双房室旁道合并Mahaim纤维

报道１例束室纤维合并双房室旁道的电生理表现。患者有心动过速史１５年，心电图示右侧游壁显性旁道，分别于三尖瓣环８点半和５点半处消融阻断旁道，原心电图发生了改变，但存在Ｄｅｌｔａ波。上述两条旁道消融前，ＰＲ间期均为０．０６ｓ，心房递增刺激Ｄｅｌｔａ波增大，房室传导无文氏现象。     

中间隔右侧旁道的特殊类型──邻希氏束旁道的定位和消融治疗

报道６例中间隔右侧旁道的特殊类型──邻希氏束旁道的射频消融治疗,心内标测和消融证实该类旁道位于中间隔右侧的前上部,邻近希氏束的影象显示其距离在０．５ｃｍ以内,有效消融靶点局部电图均记录到Ｈ波（≤０．０１ｍＶ）,其振幅明显小于希氏束电图Ｈ波振幅,Ｖ─Ａ间期短于或等于希氏束电图上的Ｖ─Ａ间期,Ｖ波与Ａ波之间有旁道电位,强调在房室折返性心动过速时放电,６例患者心动过速在放电５ｓ内终止,其中４例出现交界区早搏或短阵交界心律,２例出现窦性心动过速,停止放电后均恢复窦性心律。笔者提出恢复后的窦性心律无房室传导阻滞是旁道阻断而正常房室传导无损伤的重要依据。连续放电可完全阻断旁道。     

房室结折返性心动过速射频消融术中特殊病例分析

在２６０例房室结折返性心动过速（ＡＶＮＲＴ）射频消融中出现１１例特殊病例。其中男３例、女８例。５例属电生理现象复杂，其中１例快－慢型者Ｓ１Ｓ１５００ｍｓ心室刺激时，连续３个刺激便出现室房文氏现象，随之出现心动过速，ＡＶＮＲＴ时心室率１８２ｂｐｍ，Ｈｉｓ束电极Ａ波最先激动，呈Ａ－Ｈ－Ｖ传导，ＶＡ间期２２０ｍｓ，ＶＡ＞ＡＶ；另１例快－慢型者心内电生理诱发出典型ＡＶＮＲＴ，其频率１６２ｂｐｍ，对其慢径改良后，诱发出另一种频率的快－慢型ＡＶＮＲＴ。３例慢－慢型者心动过速较易诱发，ＡＶＮＲＴ时均以冠状静脉窦口（ＣＳＯ）Ａ波最提前，Ｈｉｓ束电极示Ｈ－Ｖ－Ａ传导。３例永存左上腔静脉，ＣＳＯ异常扩张，窦口上缘几乎接近Ｈｉｓ束水平。３例放电过程特殊者，其中１例在较大范围内消融，均出现慢交界区心律，另１例在消融中出现一个交界区心律后，便诱发ＡＶＮＲＴ，再有１例为消融时难以出现慢交界律。所有病例均消融成功（１００％）。结果提示对特殊病例除应进行详细电生理检查之外，应采取不同的消融策略     

选择性消融逆传快径治疗典型房室结折返性心动 …

设计一种新的射频消融方法（选择性消融逆传快径）对２５例反复发作的典型房这地折返性心动过速（ＡＶＮＲＴ）进行消融治疗。经股静脉插入１～２根大头电极至Ｋｏｃｈ氏三角区,于旁Ｈｉｓ束心室起搏下寻找逆传Ａ最早的靶点,靶点图上不能有或仅有极小Ｈ波,大头电极用力压向靶点出现：（１）ＶＡ分离或ＨＡ间期延长,说明逆传快径已机械刺激所阻断,立即放电１５～２５Ｗ,持续３０～９０ｓ;（２）ＡＨ间期延长,说明前传快快径已     

房室慢旁道的电生理表现及射频消融治疗

报道射频导管消融（ＲＦＣＡ）治疗慢旁道参与的房室折返性心动过速患者１１例。电生理检查和静脉注射ＡＴＰ（７例）试验发现：①增频刺激右室心尖部时，ＶＡ文氏点为１８３．２±２２．６（１６０～２３０）ｂｐｍ，达１１室房传导的最高刺激频率时最早心房激动部位的室房传导时间较基础频率刺激时最早心房激动部位的室房传导时间（ＢＶＡＥ）延长６８．８±２９．８（４６～１０９）ｍｓ，Ｐ＜０．０１。心室程控刺激时旁道阻滞前最早心房激动部位的室房传导时间较ＢＶＡＥ延长１０７．６±４１．８ｍｓ，Ｐ＜０．０１，表明慢旁道传导表现为传导速度慢以及出现频率依赖性递减传导和文氏阻滞。②连续心室刺激时静脉注射ＡＴＰ７例中有５例于注射后２０．６±２．０（１８～２３）ｓ出现完全性室房阻滞，另２例室房传导时间逐渐延长。提示ＡＴＰ可使慢旁道的室房传导发生阻滞或传导时间延长。③心动过速时逆传激动顺序异常，与Ｈ波同步刺激心室均能夺获心房。④ＲＦＣＡ可成功阻断慢旁道，有效靶点的室房传导时间为１３３．６±２１．１（１２８～１６０）ｍｓ，Ａ波超前最早参照点为２６．４±８．４（２０～４０）ｍｓ，有效靶点逆传房波前有旁道电位。结论：上述结果提示慢旁道的电生理特点和     

后间隔旁道体表心电图及心内电图的特征

总结射频消融成功的后间隔旁道３７例体表及心内电图特征，结果显示：显性后间隔旁道体表心电图Ⅱ、Ⅲ、ａＶＦ导联δ波负向，ＱＲＳ波群在Ｖ２导联呈Ｒ或Ｒｓ形时，若Ｖ１导联为ｒＳＲ或Ｒｓ形诊断为左后间隔旁道，其敏感性７３．３％、特异性９１．７％；Ｖ１导联为ＱＳ形诊断为右后间隔旁道，其敏感性５８．３％、特异性１００％。冠状窦电极为间距１ｃｍ的４极标测电极，近端电极置于窦口。心动过速时，心内电图ΔＶＡＨ－ＣＳ（ＶＡＨ与最短ＶＡｃｓ的差值）≥２５ｍｓ提示左侧，敏感性６２．８％、特异性９３．７％；ΔＶＡｃｓ（冠状窦电极记录的最长与最短ＶＡ的差值）≤１５ｍｓ提示左侧，敏感性８７．５％，特异性９５．４％。此外，左后间隔旁道逆行Ａ波最早出现在冠状窦近端（ＣＳｐ）或冠状窦中端（ＣＳｍ），且冠状窦中端Ａ波（Ａｃｓｍ）均早于希氏束远端（Ｈｉｓｄ）Ａ波（ＡＨｉｓｄ）；右后间隔旁道逆行Ａ波最早出现在Ｈｉｓｄ或ＣＳｐ处，Ａｃｓｍ均晚于ＡＨｉｓｄ。通过体表心电图和心内电图特征，可简便准确地预测间隔旁道的消融靶点。     

隐匿性慢旁束心动过速的诊断和消融

２例隐匿性慢旁束折返性心动过速的诊断依据：１、心房和心室电刺激易诱发和终止心动过速；２、心动过速时体表心电图呈窄ＱＲＳ波，递行Ｐ波及ＰＲ〈ＰＲ；３、心动过速与右心室起搏均呈同样的偏心性心房激动顺序；４、心动过速时于希司速不应期刺激心室可提前夺获心房；５、经旁速室房传导呈递减性，未发现旁束有前传能力；６、射频消融心动过速的逆传支后表现为室房分离。射频消融需在心运过速或心起搏时仔细标测三尖瓣环，寻找最     

快-慢型房室结折返性心动过速的电生理特征和射频消融治疗

报道８例快－慢型房室结折返性心动过速（ＡＶＮＲＴ）的电生理特征及射频消融治疗。其中３例为慢－快型ＡＶＮ－ＲＴ射频消融改良慢径后出现的快－慢型ＡＶＮＲＴ。８例均经消融慢径而成功终止心动过速。平均放电次数３±１．１次、平均放电时间１２０±３０．４ｓ、平均放电功率３０±１１Ｗ。随访６～２４个月，无复发。快－慢型ＡＶＮＲＴ具有以下临床电生理特征：①快径不应期短、慢径不应期长。②心内电刺激无房室结双径路现象。③心动过速能由心房刺激诱发。④心动过速时ＡＨ间期＜ＨＡ间期，冠状窦近端Ａ波最提前。熟悉快－慢型ＡＶＮＲＴ的电生理特征，对于鉴别房性心动过速及右后间隔旁道参与的房室折返性心动过速十分重要，也是指导快－慢型ＡＶＮＲＴ射频消融成功的关键。     

短P—R综合征合并室上性心动过速的电生理观察

为探讨短Ｐ－Ｒ综合征合并室上性心动过速的电生理机制,对７例短Ｐ－Ｒ综合征合并室上性心动过速的患者进行心内电生理检查。结果发现：随着心房负扫描程序刺激,６例Ａ－Ｈ间期逐渐延长,１例间歇性延长,６例有Ａ－Ｈ间期跳跃现象;室上性心动过速时６例最早心房激动部位在希氏束,Ｖ－Ａ间期〈７０ｍｓ,１例在左后游离壁,Ｖ－Ａ间期〉７０ｍｓ。提示短Ｐ－Ｒ综合征合并室上性心劝过速的电生理机制是房室结加速传导合并房室结双     

射频导管消融治疗房室结折返性心动过速中较难病例的电生理特点

目的：明确射频导管消融治疗房室结折返性心动过速（ＡＶＮＲＴ）中较难病例的电生理特点。方法：７２例行慢径射频导管消融的慢—快型ＡＶＮＲＴ病人中１１例（１５％）成功射频导管消融的放电次数超过２０次或总放电时间超过２００秒被定义为较难病例（较难组），其余的为非较难病例（非较难组）６１例（８５％）。结果：较难组１１例中有７例（６４％）短心房—希氏束间期（≤６０ｍｓ），而非较难组６１例中１４例（２３％）短心房—希氏束间期（≤６０ｍｓ，Ｐ＜０．０５）；较难组１１例中８例（７３％）短房室结逆传文氏周期（≤２８０ｍｓ）；非较难组５７例（６１例中有４例因心室刺激反复诱发心动过速不能测得逆传文氏周期）中有１５例（２６％）具有短房室结逆传文氏周期（≤２８０ｍｓ，Ｐ＜０．０１）。７２例中５５例（７６％）具有房室结前传不连续曲线。房室结前传曲线有多次“跳跃”在较难组１１例中有７例（６４％）病人，在非较难组中有１２例病人（２０％，Ｐ＜０．０１）。结论：短心房—希氏束间期、短房室结逆传文氏周期和前传曲线多次“跳跃”的病人在较难组所占的百分率明显高于非较难组，有显著差异。     

导管消融具有双向传导特性的Mahaim结室纤维

目的介绍具有双向传导特性Mahaim结室纤维的电生理机制及导管消融方法。方法患者女性,34岁,反复发作性心动过速病史7年。外院心电图示“阵发性室上性心动过速”。心动过速可被维拉帕米及普罗帕酮终止。入院各项检查排除器质性心脏病后行电生理检查及导管消融术。结果电牛理检查示窦性心律时AH=73ms、HV=42ms,QRS时限100ms。心动过速时QRS波形态与窦性心律时相似,伴有轻度电交替。心动过速在多数情况下室房呈分离状态,HV问期为42ms,与窦性节律时相同,有时室房呈1：1传导,最早心房激动位于希氏束记录处。右心室心尖部以400ms周长刺激时室房呈分离状态。心房增频刺激时QRS波逐渐增宽,直至充分预激。在QRS波增宽过程中,HV逐渐缩短直至H波融合于QRS波之中,刺激信号至QRS波的间期逐渐延长,反映了递减传导的过程。继续缩短心房刺激周长后突然旁路传导受阻,经房室结下传并出现传导跳跃现象,继传导跳跃后心动过速被诱发。心动过速可被三磷酸腺苷（ATP）终止,终止后房室经旁路前传,其QRS波形态与充分预激时相似。在心房刺激保持充分预激的前提下,沿三尖瓣环标测,于左前斜位45。三尖瓣环4点钟处标测到最早V波,此处较体表心电图QRS波提前25ms,单极记录呈Qs型,HA波与V波之间未见高频电位。于该点消融放电（60W×60℃）,2S后旁路传导消失。放电过程中未出现交界性心律。消融结束后心房程序电刺激仍有房室传导跳跃现象。随访18个月,未再有心动过速发作。结论本病例心动过速系Mahaim结室纤维所介导,该纤维具有双向传导功能,其上插入端位于房室结慢径区域,下插入端位于邻近房室沟的局部心室肌。心动过速时房室结-希氏-浦肯野系统为前传支,结室纤维作为逆传支。     

Preexcitation Secondary to Fasciculoventricular Pathways in Children: A Report of Three Cases

Fasciculoventricular Pathways in Children. Introduction: Fasciculoventricular connections are the rarest form of accessory pathways leading to preexcitation. Electrophysiologic characteristics of these pathways include ventricular preexcitation with normal PR and AH intervals and short HV intervals during sinus rhythm. In addition, atrial overdrive pacing prolongs the PR interval without affecting the HV interval or the degree of preexcitation.
Methods and Results: From March 1994 through February 1997, 3 of 59 pediatric patients referred for electrophysiologic study for preexcitation on surface ECGs were found to have iasciculoventricular pathways. Two patients had no inducible supraventricular tachycardia. One patient had successful ablation of both a left lateral pathway and a concealed antentlateral pathway that had facilitated antidromic and orthodromic supraventricuiar tachycardias, respectively.
Conclusion: Children often manifest minimal preexcitation via accessory AV pathways due to rapid AV conduction and/or left lateral pathway location. Fasciculoventricular pathways may masquerade as Wolff-Parkinson-White syndrome. Separation of the two diagnoses depends on the demonstration of specific electrophysiologic criteria.     

Permanent junctional reciprocating tachycardia (Coumel type): an unusual location of a retrograde accessory pathway

Permanent junctional reentrant tachycardia (PJRT) is an uncommon form of tachycardia that is usually due to an atrioventricular reentry via a right posteroseptal accessory pathway with decremental properties. We describe a case of PJRT that showed evidence of two accessory pathways located both left and right. A 63-year-old woman was referred to our institution for radiofrequency (RF) ablation of a permanent form of regular narrow QRS tachycardia (T) (cycle length 520 ms) with long RP interval (380 ms); P wave was negative in inferior leads, negative in D1 and flat in aVL. During sinus rhythm, AH and HV intervals were 110 ms and 50 ms respectively. The atrioventricular anterograde conduction curve was continuous. A decremental retrograde conduction via a left posterior pathway until ventricular effective refractory period (210 ms) was evident. Tachycardia inducible with both atrial and ventricular programmed stimulation was almost incessant. During tachycardia, a premature ventricular depolarization delivered when His bundle was refractory was able to advance the next atriogram, and tachycardia could be interrupted by a ventricular depolarization without atrial capture. During right atrial mapping, an earliest atrial activation was found in the mid-septal position just above the coronary sinus ostium and RF application caused a transient interruption of T (3 minutes). Tachycardia resumed with basal characteristics, but no evidence of earlier right atrial activation was found during atrial mapping. Successful RF ablation was performed via retrograde aortic catheterization in the left posterior region. This case showed evidence of a left posterior pathway causing PJRT. However, the transient successful ablation in the right mid-septal region and the lack of evidence of right early atrial activation after RF application could account for the presence of an additional right accessory pathway or a strand of the same broad left pathway.     

Successful elimination of concealed accessory pathway-mediated tachycardia by ablation of AV nodal slow pathway

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.     

Variants of Preexcitation—Specialized Atriofascicular Pathways, Nodofascicular Pathways, and Fasciculoventricuiar Pathways:

Variants of Preexcitation. introduction: In the present report, the electrophysiiologic findings in patients with different types of variants of preeexcitwtion, i.e., atriofascicualr, nodofacicular, and fasciculoventricular fibers, and the results of radiofrequency catheter ablation using different target sites are described. Methods and Results: Twelve patients (mean age 36 ± 17 years) with variants of the preexcitation syndromes underwent electrophysiologic study and radiofrequency catheter ablation. The atrial origin of atriofascicular pathways remote from the normal AV node was assessed by application of late atrial extrastimuli that advanced (“reset”) the timing of the next QRS complex without anterograde penetration into the AV node. In patients with atriofacicular pathways, ablation of the accessory pathway or the retrograde fast AV node pathway was attempted. Ablation of the atriofascicular pathways was guided by a stimulus-delta wave interval mapping in the first live patients and by recording of atriofascicular pathway activation potentials in the next five patients. A nodofascicular pathway was suggested if VA dissociation occurred during tachycardia and if atrial extrastimuli failed to reset the tachycardia without anterograde penetration into the AV node. A fasciculoventricular connection was suggested if the proximal insertion of the accessory pathway was found to arise from the His bundle or bundle branches. The PR interval was expected within normal limits during sinus rhythm and the QRS complex to he slightly prolonged with a discrete slurring of the R wave, suggesting a small delta wave. Ten of the 12 patients had evidence for atriofascicular pathways and one patient each for a nodofascicular and fasciculoventricular pathway. In six patients, the atriofascicular pathways were successfully ablated, and in two patients, the retrograde fast AV node pathway. In one patient, a concealed right posteroseptal accessory AV pathway served as the retrograde limb and was successfully ablated. The nodofascicular pathway was shown to he a bystander during AV node reentrant tachycardia. After successful fast AV node pathway ablation resulting in marked PR prolongation, no preexcitation was present during sinus rhythm because of the proximal insertion of the nodofascicular pathway distal to the delay producing parts of the AV node. The proximal insertion of the fasciculoventricular pathway was suggested to arise distal to the AV node at the site of the penetrating AV bundle. The earliest ventricular activation at the His-bundle recording site indicated the ventricular insertion of this accessory connection into the ventricular summit. The fasciculoventricular connection gave rise to a fixed ventricular preexcitation and served as a bystander during orthodromic AV reentrant tachycardia incorporating a left-sided accessory AV pathway.     

Catheter ablation from right atrium of anteroseptal accessory pathways using radiofrequency current.

Catheter ablation with radiofrequency current has recently been introduced as a therapeutic regimen for symptomatic patients with the Wolff-Parkinson-White syndrome or atrioventricular (AV) tachycardia mediated by a retrogradely conducting (concealed) accessory AV pathway. These pathways may be located, although infrequently, in the anteroseptal region of the heart in close proximity to the AV node-His bundle conduction system. Any attempt to interrupt an anteroseptal accessory pathway therefore is subject to the potential complication of inadvertent impairment of normal AV conduction. This study was conducted to establish whether abolition of anteroseptal accessory pathways by radiofrequency current aimed at the atrial as opposed to the ventricular insertion of the pathway can be achieved with preservation of AV node-His bundle conduction. Twelve patients (mean age 37 +/- 13 years; 10 with Wolff-Parkinson-White syndrome, 2 with a concealed accessory pathway) were studied. In the majority of patients, radiofrequency current (500 kHz; mean energy 577 +/- 207 J) was applied through a steerable catheter with a long tip electrode placed in the anterior septal space at the atrial aspect of the tricuspid anulus, with the intention to destroy the atrial insertion of the accessory pathway. All pathways were successfully ablated. The AV node or His bundle conduction was not impaired in any patient. Right bundle branch block was induced in two patients (17%). There were no complications related to the procedure. It is concluded that catheter ablation from the right atrium using radiofrequency current provides effective and safe interruption of anteroseptal accessory pathways with good preservation of the normal conduction system.     

Slow pathway ablation in patients with atrioventricular node reentrant tachycardia and a prolonged PR interval

Objectives. We sought to assess the safety and efficacy of selective slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with a prolonged PR interval and atrioventricular (AV) node reentrant tachycardia.Background. Although both fast and slow AV node pathways can be ablated in patients with AV node reentrant tachycardia, slow pathway ablation, by obviating the risk of AV block, appears to be safer. However, the safety and efficacy of selective slow pathway ablation using transcatheter radiofrequency energy in patients with a prolonged PR interval during sinus rhythm are unclear.Methods. The seven study patients with a prolonged PR interval (mean ± SD 237 ± 26 ms) comprised three women and four men with a mean age of 31 ± 15 years. The slow pathway was targeted in all seven patients at the posterior/inferior interatrial septal aspect of the tricuspid annulus. Two patients presented with the uncommon variety of AV node reentrant tachycardia after initial fast pathway ablation; in the remaining five patients, the AV node reentrant tachycardia was of the common variety.Results. A single radiofrequency pulse at 30 W successfully abolished the slow pathway in both the anterograde and the retrograde direction in the two patients with uncommon AV node reentrant tachycardia. A mean of 5 ± 3 radiofrequency pulses were required in the remaining five patients with reentrant tachycardia of the common variety. The postablation PR interval and AH interval remained unchanged. The shortest cycle length of 1:1 AV conduction was prolonged significantly (from 327 ± 31 to 440 ± 59 ms, p < 0.01, as was the AV node effective refractory period (from 244 ± 35 to 344 ± 43 ms, p < 0.01). During a mean follow-up interval of 20 ± 6 months, no patient developed symptoms suggestive of AV node reentrant tachycardia or had evidence of second- or third-degree AV block.Conclusions. These data suggest that the AV node slow pathway can be ablated in patients with AV node reentrant tachycardia who demonstrate a prolonged PR interval during sinus rhythm.     

Evidence that cocaine slows cardiac conduction by an action on both AV nodal and His-Purkinje tissue in the dog

The effects of intravenous cocaine (2 mg/kg) were tested on several indices of cardiac electrical activity in sedated dogs. These included sinus rate, PR, AH, and HV intervals; AV nodal effective refractory period (AVNERP); ventricular effective refractory period; QRS duration; and the QT interval. Cocaine induced significant changes in six control animals with an intact-functioning autonomic nervous systems. After pharmacologic autonomic blockade with propranolol plus propantheline, cocaine increased the PR interval (+ 11 +/- 4.0 ms, p less than 0.05), primarily by slowing conduction at the AV nodal level. However, with constant atrial pacing at a rate above the sinus cycle length, prolongation of both the AH and the HV intervals (+ 15 +/- 2.5 and 6.7 +/- 1.7 ms, respectively) occurred. There was also a significant increase in the AVNERP (+ 29 +/- 5.9 ms, p less than 0.05). Consistent with the observed rate-dependent HV prolongation, cocaine decreased the rate of rise of phase 0 of the transmembrane action potential of Purkinje fibers. These data indicate that cocaine impairs cardiac conduction by direct actions on AV nodal and His-Purkinje cells.     

Catheter Ablation of the Atrial Origin of a Decrementally Conducting Atriofascicular Accessory Pathway by Radiofrequency Current

Radiofrequency Ablation of Pseudo-Mahaim Fibers. Introduction: A young woman with refractory recurrent supraventricular tachycardia was referred for catheter ablation. Methods and Results: Electrophysiologic studies revealed the mechanism of tachycardia to be atrioventricular (AV) reentry, utilizing a decrementally conducting atriofascicular accessory pathway as the anterograde limb of the circuit and the normal intraventricular conducting system as the retrograde limb. Pace mapping in the right atrium during sinus rhythm suggested an atrial origin of the accessory pathway several centimeters distant from the AV node. Multiple radiofrequency lesions at the distal insertion of the accessory pathway in or near the right bundle branch failed to abolish preexcitation. In contrast, radiofrequency current applied to the ventricular side of the anterolateral tricuspid ring, adjacent to the atrial origin of the accessory pathway, was successful in abolishing preexcitation and inducible supraventricular tachycardia without affecting AV nodal conduction. Conclusion: Radiofrequency ablation can provide curative therapy for intractable supraventricular tachycardia due to decrementally-conducting atriofascicular accessory pathways. The risk of AV block in such patients as a consequence of the procedure should be quite low.     

Reliability of retrograde atrial activation patterns during ventricular pacing for localizing accessory pathways

Definitive localization of accessory pathways is based on atrial activation patterns during orthodromic supraventricular tachycardia when retrograde conduction occurs exclusively through the accessory pathway. In some patients, supraventricular tachycardia cannot be induced or is deleterious. To determine whether accessory pathway sites can be identified accurately during ventricular pacing, retrograde atrial activation was assessed during orthodromic supraventricular tachycardia and ventricular pacing at multiple cycle lengths in 41 patients with a single accessory pathway. To obviate retrograde fusion due to concomitant conduction through the normal atrioventricular (AV) conduction system that may obscure the location of the accessory pathway, the difference in conduction time from the site of earliest atrial activation to the His bundle atrial electrogram (delta A-SVT) was measured during orthodromic supraventricular tachycardia and compared with values observed during ventricular pacing (delta A-VP). Characteristic values for the delta A-SVT interval were identified for left lateral (66 +/- 17 ms), left posterior (50 +/- 8 ms), posteroseptal (33 +/- 7 ms), right free wall (22 +/- 15 ms) and anteroseptal (0 +/- 0 ms) accessory pathway sites. During ventricular pacing, the site with the earliest atrial electrogram was used to define the accessory pathway location only if the maximal value of the delta A-VP interval over the range of cycle lengths assessed was comparable with the value of the delta A-SVT interval characteristic of that region. Values of the delta A-SVT interval correlated closely with the maximal values of the delta A-VP interval (r = 0.91). With this approach, 40 (98%) of 41 accessory pathway sites were identified correctly during ventricular pacing.(ABSTRACT TRUNCATED AT 250 WORDS)