diagnostic pacing maneuvers for supraventricular tachycardia: part 1

REVIEW

Diagnostic Pacing Maneuvers for SupraventricularTachycardia: Part 1GEORGE D. VEENHUYZEN, M.D., F. RUSSELL QUINN, M.B.B.S., PH.D.,STEPHEN B. WILTON, M.D., ROBIN CLEGG, M.D., and L. BRENT MITCHELL, M.D.From the Libin Cardiovascular Institute of Alberta, University of Calgary, Calgary, Alberta, Canada

This two-part manuscript reviews diagnostic pacing maneuvers for supraventricular tachycardia (SVT).Part one will involve a detailed consideration of ventricular overdrive pacing (VOP), since this pacingmaneuver provides the diagnosis in the majority of cases. This will include a review of the post-VOPresponse, fusion during entrainment, the importance of the VOP site, quantitative results of entrainmentsuch as the postpacing interval, differential entrainment, and new criteria derived from features found atthe beginning of the VOP train. There is a considerable literature on this topic, and this review is by nomeans meant to be all-encompassing. Rather, we hope to clearly explain and illustrate the physiology,strengths, and weaknesses of what we consider to be the most important and commonly employeddiagnostic pacing maneuvers, that is, those that trainees in cardiac electrophysiology should be wellfamiliar with at a minimum. (PACE 2011; 34:767–782)

ablation, electrophysiology–clinical, svt, pacing

IntroductionThe approach to supraventricular tachycardia

(SVT) diagnosis can be complex because itinvolves synthesizing baseline electrophysiologicfeatures, features of the SVT, and responses topacing maneuvers. In this review, we will mainlyexplore the latter while recognizing that neitherof the former can be ignored, for they providethe context in which diagnostic pacing maneuversmust be correctly chosen and interpreted. Noneof these are without their limitations, so onemust be comfortable employing and interpretinga variety of pacing maneuvers to be proficient atSVT diagnosis.

This review will address distinguishingamong the three most common SVT mechanisms,namely, atrioventricular node reentry tachycardia(AVNRT), atrioventricular reciprocating tachycar-dia (AVRT), and atrial tachycardia (AT). Partone will involve a detailed consideration ofventricular overdrive pacing (VOP), since thispacing maneuver provides the diagnosis in themajority of cases. This will include a review of the

Dedication: This manuscript is dedicated to the memory of Dr.Michael Andrew Nault (1972–2010), a contagiously inquisitivelover of the good, the silly, and the electrocardiologic.

Address for reprints: George D. Veenhuyzen, M.D., F.R.C.P.C.,Libin Cardiovascular Institute of Alberta, University of Calgaryand Calgary Health Region, Foothills Medical Centre, Rm C836,1403–29 St. N.W., Calgary, Alberta, T2N 2T9, Canada. Fax: 403-944-1592; e-mail: [email protected]

Received August 20, 2010; revised January 30, 2011; acceptedFebruary 07, 2011.

doi: 10.1111/j.1540-8159.2011.03076.x

post-VOP response, fusion during entrainment,the importance of the VOP site, quantitative resultsof entrainment such as the postpacing interval(PPI), differential entrainment, and new criteriaderived from features found at the beginning ofthe VOP train. Part two will consider pacingmaneuvers that can be performed when VOP isnot diagnostic (scanning diastole with ventricularand/or atrial premature beats, overdrive atrialpacing) or when sustained SVT cannot be induced(apex vs base pacing, para- and pure-Hisianpacing). Challenges in SVT diagnosis, includingsome esoteric ones, will be discussed in Parttwo also. There is a considerable literature onthis topic, and this review is by no meansmeant to be all-encompassing. Rather, we hopeto clearly explain the physiology, strengths, andweaknesses of what we consider to be the mostimportant and commonly employed diagnosticpacing maneuvers, that is, those that trainees incardiac electrophysiology should be well familiarwith at a minimum.

Choosing a Pacing Maneuveror an Ablation Catheter

Let us begin by considering the usual man-ifestation of SVT: a narrow complex tachycardiawith a normal His-Ventricular (HV) interval. Thereare three tachycardia features that are useful toconsider as outlined in Table I, including (a) theVentriculo-Atrial (VA) relationship, (b) the VAinterval, and (c) the atrial activation sequence.Often, three additional features, dependant uponperturbations in the SVT, provide additionalinformation: (d) whether, when there are small

C©2011, The Authors. Journal compilation C©2011 Wiley Periodicals, Inc.

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Table I.

Six Features of SVT to Consider before Considering a Diagnostic Pacing Maneuver

Feature Details SVT Mechanism(s)

1. VA relationship V = A AVNRT, AVRT, ATV > A ± AV dissociation ONVRT, ONFRT, AVNRTV < A AVNRT, AT

2. VA interval VA > 70 ms aAVNRT, AVRT, ATVA ≤ 70 ms tAVNRT, ATVA > AV aAVNRT, AT, AVRT using slowly

conducting AP

3. Atrial activation sequence High to low ATConcentric AVNRT, AVRT, ATEccentric AVRT, AT*

4. Spontaneous termination Ends with an “A” AVNRT, AVRTEnds with a “V” AVNRT, AVRT, AT

5. HH changes precede and predictAA changes

YesNo

AVNRT, AVRTAVNRT, AVRT, AT

6. VA increase > 30 ms withfunctional BBB

Yes AVRT with free wall AP ipsilateral toBBB

No AVNRT, AVRT, AT

aAVNRT = atypical AVNRT; tAVNRT = typical AVNRT; ONVRT = orthodromic nodoventricular reciprocating tachycardia; ONFRT =orthodromic nodofascicular reciprocating tachycardia. *AVNRT with a Leftward atrionodal exit is uncommon but still possible. AT is mostlikely, but AVNRT and AVRT are theoretically still possible.

variations in tachycardia cycle length (TCL), His-His (HH) or interventricular (VV) interval changesprecede and predict interatrial (AA) intervalchanges (i.e., the His-Atrial [HA] or VA intervalis constant despite HH or VV interval changes), (e)termination of SVT on a nonpremature terminalatrial electrogram with the same atrial activationsequence as SVT, and (f) changes in the VAinterval with the appearance or disappearance offunctional bundle branch block. It is noteworthythat, after studying these features of the SVT, anablation catheter rather than a pacing maneuvermay be what is required next. For example, ifSVT has a septal VA interval <70 ms (excludingAVRT) and HH interval changes precede andpredict AA interval changes, or the SVT stopswith a nonpremature terminal atrial electrogram(excluding AT, particularly if the latter happensmore than once so that this is not a merecoincidence), a diagnosis of typical AVNRT canbe made and the slow atrioventricular (AV) nodalpathway can be targeted for ablation. On theother hand, it should not be surprising thatdifferentiating among tachycardias with a 1:1 V-A relationship, septal V-A interval >70 ms, anda central atrial activation sequence has receivedconsiderable attention in the literature, since eachof the usual SVT mechanisms may be operative.

One would want to be very sure of the correctSVT mechanism in these cases before choosingan ablation target because of the variable risk ofAV block associated with ablation at differentsites in the septum. For example, it would beunwise to mistake AVNRT for a septal AT or AVRTemploying a septal accessory pathway (AP), sinceboth of the latter mechanisms require mapping tothe earliest atrial electrogram, which, in the caseof AVNRT, could well lead one to ablate in aregion where the risk of AV block is considerablyhigher than targeting the slow AVN pathway inthe region between the coronary sinus os andthe tricuspid valve annulus. It is also noteworthythat often the correct diagnostic pacing maneuvermust be chosen after some combination of thefeatures in Table I permits the SVT mechanismto be narrowed down to only two possibilities.

Quickly Ruling AT In or OutSince AT can have any atrial activation

sequence and any VA interval, it is in thedifferential diagnosis of 12 (80%) of the 15diagnostic categories found in the extreme rightcolumn of Table I. Overdrive pacing from theright ventricle (RV) at a cycle length (CL) that is10–40 ms shorter than the TCL provides a rapidtool to rule AT in or out.1 If, during overdrive

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DIAGNOSTIC PACING MANEUVERS FOR SVT

Figure 1. Panel A: response after cessation of overdrive ventricular pacing (340 ms) in an atrialtachycardia (cycle length 360 ms). The atrial cycle length (CL) was accelerated to the ventricularpacing CL and then slowed immediately after pacing was stopped. The last atrial electrogramthat was accelerated to the pacing CL is the first atrial electrogram labeled “A.” The responseafter pacing is stopped is A-A-V, which indicates a diagnosis of AT. Also note that the septalatrial electrograms (pHIS, CS 9,10) precede the high right atrial (HRA) electrogram during pacingwith 1:1 ventriculoatrial (VA) conduction (low-to-high atrial activation), while that activation isreversed during the AT (high-to-low atrial activation). A change in the atrial activation sequenceduring overdrive ventricular pacing with 1:1 VA conduction is also consistent with a diagnosisof AT (In fact, a descending pattern of atrial activation during the tachycardia alone is sufficientto indicate a diagnosis of AT). Panel B: response after cessation of right ventricular overdrivepacing in an orthodromic atrioventricular reciprocating tachycardia (AVRT) using a concealedleft-sided accessory pathway. The atrial CL was accelerated to the ventricular pacing CL andthen slowed to the prepacing tachycardia atrial CL immediately after pacing was stopped. Theatrial activation sequence during VOP is the same as the atrial activation sequence during SVT.The last atrial electrogram that was accelerated to the pacing CL is the atrial electrogram labeled“A.” The response after pacing is stopped is A-V, which excludes a diagnosis of AT. (stimulus-to-atrial [SA] = 285 ms; VA = 210 ms; SA-VA = 75 ms; PPI = 520 ms; TCL = 380 ms; PPI-TCL =140 ms; cPPI-TCL = 120 ms. The cPPI-TCL and SA-VA differences are “borderline” because ofthe distance of the pacing site from the left sided AVRT circuit.)


VEENHUYZEN, ET AL.

ventricular pacing, the atrial CL is accelerated tothe pacing CL, and the tachycardia continues afterpacing is stopped, then a post-VOP response that isatrial-atrial-ventricular (A-A-V) rules in AT whilea post-VOP response that is atrial-ventricular (A-V) rules out AT (effectively ruling in AVRT orAVNRT). The last atrial electrogram accelerated tothe pacing CL is the first atrial electrogram countedin the interpretation of this response (Fig. 1).The main shortcoming of this pacing maneuveris that, in 50–80% of cases of AT, the atria are notaccelerated to the pacing CL (the ventricles aredissociated from the tachycardia), so the responseis technically not interpretable (though thisparticular response still excludes AVRT).2–4 Whenthis is the case, the diagnosis is usually AT,2,4

though further information would still be requiredto prove a diagnosis of AT rather than AVNRT.

It is important to understand why VOP canrule AT in or out. First consider AT: during VOP,as long as the VA block CL is not longer than theTCL, there will eventually be 1:1 VA conductionover the normal AV conduction system, andeach retrogradely conduced atrial wavefront willoverdrive, suppress, or entrain (if reentrant) theAT. The last paced retrogradely conducted atrialwavefront (which will be responsible for thefirst atrial electrogram counted in the post-VOPresponse) cannot echo back to the ventricle be-cause the AV conduction system is still refractoryfrom having just conducted that wavefront to theatrium. It seems that even when either dual AVNphysiology or a bystander AP happens also to bepresent, none of these routes are available for thelast paced retrogradely conducted atrial wavefrontto echo to the ventricle as all are penetratedby the pacing wavefront and remain refractoryto the antegrade conduction that would lead tosuch an echo beat.1 If the AT has not terminated,the next atrial electrogram (i.e., the second atrialelectrogram counted in the post-VOP response)will result from the continuation of the AT, and bythen, the AV conduction system will usually haverecovered so that the next electrogram will be a Hiselectrogram followed by a ventricular electrogram,hence, an A-A-V response (Fig. 2A).

In orthodromic AVRT, as long as the refrac-tory periods of the participating ventricle, AP,and atrium do not exceed the TCL, eventually,during VOP, there will be 1:1 VA conductionof the stimulated orthodromic wavefront (socalled because it travels in the same directionas the tachycardia circuit) via the AP (so theatrial activation sequence during VOP ought tobe identical to that of the SVT). A portion ofthat stimulated wavefront, called the stimulatedantidromic wavefront (because it travels in theopposite direction of the tachycardia circuit), will

collide with the orthodromic wavefront from thepreceding beat either in ventricular myocardiumor in the AV conduction system (Fig. 2B). Atthis point, each stimulated orthodromic wavefrontis resetting the tachycardia to the pacing CL,and each stimulated antidromic wavefront iscolliding with, or fusing with, the orthodromicwavefront from the previous beat. Thus, thetachycardia is entrained (i.e., continually resetby the pacing train). If there is fusion in theQRS complex morphology during VOP (i.e., theQRS morphology is a fusion beat combiningsome aspects of the QRS complex morphologyof a fully paced beat with some aspects of theQRS complex morphology of the SVT), thereis proof that the SVT is entrained (manifestentrainment). In the absence of evidence offusion, as long as AVRT continues after pacingis stopped, it is reasonable to assume that AVRTwas entrained (concealed entrainment). The lastpaced retrogradely conducted atrial wavefront(producing the first atrial electrogram counted inthe post-VOP response) can now revolve throughthe AVRT circuit and, because there is no newstimulated antidromic wavefront for it to collidewith, conduct back to the ventricles over thenormal AV conduction system, producing a Hiselectrogram and a ventricular electrogram, hence,an A-V response.

Exactly the same thing happens when typicalAVNRT is entrained by VOP, except that thestimulated wavefront must travel up the His-Purkinje system to reach the AV node where thestimulated orthodromic wavefront resets AVNRTvia the fast AV node pathway (and also acceleratesthe atria to the pacing CL), and the stimulated an-tidromic wavefront collides with the orthodromicwavefront from the previous beat somewherein the slow AV node pathway (Fig. 2C). Thelast retrogradely conducted stimulated wavefrontproduces the first atrial electrogram that is countedin the post-VOP response, and also revolvesaround the AV node circuit to conduct backdown the slow AV node pathway to reach thelower common pathway, His-Purkinje network,and ventricles because there is no new stimulatedantidromic wavefront for it to collide with, hence,an A-V response. Note that, during entrainment oftypical AVNRT, the collision between the stimu-lated antidromic wavefront and the orthodromicwavefront from the previous beat occurs in theAVN and cannot possibly occur in ventricularmyocardium. Accordingly, QRS complex mor-phology fusion cannot occur, and entrainmentof AVNRT cannot be proven. (See later.)

Thus, a post-VOP response that is A-Vindicates entrainment of AVRT or AVNRT andexcludes AT (though proof of entrainment of



Figure 2. Responses to ventricular overdrive pacing (VOP) for three common SVT mechanisms.In each panel, square wave = pacing site, solid arrows = antidromic paced wavefront, dashedarrows = orthodromic wavefront, dotted arrows = orthodromic wavefront from the previousbeat. Panel A: in atrial tachycardia (AT), VOP causes overdrive suppression (if focal mechanism,faded star), or entrainment (if reentrant mechanism) of the SVT. The last paced impulse conductsretrogradely to the atrium and is followed by a beat of AT (star), which then conducts antegradelyto the ventricle—hence an “A-A-V” or “A-A-H” response. Panel B: in orthodromic AVRT (shownin this case using a right free-wall pathway), the last impulse of VOP conducts via the accessorypathway to the atrium, then continues around the circuit through the AV node and conductionsystem to the ventricle—hence an “A-V” or “A-H” response. The antidromic paced impulsecollides with the orthodromic impulse from the previous beat either in the conduction system(as shown here, black bar) or in ventricular myocardium. Panel C: In typical AVNRT, the lastpaced impulse of VOP conducts retrogradely via the conduction system, enters the excitable gapin the AV nodal circuit, activates the atrium via the fast pathway, then conducts via the slowpathway back to the His-Purkinje system to activate the ventricle—hence an “A-V” or “A-H”response. Collision of the stimulated antidromic wavefront during VOP occurs in the AV nodalslow pathway (black bar).


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Figure 3. A “pseudo A-A-V response.” The atria are accelerated to the overdrive pacing cycle length (CL = 360 ms)and the tachycardia resumes after pacing is stopped (380 ms). Note that the second atrial electrogram after the lastpaced beat is the last atrial electrogram that is accelerated to the pacing CL, so this is an A-V response. Failure torecognize this could lead to counting the first atrial electrogram after the last paced beat (*) in the post ventricularpacing response, leading to an erroneous conclusion of an A-A-V response. This was, in fact, a case of fast-slowAVNRT (PPI = 565 ms; cPPI-TCL = 185 ms; SA = 415 ms; VA = 265 ms; SA-VA = 150 ms). The recordings labeledpABL and dABL are from the right atrium. The coronary sinus catheter electrodes are labeled 9,10 as proximal and1,2 as distal.

AVRT is only available when there is evidenceof fusion), while a post-VOP response of A-A-V indicates that the SVT mechanism is notcapable of echoing the last stimulated retrogradelyconducted atrial wavefront back to the ventricles,as is the case in AT. Note that the features of,and criteria for, entrainment can be studied in thecontext of familiar SVT circuits.5

Pitfalls in the interpretation of the post-VOPresponse include the following:

1. Incorrectly identifying the last atrialelectrogram that is accelerated to the pacing CL.

As mentioned above, the last atrial electro-gram accelerated to the pacing CL is the firstresponse that ought to be annotated after pacingis stopped. When the SVT mechanism is AVRTor AVNRT, but the retrograde limb of the circuitconducts slowly, as it might in atypical AVNRT(aAVNRT) (such as in so-called “slow-slow” or“fast-slow” AVNRT) or AVRT employing a slowlyconducting AP, the VA interval after the last pacedbeat may be longer than the pacing CL such thatthe second atrial electrogram after the last pacedventricular beat may in fact be the last atrial

electrogram that was accelerated to the pacing CL(Fig. 3). When this is the case, the interval betweenthe first and second atrial electrograms after thelast paced ventricular beat will be the same asthe pacing CL. If this is not recognized, thena “pseudo-A-A-V” response may be incorrectlyinterpreted as indicating a diagnosis of AT. It ispossible that the first beat of an AT may occurafter the last atrial electrogram resulting from VAconduction at a time interval that is equal to thepacing CL by pure coincidence.6 Accordingly, itis worthwhile to repeat VOP several times and atdecrementally shorter CLs whenever possible toshow that the A-A-V response is reproducible. Itis also necessary to examine whether the atrialactivation sequence during 1:1 V-A conductionis the same as during SVT,6 as a different atrialactivation sequence in this setting could be theclue that AT is present (Fig. 1).

2. When the pacing CL is not short enough,or when the TCL shortens just before or duringpacing, so that 1:1 VA conduction during pacingis not present and the tachycardia and the pacingtrain are just isorhythmically dissociated fromeach other.



Figure 4. Overdrive pacing at a CL of 340 ms during typical AVNRT (CL 380 ms). The electrogram labeled “A” isthe last atrial electrogram accelerated to the pacing CL (340 ms). Note that on the first beat after pacing stops, theHV interval exceeds the HA interval. The HA interval on the first beat after pacing can be shorter than during stableSVT because of the preceding decrement in slow pathway conduction induced by VOP, as in this case. One couldbe tempted to include the subsequent atrial electrogram (*) in the post overdrive pacing response, but this would beincorrect. Although it does precede the following ventricular electrogram, it occurs after the His bundle electrogramindicating that it could not possibly have conducted antegradely through the His-Purkinje system to produce theventricular electrogram. Only atrial electrograms that can conduct antegradely to produce the ventricular electrogramare counted in the post ventricular pacing response. For cases such as these, where the HV interval exceeds the HAinterval, the error of considering this to represent an A-A-V response can be avoided by considering the response asA-H instead. The recordings labeled pABL and dABL are from the right atrium. The coronary sinus catheter electrodesare labeled 9,10 as proximal and 1,2 as distal.

Two ways to avoid this problem include1) performing the maneuver repeatedly anddecrementing the pacing CL by 10–20 ms aftereach apparently successful attempt to acceleratethe atria to the pacing CL and 2) checking to seethat after pacing has stopped, the TCL immediatelyreturns to the longer pre-pacing TCL, or at least aCL that is longer than that to which the atria wereaccelerated during pacing (Fig. 1 and 3).

3. When the HV interval exceeds the HAinterval in AVNRT.

In AVNRT, if the HV interval exceeds theHA interval (which can happen when the HVinterval is long or when the HA interval is veryshort or even a negative value as can occur inAVNRT with a long lower common pathway), thelast entrained atrial electrogram will be followedby a ventricular electrogram but that ventricularelectrogram will be preceded by a second atrialelectrogram resulting from the ongoing AVNRT

circuit (and not from pacing) (Fig. 4). This“pseudo-A-A-V” response could lead to an errorthat can easily be avoided by considering the post-VOP response as A-A-H or A-H rather than asA-A-V or A-V.7 Doing so should also avoid thepotential for a pseudo-A-A-V response in the rarecase where the first return beat of AVNRT blocksbelow the His-bundle. Accordingly, for the rest ofthis article, we will refer to the post-VOP responseas A-H or A-A-H.

4. AVNRT with block below the lowercommon pathway on the first return beat.

Theoretically, the first return beat afterentrainment of AVNRT could block below thelower common pathway, but above the Hisbundle (so that a His potential would not berecorded), resulting in an A-A-H response inAVNRT. Accordingly, the post-VOP response maybe unreliable in cases where there is spontaneousAV block during SVT. We are not aware of a


VEENHUYZEN, ET AL.

case where this has happened, and so we believethat the chances of block occurring below thelower common pathway on only the first returnbeat after overdrive ventricular pacing are lowenough that such a response should prompt strongconsideration of a diagnosis of AT. Other featuresor pacing maneuvers may need to be considered ifAVNRT is otherwise suggested.

5. Coexistence of AVNRT or AVRT withan AT

An A-H response indicates that either AVNRTor AVRT are present, but does not exclude thepossibility that an AT may also be present. Itis always prudent to test for the inducibility ofother forms of SVT after one substrate has beeneliminated.

What Next?If AT is ruled in by VOP, then the next step

would be mapping and ablation of the AT. If ATis ruled out by VOP, the diagnosis of AVNRTor AVRT may be clear, based on the featuresin Table I. When the atrial activation sequenceis concentric, and the VA interval is >70 ms,more information will be required to distinguishbetween AVRT employing a septal AP andaAVNRT. Thankfully, that information is oftenalready present in other features of the responseto VOP. For the remainder of the discussion,unless otherwise stated, only tachycardias withconcentric atrial activation (aAVNRT with a VA>70 ms and AVRT employing a septal AP) areconsidered.

Fusion during EntrainmentAs mentioned above, a post-VOP response

of A-H indicates entrainment of either AVNRTor AVRT and, in the case of entrainment ofAVRT, there is an opportunity to observe QRScomplex fusion due to collision of the stimu-lated antidromic wavefront with the orthodromicwavefront from the previous beat occurring inventricular myocardium (Fig. 5). Because QRScomplex fusion is impossible during entrainmentof AVNRT, the presence of QRS complex fusiondistinguishes AVRT from AVNRT. Unfortunately,like most diagnostic features for SVT, QRScomplex fusion during entrainment is specific forAVRT, but not sensitive. That is, during VOP,entrainment of AVRT is usually concealed: theQRS complex morphology is that of a pacedbeat because the orthodromic wavefront fromthe previous beat collides with the stimulatedantidromic wavefront in the AV conductionsystem, and fusion (and therefore proof ofentrainment) is not present (e.g., as depicted inFig. 2B). This is called “concealed entrainment”(the tachycardia is entrained, but entrainment

cannot be proven, since proof of entrainmentrequires the demonstration of fusion).

To maximize the opportunity to detect fusionduring entrainment of AVRT by VOP (i.e., toincrease the sensitivity of fusion for AVRT),one can also include evidence of fusion inthe intracardiac tracings rather than just in thesurface QRS complex morphology. The presenceof an orthodromically captured His or rightbundle potential during VOP indicates that theorthodromic wavefront from the previous beat hasreached the AV conduction system and will surelycollide with the stimulated antidromic wavefront(Fig. 5). This collision point may occur within thedistal AV conduction system or within ventricularmyocardium before the orthodromic wavefrontfrom the previous beat has depolarized a sufficientamount of ventricular myocardium to affect thepaced QRS complex morphology. It is worthemphasizing this point: in the latter two cases theQRS complex morphology will either be identicalto, or virtually indistinguishable from, the QRScomplex morphology of a fully paced beat, yet thepresence of an orthodromically captured His po-tential is intracardiac evidence that fusion is tak-ing place in the circuit somewhere distal to the Hisbundle, thus indicating that the circuit is AVRT.

The Importance of the Pacing Site in PermittingFusion during Entrainment of AVRT by VOP

Another way to increase the sensitivity of QRScomplex morphology fusion during entrainmentof AVRT is to permit the orthodromic wavefrontfrom the previous beat to depolarize as muchventricular myocardium as possible before col-liding with the stimulated antidromic wavefront.Because the orthodromic wavefront from theprevious beat begins to depolarize ventricularmyocardium as it exits the His-Purkinje network,the pacing location that would permit thatwavefront to depolarize as much ventricularmyocardium as possible before colliding withthe stimulated antidromic wavefront is the onefarthest from the interface of the His-Purkinjenetwork and ventricular myocardium, while stillclose to the AVRT circuit. That is, as close aspossible to the ventricular insertion of the AP,on the ventricular side of the AV groove oppositethe earliest atrial electrogram in SVT (Fig. 6).The closer the pacing site is to the ventricularinsertion of the AP, the more likely fusionbecomes, perhaps to the point of concealed fusion(where the paced QRS complex morphology isthe same as the QRS complex morphology ofthe tachycardia) (Fig. 7). Accordingly, when VOPis performed from the right ventricular apex,manifest entrainment (QRS complex fusion duringentrainment) is appreciable in the majority of



Figure 5. Manifest entrainment of orthodromic AVRT employing a left free wall AP (CL = 340 ms)with fusion. Panel A: The atria are accelerated to the pacing CL (320 ms) and the tachycardiacontinues after pacing is stopped. Note that the pacing site is the basal LV via a branch of theCS. The post-VOP response is A-H. There is an orthodromically captured His potential duringpacing that is visible just after the pacing stimulus, indicating entrainment with intracardiacelectrogram evidence of fusion. The PPI-TCL difference is 90 ms (430–340 ms). The first returnAH interval is 240 ms, which is 60 ms longer than the AH interval during tachycardia (due todecremental conduction slowing through the AV node at the shorter pacing CL), so the correctedPPI-TCL difference is only 30 ms (90–60 ms). The SA-VA interval difference is −20 ms. PanelB: QRS complex morphology of purely paced beats from the same pacing site that was used forVOP. Note that the QRS complexes during VOP (left side of Panel A) are narrower than those ofa purely paced beat, and have an intermediate morphology between fully paced beats and beatsof the SVT. LA = left atrial; LV = left ventricular. (The PPI is measured from the pacing stimulusto the first return ventricular electrogram recorded by the pacing channel. The SA interval ismeasured from the pacing stimulus to a consistent atrial electrogram, usually the earliest atrialelectrogram. The VA interval is measured from the beginning of the earliest QRS complex in SVTto the same atrial electrogram that was used to measure the SA interval.)

AVRTs employing septal or right-sided APs, butis rarely evident for AVRTs employing a left-sided AP.4 Similarly, when VOP is performed fromthe left ventricle (LV), manifest entrainment isappreciable in the majority of AVRTs employingleft-sided APs.4

Note that when VOP is performed from thebasal septum, inadvertent His bundle capture(or proximal right or left bundle capture) couldproduce a narrow QRS complex that could mimicfusion. This can be avoided by pacing superior orinferior to the His and right bundles.

Entrainment, Fusion, and “Bystander” APsThis discussion has indicated that transient

entrainment by VOP that results in manifest

fusion proves that the SVT is reentrant, that anAP is participating, and that the ventricle is arequired component of the circuit, excluding bothAVNRT and AT. Theoretically, a simultaneous AToriginating close to the atrial aspect of an AP, ora simultaneous AVNRT with an atrial exit closeto an AP, are not excluded by these findings.Such an exceptional circumstance would requirea double tachycardia or a double loop tachycardiawhere one of the tachycardias is orthodromicAVRT. Accordingly, such an AP could notstrictly be considered a “bystander.” Ablationof the AP would ultimately be required bothclinically and to unmask the second tachycardiamechanism. Thus, entrainment of SVT with fusionindicates that orthodromic AVRT is present;


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Figure 6. Importance of pacing site to demonstrationof QRS complex fusion. In panel A, with VOP froman apical site, collision of the stimulated antidromicwavefront (solid arrow) with the orthodromic impulsefrom the previous beat (dotted arrow) occurs withinthe conduction system (black bar). Thus the ventricleis activated entirely by the paced wavefront and QRScomplex fusion will not be seen. In panel B, the pacingsite has been moved to the base, close to the siteof earliest atrial activation. In this case, the impulsefrom the previous beat (dotted arrow) has the greatestchance to exit the His-Purkinje system and activatemost of the ventricle. The collision of the antidromicimpulse and the prior orthodromic impulse occurs inventricular myocardium. Manifest QRS fusion, or evenconcealed fusion (where the QRS morphology matchesthat of the tachycardia), will be apparent. The lattermust be distinguished from isorrhythmic dissociation ofthe pacing stimulus from the tachycardia (i.e., when thetachycardia is not actually accelerated to the pacing CL,but rather, the pacing CL is the same as the tachycardiaCL because an inappropriately long pacing CL waschosen or the tachycardia accelerated as pacing wasinitiated).

nevertheless, other SVT mechanisms could also bepresent.

Beyond Fusion: The Need for QuantitativeFeatures of Entrainment of SVT by VOPDespite considering evidence of fusion in

intracardiac electrograms and pacing from ventric-ular sites close to the ventricular insertion of theoperative AP, fusion during entrainment of AVRTis not always appreciable (i.e., only concealedentrainment may be possible). Nevertheless,AVRT and AVNRT can reliably be distinguishedby studying certain quantitative features of theirentrainment, including the difference betweenthe PPI and the TCL (the PPI-TCL difference),and the difference between the stimulus to atrialelectrogram (SA) interval and the tachycardia VAinterval (the SA-VA interval difference).

The PPI-TCL DifferenceThe PPI is the time required for the last

stimulated orthodromic wavefront to propagateto an excitable gap in a reentrant circuit, makeone revolution around that circuit, and return tothe pacing site. Accordingly, if the pacing siteis in the circuit, the PPI should approximatethe TCL, and the PPI-TCL difference shouldonly be 0–30 ms. The PPI-TCL difference shouldincrease as the distance of the pacing site fromthe circuit increases. A portion of ventricularmyocardium is “in circuit” for AVRT, whileventricular myocardium is relatively far fromAVNRT circuits, separated from them by theintervening His-Purkinje network that must betraversed twice during entrainment of AVNRT byVOP: once to reach the AVN circuit, and once toget back to ventricular myocardium. Accordingly,the PPI-TCL difference should be considerablylonger after entrainment of AVNRT than afterentrainment of AVRT by VOP8 (Fig. 8).

The Corrected PPI-TCL DifferenceWhile the PPI will increase as the distance of

the pacing site from the circuit increases, it mayalso increase if overdrive pacing causes decremen-tal (i.e., rate dependent) conduction slowing. Thisis most likely to occur in the AV node becausethe AV node typically displays decrementalconduction properties. During entrainment ofAVRT by VOP, the atria are accelerated to thepacing CL. Therefore, the input to the AV node isalso accelerated to the pacing CL and the AV nodeconduction time will increase in keeping with itsdecremental conduction properties. Thus, whenAVRT is entrained by VOP, the first Atrio-His (AH)interval (or, assuming that the His-ventricularinterval remains more or less constant, the firstAV interval) after entrainment is often prolongedcompared to the AH (or AV) interval during AVRT.This increase in the subsequent PPI is unrelated tothe distance of the pacing site to the circuit. ThePPI-TCL difference can be corrected for the degreeof decremental conduction slowing by subtractingthe magnitude of the increase in the AH (orAV) interval on the first return beat comparedto the AH (or AV) interval during spontaneousAVRT from the PPI-TCL difference9 (Fig. 5). Theoverlap between PPI-TCL differences in patientswith AVNRT and patients with AVRT employing aseptal AP disappears when the corrected PPI-TCLdifference (cPPI-TCL) is considered: a cPPI-TCLdifference <110 ms is consistent with a diagnosisof AVRT employing a septal AP while a cPPI-TCLdifference >110 ms is consistent with a diagnosisof AVNRT (Fig. 3).9 The cPPI-TCL difference maybe >110 ms in a case of AVRT if the pacing site



Figure 7. Manifest entrainment of orthodromic AVRT employing a left free wall AP with near concealed fusion. Theatria are accelerated to the pacing CL (340 ms) and the tachycardia resumes at a longer CL (355 ms) immediatelyafter pacing stops. The post-VOP response is AV. Note that the QRS complexes during VOP are almost identical tothe QRS complexes during tachycardia. There is only a slight difference in the end of the QRS complexes in leads IIIand V1 during entrainment. Note that the pacing site is the posterobasal LV.

is far from the circuit (as is the case when AVRTusing a left-sided AP is entrained by VOP fromthe right ventricular apex—Fig. 1B) or if the APhas decremental conduction properties (as mightbe encountered during a long RP interval SVT).

Correction of the PPI-TCL difference asdescribed above will also avoid a similar problemwith the uncorrected PPI-TCL difference thatcan arise in patients with both dual AV nodephysiology and AVRT employing a septal AP.During entrainment of AVRT that uses the fastAVN pathway as the antegrade limb, the pacingCL may encroach upon a fast AV node pathwayrefractoriness so that the stimulated orthodromicwavefront may be forced to use a slow AV nodepathway. The AH interval on the first return beatwould be considerably prolonged in such a case.This would prolong the PPI-TCL difference notbecause of decremental conduction in the AV nodebut because of a “jump” to the slow AVN pathwayduring entrainment.10

The SA-VA DifferenceDuring AVNRT the ventricle and atrium are

activated in parallel, while during entrainmentof AVNRT by VOP, their activation is in series.

In contrast, both during orthodromic AVRT andduring entrainment of orthodromic AVRT byVOP, the ventricle and atrium are activatedin series. Accordingly, the difference betweenthe VA interval during entrainment and SVTshould be longer for AVNRT than for AVRT(Fig. 8). The VA interval during entrainmentis measured from the pacing stimulus, so itis called the SA interval. SA-VA differences<85 ms are consistent with AVRT (Fig. 5) whileSA-VA differences >85 ms are consistent withAVNRT.8

SA-VA differences have tended to di-chotomize patients with AVNRT and AVRT lesswell than PPI-TCL and cPPI-TCL differenceswhen VOP is performed from or near the RVapex.8,9 While the SA-VA difference is not subjectto decremental conduction slowing through theAV node during the A-H response, the SA-VAdifference could be relatively long (close to or>85 ms) if the pacing site is far from the operativeAP (for instance, in the case of entrainment oforthodromic AVRT using a left-sided AP by pacingfrom the RVA) or if the AP has decrementalconduction properties (as might be encounteredduring a long RP interval SVT).


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Figure 8. Quantitative features of entrainment of SVTby VOP. A, left panel: tachycardia circuit in orthodromicAVRT (shown here using a right-sided accessorypathway). The VA interval will be the time from initialventricular activation (breakout from the His-Purkinjesystem, marked “V”) to earliest atrial activation (atrialbreakout from the accessory pathway, marked “A”). A,right panel: last beat of VOP, with an apical pacing siteclose to the circuit. The stimulus-to-atrial (SA) intervalwill be similar to the VA interval since the impulse istravelling over the same route in each. Note that duringSVT and VOP, the atrium and ventricle are activatedin series. The postpacing interval (PPI, time from thelast paced stimulus to the return electrogram at thatsite) will also approximate the tachycardia cycle length(TCL). Thus the PPI-TCL and SA-VA differences willbe relatively short. B, left panel: tachycardia circuit intypical AVNRT. The VA interval during SVT is shortsince the two chambers are activated in parallel. B,right panel: last beat of VOP. The SA interval will belonger than the VA interval during tachycardia sinceactivation of V and A is forced to occur in series. The PPIwill also be longer than the TCL since the impulse musttravel retrogradely up the conduction system, completeone revolution of the AVNRT circuit, then conductantegradely again to the ventricular pacing site. Thus,PPI-TCL and SA-VA will be relatively long. See text fordetails.

The Importance of the Pacing Site with Respectto the cPPI-TCL and SA-VA DifferencesCompared to apical ventricular pacing sites,

pacing sites close to the AV groove should becloser to an AP that operates in a conventionalAVRT circuit (if close to the region with early atrialactivation), yet farther from AV nodal circuits

Figure 9. Influence of pacing site on PPI-TCL and SA-VA differences. Panel A: in orthodromic AVRT (shownhere using a left free-wall accessory pathway), animpulse from an RV apical pacing site (square wave1) may have a larger distance to travel to enter thetachycardia circuit (solid arrow), compared to a basalsite close to the site of earliest atrial activation (squarewave 2). The latter site should thus give shorter PPI-TCLand SA-VA differences. Panel B: in contrast, in AVNRTthe apical site is “electrically closer” to the circuit thana basal site, since in the latter case the impulse mustfirst travel through ventricular myocardium (grey arrow)before entering the distal arborizations of the Purkinjesystem. In the case of the PPI, it must also travel thisdistance a second time to get back to the pacing site.Thus, in AVNRT a basal pacing site will cause PPI-TCLand SA-VA differences to be greater.

(because of the extra distance required for abasal pacing stimulus to reach the more apicalarborization that appears to be the usual input tothe His-Purkinje network) (Fig. 9). Accordingly,compared to apical pacing sites, basal pacingsites would be expected to (1) increase the cPPI-TCL and SA-VA differences for a given AVNRTcircuit and (2) decrease the SA-VA difference for agiven AVRT circuit. Basal pacing sites should alsodecrease the cPPI-TCL difference for a given AVRTcircuit to the extent that the basal site, being closerto the operative AP, may be closer to the circuit(Fig. 9). These hypotheses have been born outby a prospective study where, interestingly, thediscriminatory value for the cPPI-TCL difference(110 ms) and the SA-VA difference (85 ms)remained essentially unchanged (110 ms and80 ms, respectively), but the spread between thehighest values in AVRT and the lowest valuesin AVNRT increased significantly. In addition,there was no overlap between these values incases of AVNRT and these values in cases ofAVRT, regardless of the location of the AP,when basal VOP was performed. These resultsindicate that cPPI-TCL and SA-VA differencesobtained from entrainment by VOP from basal



Figure 10. Onset of ventricular overdrive pacing at aCL of 280 ms during SVT with a CL of 300 ms. Thefirst four paced beats show progressive QRS complexmorphology fusion. The fifth paced beat is the first beatto have fixed QRS complex morphology as determinedby studying all 12 leads at the onset of pacing (notshown here). Thus, the transition zone begins with thefirst pacing stimulus and ends with the fifth paced beat.Note that the atrial CL is accelerated to the pacingCL in the transition zone after the second paced beat,which is fused. The arrows indicate a fixed stimulus-atrial (SA) interval, which is also established in thetransition zone. If the diagnosis were AVNRT, onewould not expect the atrial CL to be perturbed or afixed SA interval to be established until one or morebeats after the transition zone. As we will discuss inPart two of this review, the second pacing stimulusresults in a His-refractory ventricular premature beat (itmust be His-refractory since the QRS complex is fused,indicating that the stimulated antidromic wavefrontcollided with the orthodromic wavefront from theprevious beat in ventricular myocardium after it hadto exit the His-Purkinje network) that preexcites theatrium by 20 ms without a change in the atrial acti-vation sequence, indicating a diagnosis of orthodromicAVRT.

sites better dichotomize AVNRT circuits fromAVRT circuits.4 As discussed earlier, basal pacingsites close to the earliest atrial activation arealso most likely to permit the identification offusion (Fig. 6). Compared to RV apical pacingsites, basal ventricular pacing sites are not as easyto access with stability and without inadvertentatrial or His bundle capture. Accordingly, wereserve VOP from basal sites for those instanceswhen VOP from the RV apex results in anA-H response with concealed entrainment andborderline or questionable cPPI-TCL and/or SA-VA differences.

Differential EntrainmentBased on the results of apex versus base

pacing (to be discussed in detail in Part two ofthis review) by Martinez-Alday et al.,11 we hypoth-esized that the SA-VA and PPI-TCL differencesafter entrainment of AVNRT by basal VOP oughtto be at least 10 and 20 ms longer, respectively,than after apical VOP. These differences should bespecific for AVNRT provided that long and similarpacing CLs are employed at both sites to avoidany increases that might be due to decrementalconduction slowing during VOP. We coined theterm “differential entrainment”12 to describe thisphenomenon.

Our colleagues at the University of WesternOntario provided further proof of this concept.13

Apical VOP was performed with the RV catheteradvanced as far out to the RV apex as possible.Basal VOP was performed by advancing a steerableablation catheter just beyond and superior tothe His bundle where inadvertent atrial andHis bundle capture could be reliably avoided.The differential cPPI-TCL values and differentialSA-VA (which they called the differential VA)interval values were defined as those valuesobtained after VOP from the RV apex subtractedfrom those values obtained after VOP from theRV base. The differential VA interval could becalculated even in cases where VOP consistentlyterminated the SVT if VOP did acceleratethe atria to the pacing CL prior to termination (seenumber 2 below). All patients with differentialVA and differential cPPI-TCL values >20 and30 ms, respectively, had AVNRT, while all thosewho did not had AVRT. Differential entrainmentperformed in this way has the strength ofnot requiring knowledge of the site of earliestatrial activation, which might be particularlyvaluable if a coronary sinus (CS) catheter isnot routinely used, or if the CS cannot becannulated.


VEENHUYZEN, ET AL.

Figure 11. A supraventricular tachycardia with a long RP interval and earliest atrial activation along the mitralannulus. Overdrive posterobasal left ventricular pacing is initiated about half way through the tracing. The secondpacing stimulus captures enough ventricular myocardium to result in a fusion beat. Note that the QRS complexmorphology associated with the second pacing stimulus is partly that of the QRS complex morphology of thenative tachycardia (compare to the QRS complex morphology of the preceding beats) and partly that of the QRScomplex morphology of a fully paced beat (compare to the QRS complex morphology of the subsequent paced beats).Importantly, the second pacing stimulus is followed by abrupt VA block, which terminates the SVT. Ventricular pacingwith 1:1 VA conduction ensues. The atrial CL was perturbed (termination with abrupt VA block) in the transitionzone. As we will discuss in Part two of this review, the second pacing stimulus results in a His-refractory ventricularpremature beat (it must be His-refractory since the QRS complex is fused indicating that the stimulated antidromicwavefront collided with the orthodromic wavefront from the previous beat in ventricular myocardium after it hadto exit the His-Purkinje network) that terminates the SVT without conduction to the atrium. If one only studied theend of this overdrive pacing train and found that SVT had stopped, one would miss this information, indicating adiagnosis of orthodromic AVRT (in this case, employing a slowly conducting left free-wall accessory pathway).

What if the Response to VOP Is NotInterpretable?

Three responses to VOP, while often consid-ered uninterpretable, may still provide importantdiagnostic information.

1. The atria are not accelerated to thepacing CL: As already discussed, repeated failureto accelerate atrial activation to the ventricularpacing CL suggests, but does not prove, that theSVT is an AT.

2. The atria are accelerated to the pacingCL, but SVT fails to continue after VOP stops.In this situation, the reason that the SVT stopsis because the VOP CL has encroached upon theantegrade refractory period of the AVN, so that

the last retrogradely conducted atrial wavefrontcannot echo back to the ventricles to produce anAH response after VOP. Often, this problem canbe overcome by shortening the refractory periodof the AVN by intravenous isoproterenol. If thisproblem cannot be overcome, the response canstill be helpful diagnostically, particularly whenit is part of differential entrainment as discussedabove. (In this instance, the term “differentialentrainment” is inappropriate, since the SVTcannot be said to be entrained if VOP results inits termination.)

Recently, three retrospective studies havereported that resetting of the timing of atrialactivation (usually advancement; less commonly



Figure 12. A proposed flow chart for the use of ventricular overdrive pacing in the diagnosis ofSVT. * = closest to the site of earliest atrial activation.

delay or tachycardia termination without atrialactivation) during the early portion of VOP candifferentiate AVNRT (typical or atypical) fromAVRT (regardless of AP location) with a veryhigh degree of sensitivity and specificity.14–16

When VOP is initiated, there is usually a gradualchange from the tachycardia QRS morphology,through a transition zone of varying degrees offusion, to a final stable paced QRS complexmorphology (which may be either fully pacedor represent stable fusion) (Figs. 10 and 11).Definition of the first stable QRS morphology beatis central to this discriminator and should useall 12 surface electrocardiogram leads. In these

studies, the positive predictive value of resettingof the timing of atrial activation either beforeor at the time of the first beat showing finalpaced QRS morphology for AVRT and the positivepredictive value of resetting of the timing of atrialactivation after the first beat showing final pacedQRS morphology for AVNRT both exceed 90%.In AVRT, VOP impulses will reach the atria assoon as the ventricular paced impulses reach theAP and traverse it. In AVNRT, VOP impulses willnot reach the atria until the ventricular pacedimpulses reach the input to the distal His-Purkinjesystem and traverse the His-Purkinje systemand the AVN retrogradely. This discriminator


VEENHUYZEN, ET AL.

between AVRT and AVNRT is attractive be-cause it does not require that the tachycardiacontinue after termination of VOP. Accordingly,prospective studies of this discriminator seemwarranted.

Potential pitfalls should be kept in mind,including variable TCLs, pacing at a CL shorterthan 40 ms less than TCL (where the pacedwavefront could penetrate the His bundle andAV node and perturb the atrial CL during ATor AVNRT in fewer beats), decremental APs(where the paced wavefront could take morebeats to perturb the atrial CL in AVRT), thepresence of bystander APs (which could providea route to readily perturb the atrial CL duringAT or AVNRT), and difficulties in identifyingthe first paced beat with a stable QRS complexmorphology, for which interobserver agreementappears to be around 80%.16 For the same reasonsdiscussed above, one would expect the diagnosticyield of findings at the beginning of VOP to beimproved by basal VOP close to the earliest atrialactivation in challenging or borderline cases. Thatis, one would expect that the atrial CL would beperturbed earlier in the transition zone for casesof AVRT, and even longer after the transition zone

for cases of AVNRT, if VOP were performed atbasal ventricular sites, especially ones close to theearliest atrial activation.

A proposed flow chart employing VOP forSVT diagnosis is presented in Fig. 12.

When SVT repeatedly terminates during VOP,it may also be useful to burst pace the ventricle for3–6 beats at a CL of 200–250 ms. Around 60% ofthe time, the ventricles will be dissociated fromthe SVT mechanism (excluding AVRT) or the SVTwill terminate without conduction to the atrium(excluding AT).2

ConclusionVOP during sustained, stable SVT is quick

and easy to perform. Because it is qualitativelyand quantitatively information rich, it can providea diagnosis of SVT mechanism in a majority ofcases. Basal VOP and differential entrainment canbe useful in cases where the results of VOP fromthe RVA are borderline. A good understandingof VOP as a diagnostic tool will provide a solidfoundation for understanding SVT mechanisms,the principles of entrainment, and other diagnosticpacing maneuvers, which will be discussed in Parttwo of this review.

References1. Knight BP, Zivin A, Souza J, Flemming M, Pelosi F, Goyal R,

Man KC, et al. A technique for the rapid diagnosis of atrialtachycardia in the electrophysiology laboratory. J Am Coll Cardiol1999; 33:775–781.

2. Knight BP, Ebinger M, Oral H, Kim MH, Sticherling C, Pelosi F,Michaud GF, et al. Diagnostic value of tachycardia features andpacing maneuvers during paroxysmal supraventricular tachycardia.J Am Coll Cardiol 2000; 36:574–782.

3. Maruyama M, Kobayashi Y, Miyauchi Y, Ino T, Atarashi H, KatohT, Mizuno K. The VA relationship after differential atrial overdrivepacing: A novel tool for the diagnosis of atrial tachycardia in theelectrophysiologic laboratory. J Cardiovasc Electrophysiol 2007;18:1127–1133.

4. Veenhuyzen GD, Coverett K, Quinn FR, Sapp JL, Gillis AM,Sheldon R, Exner DV, et al. Single diagnostic pacing maneuverfor supraventricular tachycardia. Heart Rhythm 2008; 5:1152–1158.

5. Veenhuyzen GD, Quinn FR. Principles of entrainment: Diagnosticutility for supraventricular tachycardia. Indian Pacing Electrophys-iol J 2008; 8:51–65.

6. Sticherling C, Knight BP. A long RP tachycardia. What isthe tachycardia mechanism? J Cardiovasc Electrophysiol 2001;12:115–117.

7. Vijayaraman P, Lee BP, Kalahasty G, Wood MA, EllenbogenKA. Reanalysis of the “pseudo A-A-V” response to ventricularentrainment of supraventricular tachycardia: Importance of his-bundle timing. J Cardiovasc Electrophysiol 2006; 17:25–28.

8. Michaud GF, Tada H, Chough S, Baker R, Wasmer K, SticherlingC, Oral H, et al. Differentiation of atypical atrioventricular nodere-entrant tachycardia from orthodromic reciprocating tachycardiausing a septal accessory pathway by the response to ventricularpacing. J Am Coll Cardiol 2001; 38:1163–1167.

9. Gonzalez-Torrecilla E, Arenal A, Atienza F, Osca J, Garcia-Fernandez J, Puchol A, Sanchez A, et al. First postpacing intervalafter tachycardia entrainment with correction for atrioventricularnode delay: A simple maneuver for differential diagnosis ofatrioventricular nodal reentrant tachycardias versus orthodromicreciprocating tachycardias. Heart Rhythm 2006; 6:674–679.

10. Veenhuyzen GD, Stuglin C, Zimola KG, Mitchell LB. A tale of twopost pacing intervals. J Cardiovasc Electrophysiol 2006; 6:687–689.

11. Martinez-Alday JD, Almendral J, Arenal A, Ormaetxe JM, PastorA, Villacastin JP, Medina O, et al. Identification of concealedposteroseptal Kent pathways by comparison of ventriculoatrialintervals from apical and posterobasal right ventricular sites.Circulation 89:1060–1067.

12. Platonov M, Schroeder K, Veenhuyzen GD. Differential en-trainment: Beware from where you pace. Heart Rhythm 2007;8:1097–1099.

13. Segal OR, Gula LJ, Skanes AC, Krahn AD, Yee R, Klein GJ.Differential ventricular entrainment: A maneuver to differentiateatrioventricular node reentrant tachycardia from orthodromicreciprocating tachycardia. Heart Rhythm 2008; 6:493–500.

14. Dandamudi G, Mokabberi R, Assal C, Das MK, Oren J, StormR, Vijayaraman P, et al. A novel approach to differentiatingorthodromic reciprocating tachycardia from atrioventricular nodalreentrant tachycardia. Heart Rhythm 2010; 7:1326–1329.

15. Almahameed ST, Buxton AE, Michaud GF. New criteria during rightventricular pacing to determine the mechanism of supraventriculartachycardia. Circ Arrhythm Electrophysiol 2010; 3:578–584.

16. Rosman JZ, Roy MJ, Stevenson WG, Epstein LM, Tudrow UB,Koplan BA, Albert CM, et al. Resetting criteria during ventricularoverdrive pacing successfully differentiate orthodromic reentranttachycardia from atrioventricular nodal reentrant tachycardiadespite interobserver disagreement concerning QRS fusion. HeartRhythm 2011; 8:2–7.


diagnostic pacing maneuvers for supraventricular tachycardia: part 1

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