Role of extrastimulus site and tachycardia cycle length in inducibility of atrial preexcitation by premature ventricular stimulation during reciprocating tachycardia

Role of ExtrastimulusSite and Cyclelength in lnducibilityo Preexcitationby PrematureVentricular StimulationDuring Reciprocatin DAVID G. BENDlIT, MD, D. WOODROW BENS ANN DUNNIGAN, MD, CHARLES C. GORNICM, MD, ADRIAN ALMQUIST, MD, H. GARETH TOBLER,

Preexcitation of the atria during reciprocating tachycardia (RT) by a premature ventricular complex occurring when the His bundle is refractory provides direct evidence of the presence of accessory atrioventricular (AV) connection. The impact of ventricular stimulation site and RT cycle length on inducibility of atrial preexcitation was assessed in 38 patients with RT utilizing a single accessory AV connection (right free wall in 5 patients, left free wall in 21 and posterior septal/paraseptal in 12). Extrastimuli were inserted at right ventricular (RV) apical, left ventricular (LV) septal and LV free wall sites. lnducibility of and magnitude of atrial preexcitation increased as stimulation site approached accessory AV connection site. Thus, for RV free wall connections, RV extrastimuli preexcited the atria in 5 of 5 patients, LV septal in 1 of 5 and LV free wall

I

n the electrophysiologic evaluation of patients with paroxysmal reciprocating tachycardias (RT), a premature ventricular complex interpolated into the tachycardia cycle at a time when the His bundle is refractory advances (preexcites) the subsequent atria1 cycle. This event provides direct evidence of the presence of an accessory atrioventricular (AV) connection.1-4 FurFrom the Departments of Medicine, Pediatrics and Surgery, University of Minnesota Medical School, Minneapolis, Minnesota. This work was supported in part by fellowship grants from the North American Society of Pacing and Electrophysiology and Grant 5F32HL06593 from the National Institutes of Health, Bethesda, Maryland. Manuscript received march 24, 1987; revised manuscript received and accepted June 5, 1987. Address for reprints: David 6. Benditt, MD, University of Minnesota, Box 341 UMHC, Minneapolis, Minnesota 55455.

in 0 of 4. For LV free wall accessory connections, RV extrastimuli preexcited the atrla in only 3 of 218 patients, compared with 12 of 17 with LV septal and 20 of 21 with LV free wall stimulation. Additionally, the magnitude of atrial preexcitation achieved was related to RT cycle length, diminishing as cycle length shortened. Finally, in a few instances both RV apical and LV free wall extrastimuli failed to elicit preexcitation in patients with a posterior sept connection. Thus, ventricular pacing site and RT cycle length contribute importantly to induction of atrlal preexcitation by ventricular extrastimulation technique and should be considered during evaluation of patients with RT in whom accessory AV connections may be present. (Am J Cardiol 1987;60:811-81

ther, concordance of the retrograde atria1 activation sequence of the preexcited atria1 cycle with preceding tachycardia cycles implicates participation of the accessory AV connection in the reentry circuit. Initiation of appropriately timed ventricular premature complexes during tachycardia is usually undertaken as part of the electrophysiologic testing procedure by insertion of progressively premature extrastimuli scanning the cardiac cycle from the right ventricular (RV) apex. However, RV apical stimulation may be inadequate to elicit clear-cut%trial preexcitation in many patients with left-sided accessory AV connections.4 Also, achieving atria1 preexcitation may be difficult in the presence of rapid tachycardias5 Consequently, failure to induce atria1 preexcitation by RV apical extrastimuli may not unequivocally exclude an accessory AV connection. We assessed the impact

ATRIAL

812

PREEXCITATION

IN RECIPROCATING

TACHYCARDIA

of both stimulation site and tachycardia cycle length on inducibility of atria1 preexcitation by ventricular extrastimulus testing during electrophysiologic study.

Methods Patients: Patients presenting sequentially for electrophysiologic assessment of tachyarrhythmias were included in this study if they met the study criteria: (1) evidence for presence of orthodrotiic RT utilizing a single accessory AV connection; (2) less than 10 ms of beat-to-beat RT cycle length vaiiation during insertion of premature ventricular extrastimuli at any single site;

A- A-AHis A

A A-A

RA v

RV

r

v

1

y

A-A

r

y

v

y

V

1

A

A-A,+*

A

A-A’ c A-A ,

Iv

Y

= [A-AI-CA-A’)

S=StimuIus

Coincident

with

Upstroke

of His Potential

8. A-Amax A

A A-A

RA v

A-A~~~

v

v

A-A’
Y,,

w

A

A

,,’

A-A

V

Y

V

= IA-A)-(A-A’)

S = Earliest Premature Stimulus with His Potential Clearly Discernible FIGUPE 1. Atrial preexcitation measureinents used in this study. Top to botfom, surface electrocardiogram (ECG) and right atrial (RA), right ventricular (RV) and His bundle electrograms (HBE). A, RV extrastimulus (S) coincides with the upstroke of the His bundle potential (H). The subsequent atrial cy$le is advanced (preexcited) is insertby an interval designated AA-A”,,. e, the RV extrastimulus ed at the shortest coupling intervpl consistent with continued ability !o recognize that the His bundle pitential (generated by conduction in the anterograde dir&on) has not bee? altered in its timing relative to the tachycardia.‘The latter extrastimuius results in maximum achievable advancement (preexcitation) of the subsequent atrial cycle and the magnitude of advanc$ment is designated AAA’ Ill%.

(3) insertion of ventricular extrastimuli scanning the RT cycle at both RV [RV apical) and LV (LV apical or LV septal] sites; and (41 absence of cardioactive medications for a period of at least ? drug half-lives before study. Indications for electrophysiologic study were recurrent symptomatic (31 patients) or life-threatening (7 patients) tachycardias. Three patients had associated cardiac disease but had no clinically significant symptoms from these conditions: coronary artery disease in patient 21, cardiomyopathy in patient 34 and valvular heart disease in patient 36. Patients gave written informed consent before initiation of electrophysiologic studies. Clinical electrophysiologic procedures: The electrophysiologic techniques have been summarized previously6 and iriclude monitoring systemic arterial p?essure by means of percutaneous cannulation of either the right or left femoral artery (No. 7Fr cannula). In this study the arterial cannula was also used to advance a No. 6Fr multipolar electrode catheter retrogradely across the aortic valve. All patients received heparin, 5,000 to 10,000 U, during the course of invasive studies. Neither thrombotic nor hemorrhagic complications occurred. Electrical stimulation of the heart was performed using a stimulus amplitude of twice diastolic threshold and pulse width of 2 ms generated by a custom-designed, constant-current pulse generator with optically-isolated outputs. Electrograms were recorded at a paper speed of 100 mm/s (Electronics for Medicine VR-16 recorder, filter settings 50 to 1000 Hz for intracardiac electrograms). All electrical equipment was carefully grounded. Ventricular extrastimulus protocol: During RT, single premature ventricular complexes were induced (approximately every 8 to 10 cardiac cycles] by programmed ventrictilar extrastimuli at progressively shorter coupling intervals (lo-ms decrements) beginning at a coupling interval approximately equal to, RT cycle length, and, terminating with failure of ventricular capture. Further, a zone approximately 100 ms in duration centered on the initial deflection of the His bundle electrogram was scanned 2 to 5 additional times to improve chances of obtaining a reco?ding at a time when the His bundle electrogram was clear. Using fluoroscopy for confirmation of catheter position, ventricular extrastimuli were inserted at the RV apex in all 38 patients, and at base of the LV lateral free wall (LV free wall site) in 37, and on the midportion of the LV endocardial surface of the ventricular septum (LV septal site) in 32. The LV septal stimulation site was chosen to approximafe ventricular insertion of both left paraseptal and posteroseptal accessory AV connections.7 Definitions: Orthodromic RT was considered present if at least 2 of the following criteria were satisfied6s8: premature ventricular complexes iqduced during tachycardia (from at least 1 test site] at a time when the His bundle was refractory advanced [preexcited) the subsequent atria1 cycle with an atria1 activation sequence. identical to that of the tachycarditi; min-

October

1, 1987

imum ventriculoatrial interval more than 61 ms*; and ventriculoatrial interval increased after transient development of functional bundle branch block during tachycardiaaQ Atria2 p?eexcitation by a ventricular extrastimulus during tachycardia was considered present if atria1 activation at the electrode catheter site closest to the presumed accessory AV connection was reproducibly advanced at least 10 ms at a time when the His bundle was refractory [Fig. 1). Atria1 preexcitation with ventricular extrastimulus depolarization coincident with the His bundle electrogram was defined as the magnitude of atria1 cycle advancement observed at a time when onset of the induced premature ventricular complex coincided with the initial portion of the His bundle electrogram. Maximum atrial preexcitation was defined as the maximum atria1 cycle advancement achieved. Endocardial localization of accessory atrioventricular connections: In all patients atria1 activation sequences were recorded during RT by conventional electrode catheter techniques.lJr8J0 In the case of atrial insertion of left-sided accessory AV connections the approximate distance of the accessory AV connection from the coronary sinus OSwas determined using the interelectrode separation on the electrode catheter as an index of distance, and the site of minimum recorded ventriculoatrial interval as the point of reference for accessory AV connection location. Defining the location of the coronary sinus OSis imprecise. LV free wall accessory AV connections were defined as those in which the ventriculoatrial interval increased by at FIGURE

2.

THE AMERICAN

JOURNAL

OF CARDIOLOGY

Volume

SO

least 35 ms with development of functional left bundle branch block during RT,*l or those more than 2 cm from the coronary OS.Accessory connections crossing the atrioventricular groove in the distal third of the coronary sinus were considered to be lateral, while those crossing in the region of the middle third of the coronary sinus were considered posterolateral. Accessory AV connections in which ipsilateral functional bundle branch block resulted in prolongation of the ventriculoatrial interval less than 35 msll or those crossing the AV groove less than 2 cm from coronary sinus OSwere categorized as posterior septal/paraseptal. In patients with overt preexcitation, the ventricular insertion site of accessory connections was further confirmed by analysis of delta wave vectors during pacing-induced maximal preexcitation.lJ Multiple accessory atrioventricular connections: Patients, were excluded if any of the following observations suggesting the presence of more than 1 accessory AV connection were present? electrocardiographic evidence of more than 1 form of preexcited QRS morphologic pattern; occurrence during orthodromic RT of varying retrograde atria1 activation sequences; presence of RT with differing cycle lengths in the absence of change in QRS morphologic characteristics; and antidromic RT with an eccentric retrograde atria1 activation sequence. Findings in 3 patients were excluded based on 1 or more of these findings. Statistical analysis: The effect of altering ventricular extrastimulation site on inducibility of atria1 preexcitation and on the magnitude of atria1 preexcitation achieved was assessed by Student t test for intrapatient

Electrocardiograph-

ic and intracardiac recordings showing maximum atrial preexcitation achieved by extrastimuli at each of the 3 stimulation sites tested in a patient with a right anterolateral accessory atrioventricular (AV) connection (patient 4). Top to boffom, leads VI, I, II, Ill and aVR, and Intracardiac electrograms from the right atrium (RA), His bundle (HBE), right ventricular apex (RV), left ventricle (LV) and proximal and distal coronary sinus (PCS and DCS). Time line marklngs in all figures are at l-second intervals. A, an extrastimulus delivered just before inscription of the His potential (H) resulted in maximum atrial preexcitation (AA-A,,,) of 70 ms. The LV electrogram is f;om the LV septal surface. In panels /3 (LV septal site) and C (LV free wall site), maximal atrial preexcitation achieved by extrastimuli not obscuring the HIS electrogram was 0 ms.

A. RV Apex:

A A-A,,,

q 70 ms

“1 I II m aVR RA HBE RV LV PCS OCS

0.

LV Septal:

AA-A,,,=0

ms

C. LV Free-wall: “1

,”

A A-A,,,

=Q ITS I

2:

Patient %4

814

ATRIAL

PREEXCITATION

IN RECIPROCATING

TACHYCARDIA

paired samples.The relation between the magnitude His bundle electrogram preexcited the atria in al! of atria1 pieexcitation achieved and both RT cycle cases[range20to 40 ms).Comparablytimed LV septal length and‘the degreeto which local ventricular acti- and LV freewall extrastimuli were ineffectiire in 5 and vation was advancedby extrastimuli was evaluatedby 4 patients, respectively (i.e., preexcitation = 0 ms). In linear regressionanalysis.Data are presenteeasmean al? 21 LV free wall patients,,RV apical extrastimuli f standarddeviation. Statisticalsignificancelevel was c;oindidentwith the His bundle electrogram failed to induce atria1 preexcitation. LV septal extras@uli set at p IQ.05. were effective in 12of 17patientstested(preexcitation Results 23 f 23 ms, p x0.01 vs RV apical stimulation),while LV Patient subgroups: Thirty-eight patients (14 wom- free wall stimulation was effective in 20 of 21 patienti en, 24 men, dged 7 to 63 years] constituted the study (preexcitation42 f 22 ms, p
ms

"I

I It m aVR

HBE PCS DCS

B. LV S&al:

A A-A,,,

= 30 mu

C. LW Free-wall: A A-A,,,

v,

“I

I

I II

II m aVp

= 95 mu

induce atrial preexcitation (AAA max = 0 ms). Band C, extrastimuli inserted at the left ventricular (LV) septal and LV free wall sites induced maximum atrial preixcitaiion of ;O ms and 95 ms, respectively.

Ill aVR

LV

LV

RV

RV

RA

RA

HBE

HBE

PCS

PCS

DCS

DCS

FIGURE 3. Electrocardiographk and intracardiac recordings illustrating maximum atria! preexcitation achieved from each stlmulation site in a patient with a left free wall accessory atrioventricular (AV) connection (patient 12). Format is similar to that of Figure 2. A, a right ventricular (RV) apical extrastimulus delivered approximately 270 ms after the pre ceding RV electrogram failed to

Patient

l 12

TABLE

Pt

I

Clinical

Age olr) & sex

and

E~ectrophysiolog~c

Findin

Accessory AV Connection RT CL

Site

WV AA-AH,.

LV Septal AA-&

Right Free Wall Accessory 1 2 3 4 5

9M 29M 33M 31M 14M

225-235 300 235-240 330-340 320-340

A-L L P A-L A-L

20 30 40 40 35 Left Free

6 7 8 9 10 11 12 13 14 15 16 17 ia 19 20 21 22 23 24 25 26

19M 26F 40M 17M 48M 34M 17F 18M 24M 22F 40M 24F 40M 49F 59M 63M 60M 22M 14F 37M 13M

265-310 315330 400 350-360 320-345 380-410 320 260-330 250-270 340 315 360 275-290 290-315 305-330 480 340 300 250 350-360 300

L L L L L L A-L L P-L P-L P-L P-L P P-L P P-L P-L P-L L L L

Wall Accessory 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

14F 7F 25F 25F 46M 25M 24F 27M 21F 63M 20F 20F

330 260-300 290-330 290-330 260 260 280-340 305-320 440-470 330-355 275 280

PS PS PS PS PS PS Ps Ps PS PS PS PS

(left)

(left) (left) (left) (left)

0 0 0 0 0 0 0 0 0 40 IO 15

AA-A,,

AA-A”!,

Wall AA-A,,

Connections 30 30 40 70 70

SeptabParaseptal 27 28 29 30 31 32 33 34 35 36 37 38

AA-&s

LV Free

0” 0 0 0 0

0” 0* 0’ 0 50

0 0 ND 0 0

0 0 ND 0 0

65 10 35 ND ND ND IO ND 20 0 60 50 0 0 45 IO 25 60 0 0 IO

65 10 65 ND ND ND 30 ND 25 10 60 50 30 25 55 60 45 50 35 40 50

50 50 65 65 45 IO 40 IO 30 70 65 50 45 30 0” 30 60 10 25 50 30

90 50 100 100 a5 50 95 45 35 90 75 70 45 65 20 60 60 10 75 a0 40

20 25 0 ND 20 ND 0 15 75 50 10 35

60 70 20 No 60 ND 30 45 115 80 25 35

20 0 0 0 0 0 0 0 0 0 0 0

60 15 0 45 IO 20 0 25 45 35 IO 15

Connections 0 0 0 0 0 0 0 0 0 0 30 55 0 0 0 IO 0 0 0 0 0

Accessory 45 0 0 0 15 25 40 0 45 45 25 20

Connections

“Preexcitation of
and LV free wall extrastimuli 0 of 4 [WO) (Fig. 2). In patients with left-sided free wall accessory AV connections, RV apical extrastimuli were effective in only 3 of 21 patients (14%) (patients 16, 17 and 21), compared with 12 of 17 (71%) for LV septal stimulation and 20 of 21 (95%] for LV free wall stimulation [Fig. 3). In the 1 patient with a LV free wall connection in whom LV free wall stimulation failed to advance atria1 activation longer than 10 ms (patient 201, LV septal stimulation preexcited the atria by 45 ms. Thus, for LV free wall patients the combined yield for both LV stimulation sites was 21 of 21 (lOO%] (p
cal stimulation in 8 of 12 [66%j, by LV septal stimulation in 10 of 10 (lOO%] and by LV free wall stimulation in 9 of 12 (75%) (Fig. 4. In patients 29 and 30, RV stimulation failed to detect the presence of a posterior septal connection, while LV extrastimuli a vanced the atria1 cycle by up to 20 ms and 70 ms, respectively [Fig. 5). Maximum atrial preexcitation achieved: Figure 6 shows the relation between maximum atria1 preexcitation induced from each extrastimulus site and the proximity of the stimulation site to the accessory connection. In patients with RV free wall connections, RV extrastimuli resulted in maximal preexcitation of 30 to 70 ms. On the other hand, attempts to induce preexci-

818

ATRIAL

PREEXCITATION

IN RECIPROCATING

TACHYCARDIA

tation were nondiagnosticin 4 of 5 RV free wall patients with LV septalstimulation and in 3 of 4 RV free wall patientswith LV free wall stimulation. In patients with LV free wall connections,RV extrastimuli resulted in atria1preexcitationin only 3 of 21 (patients16, 17 and 21), with maximal values of 30, 55 and 10 ms, respectively. Maximal preexcitation with LV septal stimulation rangedfrom 10to 65ms in 17 of 21 patients tested(mean 42 f 16 ms, p
AV connectionwas measuredon the‘RV electrogram for patients with right-sided accessoryconnections, the LV electrogram(or the coronarysinus ventricular electrogram)for patients with left free wall accessory connections and at the base of the interventricular septum(ventricular componentof the His bundle electrogram) for patients with septal/paraseptalconnections. Similarly, the relation between RT cycle length and magnitude of preexcitation induced by ventricular stimulation at the site closestto the accessoryAV connectionis depicted in Figure 6. Findings from all 3 patient groups were combined, and although wide scatterof data points is evident, there appearsto be a direct relation between tachycardia cycle length and magnitude of atria1preexcitation induced.

Discussion This study assessedthe impact of both stimulation site and tachycardia rate on the successwith which atria1 preexcitation could be induced by ventricular stimulation during RT in patientswith known accessory AV connections.1-5J4-16 Our findings indicate that the ability to induce atria1preexcitation and the magnitude of atria1preexcitation achieved is directly dependent on both proximity of the extrastimulussite to

ms

“1

I P m aVR

B. LV SeqWAA-A,=70

ms

C. LV Free-wall:AA-A,,=15

ms

"1 I II m aVR

RA

Patient

+27

FIGURE 4. Effect of proximity of the extrastlmulus slte to the accessory connection on AA-A,, In a patient with a posteroseptal connectlon (patient 27). Rlght ventricular (RV) apical extrastlmuli coincident with the Initial deflection of the His bundle eiectrogram failed to induce atrlai preexcitation (AA-A,,,,,,= 0 ms). Both left ventrlcuiar (LV) septal and LV free wall stimulation sites resulted in atriai preexcltatlon ( AA-hnax = 70 ms and 15 ms, respectively).

October

s, 1987

‘HE

AMERICAN

JOURNAL

A. RV

A-A,,,sl

OF CAADiOLOGY

Volume

60

=O ms

FIGURE 6. Failure of right ventricular (RV) apical and left ventricular (LV) free wail extrastimuli to induce atriai preexcitation In a patient with a posteroseptai accessory atrioventricuiar (AV) connection (patient 29). Format of the figure is similar to that of Figure 2. in this patient demonstration of atriai preexcitatlon during reciprocating tachycardia (RT) by LV septai stimulation was critical to substantiate presence of the accessory connection and thereby suggest that the arrhythmia was not due to reentry within the atrioventricuiar node. The apparent difference in right atriai

B. LV Septal:

d A-A,,,

= 20 ms

C.

LV Free-wall:

4 A-Amax=

0 ms

(FM) activation time in panel C compared with that of panels A and B probably reflects a minor degree of catheter movement within the atrium.

the accessory AV connection and the tachycardia cycle length. Additionally, findings in this study indicate that in a few instances neither RV apical nor LV free wall extrastimuli are adequate to exclude presence of posterior septal/paraseptal accessory AV connections, and in these instances the LV septal site may be helpful in distinguishing the presence of these accessory connections. Identification of accessory atrioventricular connections: Both electrocardiographic and electrophysiologic observations may suggest the presence of accessory AV connections in patients presenting with paroxysmal RT. For instance, ventricular preexcitation during sinus rhythm, initiation of RT after acceleration of sinus rate, occurrence of QRS alternans during tachycardia, and prolongation of tachycardia cycle length or lengthening of the ventriculoatrial interval after development of functional bundle branch block during tachycardia have been reported to suggest participation of an accessory AV connection in tachycardia.8J1J7 However, apart from development of ventriculoatrial interval prolongation with functional bundle branch block during tachycardia, these observations do not unequivocally implicate participation of accessory connections in a reentry circuit. Similarly, recognition of an eccentric atria1 activation sequence during electrophysiologic study suggests, but alone does not conclusively substantiate, the presence of an accessory AV connection,lJ since an ectopic atria1 tachycardia may result in the same finding. Consequently, obtaining direct evidence for the presence of an accessory AV connection by utilization of ventricular extrastimulus testing to induce atria1 preexcitation is usually a

critical element in evaluating patients with paroxysmal tachycardias. Induction of atrial preexcitation by ventricular extrastimuli: The diagnostic value of observing atrial preexcitation after premature ventricular depolarizations closely preceding or coinciding with the His bun-

90

A-4 0-o C--O

80 70 t

RV Freewall Patients LV Freewall Patients Septal /Paraseptal Patients

-

gs50 2

40

$

30

3 60 20

I

10

0 t

___ RV Apex

___ LV Septal

Extrastimulus

___ LV Freewall

Site

FIGURE 6. influence of extrastimulus site-accessory connection proximity on maximum atriai preexcitation induced (AA-A,,,) for right ventricular (RV) free wail connections (filled diamonds, solid lines), left ventricular (LV) free wail connections (filled circles, solid Hnes), and septailparaseptal connections (unfilled circles, hafched hes). The magnitude of maximal preexcitation achieved increases as the stimulation site approaches the accessory connection site.

818

ATRIAL

PREEXCITATION

IN RECIPROCATING

TACHYCARDIA

dle electrogramwas initially noted in casestudiesdescribing the early development of electrode catheter techniquesfor evaluation of patientswith paroxysmal supraventriculartachycardias,14-I6 and its importance during clinical electrophysiologicstudieswas substantiated by Sellers et a1.4However, in the latter study RV apical stimulation often failed to elicit atria1preexcitation in patients with left-sided accessoryAV connections [4 successfulattemptsin 20patients,20%] unless the extrastimuli were inserted at a time when spontaneous functional left bundle branch block had occurred (5 of 5 successful).Presence of left bundle

A. Right Freewall 120r

Accessory

Connections

branch block presumablypermitted RV apical activation by the extrastimulus sufficient time to proceed transseptally and engagethe reentry circuit. Unfortunately, spontaneousdevelopment of functional left bundle branch block of sufficient duration to permit insertion of programmedventricular extrastimuli scanningthe cardiac cycle may not occurduring electrophysiologicstudy (e.g.,5 instancesin the 31patients reported by Sellers et a14).Furthermore, in instances where both normal QRS and left bundle branch block QRS tachycardiaare observed,the resulting ventriculoatrial interval changesmay in themselvesbe diagnostic [or in the caseof left paraseptalconnections,be highly suggestive)of a left-sided accessoryAV connection g-11 dur findings suggestthat in patients with septal/ paraseptal connections, the LV septal endocardial stimulation site is more effective than either RV apical A. Relation of AA-A&o

,5A-Alur

6. Left Freewall

RT Cycle Length

(me)

Accessory Connections b’\-*~X..~3~“-YI.,-1.~~

300 RT Cycle

400 Length

(ms)

0 RV Freewall Patients n TV Fr~e~sll Patients A SeptallPsraseptal Patients

SeptallParaseptal

Accessory

B. Relation of AA-A maxto RT Cycle Length

Connections

w-22.1

0

20

40 80 100 aA-A.,6:ha)

FIGURE 7. Relations between maximum atriai preexcitation induced and maximum local ventricular prematurity induced by extrastimuius testing (AV,-V2,,, ) for each stimulation site. Right ventricular (RV) apical stimulation site is indicated by circ/es, left ventricular (LV) septai stimulation by filled Wang/es and LV free wail stimulation by unfilled boxes.

A . 0 200 FIGURE AA-A,,,,,

III1’IIII’InII

300

400

RT Cycle Length (ms) 8. Relation of induced atriai preexcitation, (B) and reciprocating tachycardia (RT)

500 hA-AHb (A) and cycle length (CL).

October

or LV free wall sites for eliciting atria1 preexcitation. Indeed, in 2 patients proved to have posterior septal accessory AV connections (patients 29 and SO), RV apical stimulation failed to induce atria1 preexcitation, whereas at least one of the LV stimulation sites was successful in each case. Also, in patient 29, neither RV apical nor LV free wall extrastimuli were diagnostic [Fig. 5). In the latter instance, only the LV septal stimulation site substantiated the presence of an accessory AV connection (LV septal, maximum preexcitation = 20 ms). These observations are consistent with recent understanding of the anatomy of posteroseptal accessory connections.7 Specifically, theventricular attachment of the connection is typically located on the posterior inferior process of the left ventricle, with the atria1 attachment to the adjacent right atrium. Consequently, it should not be surprising that premature ventricular complexes of RV origin may sometimes fail to identify the presence of an accessory AV connection in a posteroseptal location. Recently, Weiss et all* noted that careful measurement of the ventriculoatrial interval associated with ventricular premature complexes may be useful for differentiating septal from left free wall accessory AV connections. Specifically, a ventriculoatrial interval of an induced RV extrasystole exceeding that of a typical tachycardia cycle by more than 15 ms tended to be associated with left free wall connections. However, our observations suggest that unequivocal induction of atria1 preexcitation at a time when the His electrogram is clearly undisturbed may be difficult to achieve in left free wall connections, limiting the value of this observation. Presumably, the long ventriculoatrial conduction time required of RV apical extrasystoles in order to induce atria1 preexcitation diminishes the magnitude of atria1 preexcitation achievable. In the 1 example provided by Weiss et al,l* the maximum achievable atria1 preexcitation for a left free wall connection was only 10 ms, a value that we consider to border on the precision of reliable measurement capability. This opinion appears to be supported by Miles et al,lg who similarly required atria1 preexcitation to be at least 10 ms in their study of preexcitation index. However, the specificity of the preexcitation index for identification of accessory AV connections is somewhat suspect in that the technique is both described and generally used without regard for clearcut identification of undisturbed anterograde His bundle depolarization.lg The method in the present study was specifically designed to capitalize on the unequivocal information obtained when it is clear that the His bundle is refractory to retrograde penetration by the premature ventricular complex.l-* Clinical implications: Attempting to elicit atria1 preexcitation by interpolation of ventricular extrasystales during RT is an important diagnostic tool for identification of accessory AV connections in patients with paroxysmal tachycardia, and the effectiveness of this technique is optimized by insertion of extrastimuli in close proximity to the accessory connection site. Therefore, if the presence of a suspected accessory AV connection cannot be substantiated by premature stimulation from the RV apex, insertion of premature

1, 1987

THE AMERICAN

JOURNAL

OF CARDIOLOGY

Volume

60

extrastimuli at other ventricular sites should be considered. The latter procedure would be particularly useful for distinguishing reentry within the AV node from reentry utilizing a concealed posterior septal accessory AV connection, and would be warranted in those circumstances in which unequivocal identification of an accessory connection would lead to consideration of a surgical or electrode catheter ablation procedure. Acknowledgment: We acknowledge the assistance provided by the staff of the cardiac catheterization laboratory and the many cardiology fellows who participated in these studies. We are grateful to Barry L.S. Detloff and Barbara Borgwardt for technical assistance and to Wendy Markuson for preparing the manuscript.

References 1. Gallagher JJ, Gilbert M, Svenson RH, Sealy WC, Kasell J, Wallace AG. Wolff-Parkinson-White syndrome: the problem, evaluation, and surgical correction. Circulation 1975;51:767-785. 2. Gallagher II, Pritchett ELC, Scaly WC, Kasell 1, Wallace AG. The preexcitotion svnhroies. Pron Cordiovosc-Dis 1978:2O:i85-327. 3. P&tow&y EN, &es WM, Heger JJ, Zipes DP. Preexcitotion syndromes. n/Iechonism and management. Med CJin North Am 1984;68:831-893. 4. Sellers TD Tr, Gallagher JJ, Cope GD, Tonkin AM, Wallace AG. Retrograde otriof preexcitotion following premature ventricular beats during reciprocoting tochycordio in the Wolff-Parkinson-White syndrome. Eur J Cordiol 1976;4:283-294. 5. Wellens HJJ. Electrical Stimulation of the Heart in the Study and Treatment of Tochycordias. Baltimore: University Park Press, 1971:14-22. 6. Benditt DG, Epstein ML, Arentzen Cg, Kriett JM, Klein GJ. Enhanced atrioventriculor conduction in patients without preexcitalion syndrome: relation to heart rote in paroxysmal reciprocating tochycardia. Circulation 1982:65:1474-1479. 7. Ghiraudon GM, Klein GJ, Sharma AD, Jones DL. Surgical treatment of Wolff-Parkinson-White syndrome: the epicardial approach. In: Benditt DG, Benson DW [r, eds. Cardiac Preexcitotion Syndromes. Origins, Evaluation and Treatment. Boston: Martinus-Nijhoff, 1986:535-541. 8. Benditt DG, Prichett ELC, Smith WM, Gallagher JJ. VentricuJootrioJ intervals: diagnostic use in paroxysmal suproventriculor lochycordio. Ann Intern Med 1979;91:161-166. 9. Pritchett ELC, Tonkin AM, Dugan FA, Wallace AG, Gallagher JJ, VentricuJootrial conduction time during reciprocating tochycardio with intermittent bundle-branch block in Wolff-Parkinson-White syndrome. Br Heart [ 1976; 38:1058-1064. 10. Gallagher JJ, Pritchett ELC, Benditt DG, Tonkin AM, Campbell RWF, Duean FA. Bashore TM. Wallace AG. New catheter techniaues for onolvsis of the”sequence of retrograde otriol octivotion in mon. Eur r C&d&J 1977;b?-14. 11. Kerr CR, Gallagher 11, German LD. Changes in ventriculo-otriol intervals with bundle-branch bJ&k aberration during reciprocating tochycordia in patients with accessory otrio-ventricular pathways. Circulation 1982;66:196201. 12. Gallagher JJ, Scaly WC, Wallace AG, Kasell J. CorreJotion between cotheter electrophysiologicol studies and findings on mopping of ventricular excitation in the WPW syndrome. In: WeJJens HI/, Lie KI, fonse MI, eds. The Conduction System of the Heart. The Netherlands: H.E. Stenfert Kroese BV, 1976;588-61’2. 13. Tobler HG, Anderson RW, Ring WS, Benditt DG. Techniques for introoperative mopping of tochyorrhythmias in preexcitotion syndromes. In: Ref. 7:507-526. 14. Zipes DP, Dejoseph RL, Rothbaum DA. Unusual properties of accessory pathways. Circulation 1974;49:1200-1211. 15. Neuss H, Schlepper M, Thormann J, Analysis of re-entry mechanisms in three patients with concealed Wolff-Parkinson-White syndrome. Circulation 1975;51:75-81. 16. Tonkin AM, Gallagher IJ, Svenson RH, Wallace AG, Sealy WC. Anterograde block in accessory pathways with retrograde conduction in reciprocoting tochycordia. Eur r Cardiol 1975;3:143-152. 17. Morady F. The spectrum of tochyorrhythmios in preexcitation syndromes. In: Ref. 7:119-139. 18. Weiss I. Brueada P. Rev D. Bar FWHM. Wellens HIT. Localization of the accessory pathway in the Wolff-Parkinson-White syndrome from the ientriculootriol conduction time of right ventricular apical extrosystoles. PACE 1983;6:260-267. 19. Miles WM, Yee R, Klein GJ, Zipes DP, Prystowsky EN. The preexcitotion index: an aid in determining the mechanism of suproventriculor tachycardio and localizing accessory pathways. Circulation 1986;74:493-500. ~ , ,

-

. I

I I