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Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian AV block
Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian block
AV
The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:l supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:l AV conduction, but despite prompt termination of tachycardia in both cases, 2:l AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block-that is, the “final common pathway” of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node. (AM HEART J 107:431, 1984.)
Angas W. F. Hamer, M.D., Carol A. Zaher, M.D., Thomas William J. Mandel, M.D. Los Angeles, Calif.
Reentry within the region of the atrioventricular (AV) node has been described as a regular tachycardia with almost simultaneous activation of the atria and ventricles.* The occurrence of AV block in association with regular atrial activity favors the
diagnosis of an atrial rather than an AV nodal arrhythmia. Nonetheless, a few examples of arrhythmias felt to represent AV node reentry, with either retrograde
block to the atria2m4 or anterograde
block
to the ventricles,3, 5-7have been described. The site of anterograde
block
to the ventricles
haa generally
been the His bundle
or bundle branches,3.5*7 and block appears to be very uncommon.3~7
supra-Hisian Consequently, little if any information is available concerning the effects of drugs on AV node reentry with supra-Hisian block. The purpose of this com-
munication, patients
From Funded Center, Received
then, is to describe the features of two with
the Division
supraventricular
of Cardiology,
tachycardia
Cedars-Sinai
in part by Los Angeles,
E.C.H.O. Calif.
Research
for publication
July
13, 1983;
Medical Fund
accepted
Reprint requests: William J. Mandel, M.D., Cedars-Sinai Medical Center, 8700 Beverly 90048.
and
due to AV node reentry and intermittent Hisian
2:l supraAV block, in order to add to the documenta-
tion of this arrhythmia and in addition to describe the effects of verapamil, a calcium channel blocking drug with particular affinity for the AV node, on this arrhythmia. METHODS Patients. Two patients were studied, one female and one male, aged 27 and 42 years, respectively. Neither had evidence for cardiac disease apart from his or her arrhythmias. Their resting ECGs were normal. One patient has been included in a previous report from this laboratory, but without a detailed analysis of these issues. Electrophysiologic studies. With each patient’s informed consent, electrophysiologic studies were performed in a fasting state, after premeditation with 100 mg of secobarbital. The study protocol used conventional methodology, as previously described.8 All cardioactive drugs were stopped for a minimum of 5 half-lives prior to these studies. RESULTS
Center.
of Cedars-Sinai Aug.
(SVT)
Peter, M.D.,
Medical
17, 1983.
Division of Cardiology, Blvd., Los Angeles, CA
Some of the measured
electrophysiologic
ables before and after the administration pamil are given in Table I. Included
pertaining node
to the sinus cycle length,
refractory
periods,
AV
node
variof veraare data
atrial and AV Wenckebach 431
432
Hamer
et al.
American
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March, 1984 Heart Journal
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Fig. 1. This panel shows nonsustained high right atria1 tachycardia initiated in patient No. 1. The panel is arranged with surface ECG leads I, aVr, and V, above intracardiac recordings from the high right atrium (HRA), His bundle region (HBE), and from the distal coronary sinus (CS). The patient is in sinus rhythm (cycle length = 680 msec), and a premature right atria1 stimulus (S& at a coupling interval of 250 msec evokes three atria1 tachycardia complexes (cycle length = 430 to 530 msec) before sinus rhythm resumes. The atria1 activation sequence (measured in milliseconds from the dotted vertical line through the His deflection to the most rapid atria1 deflection [A]) of the atria1 tachycardia is similar to, but not identical to that in sinus rhythm, and the HRA polarity differs. A = atria1 electrocardiogram; H = His deflection; V = ventricular electrogram. Time lines are 1000 msec apart.
Table
I. Electrophysiologic
variables
before and after verapamil
No.
Sinus cycle length
Atria1 * ERP
AV node’ ERP
c
600
180
<210
380
320
520 935 800
270 290 260
300 <295 350
470 470 400
400 420 360
AV node* FRP
A V node Wenckebach
1
v 2:
ERP = effective refractory period, *Measured at a drive cycle length tSingle atria1 echoes only.
FRP = functional of 550 msec.
refractory
period;
SVT
threshold, the echo zones denoting the atrial coupling intervals for single atrial echo or tachycardia initiation, and variables describing retrograde ventriculoatrial (VA) conduction and refractoriness. Inducible arrhythmias. Patient No. 1 had two distinct arrhythmias: (1) nonsustained atria1 tachycardia, cycle length 430 to 530 msec, induced by single right atria1 premature stimuli during sinus rhythm (Fig. 1) and also during right atrial pacing. The sequence of atria1 activation was similar to, but not exactly the same as that for sinus rhythm, suggesting an origin in the high right atrium but not necessarily in the region of the sinus node. (2) Sustained SVT, with either 1:l conduction (Fig. 2) or 2:l AV block (Fig. 3), the latter being supraHisian. The atria1 activation sequence during this arrhythmia was low (septal) right atrium preceding simultaneous activation of the high right atrium and distal coronary sinus. This activation sequence was the same as that seen during right ventricular pacing.
= supraventricular
SVT echo zone 1:l AV 210-260 2:l AV 270-320 300-380t 370-380t 295-320
tachycardia,
Paced VA*
VA block
VA ERP
VA FRP
90
260
<260
360
165
290 280
<260 300
340
c = coronary;
v = venous.
The atrial cycle length during SVT was constant (250 to 270 msec), regardless of the presence or absence of AV block. SVT with 1:l AV conduction was initiated on six occasions by single premature right atrial stimuli during sinus rhythm and during atrial pacing, and by rapid right atrial pacing. However, only between two and seven atrial echo beats were inducible from the coronary sinus. SVT with 2:l AV block was only initiated by right atrial premature stimuli a total of 13 times. Neither form of tachycardia was initiated by right ventricular pacing. At a pacing cycle length of 550 msec, the atrial echo zone for SVT with 1:l conduction was between 270 and 290 msec (H,H, = 415 to 430 msec), and the echo zone for SVT with 21 AV block was between 210 and 260 msec (H,H, = 400 to 410 msec), the inner limit being the atrial functional refractory period (Fig. 4). Dual AV node pathways could not be identified, however. Single ventricular premature stimuli scanning diastole during SVT with 1:l AV conduction neither
Volume Number
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Verapamil
in AV reentry
SVT
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block
433
Fig. 2. This panel showsthe initiation of SVT with 19 AV conduction in patient No. I. The panel is arranged similar to Fig. 1, with addition of a ladder diagram below, suggestingthe mechanismfor the observed events. The patient is in sinusrhythm (cycle length = 635 msec)when a premature right atrial stimulus (S& at a coupling interval of 265 msecinitiates reentry tachycardia with an H,H, interval of 425 msec. The atria1 and ventricular cycle lengths stabilize at 260 to 265 msec, and atrial and ventricular activation appear simultaneous, consistent with a diagnosis of AV nodal reentry. The septal atria1 electrogram, buried between the His deflection (H) and the QRS, precedesatrial activation in the HRA and distal CS.
3. This panel showsinitiation of SVT with variable AV block in patient No. 1. The panel is arranged similar to those in Figs. 1 and 2. The patient is in sinusrhythm (cycle length 615 msec)when a right atrial premature stimulus (SJ at a coupling interval of 225 msecinitiates a tachycardia after an H,H, interval of 405 msec.The atria1 activation sequenceis identical to that in Fig. 2, with an atrial cycle length of 245 to 270 msec.The ventricular response,however, initially showeda Wenckebach sequenceuntil 2:l AV block was establishedproximal to the His bundle. This arrhythmia was diagnosedas AV node reentry with variable and later 2:l supra-Hisian AV block. Fig.
advanced atria1 activity
nor terminated
mia. Spontaneous premature ventricular
the arrhythcomplexes
during SVT with 2:l AV block had a variable effect,, depending on their prematurity: no effect, conversion of 2:l AV block to 1:l AV conduction, or advancement of atria1 activation with termination of the arrhythmia (Fig. 5). Following conversion of SVT with 2:l AV block to 1:l AV conduction by a premature ventricular complex, transient left or right bundle branch block aberration was frequently seen, for up to 12 complexes. Both forms of SVT could be terminated by bursts of rapid right atrial pacing, but during the initial second of pacing the
timing of all atrial recording sites could be advanced without disturbing the tachycardia. Patient No. 2 also had two distinct inducible arrhythmias: (1) atrial flutter, cycle length 190 to 225 msec induced by rapid right ventricular pacing with 1:l VA conduction and alao by closely coupled right atrial premature stimuli (Fig. 6); (2) SVT with 1:l conduction (Fig. 7), and on one occasion 2:l supra-Hisian AV block (Fig. 8). The atrial cycle length was usually between 300 and 310 msec regardless of the state of the AV conduction, and the atrial activation sequence was low (septal) right atrium followed by distal coronary sinus, and fInally
434
Hamer et al.
American
(A) I
SI
550
Sl250
RA PACING
.n.
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A SVT 2~1 AV BLOCK
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March, 1984 Heart Journal
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Fig. 4. This panel shows the initiation of SVT with 21 AV block and 1:l AV conduction by the extrastimulus technique in the right atrium. The panels are arranged as in the previous figures. The left panel (A) shows that following the last of eight right atria1 (RA) stimuli (SJ at a cycle length of 550 msec, a premature stimulus (S,, at a coupling interval of 250 msec intiates SVT with 2:l AV block with an atria1 cycle length that initially varies from 230 to 330 msec. The ventriculoatrial relationship remains fixed, however (His [H-A] in the HRA = 55 msec). The right panel (I31 shows that a slightly longer coupling interval for S, (285 msec) initiates SVT with 1: 1 conduction, with an atria1 cycle length varying from 245 to 320 msec. Again, ventriculoatrial relationships remain fixed (H-A = 55 msec). The H,H, interval for initiation of SVT with 2:l AV block was shorter (400 msec) than for SVT with 1:l AV conduction (430 msec) .
the lateral right atrium. This was similar to that seen with right ventricular pacing. SVT with 1:l AV conduction was initiated eight times by rapid right atria1 pacing and by single premature atrial stimuli in the right atrium and coronary sinus, but not by right ventricular pacing. At a right atrial pacing cycle length of 550 msec, the atrial echo zone was between 290 and 320 msec, the inner limit being the atria1 functional refractory period. Dual AV nodal pathways were not evident. SVT with 2:l AV block was only initiated once, following a period of rapid right atrial pacing during which AV node Wenckebach block became 21 AV block, continuing as the pacing was turned off and the tachycardia ensued (Fig. 8). Similar to patient No. 1, SVT with 2:l AV block was converted to 1:l AV conduction by a spontaneous premature ventricular complex. SVT with 1:l AV conduction was readily terminated by rapid coronary sinus or right atria1 pacing. Effects of verapamil on sustained supraventricular tachycardia. Ten milligrams of intravenous verapa-
mil was given to both patients during sustained SVT with 1:l AV conduction. SVT was terminated following an atria1 complex in both circumstances, 50 and 81 seconds, respectively, after beginning a 30second infusion of verapamil. Prior to conversion, patient No. 1 showed an increase in the SVT cycle length from 260 msec to alternating short and long R-R cycles, varying from 280 to 350 msec just prior to termination (Fig. 9). Patient No. 2 also showed
varying cycle lengths just prior to termination, with an increase from 300 to between 310 and 360 msec after verapamil. Verapamil did not induce 2:l AV block in either patient. Following termination of SVT by verapamil, single atria1 echo beats were all that could be induced by pacing in either patient, with increases in the outer limit of the atria1 echo zones as well as increases in the inner limit, associated with an increase in AV node refractoriness. The relative timing of ventricular and atrial complexes remained fixed, however, despite the longer atrial echo cycle length (Fig. 10). Retrograde conduction times and refractoriness were assessed after verapamil only in patient No. 2, and although the VA effective refractory period appeared to have prolonged, functional properties of retrograde conduction such as the VA conduction time and the ventricular pacing cycle length for VA block remained essentially unchanged, with a 25 msec increase in VA conduction times both before and after verapamil over the range of ventricular pacing cycle lengths. Findings supportive with intermittent 2:l
of diagnosis supra-Hisian
of AV node reentry block. Since both
patients had clear evidence for atrial arrhythmias as well as sustained SVT, low atrial reentry tachycardia with a prolonged PR interval must be considered as a differential diagnosis for their SVT. Also, it is necessary to closely examine the evidence for the site of intermittent 2:l block as being located above the His-Purkinje system. Using conventional rea-
Volume Number
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Verapamil
(A) I-
+---1000mc -I * L -
in AV reentry SVT with supra-Hisian
block
435
(B) SNUS
RtiW
5. A and B, These panelsshowthe variable effects of spontaneouspremature ventricular complexes during SVT with 21 AV block in patient No. 1. The panelsare arranged asin previous figures.The top left panel (A) showsa spontaneouspremature ventricular complex (PVC*), occurring 180 msec after the previous QRS, transiently converting 2:l AV block to 3:l block before 21 AV block resumes.The atria1 cycle length remains essentially unchanged (255 to 260 msec). The top right panel (B) showsthat a spontaneousPVC (*), 280msecafter a QRS, was ableto advance atrial activation (260 - 220msec)ahead of the anterograde reentry wave front and the reentry cycle sufficiently to lead to anterograde AV nodal block and termination of the tachycardia shortly after. C, This panel showsthat an even later premature ventricular complex (*) 325msecafter a QRS doesnot alter the atria1 cycle length during the tachycardia, but following the transient conversion of 2:l to 3:l AV block by retrograde penetration of the lower AV node, the electrophysiologic properties of the lower AV node are altered sufficiently to allow 1:l AV conduction thereafter. Right bundle branch block aberration is seenin the secondventricular complex after the premature ventricular complex, possibly due to the relatively long preceding R-R interval. Fig.
soning, one would attempt to differentiate atrial reentry from AV node reentry on the basis of a reliance on critical atrial coupling intervals for initiation in the former, rather than critical A,H, intervals in the latter5 However, this differentiation was not possible prior to initiation verapamil, as in both patients the atrial echo zones extended from the atrial functional refractory periods outwards. After verapamil, however, echo zones were at longer atrial coupling intervals, and most importantly, the inner aspect was limited by AV node refractoriness rather
than by atria1 refractoriness or a critical atrial coupling level. This favored AV node reentry as the diagnosis. AV node reentry was also favored by the fact that the timing of all atrial recording sites (including the septal site in the His bundle recording) could be advanced by right atrial pacing without effect on the tachycardia cycle length. In addition to the above, perhaps the single most convincing feature of these studies suggesting a diagnosis of AV node reentry for the sustained SVT was the lack of effect of cycle length changes on VA
March.1984 436
Hamer
et al.
American
Heart
Journal
HBE
6. This panel showsinitiation of atrial flutter (cycle length 190to 225msec)with variable AV block in patient No. 2. Atrial flutter wasinitiated by a premature stimulus (SJ at a coupling interval of 225 msec following eight pacedstimuli (Sb at a cycle length of 550 msecdelivered to the distal coronary sinus.The panel is arranged similarly to the previous figures except the right atria1 recordings were taken from the lateral right atrium rather than the high right atrium and there is no distal coronary sinusrecording. In the right atrium, the lower atria1 recording (A in HBE) just precedesthe activation in the lateral RA, as measuredfrom the vertical dotted line. Fig.
VI Lalerd RA Distd cs I-BE 7. This panel showsthe initiation of SVT with 1:l AV conduction by rapid atria1 (RA) pacing (S) at a cycle length of 300 msecin patient No. 2. The panel is arranged asin Fig. 6, with the addition of a distal CS recording. The atria1 cycle length during the initial few cycles of the supraventricular tachycardia varied from 240 to 425 msec,and atria1 activation (A) in the lateral RA followed that in the distal CS, as indicated by the atria1 activation times measuredfrom the vertical dotted line passingthrough the His deflection. (His [H-AcJ = 105 msec,H-A,,,,* = 125 msec.)Septal RA activation could not be discerned. The ventriculoatrial relationship suggested AV nodal reentry, and despite changes in atria1 and ventricular cycle lengths, the VA relationship remained fixed. Fig.
relationships during SVT (Figs. 4, 7, and lo), a feature previously noted by Ahktars Verapamil, in
particular, caused changes in cycle length by altering the AH intervals during SVT (Fig. 9) without changing the relationship between the subsequent ventricular and atrial depolarizations (fixed HA intervals). Cycle length alternation is a common finding in cases of AV nodal reentry following verapamil administration. Verapamil has not been reported to commonly cause such obvious changes in atrial reentry tachycardia, and it is almost inconceivable that changes in atrial cycle length would be exactly matched by secondary changes in antero-
grade AV node conduction times to allow VA relationships coincidentally to remain unchanged. Resolution of the second issue, addressing the site of intermittent AV block, depends solely on the findings of a supra-Hisian Wenckebach sequence without changes in the HV interval prior to development of SVT with 2:l AV block during the first few seconds of tachycardia in patient No. 1 (Fig. 3), and during atrial pacing prior to tachycardia in patient No. 2 (Fig. 8). During established 2:l AV block in SVT, absence of a QRS was associated with the concurrent absence of a His deflection, also suggesting a supra-Hisian site for the block. The presence of
Volume Number
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Verapamil
in AV reentry SVT with supra-Hisian
block
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Fig. 8. This figure showsinitiation of SVT with 2:l AV block by right atria1 pacing (S,) with a cycle length of 300 msec in patient No. 2. The panel is arranged as for Fig. 7, with the addition of a ladder diagram below, suggestinga possiblemechanismfor the observedfindings. The first atria1 paced complex is shownto the left of the panel, and subsequentlyan AV Wenckebach pattern is established,followed by 2:l AV block proximal to the His bundle, An aberrant QRS is seenon one occasion(*). Upon termination of the pacing, tachycardia ensues,with an atrial cycle length of 300to 315 msec,with 2:l supra-Hisian AV block. Although the site of AV block during pacing is presumedto be in the AV node, whether it is in the upper or lower AV node, or both during pacing could not be determined. Hencethe ladder diagram is only one of several possibleexplanations. After pacing, however, the supra-Hisian block must be below the AV nodal reentry circuit.
t-1 98c+
SVT
AVF+W&+
SVT
+ 5os8c
I
POSt
VERAPAhL
SINUS
RHYTHM
m
Fig. 9. This panel showsthe effects of 10mg of intravenous verapamil on SVT with 1:l AV conduction in patient No. 1. The panel is arranged as in Fig. 1. Prior to verapamil (left hand side), the atria1 and ventricular cycle lengths were 260 msec.Fifty secondsafter beginning a 30-secondinjection of verapamil, tachycardia terminated following an atria1 complex (A), presumably by anterogradeAV node block. Just prior to termination, cycle length alternation (280 to 350 msec)in atria1 A-A intervals were matched by ventricular R-R intervals, suggestinga fixed ventriculoatrial relationship. This behavior was consistent with AV nodal reentry, and helped exclude a low atrial tachycardia with a long PR interval as an alternative diagnosis.
a Wenckebacb sequence alone, however, is not pathognomonic for this level of block, since it has been demonstrated to occur preceding the onset of 2:l infra-Hisian block during AV node reentry.3v7 Despite the presumption that the origin of the site of block is in the lower AV node proximal to the His-Purkinje system, the site of block appeared relatively insensitive to verapamil. The conversion of SVT with 23 block to 1:l AV conduction typically
followed a spontaneous premature ventricular complex (Fig. 5). The presumed mechanism for this was that the premature ventricular complex was associated with concealed retrograde penetration of the lower AV node, resulting in anterograde block of the next tachycardia reentry wavefront, and this resulted in readjustment of the conduction properties of the distal AV node to accept continuous 1:l AV conduction during subsequent reentry cycles.
March,
438
Hamer et al.
American
PRE VERAPAMIL
Heart
1984 Journal
POST VERAPAMIL
I AVF VI Lateral RA Distal CS HBE Fig. 10. This figure showssingle atria1 echoesinduced before and after verapamil in patient No. 2. The panel is arranged asin Fig. 7. Following a period of right atria1 pacing (S,) at a cycle length of 550msec,a premature stimulus (SJ at the samecoupling interval of 320 msecinducesa singleatria1 echo (Ae) in each case.Before verapamil (left-hand panel), the atria1 coupling interval of the echo measuredin the coronary sinus (A,-AeCS) was 285 msec.Following verapamil, the sameatria1 coupling interval had lengthened to 350 msec.Despite this, the atria1 activation sequence(measuredfrom the vertical dotted line through to the His deflection) remained fixed and identical (Hz-AeCS = 105 msec,H,-AeLatRA = 125 msec). This suggestedthe predominant effect of verapamil was on anterograde AV nodal conduction proximal to the point of retrograde reentry in the AV node, without significant effects on the retrograde limits of the reentry circuit or the final common pathway distal to the circuit.
DISCUSSION
AV node and the His bundle has been demonstrated in an isolated rabbit heart preparation by Janse et al.‘O Clinical evidence for this arrhythmia may have been present in the case study of Zeft et aL6 although analysis of the surface ECGs did not allow differentiation between supra- and infra-Hisian AV block during AV node reentry tachycardia. However, it was not until the advent of His bundle recordings and programmed stimulation techniques designed to initiate AV node reentry in susceptible individuals that demonstrations of AV node reentry with infraHis block appeared,5 and subsequently reentry with supra-Hisian block.3 Overall, AV nodal reentry with supra-Hisian block appears to be an unusual form of this arrhythmia, occurring in 2 out of 67 (3%) consecutive patients referred to Wellens et al3 for an electrophysiologic study. Several of the features of the tachycardias we have described concur with those noted by Wellens et al.,3 namely (1) 2:l AV block frequently occurred at the time of onset of SVT; (2) the echo zone for SVT with 1:l AV conduction was at longer A,A, coupling intervals than for SVT with 2:l AV conduction; (3) 2:l AV block was converted to 1:l AV conduction by premature ventricular complexes (one premature ventricuAV node
reentry
with supra-Hisian
block.
reentry with block between the reentry circuit
lar complex in our patients, two premature ventricular complexes in those of Wellens et al.), and frequently was followed by a brief period of aberrant intraventricular conduction during SVT; and (4) p waves during SVT, best seen during periods of AV block, were “flat” in lead I, negative in aVr, and positive in V,. Our findings varied in relatively minor ways, however, in that tachycardia in patient No. 1 could be terminated by one ventricular premature complex, not two (as Wellens et al. found), and we did not observe a spontaneous rate-related or pacinginduced transition from 1:l to 2:l AV conduction. We did not find the atria1 rate during tachycardia significantly different between periods of 1:l and 2:l AV conduction either. Another of our findings not specifically mentioned for a case of AV node reentry with supra-Hisian block by Wellens et al. but noted by Castellanos et a1.,7 was the development of Wenckebach periodicity prior to 2:l AV block during tachycardia. Effects of verapamil. Although many of our observations appear merely to support those of others, we believe the effects of verapamil on this arrhythmia provide some new and interesting insights into AV node function during AV node reentry tachycardia. Although 2:l AV node block could be initiated by certain forms of atria1 pacing prior to verapamil
Volume Number
107 3
Verapamil
administration, a bolus injection of 10 mg of verapamil was able to lengthen conduction time in and eventually block the anterograde AV node conduction pathway used for AV node reentry, without initiating 2:l block distal to the reentry pathway. This was despite the fact that cycle length changes after verapamil showed short cycles within 20 msec of baseline. The fixed VA relationship maintained after verapamil also suggested that either verapamil had no effect on both the final common pathway in the AV node and the retrograde reentry pathway, or less likely, that it prolonged conduction time in each to an equal extent. We favor a hypothesis that the site of supra-Hisian block distal to the reentry pathway is in the AV node but is relatively insensitive to verapamil. As such, these findings would support some of the hypothetical mechanisms of verapamil’s action on anterograde conduction through the AV node that we have proposed elsewhere, wherein verapamil frequently affects anterograde conduction in the upper part of the AV node but not in the lower final common pathway.* Data from both these patients would also support the contention that verapamil may have no effect on retrograde conduction to the atria during supraventricular tachycardia, a finding consistent with many previous studies, and evidence from patient No. 2 suggested that verapamil had no effect on retrograde conduction during ventricular pacing. The latter finding, however, does not mean that verapamil cannot have a differential effect on anterograde and retrograde conduction in the final common pathway of the AV node, since previous data from our laboratory8 have shown that effects of verapamil on retrograde conduction and refractoriness during ventricular pacing can be present despite lack of such an effect during SVT. In five out of nine patients with unchanged retrograde conduction times during SVT prior to anterograde block and termination of the SVT by verapamil, the cycle length for retrograde AV nodal block during subsequent ventricular pacing was similar to or longer than the SVT cycle length. This suggested effects of verapamil on retrograde (but not anterograde) conduction and refractoriness through the final common pathway of the AV node, below the site of reentry. Clinical significance. Wellens and Farre” have suggested that AV block during AV nodal reentry is less likely to occur clinically than in the catheter laboratory. Part of this may be due to the fact that AV block usually occurs at the time of onset of SVT, and subsequently the arrhythmia may not be clinically recognized because of the relatively slow ventricular
in AV reentry
SVT
with supra-ffisian
block
439
rate or it is only noted when it spontaneously regains 1:l AV conduction. In addition, the arrhythmia may be mistakenly diagnosed as an atria1 tachycardia in many instances, despite atypical timing of the p waves.” The bolus injection of a relatively standard dose of verapamil did not appear to precipitate AV block during SVT in these patients. This was due to a lack of effect on the final common pathway in the AV node, and although spontaneous rate-related AV block has been noted by Wellens et al3 in these patients, slowing of the rate of AV nodal reentry tachycardia by verapamil may prevent this also. Thus it follows that if verapamil is administered during a regular SVT of unknown mechanism, the occurrence of AV block would favor a diagnosis of an atrial rather than an AV node arrhythmia. The authors express their gratitude assistance, to Lance Laforteza for Edwards and Rosa Goldsmith.
to Joye Nunn for editorial graphics, and to Patricia
REFERENCES
1. Wu D, Denes P, Amat-Y-Leon F, Wyndham C, Dhingra R, Rosen KM: Clinical electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol 41:1045, 1978. 2. Bauernfeind RA, Wu D, Denes P, Rosen KM: Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia. Am J Cardiol 42:499, 1978. 3. Wellens HJJ, Wesdorp JC, Duren DR, Lie KI: Second degree block during reciprocal atroventricular nodal tachycardia. Circulation 53:595, 1976. 4. Coumel P, Motte G, Gourgon R, Fabiato A, Slama R, Bouvrain Y: Les tachycardies supraventriculaires par rhythm reciproque en deliors du syndrome de Wolff Parkinson White. Arch Ma1 Coeur 63:35, 1970. 5. Goldreyer BN, Damato AN: The essential role of atrioventricular conduction delay in the initiation of paroxysmal supraventricular tachycardia. Circulation 43:679, 1971. 6. Zeft HS, McGowan RL: Termination of paroxysmal junctional tachycardia by right ventricular stimulation. Circulation 40:919, 1969. 7. Castellanos A, Zaman L, Rozanski JJ, Garcia N, Myerburg RJ: Conduction delay and block distal to the A-V nodal reentry circuit: Relationship of electrophysiologic manifestations to underlying mechanisms (abstr). Circulation 66:II268, 1982. A, Peter T, Mandel W: Atrioventricular node reentry. 8. Hamer Intravenous verapamil as a method of defining multiple electrophysiological types. AM HEART J 105:629, 1983. 9. Ahktar M: Paroxysmal atrioventricular nodal reentrant tachycardia. In Narula OS, editor: Cardiac arrhvthmias. Electrophysiology, diagnosis and management. Baltimore, 1979. The Williams & Wilkins Co. n 294. 10. Jan& MJ, van Capelle FJL, Gre;‘d GR, Durrer D: Circus movement within the A-V node as a basis for supraventricular tachycardia as shown by multiple microelectrode recordina in the isolated rabbit heart. Circ Res 28:403. 1971. 11. Wellens HJJ, Farre J: The value of the electrocardiogram in diagnosing site of origin and mechanism of supraven&icular tachvcardia. In Wellens HJJ, Kulbertus HE. editors: What’s new-in electrocardiography. Boston, 1981, Martinus Nijhoff, p 131.
AV
The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:l supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:l AV conduction, but despite prompt termination of tachycardia in both cases, 2:l AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block-that is, the “final common pathway” of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node. (AM HEART J 107:431, 1984.)
Angas W. F. Hamer, M.D., Carol A. Zaher, M.D., Thomas William J. Mandel, M.D. Los Angeles, Calif.
Reentry within the region of the atrioventricular (AV) node has been described as a regular tachycardia with almost simultaneous activation of the atria and ventricles.* The occurrence of AV block in association with regular atrial activity favors the
diagnosis of an atrial rather than an AV nodal arrhythmia. Nonetheless, a few examples of arrhythmias felt to represent AV node reentry, with either retrograde
block to the atria2m4 or anterograde
block
to the ventricles,3, 5-7have been described. The site of anterograde
block
to the ventricles
haa generally
been the His bundle
or bundle branches,3.5*7 and block appears to be very uncommon.3~7
supra-Hisian Consequently, little if any information is available concerning the effects of drugs on AV node reentry with supra-Hisian block. The purpose of this com-
munication, patients
From Funded Center, Received
then, is to describe the features of two with
the Division
supraventricular
of Cardiology,
tachycardia
Cedars-Sinai
in part by Los Angeles,
E.C.H.O. Calif.
Research
for publication
July
13, 1983;
Medical Fund
accepted
Reprint requests: William J. Mandel, M.D., Cedars-Sinai Medical Center, 8700 Beverly 90048.
and
due to AV node reentry and intermittent Hisian
2:l supraAV block, in order to add to the documenta-
tion of this arrhythmia and in addition to describe the effects of verapamil, a calcium channel blocking drug with particular affinity for the AV node, on this arrhythmia. METHODS Patients. Two patients were studied, one female and one male, aged 27 and 42 years, respectively. Neither had evidence for cardiac disease apart from his or her arrhythmias. Their resting ECGs were normal. One patient has been included in a previous report from this laboratory, but without a detailed analysis of these issues. Electrophysiologic studies. With each patient’s informed consent, electrophysiologic studies were performed in a fasting state, after premeditation with 100 mg of secobarbital. The study protocol used conventional methodology, as previously described.8 All cardioactive drugs were stopped for a minimum of 5 half-lives prior to these studies. RESULTS
Center.
of Cedars-Sinai Aug.
(SVT)
Peter, M.D.,
Medical
17, 1983.
Division of Cardiology, Blvd., Los Angeles, CA
Some of the measured
electrophysiologic
ables before and after the administration pamil are given in Table I. Included
pertaining node
to the sinus cycle length,
refractory
periods,
AV
node
variof veraare data
atrial and AV Wenckebach 431
432
Hamer
et al.
American
I I
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kk SNJS
RHYTHM
AVF __uZr
ATRIAL ce
I
I
TACHYCPRMP, ”
SIWS
March, 1984 Heart Journal
RHYTW
”
”
Fig. 1. This panel shows nonsustained high right atria1 tachycardia initiated in patient No. 1. The panel is arranged with surface ECG leads I, aVr, and V, above intracardiac recordings from the high right atrium (HRA), His bundle region (HBE), and from the distal coronary sinus (CS). The patient is in sinus rhythm (cycle length = 680 msec), and a premature right atria1 stimulus (S& at a coupling interval of 250 msec evokes three atria1 tachycardia complexes (cycle length = 430 to 530 msec) before sinus rhythm resumes. The atria1 activation sequence (measured in milliseconds from the dotted vertical line through the His deflection to the most rapid atria1 deflection [A]) of the atria1 tachycardia is similar to, but not identical to that in sinus rhythm, and the HRA polarity differs. A = atria1 electrocardiogram; H = His deflection; V = ventricular electrogram. Time lines are 1000 msec apart.
Table
I. Electrophysiologic
variables
before and after verapamil
No.
Sinus cycle length
Atria1 * ERP
AV node’ ERP
c
600
180
<210
380
320
520 935 800
270 290 260
300 <295 350
470 470 400
400 420 360
AV node* FRP
A V node Wenckebach
1
v 2:
ERP = effective refractory period, *Measured at a drive cycle length tSingle atria1 echoes only.
FRP = functional of 550 msec.
refractory
period;
SVT
threshold, the echo zones denoting the atrial coupling intervals for single atrial echo or tachycardia initiation, and variables describing retrograde ventriculoatrial (VA) conduction and refractoriness. Inducible arrhythmias. Patient No. 1 had two distinct arrhythmias: (1) nonsustained atria1 tachycardia, cycle length 430 to 530 msec, induced by single right atria1 premature stimuli during sinus rhythm (Fig. 1) and also during right atrial pacing. The sequence of atria1 activation was similar to, but not exactly the same as that for sinus rhythm, suggesting an origin in the high right atrium but not necessarily in the region of the sinus node. (2) Sustained SVT, with either 1:l conduction (Fig. 2) or 2:l AV block (Fig. 3), the latter being supraHisian. The atria1 activation sequence during this arrhythmia was low (septal) right atrium preceding simultaneous activation of the high right atrium and distal coronary sinus. This activation sequence was the same as that seen during right ventricular pacing.
= supraventricular
SVT echo zone 1:l AV 210-260 2:l AV 270-320 300-380t 370-380t 295-320
tachycardia,
Paced VA*
VA block
VA ERP
VA FRP
90
260
<260
360
165
290 280
<260 300
340
c = coronary;
v = venous.
The atrial cycle length during SVT was constant (250 to 270 msec), regardless of the presence or absence of AV block. SVT with 1:l AV conduction was initiated on six occasions by single premature right atrial stimuli during sinus rhythm and during atrial pacing, and by rapid right atrial pacing. However, only between two and seven atrial echo beats were inducible from the coronary sinus. SVT with 2:l AV block was only initiated by right atrial premature stimuli a total of 13 times. Neither form of tachycardia was initiated by right ventricular pacing. At a pacing cycle length of 550 msec, the atrial echo zone for SVT with 1:l conduction was between 270 and 290 msec (H,H, = 415 to 430 msec), and the echo zone for SVT with 21 AV block was between 210 and 260 msec (H,H, = 400 to 410 msec), the inner limit being the atrial functional refractory period (Fig. 4). Dual AV node pathways could not be identified, however. Single ventricular premature stimuli scanning diastole during SVT with 1:l AV conduction neither
Volume Number
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SVT
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433
Fig. 2. This panel showsthe initiation of SVT with 19 AV conduction in patient No. I. The panel is arranged similar to Fig. 1, with addition of a ladder diagram below, suggestingthe mechanismfor the observed events. The patient is in sinusrhythm (cycle length = 635 msec)when a premature right atrial stimulus (S& at a coupling interval of 265 msecinitiates reentry tachycardia with an H,H, interval of 425 msec. The atria1 and ventricular cycle lengths stabilize at 260 to 265 msec, and atrial and ventricular activation appear simultaneous, consistent with a diagnosis of AV nodal reentry. The septal atria1 electrogram, buried between the His deflection (H) and the QRS, precedesatrial activation in the HRA and distal CS.
3. This panel showsinitiation of SVT with variable AV block in patient No. 1. The panel is arranged similar to those in Figs. 1 and 2. The patient is in sinusrhythm (cycle length 615 msec)when a right atrial premature stimulus (SJ at a coupling interval of 225 msecinitiates a tachycardia after an H,H, interval of 405 msec.The atria1 activation sequenceis identical to that in Fig. 2, with an atrial cycle length of 245 to 270 msec.The ventricular response,however, initially showeda Wenckebach sequenceuntil 2:l AV block was establishedproximal to the His bundle. This arrhythmia was diagnosedas AV node reentry with variable and later 2:l supra-Hisian AV block. Fig.
advanced atria1 activity
nor terminated
mia. Spontaneous premature ventricular
the arrhythcomplexes
during SVT with 2:l AV block had a variable effect,, depending on their prematurity: no effect, conversion of 2:l AV block to 1:l AV conduction, or advancement of atria1 activation with termination of the arrhythmia (Fig. 5). Following conversion of SVT with 2:l AV block to 1:l AV conduction by a premature ventricular complex, transient left or right bundle branch block aberration was frequently seen, for up to 12 complexes. Both forms of SVT could be terminated by bursts of rapid right atrial pacing, but during the initial second of pacing the
timing of all atrial recording sites could be advanced without disturbing the tachycardia. Patient No. 2 also had two distinct inducible arrhythmias: (1) atrial flutter, cycle length 190 to 225 msec induced by rapid right ventricular pacing with 1:l VA conduction and alao by closely coupled right atrial premature stimuli (Fig. 6); (2) SVT with 1:l conduction (Fig. 7), and on one occasion 2:l supra-Hisian AV block (Fig. 8). The atrial cycle length was usually between 300 and 310 msec regardless of the state of the AV conduction, and the atrial activation sequence was low (septal) right atrium followed by distal coronary sinus, and fInally
434
Hamer et al.
American
(A) I
SI
550
Sl250
RA PACING
.n.
SP
A SVT 2~1 AV BLOCK
‘Bs,,
s2
March, 1984 Heart Journal
+-----D33mc+
AA-. SVT I :I CPJCONDUCTION
AVF-y/
Fig. 4. This panel shows the initiation of SVT with 21 AV block and 1:l AV conduction by the extrastimulus technique in the right atrium. The panels are arranged as in the previous figures. The left panel (A) shows that following the last of eight right atria1 (RA) stimuli (SJ at a cycle length of 550 msec, a premature stimulus (S,, at a coupling interval of 250 msec intiates SVT with 2:l AV block with an atria1 cycle length that initially varies from 230 to 330 msec. The ventriculoatrial relationship remains fixed, however (His [H-A] in the HRA = 55 msec). The right panel (I31 shows that a slightly longer coupling interval for S, (285 msec) initiates SVT with 1: 1 conduction, with an atria1 cycle length varying from 245 to 320 msec. Again, ventriculoatrial relationships remain fixed (H-A = 55 msec). The H,H, interval for initiation of SVT with 2:l AV block was shorter (400 msec) than for SVT with 1:l AV conduction (430 msec) .
the lateral right atrium. This was similar to that seen with right ventricular pacing. SVT with 1:l AV conduction was initiated eight times by rapid right atria1 pacing and by single premature atrial stimuli in the right atrium and coronary sinus, but not by right ventricular pacing. At a right atrial pacing cycle length of 550 msec, the atrial echo zone was between 290 and 320 msec, the inner limit being the atria1 functional refractory period. Dual AV nodal pathways were not evident. SVT with 2:l AV block was only initiated once, following a period of rapid right atrial pacing during which AV node Wenckebach block became 21 AV block, continuing as the pacing was turned off and the tachycardia ensued (Fig. 8). Similar to patient No. 1, SVT with 2:l AV block was converted to 1:l AV conduction by a spontaneous premature ventricular complex. SVT with 1:l AV conduction was readily terminated by rapid coronary sinus or right atria1 pacing. Effects of verapamil on sustained supraventricular tachycardia. Ten milligrams of intravenous verapa-
mil was given to both patients during sustained SVT with 1:l AV conduction. SVT was terminated following an atria1 complex in both circumstances, 50 and 81 seconds, respectively, after beginning a 30second infusion of verapamil. Prior to conversion, patient No. 1 showed an increase in the SVT cycle length from 260 msec to alternating short and long R-R cycles, varying from 280 to 350 msec just prior to termination (Fig. 9). Patient No. 2 also showed
varying cycle lengths just prior to termination, with an increase from 300 to between 310 and 360 msec after verapamil. Verapamil did not induce 2:l AV block in either patient. Following termination of SVT by verapamil, single atria1 echo beats were all that could be induced by pacing in either patient, with increases in the outer limit of the atria1 echo zones as well as increases in the inner limit, associated with an increase in AV node refractoriness. The relative timing of ventricular and atrial complexes remained fixed, however, despite the longer atrial echo cycle length (Fig. 10). Retrograde conduction times and refractoriness were assessed after verapamil only in patient No. 2, and although the VA effective refractory period appeared to have prolonged, functional properties of retrograde conduction such as the VA conduction time and the ventricular pacing cycle length for VA block remained essentially unchanged, with a 25 msec increase in VA conduction times both before and after verapamil over the range of ventricular pacing cycle lengths. Findings supportive with intermittent 2:l
of diagnosis supra-Hisian
of AV node reentry block. Since both
patients had clear evidence for atrial arrhythmias as well as sustained SVT, low atrial reentry tachycardia with a prolonged PR interval must be considered as a differential diagnosis for their SVT. Also, it is necessary to closely examine the evidence for the site of intermittent 2:l block as being located above the His-Purkinje system. Using conventional rea-
Volume Number
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Verapamil
(A) I-
+---1000mc -I * L -
in AV reentry SVT with supra-Hisian
block
435
(B) SNUS
RtiW
5. A and B, These panelsshowthe variable effects of spontaneouspremature ventricular complexes during SVT with 21 AV block in patient No. 1. The panelsare arranged asin previous figures.The top left panel (A) showsa spontaneouspremature ventricular complex (PVC*), occurring 180 msec after the previous QRS, transiently converting 2:l AV block to 3:l block before 21 AV block resumes.The atria1 cycle length remains essentially unchanged (255 to 260 msec). The top right panel (B) showsthat a spontaneousPVC (*), 280msecafter a QRS, was ableto advance atrial activation (260 - 220msec)ahead of the anterograde reentry wave front and the reentry cycle sufficiently to lead to anterograde AV nodal block and termination of the tachycardia shortly after. C, This panel showsthat an even later premature ventricular complex (*) 325msecafter a QRS doesnot alter the atria1 cycle length during the tachycardia, but following the transient conversion of 2:l to 3:l AV block by retrograde penetration of the lower AV node, the electrophysiologic properties of the lower AV node are altered sufficiently to allow 1:l AV conduction thereafter. Right bundle branch block aberration is seenin the secondventricular complex after the premature ventricular complex, possibly due to the relatively long preceding R-R interval. Fig.
soning, one would attempt to differentiate atrial reentry from AV node reentry on the basis of a reliance on critical atrial coupling intervals for initiation in the former, rather than critical A,H, intervals in the latter5 However, this differentiation was not possible prior to initiation verapamil, as in both patients the atrial echo zones extended from the atrial functional refractory periods outwards. After verapamil, however, echo zones were at longer atrial coupling intervals, and most importantly, the inner aspect was limited by AV node refractoriness rather
than by atria1 refractoriness or a critical atrial coupling level. This favored AV node reentry as the diagnosis. AV node reentry was also favored by the fact that the timing of all atrial recording sites (including the septal site in the His bundle recording) could be advanced by right atrial pacing without effect on the tachycardia cycle length. In addition to the above, perhaps the single most convincing feature of these studies suggesting a diagnosis of AV node reentry for the sustained SVT was the lack of effect of cycle length changes on VA
March.1984 436
Hamer
et al.
American
Heart
Journal
HBE
6. This panel showsinitiation of atrial flutter (cycle length 190to 225msec)with variable AV block in patient No. 2. Atrial flutter wasinitiated by a premature stimulus (SJ at a coupling interval of 225 msec following eight pacedstimuli (Sb at a cycle length of 550 msecdelivered to the distal coronary sinus.The panel is arranged similarly to the previous figures except the right atria1 recordings were taken from the lateral right atrium rather than the high right atrium and there is no distal coronary sinusrecording. In the right atrium, the lower atria1 recording (A in HBE) just precedesthe activation in the lateral RA, as measuredfrom the vertical dotted line. Fig.
VI Lalerd RA Distd cs I-BE 7. This panel showsthe initiation of SVT with 1:l AV conduction by rapid atria1 (RA) pacing (S) at a cycle length of 300 msecin patient No. 2. The panel is arranged asin Fig. 6, with the addition of a distal CS recording. The atria1 cycle length during the initial few cycles of the supraventricular tachycardia varied from 240 to 425 msec,and atria1 activation (A) in the lateral RA followed that in the distal CS, as indicated by the atria1 activation times measuredfrom the vertical dotted line passingthrough the His deflection. (His [H-AcJ = 105 msec,H-A,,,,* = 125 msec.)Septal RA activation could not be discerned. The ventriculoatrial relationship suggested AV nodal reentry, and despite changes in atria1 and ventricular cycle lengths, the VA relationship remained fixed. Fig.
relationships during SVT (Figs. 4, 7, and lo), a feature previously noted by Ahktars Verapamil, in
particular, caused changes in cycle length by altering the AH intervals during SVT (Fig. 9) without changing the relationship between the subsequent ventricular and atrial depolarizations (fixed HA intervals). Cycle length alternation is a common finding in cases of AV nodal reentry following verapamil administration. Verapamil has not been reported to commonly cause such obvious changes in atrial reentry tachycardia, and it is almost inconceivable that changes in atrial cycle length would be exactly matched by secondary changes in antero-
grade AV node conduction times to allow VA relationships coincidentally to remain unchanged. Resolution of the second issue, addressing the site of intermittent AV block, depends solely on the findings of a supra-Hisian Wenckebach sequence without changes in the HV interval prior to development of SVT with 2:l AV block during the first few seconds of tachycardia in patient No. 1 (Fig. 3), and during atrial pacing prior to tachycardia in patient No. 2 (Fig. 8). During established 2:l AV block in SVT, absence of a QRS was associated with the concurrent absence of a His deflection, also suggesting a supra-Hisian site for the block. The presence of
Volume Number
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Verapamil
in AV reentry SVT with supra-Hisian
block
437
Fig. 8. This figure showsinitiation of SVT with 2:l AV block by right atria1 pacing (S,) with a cycle length of 300 msec in patient No. 2. The panel is arranged as for Fig. 7, with the addition of a ladder diagram below, suggestinga possiblemechanismfor the observedfindings. The first atria1 paced complex is shownto the left of the panel, and subsequentlyan AV Wenckebach pattern is established,followed by 2:l AV block proximal to the His bundle, An aberrant QRS is seenon one occasion(*). Upon termination of the pacing, tachycardia ensues,with an atrial cycle length of 300to 315 msec,with 2:l supra-Hisian AV block. Although the site of AV block during pacing is presumedto be in the AV node, whether it is in the upper or lower AV node, or both during pacing could not be determined. Hencethe ladder diagram is only one of several possibleexplanations. After pacing, however, the supra-Hisian block must be below the AV nodal reentry circuit.
t-1 98c+
SVT
AVF+W&+
SVT
+ 5os8c
I
POSt
VERAPAhL
SINUS
RHYTHM
m
Fig. 9. This panel showsthe effects of 10mg of intravenous verapamil on SVT with 1:l AV conduction in patient No. 1. The panel is arranged as in Fig. 1. Prior to verapamil (left hand side), the atria1 and ventricular cycle lengths were 260 msec.Fifty secondsafter beginning a 30-secondinjection of verapamil, tachycardia terminated following an atria1 complex (A), presumably by anterogradeAV node block. Just prior to termination, cycle length alternation (280 to 350 msec)in atria1 A-A intervals were matched by ventricular R-R intervals, suggestinga fixed ventriculoatrial relationship. This behavior was consistent with AV nodal reentry, and helped exclude a low atrial tachycardia with a long PR interval as an alternative diagnosis.
a Wenckebacb sequence alone, however, is not pathognomonic for this level of block, since it has been demonstrated to occur preceding the onset of 2:l infra-Hisian block during AV node reentry.3v7 Despite the presumption that the origin of the site of block is in the lower AV node proximal to the His-Purkinje system, the site of block appeared relatively insensitive to verapamil. The conversion of SVT with 23 block to 1:l AV conduction typically
followed a spontaneous premature ventricular complex (Fig. 5). The presumed mechanism for this was that the premature ventricular complex was associated with concealed retrograde penetration of the lower AV node, resulting in anterograde block of the next tachycardia reentry wavefront, and this resulted in readjustment of the conduction properties of the distal AV node to accept continuous 1:l AV conduction during subsequent reentry cycles.
March,
438
Hamer et al.
American
PRE VERAPAMIL
Heart
1984 Journal
POST VERAPAMIL
I AVF VI Lateral RA Distal CS HBE Fig. 10. This figure showssingle atria1 echoesinduced before and after verapamil in patient No. 2. The panel is arranged asin Fig. 7. Following a period of right atria1 pacing (S,) at a cycle length of 550msec,a premature stimulus (SJ at the samecoupling interval of 320 msecinducesa singleatria1 echo (Ae) in each case.Before verapamil (left-hand panel), the atria1 coupling interval of the echo measuredin the coronary sinus (A,-AeCS) was 285 msec.Following verapamil, the sameatria1 coupling interval had lengthened to 350 msec.Despite this, the atria1 activation sequence(measuredfrom the vertical dotted line through to the His deflection) remained fixed and identical (Hz-AeCS = 105 msec,H,-AeLatRA = 125 msec). This suggestedthe predominant effect of verapamil was on anterograde AV nodal conduction proximal to the point of retrograde reentry in the AV node, without significant effects on the retrograde limits of the reentry circuit or the final common pathway distal to the circuit.
DISCUSSION
AV node and the His bundle has been demonstrated in an isolated rabbit heart preparation by Janse et al.‘O Clinical evidence for this arrhythmia may have been present in the case study of Zeft et aL6 although analysis of the surface ECGs did not allow differentiation between supra- and infra-Hisian AV block during AV node reentry tachycardia. However, it was not until the advent of His bundle recordings and programmed stimulation techniques designed to initiate AV node reentry in susceptible individuals that demonstrations of AV node reentry with infraHis block appeared,5 and subsequently reentry with supra-Hisian block.3 Overall, AV nodal reentry with supra-Hisian block appears to be an unusual form of this arrhythmia, occurring in 2 out of 67 (3%) consecutive patients referred to Wellens et al3 for an electrophysiologic study. Several of the features of the tachycardias we have described concur with those noted by Wellens et al.,3 namely (1) 2:l AV block frequently occurred at the time of onset of SVT; (2) the echo zone for SVT with 1:l AV conduction was at longer A,A, coupling intervals than for SVT with 2:l AV conduction; (3) 2:l AV block was converted to 1:l AV conduction by premature ventricular complexes (one premature ventricuAV node
reentry
with supra-Hisian
block.
reentry with block between the reentry circuit
lar complex in our patients, two premature ventricular complexes in those of Wellens et al.), and frequently was followed by a brief period of aberrant intraventricular conduction during SVT; and (4) p waves during SVT, best seen during periods of AV block, were “flat” in lead I, negative in aVr, and positive in V,. Our findings varied in relatively minor ways, however, in that tachycardia in patient No. 1 could be terminated by one ventricular premature complex, not two (as Wellens et al. found), and we did not observe a spontaneous rate-related or pacinginduced transition from 1:l to 2:l AV conduction. We did not find the atria1 rate during tachycardia significantly different between periods of 1:l and 2:l AV conduction either. Another of our findings not specifically mentioned for a case of AV node reentry with supra-Hisian block by Wellens et al. but noted by Castellanos et a1.,7 was the development of Wenckebach periodicity prior to 2:l AV block during tachycardia. Effects of verapamil. Although many of our observations appear merely to support those of others, we believe the effects of verapamil on this arrhythmia provide some new and interesting insights into AV node function during AV node reentry tachycardia. Although 2:l AV node block could be initiated by certain forms of atria1 pacing prior to verapamil
Volume Number
107 3
Verapamil
administration, a bolus injection of 10 mg of verapamil was able to lengthen conduction time in and eventually block the anterograde AV node conduction pathway used for AV node reentry, without initiating 2:l block distal to the reentry pathway. This was despite the fact that cycle length changes after verapamil showed short cycles within 20 msec of baseline. The fixed VA relationship maintained after verapamil also suggested that either verapamil had no effect on both the final common pathway in the AV node and the retrograde reentry pathway, or less likely, that it prolonged conduction time in each to an equal extent. We favor a hypothesis that the site of supra-Hisian block distal to the reentry pathway is in the AV node but is relatively insensitive to verapamil. As such, these findings would support some of the hypothetical mechanisms of verapamil’s action on anterograde conduction through the AV node that we have proposed elsewhere, wherein verapamil frequently affects anterograde conduction in the upper part of the AV node but not in the lower final common pathway.* Data from both these patients would also support the contention that verapamil may have no effect on retrograde conduction to the atria during supraventricular tachycardia, a finding consistent with many previous studies, and evidence from patient No. 2 suggested that verapamil had no effect on retrograde conduction during ventricular pacing. The latter finding, however, does not mean that verapamil cannot have a differential effect on anterograde and retrograde conduction in the final common pathway of the AV node, since previous data from our laboratory8 have shown that effects of verapamil on retrograde conduction and refractoriness during ventricular pacing can be present despite lack of such an effect during SVT. In five out of nine patients with unchanged retrograde conduction times during SVT prior to anterograde block and termination of the SVT by verapamil, the cycle length for retrograde AV nodal block during subsequent ventricular pacing was similar to or longer than the SVT cycle length. This suggested effects of verapamil on retrograde (but not anterograde) conduction and refractoriness through the final common pathway of the AV node, below the site of reentry. Clinical significance. Wellens and Farre” have suggested that AV block during AV nodal reentry is less likely to occur clinically than in the catheter laboratory. Part of this may be due to the fact that AV block usually occurs at the time of onset of SVT, and subsequently the arrhythmia may not be clinically recognized because of the relatively slow ventricular
in AV reentry
SVT
with supra-ffisian
block
439
rate or it is only noted when it spontaneously regains 1:l AV conduction. In addition, the arrhythmia may be mistakenly diagnosed as an atria1 tachycardia in many instances, despite atypical timing of the p waves.” The bolus injection of a relatively standard dose of verapamil did not appear to precipitate AV block during SVT in these patients. This was due to a lack of effect on the final common pathway in the AV node, and although spontaneous rate-related AV block has been noted by Wellens et al3 in these patients, slowing of the rate of AV nodal reentry tachycardia by verapamil may prevent this also. Thus it follows that if verapamil is administered during a regular SVT of unknown mechanism, the occurrence of AV block would favor a diagnosis of an atrial rather than an AV node arrhythmia. The authors express their gratitude assistance, to Lance Laforteza for Edwards and Rosa Goldsmith.
to Joye Nunn for editorial graphics, and to Patricia
REFERENCES
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