REVIEW
Diagnostic Pacing Maneuvers for Supraventricular Tachycardias:Part2
GEORGE D.VEENHUYZEN,M.D.,F.RUSSELL QUINN,M.R.C.P.,P H.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 and Calgary Health Region,Alberta,Canada The approach to supraventricular tachycardia(SVT)diagnosis can be complex becau it involves synthesizing baline electrophysiologic features,features of the SVT,and the respon(s)to pacing maneuvers.In this two-part review,we will mainly explore the latter while recognizing that neither of the former can be ignored,for they provide the context in which diagnostic pacing maneuvers must be correctly chon and interpreted.Part1involved a detailed consideration of ventricular overdrive pacing,since this pacing maneuver provides the diagnosis in the majority of cas.In Part2,other diagnostic pacing maneuvers that might be helpful when ventricular overdrive pacing is not diagnostic or appropriate,including attempts to ret SVT with single atrial or ventricular beats,para-Hisian pacing, apex versus ba pacing,and atrial overdrive pacing,are discusd,as are some specific diagnostic SVT challenges encountered in the electrophysiology lab.There is considerabl
e literature on this topic,and this review is by no means meant to be all-encompassing.Rather,we hope to clearly explain and illustrate the physiology,strengths,and weakness of what we consider to be the most important and commonly employed diagnostic pacing maneuvers,that is,tho that trainees in cardiac electrophysiology should be well familiar with at a minimum.(PACE2012;35:757–769)
ablation,electrophysiology-clinical,SVT,pacing
In part1of this review on diagnostic pac-ing maneuvers for supraventricular tachycardia (SVT),we explored ventricular overdrive pacing (VOP)in detail,since it provides afirm SVT diagnosis in the majority of cas.1We will now consider pacing maneuvers that can be performed when VOP is not diagnostic,including ones that can be performed when sustained,regular SVT cannot be induced.The will include single-paced ventricular beats during ongoing SVT,para-Hisian pacing,and apex versus ba pacing. We will also explore some challenging specific situations in SVT diagnosis including differen-tiating atrioventricular node reentry tachycardia (AVNRT)from atrial tachycardia(AT)and junc-tional tachycardia(JT),SVT with atrioventricular (AV)dissociation,and differentiating AVNRT with a leftward atrionodal exit from orthodromic atrioventricular reciprocating tachycardia(AVRT) employing a left-sided accessory pathway(AP).
电影院英文
Address for reprints:George D.Veenhuyzen,M.D.,F.R.C.P.C., Libin Cardiovascular Institute of Alberta,University of Calgary and Calgary Health Region,Foothills Medical Centre,Rm C836, 1403-29St.N.W.,Calgary,Alberta,T2N2T9,Canada.Fax:403-944-1592;e-mail:george.veenhuyzen@calgaryhealthregion.ca Received September19,2011;revid December22,2011; accepted January5,2012.
doi:10.1111/j.1540-8159.2012.03352.x Scanning diastole with ventricular premature beats(VPBs)
Single VPB introduced decrementally during diastole in SVT offer an opportunity to determine the relationship between altered timing of ven-tricular depolarization and the timing of atrial depolarization.For example,if a VPB is able to terminate tachycardia without atrial depolariza-tion,then AT can be excluded,provided this is not a coincidence.Furthermore,VPBs that occur during SVT at a time when the stimulated wavefront would be expected to collide with the SVT wavefront in the His-Purkinje network or in ventricular myocardium cannot possibly affect atrial timing during either AVNRT or AT(unless a bystander AP is prent).Accordingly,such His-refractory VPBs(HRVPBs)should only be capable of affecting AVRT circuits(again,in the abnce of a bystander AP).VPBs that occur before His bundle refractoriness are potentially capable of affecting atrial timing(including terminating SVT) in any of AT,AVNRT,or AVRT.
How does one determine if a paced VPB is His-refractory?If the QRS complex morphology of the VPB shows evidence of ,the QRS complex morphology of the VPB shows some features of the QRS complex morphology of a paced VPB and some features of the QRS complex morphology of the SVT),then the paced VPB must be His-refractory,since the SVT wavefront that the卜算子送鲍浩然之浙东的意思
C 2012,The Authors.Journal compilation C 2012Wiley Periodicals,Inc.
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Figure1.Advancement of atrial activation by a fud His-refractory ventricular premature beat(HRVPB). Panel A:During supraventricular tachycardia with a stable cycle length of444ms,one-to-one atrioven-tricular relationship,and an earlier atrial electrogram recorded in the right atrium(where the ablation catheter,ABLp/d,is located)than in the ptum (d/pHIS)or coronary sinus(proximal CS9,10through distal CS1,2),a paced premature beat is delivered by electrodes at the right ventricular apex(RVd).The subquent atrial activation is advanced by19ms. The paced premature ventricular beat is His-refractory (HRVPB)becau(1)it is fud:note QRS complex morphology features and duration(122ms)that are intermediate between tho of the conducted SVT (narrow complex)and of a purely paced QRS complex (Panel B,QRS complex duration=144ms)and(2)the pacing stimulus is delivered at precily the time of the expected His bundle potential(arrow).A ventricular paced beat can be considered His-refractory if it occurs up to35–55ms earlier than the anticipated His bundle potential.Advancement of atrial activation without a change in the atrial activation quence by an HRVPB indicates that an accessory pathway(AP)is prent and almost certainly participating in orthodromic AVRT,in this ca,employing a right-sided AP.
stimulated wavefront is fusing with in ventricular myocardium must have exited the His-Purkinje network(Fig.1).If the pacing stimulus occurs just after a discernible antegrade His potential, then the paced VPB is obviously His-refractory. Finally,if the paced VPB occurs no more than 35–55ms earlier than the anticipated timing of the antegrade His potential,in the time that would be required for that stimulated wavefront to enter the distal arborization of the His-Purkinje network and travel retrogradely to the His bundle,the tachycardia wavefront would have reached the His bundle where the wavefronts would collide.2 When the paced VPB occurs more than35–55ms earlier than the anticipated timing of the antegrade His potential,it would not be considered to be His-refractory,but rather,prior to His bundle refractoriness.
There are three respons to an HRVPB that are diagnostically uful:
(1)SVT terminates without conduction to the atrium.This respon indicates a diagnosis of AVRT,provided that this event is not a coincidence,as could be the ca if the SVT frequently spontaneously terminates.The fact that an HRVPB can affect the SVT indicates that an AP is prent,and the fact that the SVT terminates with ventriculoatrial(VA)block indicates that ventricular and atrial activation must be linked so that if conduction to the atrium does not occur via the AP,the circuit is interrupted. This cannot be the ca with AT or AVNRT, even if a bystander AV AP is prent.
That is, the AP must also be participating in the SVT mechanism.Theoretically,this respon could be obrved given the coexistence of AVNRT and a bystander nodoventricular AP,but this occurrence has not been convincingly demonstrated to our knowledge,and would have to be extremely rare.
As we discusd in Part1,sometimes VOP results in an apparently noninterpretable respon when VOP repeatedly terminates the SVT.VOP may be considered as a ries of concutive VPBs.When the SVT repeatedly stops during VOP becau of VA block,if the paced beat that precedes VA block is His-refractory,and the atrial timing has not changed prior to that VPB,this constitutes an equivalent of an HRVPB terminating SVT without conduction to the atrium,thereby establishing a diagnosis of AVRT(e“What if the respon to VOP is not interpretable?”in Part I).
(2)Atrial activation is delayed without a change in the atrial activation quence.This respon indicates a diagnosis of AVRT employing a decremental AP(Fig.2).As above,the fact that an HRVPB can affect the SVT indicates that an AP is prent and delay of atrial timing indicates that atrial activation is decrementally linked to ventricular activation.This cannot be the ca with either AT or AVNRT even if a bystander AV AP is prent;the decremental AP must also be participating in the SVT mechanism. Note that for this respon to be appreciated, the degree of decremental conductio
n slowing must exceed the prematurity of the HRVPB;if they are matched,AVRT employing a decremental AP could be prent but becau no change in atrial timing would occur,one would conclude that the VPB had no effect on the SVT and the diagnosis could be misd.Accordingly,it is worth studying the effects of multiple HRVPBs
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Figure2.Delay of atrial activation by a His-refractory ventricular premature beat(HRVPB).During a long R-P interval supraventricular tachycardia with a stable cycle length of473ms,a paced premature beat is delivered by electrodes at the right ventricle.The subquent atrial activation is delayed by20ms without a change in the atrial activation quence.The paced premature ventricular beat is His-refractory becau it occurs virtually simultaneously with and certainly not more than35–55ms earlier than the expected inscription of the anterograde His bundle potential(arrow).This respon indicates that an accessory pathway(AP)is prent and participating in orthodromic AVRT,in this ca,employing a slowly conducting concealed ptal AP.(Tracing courtesy of Dr.G.Neal Kay.) introduced throughout the His-refractory diastolic window to minimize this potential pitfall of
studying only one HRVPB that had no apparent effect.Theoretically,delayed atrial timing after an HRVPB could be obrved in the tting of AVNRT with a bystander nodoventricular AP.3This is so rare that delay of atrial timing by an HRVPB without a change in the atrial activation quence should be considered extremely strong evidence that the SVT mechanism is AVRT employing a decremental AP.
transactionIt is often the ca that AVRT employing a decremental AP manifests as a long RP interval SVT.If the AP ud for retrograde conduction has decremental conduction properties,entrain-ment by VOP could be associated with long corrected postpacing interval-tachycardia cycle length(cPPI-TCL)and stimulus-atrial(SA)-VA interval values that would normally be considered evidence of atypical AVNRT.Fusion during entrainment would still provide proof that the mechanism is AVRT but,if fusion is not prent, it is important to scan diastole with VPBs during long RP interval SVTs,even if entrainment by VOP is associated with long cPPI-TCL and SA-VA interval values.In such a situation,thefinding that an HRVPB delays atrial timing(indicating a diagnosis of AVRT,Fig.2)has a greater diagnostic value than thefinding of long cPPI-TCL or SA-VA interval values(suggesting a diagnosis of AVNRT).
Application of this maneuver requires that any apparent delay in atrial timing exceeds the spontaneous variability in the SVT cycle length (CL).Accordingly,this maneuver may not be reliable in irregular SVTs.
(3)Atrial activation is advanced without a change in the atrial activation quence.The fact that an HRVPB can affect atrial timing indicates that an AP is prent.If the atrial activation quence is unaltered,one can conclude with confidence,but not with certainty,that the AP is participating in the S
VT mechanism,establishing a diagnosis of AVRT(Fig.1).Theoretically,AT or AVNRT could be advanced by conduction over a bystander AP,and if the bystander AP were clo to the AT origin or atrionodal exit, respectively,the atrial activation quence may not change appreciably.This situation is so rare that thisfinding is considered very strong evidence (but not proof)that the SVT mechanism is AVRT.
丈夫的英文
As before,application of this maneuver requires that any apparent change in atrial timing exceeds the degree of spontaneous variability in the SVT CL.Accordingly,this maneuver may not be reliable in irregular SVTs.
Unfortunately,while the respons to HRVPBs are specific(or,in the third ca,nearly specific)for AVRT,they are not particularly nsitive.If the pacing site is far from the participating AP,the orthodromic wavefront of the VPB may not have had enough time to reach the AP and affect the AVRT circuit when delivered late enough to be His-refractory.The classic situation in which an HRVPB delivered from the right ventricular(RV)apex does not affect an AVRT circuit becau of the distance of the RV apex to the AP occurs when a left free wall AP is operative; nevertheless,this problem may ari when a relatively nearby ptal AP is involved.4As is the ca with fusion during VOP,the nsitivity of the three respons to HRVPBs described earlier can be incread by moving measured
the pacing site clo to the AP,that is,to a basal ventricular site clo to the site of earliest atrial activation.This is not surprising,since fusion during VOP constitutes the continuous retting of an AVRT circuit by a ries of concutive HRVPBs;the fact that they are fud proves that they are His-refractory,as discusd earlier.
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It is commonly taught that if none of the three respons to HRVPBs described earlier is obrved,no conclusion regarding the SVT mechanism can be drawn.However,it has been suggested that,in the ca of a short RP interval SVT,advancing the local ventricular activation adjacent to the earliest atrial activation by more than30ms without affecting atrial timing should exclude the participation of a conventional AP from the SVT mechanism.5Similarly,in the ca of a long RP interval SVT,advancing the local ventricular activation adjacent to the earliest atrial activation by more than60ms without affecting atrial timing should exclude the participation of a decremental AP from the SVT mechanism.5 Regarding the HRVPB maneuver,one point ems to be underappreciated:if an SVT that rembles typical AVNRT is induced(central atrial activation and p
tal VA<70ms), this maneuver will not add further diagnostic information as it cannot distinguish AVNRT from AT(e one exception for this in the ction on AV-dissociated SVT).If the diagnosis is not clear fromfindings during spontaneous perturbations in the SVT,the pacing maneuver of choice in this situation is VOP.
Para-Hisian&Pure-Hisian Pacing
The pacing maneuvers described earlier rely on studying the respon to an induced perturbation(VOP or single premature beats)of a stable tachycardia.However,it is common to encounter SVTs that are difficult to induce, nonsustained,irregular,or repeatedly terminate during pacing protocols.Such circumstances may prevent diagnostic pacing maneuvers from being performed,or can limit interpretation of their results.
In a patient with documented SVT,but no preexcitation on their baline ECG,one of the goals at an electrophysiologic study is to determine the prence or abnce of a concealed AP.Sometimes programmed stimulation from the RV apex(or even catheter-induced PVCs)can quickly give a clue:if the atrial activation quence is clearly“eccentric”(either right or left free wall), then an AP is very likely to be prent.Further characterization of the conduction properties will be required to be more
certain,but with little effort,something of interest will have been discovered and further investigations can be directed accordingly.A CS catheter is commonly placed at the start of an electrophysiology study,so this works well for detecting nonptal left-sided APs,which account for around50%of all APs.6 The remainder of APs can be harder to detect by this method.With“standard”catheter positions there is not usually a catheter recording from sites all around the tricuspid annulus,so both ptal and right free wall APs,as well as retrograde AV nodal conduction,can show earliest atrial activation on the His catheter or at the proximal CS.Another pacing maneuver—para-Hisian pacing—can be uful in the circum-stances.7The basic concept is simple—pacing is performed next to the His bundle/proximal right bundle(HB-RB)and the respon is studied when the HB-RB and adjacent myocardium are captured,versus when local myocardium alone is captured.This is usually achieved by varying the pacing output and examining the surface QRS duration and,where possible,the stimulus-His(SH)interval.HB-RB capture will produce a narrow QRS complex and short SH interval, whereas loss of HB-RB capture will produce a wider QRS complex and lengthening of the SH interval.In the latter circumstance,the His bundle will only be activated after excitation has traveled through ventricular myocardium,penetrated the distal Purkinje network,and traveled retrogradely through the conduction system.Often,with HB-RB capture,the His potential is difficult to discern (particularly when a single catheter is ud for pacing and recording),either due to saturation
of the His channel by the pacing stimulus,or masking by the local ventricular potential.Appearance of a clear retrograde His potential,however,is usually an indication that HB-RB capture has been lost.
We can now consider the respon(timing and pattern of retrograde atrial activation)in the abnce and prence of an AP(Fig.3).If AV nodal conduction alone is prent then loss of HB-RB capture will cau a lengthening of the stimulus-atrial(SA)interval(becau excitation has a longer path to travel back to the atrium),without a change in the atrial activation quence.The change in SA interval should match the change in the SH interval,when this can be measured, and the His-atrial(HA)interval should be the same.If AP conduction alone is responsible for retrograde atrial VA conduction is prent through the AV node),then loss of HB-RB capture should have little or no effect on the SA interval and no change in the pattern of atrial activation.The SH interval will still lengthen when HB-RB capture is lost,thus the HA interval will shorten,since atrial timing depends only on conduction over the AP.When both AV nodal and AP conduction is prent then a more complex respon may be obtained,depending on the proximity of the AP to the pacing site and the conduction properties of the AP and the AV node/conduction system.Generally,a change in the retrograde atrial activation quence should be en,although this will depend on how much of the atrium is activated via the AP versus the
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Figure 3.Respons to para-Hisian pacing.In both panels,pacing is being performed from the distal poles of the His catheter(dHis).Thefirst beat in each panel captures the His bundle and local ventricular myocardium(narrow QRS complex),whereas the cond beat los His capture and only
stimulates ven-tricular myocardium.Panel A shows the respon when retrograde conduction is occurring over a concealed accessory pathway;with loss of His capture there is no change in the SA interval(the time from stimulus [dotted line]to earliest atrial activation[dashed line]), nor is there a change in the atrial activation quence. In this ca,a right para-Hisian pathway was prent, with earliest atrial activation on the HRA catheter.Panel B shows the respon after successful ablation of the accessory pathway,demonstrating the respon when purely AV nodal retrograde conduction is prent.With loss of His capture the SA interval extends by61ms since the stimulated wavefront must now travel through ventricular myocardium,penetrate the distal branches of the His-Purkinje system,then travel retrogradely through the AV node.Earliest atrial activation is tied between the proximal bipole of the His catheter(pHis) and the CS os(CS9–10).HRA=high right atrium;CS= coronary sinus;RVA=right ventricular apex;QRSd= QRS complex duration(ms);SA=time from stimulus to atrial electrogram(ms).
AV node,relative to the position of the recording sites in the where fusion is occurring in the atrium in each ca).Demonstrating this change is facilitated by having a catheter clo to the site of earliest retrograde atrial activation (i.e.some additional mapping in the atrium may be required).If the AP is clo enough to the pacing site and has sufficiently rapid conduction then the S
A interval should remain the same with loss of HB-RB capture,but there will be a change in the atrial activation quence.For example,if a posteroptal AP is prent then loss of HB-RB capture may lead to a similar SA interval on proximal poles of the CS catheter but some delay in atrial timing on the His catheter.
Pitfalls
(1)APs distant from the pacing site:Inter-pretation of the respon to para-Hisian pacing has been shown to be reliable for ptal and right free wall APs,but can be misleading for left lateral APs. In the latter ca,the pathway may be so far from the pacing site that the atria are entirely activated via the AV node whether the HB-RB is captured or not(assuming AV nodal conduction is sufficiently rapid).However,as previously mentioned,an eccentric atrial activation quence may be clearly apparent for left-sided APs simply with RV apical pacing or programmed stimulation.
(2)Slowly-conducting APs:Similarly,if conduction over an AP is slow relative to AV nodal conduction then the respon to para-Hisian pacing may fally suggest AV nodal conduction alone.7,8heel
(3)Lack of ventricular capture during HB-RB pacing:Occasionally,pure-Hisian pacing can occur,without capture of the local ventricular myocardium(sometimes called“rever para-Hisian paci
ng”).This phenomenon is usually transient,but can be associated with changes in the QRS duration and if not recognized can lead to a misinterpretation of the respon.If it is recognized,then the respon can be analyzed and can also give diagnostic information.9
(4)Prence of a fasciculoventricular con-nection:The rare pathways connect the prox-imal conduction system to basal ptal my-ocardium and,if prent,can prevent low output pacing from capturing myocardium alone;even with loss of direct His bundle capture,excitation can still reach the conduction system so little change in QRS duration may be en.10
(5)Loss of capture of the proximal left bundle branch alone:This can cau QRS widening without loss of retrograde conduction to the AV node and if not recognized could lead to misinterpretation of the respon.11
(6)Inadvertent atrial capture:This can give the impression that retrograde conduction is via the AV node when a ptal AP is prent,and it can also give the impression that retrograde conduction is via a ptal AP when no such AP is prent.Atrial capture is best identified by noting a change in atrial timing when adjusting the catheter basally(to deliberately capture the atrium and reduce the interval from the pacing stimulus to a ptal atrial electrogram)or apically (to deliberately lo captur
far and awaye of the atrium and prolong the interval from the pacing stimulus to a ptal atrial electrogram by more than
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