房室传导阻滞需植入永久性心脏起搏器2例（0．2％）,术后5d心源性猝死1例,为长期中风卧床者,为手术非相关死亡。结论经导管射频消融为阵发性室上性心动过速安全有效的治疗方法。     

室上性心动过速161例食管心房调搏资料分析

对161例SVT食管心房调搏资料的分析表明:1.预激综合征(包括隐匿性)是SVT最常见的原因,本组占50%(81/161);其次是房室结双径路,占43%(70/161)。2.食管心房调搏诱发SVT 112例(诱发率70%),其电生理机制以AVRT为第一位,占54%;AVNRT为第二位,占38%,证实国人SVT电生理机制情况与国外相比有不同的特点。3.用食管心房调搏可对SVT进行电生理分型,并作出无创性鉴别诊断。     

Electrophysiological characteristics of junctional rhythm during ablation of the slow pathway in different types of atrioventricular nodal reentrant tachycardia

BACKGROUND: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. METHODS: Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. RESULTS: In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). CONCLUSIONS: In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.     

Coincident Idiopathic Left Ventricular Tachycardia and Atrioventricular Nodal Reentrant Tachycardia: Control by Radiofrequency Catheter Ablation of the Slow Atrioventricular Nodal Pathway

A healthy 37-year-old male presented with a history of frequent palpitations and sustained wide QRS complex tachycardia with a right bundle branch block and left axis morphology. Serial electrophysiological studies revealed two inducible tachycardias, which were shown to represent atrioventricular nodal reentrant tachycardia and idiopathic left ventricular tachycardia. Transformation from one tachycardia to the other occurred spontaneously as well as following atrial or ventricular pacing. Radiofrequency catheter ablation of the slow atrioventricular nodal pathway resulted in cure of atrioventricular nodal reentrant tachycardia and the prevention of spontaneous recurrence of ventricular tachycardia, suggesting a role of atrioventricular nodal reentrant tachycardia in triggering the clinical episodes of ventricular tachycardia. The patient has remained asymptomatic without antiarrhythmic therapy for 8 months.     

Radiofrequency Catheter Ablation of AV Nodal Reentrant Tachycardia in Situs Inversus Totalis

A 41‐year‐old male with situs inversus totalis had paroxysmal supraventricular tachycardia. On electrophysiology study, the mechanism of the tachycardia was determined as slow/fast atrioventricular nodal reentrant tachycardia and slow pathway was successfully performed under fluoroscopic guidance.     

A Wide QRS Complex Tachycardia with Different Initiation Patterns: What is the Mechanism?

A 47-year-old man with palpitations underwent electrophysiologic testing (EPS). Burst atrial pacing while infusing isoproterenol induced non-reproducible wide QRS tachycardias with an unusual pattern of an H-A-V activation with the same tachycardia cycle length and two different initiation patterns. The tachycardia had the earliest atrial activation at the His bundle region. No dual atrioventricular (AV) nodal physiology was demonstrated by programmed atrial stimulation. Though a definite diagnosis of AV nodal reentrant tachycardia was not obtained, slow pathway ablation was performed in order to avoid inadvertent AV block as a complication. Thereafter, no tachycardias were induced by repeat burst atrial pacing.     

Intravenous 3-Methoxy-O-Desmethyl-Encainide in Reentrant Supraventricular Tachycardia: A Randomized Double-Blind Placebo-Controlled Trial in Patients Undergoing EP Study

Encainide is an agent effective in atrioventricular and atrioventricular nodal reentrant tachycardia. The metabolites O-desmethyl encainide and 3-methoxy-O-desmethyl encainide (MODE) are responsible for the clinical effects of encainide in most patients. In this study, intravenous MODE was evaluated in eight patients with reentrant supraventricular tachycardia undergoing electrophysiological testing. After tachycardia was induced at least twice to ensure reproducibility, MODE (30 micrograms/kg/min x 15 min, then 7.5 micrograms/kg/min) or placebo was administered in a double-blind fashion. If tachycardia remained inducible, the infusion was unblinded; in nonresponding subjects who received placebo, MODE was then administered. Placebo was ineffective in 3/3 patients. MODE prevented tachycardia induction in 5/8 patients and increased the tachycardia cycle length from 302 +/- 38 to 413 +/- 67 msec in the other three. At a mean concentration of 774 +/- 229 ng/ml, MODE prolonged PR, AH, HV, QRS, and QT intervals, right ventricular and accessory pathway effective refractory periods, and slowed or blocked antegrade accessory pathway conduction. Changes in intracardiac conduction were rate independent between cycle lengths 400 to 600 msec, while changes in ventricular effective refractory periods were most pronounced at rapid pacing rates. No adverse effects, hemodynamic changes, or conduction disturbances occurred. Thus, MODE can modify or suppress induction of reentrant atrioventricular or atrioventricular nodal tachycardia. The study design used here is well suited for the evaluation of newer antiarrhythmic agents by electrophysiological testing.     

A Latent Atrioventricular Decrementally Conducting Accessory Pathway Mimicking a Bystander Nodoventricular Fiber

A 41‐year‐old woman with recurrent wide‐QRS tachycardia is reported. Electrophysiologic findings were consistent with the diagnosis of a preexcited atrioventricular nodal reentrant tachycardia due to a bystander nodo‐ventricular fiber. However, slow pathway ablation did not preclude tachycardia recurrence. A second electrophysiology study shed light on the correct mechanism and eventually a successful ablation was achieved. (PACE 2010; e76–e80)