Sudden Wenckebach Periods and TheirRelationship to Neurocardiogenic Syncope

AGUSTIN CASTELLANOS, FEDERICO MOLEIRO. HELBERT ACOSTA,ALEXANDRE FERREIRA, MARILYN M. COX, ALBERTO INTERIAN, JR..and ROBERT J. MYERBURG

From the University of Miami School of Medicine, Division of Cardiology, Miami, Florida

CASTELLANOS, A., ET AL.: Sudden Wenckebach Periods and Their Relationship to NeurocardiogenicSyncope. Throughout a 9-month period during which 1,125 Hoiter tapes were reviewed prospectively weidentified 13 nonmedicated patients with an arrhythmia, which for the purposes of this presentation wascategorized, because of their mode of initiation, as sudden Wenckebach periods (WP). The episodesemerged abruptly from a normal f< 200 ms) PR interval with sudden prolongation of PR and PP intervals(and reversed PR-RP relationship)that took place over 1-8 cycles. The postpaced PR interval was shorterthan that of the last conducted beat. The episodes were separated into two groups. Group I included 11patients with symptoms other than syncope and Group 11 included 2 patients with syncope. There were 26episodes of sudden WP in Group 1. Twenty-five terminated in a single (and one in double) blocked Pwaves. Most episodes occurred between 10 PM and 7 AM. Symptoms did not correlate with the episodes.Mean 24-hour rates were < 90. In Group II there were 22 episodes, al! occurring between 6 AM and 10 PM.The mean sinus cycle lengths before the phenomenon started to occur in Group I (861 ±185 ms) as wellas the cycle lengths at the onset of block (1,096 ± 215 ms) were statistically longer than those in Group II(591 ± 40 ms and 747 ± 63 ms, respectively, P < 0.0001). Although the mode of onset in the episodes inGroup II was similar to Group I, 16 episodes terminated in 2-6 blocked P waves. Thus, the entire numberof episodes could be categorized as an unusual type (because ofthe PR prolongation) of paroxysmal, oradvanced second degree AV block. Because these patients had negative electrophysiological studies, pos-itive tilt tests, and absent syncope after oral propranolol therapy, they were considered as having neuro-cardiogenic syncope. In addition, the faster than normal (> 100) mean 24-hour rates) suggested that theyalso had so-called inappropriate sinus tachycardia. In summary. Group I consisted of patients with a nor-mal, benign, vagal-induced second-degree AV block, whereas the Hoiter findings in Group II appeared torefiect unusual (but natural, i.e., nonprovoked) electrocardiographic manifestations of certain patientswith neurocardiogenic syncope. (PAGE 1998; 21:1580-1588)

neurocardiogenic syncope, type I AV block, apparent type II AV block, paroxysmal A V block, vagalblock

Introduction

Episodes of type I second degree atrioven-tricular (AV) block, hereafter referred to simplyas Wenckebach periods (WP) are discussed in allarticles and chapters of electrocardiographic text-books dealing with AV conduction defects.^"^ It

Address for reprints: Agustin Castellanos, M.D., University ofMiami School of Medicine. Division of Cardiology (D-39). P.O.Box 016960, Miami, Florida 33101. Fax: (305) 585-5825.

Received January 2. 1997; revised June 9, 1997; accepted July14. 1997.

is also well known that most episodes are nottypical.^ Interestingly, there is an atypical formthat has not been extensively discussed but thatwas considered frequent enough to be includedin a recent Electrocardiography Self-AssessmentProgram (examination book) of the American Col-lege of Cardiology.^ However, this atypicity,which for the purposes of this article was calledsudden WP (see below), in turn, has variants thatcan (and have been) a source of mis-(interpreta-tion or) representation.^*'"^* Because ofthe latter,and due to the fact that its incidence and, even,dynamics have not been reported we decided to

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perform a prospective study of this conductiondisturbance.

Terminology

Mainly for didactic reasons and because oftheir not infrequent interchangeable use (a poten-tial source of misunderstanding) the followingdefinitions were used:

Constant (or stable) PP intervals: Unchangingor slightly varying (within the ranges oi normal si-nus arrhythmia) PP intervals.

Sudden WP: Mode of onset of episodes (irre-spective of the number of P waves in which it ter-minated) emerging from a normal (< 200 ms) PRinterval characterized by sudden prolongation ofthe PP and PR intervals (displaying a reversed RP-PR relationship; that is, longer RP associated withlonger PR) occurring over 1-7 cycles and withpostpause PR intervals shorter than the last con-ducted PR interval. QRS complexes were narrow(Fig. IA).

Apparent Mobitz type II AV block: Episodes(with narrow QRS complexes) of second-degreeAV block emerging from a normal PR interval withsudden prolongation of the PP interval but with-out detectable PR prolongation (at conventionalelectrocardiographic paper speed) occurring overa few cycles (Figure 1B).̂ °

PR 2«0

790 810 880 1000

PR 130 130 130 130

980

Figure 1. A. Sudden Wenckebach period. Obtainedfrom a Group I Patient. PR interval is prolonged only intbe beat preceding the blocked P wave. The P-P intervalbetween the latter and tbe last conducted P wave islonger than the previous ones. B. Apparent Mobitz typeII block. Although tbe PP intervals became longer thereis no prolongation of the PB interval prior to tbe blockedP wave. Botb arrhythmias are vagally mediated.

Pseudo-Mobitz II AV block: Episodes of WPwith high AV conduction ratios in which at leastthe last three PR intervals show a relatively con-stant (> 20 ms in the surface leads) duration andin which the first PR interval following theblocked P wave is shorter than the last conductionPR interval by 40 ms or more/

Mobitz type II block: Episodes of rate inde-pendent second-degree AV block (usually withwide QRS complexes) in which the first blocked Pwave is preceded by constant (as defined) PP andPR intervals with postblock PR intervals equal tothe last preblock PR intervals.'^'^'^'^^The diagno-sis of type I and type II block requires at least 3:2

Paroxysmal AV block: Episodes (usually withwide QRS complexes) characterized by the sud-den occurrence of repetitive block of the atrial im-pulse resulting in a transient interruption of AVconduction. '̂̂ • '̂'•^^ According to Fisch'* it can oc-cur with either an increase, a decrease, or nochange in atrial rate but without any recognizablechange in the PR interval.

Advanced second-degree AV block: A blockof two or more consecutive P waves (according tothe American College of Cardiology/AmericanHeart Association guidelines for implantation ofcardiac pacemakers.)^^ Some authors also con-sider the following as advanced AV block: 2:1,3:1, 4:1 AV block, etc.^^ Pick and Langendorf (intheir Fig. V-D-15) have used this term when whatseems to be complete AV block is interruptedby captures occurring during the supernormalperiod.

Materials and Methods

A total of 1.125 Holter tapes obtained duringa 9-month period were prospectively scanned by atrained technician or nurse. Those with any typeof AV block, or when doubts existed, were res-canned by one, or (rarely) two, physicians. Thir-teen tapes showing episodes of sudden WP wereidentified (Fig. lA). Not included were threeepisodes of apparent Mobitz type II AV block (Fig.lB).^'' Also excluded were tapes showing WP oc-curring in 12 other patients with persistent first-degree AV block (PR ^ 210 msec). All episodeswere recorded at conventional, half, and full dis-closure, paper speeds.

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Patients

The ages ranged between 19-48 years. Therewere 8 males and 5 females. The symptoms re-ported (with 1 patient reporting more than onesymptom) were: palpitations (10 patients); dizzi-ness (8 patients), atypical chest pain (2 patients),and syncope (2 patients). The episodes were sepa-rated into: Group I that includes 11 patients withsymptoms other than syncope, and Group II, con-sisting of 2 patients with syncope. Ten of 11 pa-tients without syncope and 2 patients with syn-cope had no demonstrable structural heartdisease. One patient had coronary artery disease(noncritical distal right coronary artery stenosis).Electrophysiological studies and tilt tests wereperformed in the 2 patients with syncope.

Results

Group I

Twenty-six episodes of sudden WP and threeepisodes of apparent Mohitz II hlock (excludedfrom the study) were observed in this group.Twenty-five episodes of sudden WP terminated inone (and one episode in two) blocked P waves.Ventricular pauses, not interrupted by escapebeats, were < 2.5 seconds. The number of beatsshowing PR interval prolongation (hefore theblocked P wave) above the control PR intervalwere (with number of episodes in parentheses):1(8). 2(12), 3(1), and 4(5). The sinus cycle lengthsbefore this occurrence ranged between 1,460-620ms (mean 861) (Table I). Since the PP intervals

Table I.

Differences (in msec) Between Sinus Cycie Lengthsin Groups 1 and 2

Cycle Lengths* Cycle Lengths^

Mean SD Mean SD

Group 1Group 2p value

861 ± 185591 ± 40< 0.0001

1096 ± 215747 ± 63< 0.0001

' Prior to the beginning of PR and PP interval prolongation-T Given by the interval between the iast conducted, and the firstblocked, P wave.

lengthened concomitantly with the PR intervals,the sinus cycle lengths at the moment ofthe event,given by the interval between the last conducted,and the first blocked P wave, were longer (range1,600-630; mean 1,096). The average heart ratesfor the entire (24-hour) monitoring time were < 90beats/min. Twenty-one episodes occurred be-tween 10 PM and 7 AM and five episodes between11 a.m. and 8 p.m. All patients had symptoms thatwere not related to the episodes of AV block.

Group II

Twenty-two episodes were detected in the 2patients with syncope. In contrast to Group I, only6 terminated in 1 blocked P wave. Six, 3, 1, and 6episodes ended in 2, 3, 5, and 6 consecutivelyblocked P waves, respectively. Moreover, ventric-ular pauses exceeded 3 seconds in five episodes,with escape heats interrupting six episodes. Eval-uation ofthe sinus cycle lengths during the 60 sec-onds preceding the event revealed a pattern con-sisting of cycles between 550 and 720 ms (mean591) that decreased to 600-920 ms (mean 747) atthe moment (the beginning, as previously defined)ofthe event (Tahle I, Figs. 2 and 3). Differences be-tween these intervals and those of Group I werestatistically significant (Table I). The number ofbeats showing PR prolongation above the controlPR intervals were 1 in eight episodes, 2 in fiveepisodes, 3 in one episode, 4 in one episode, 5 intwo episodes, 7 in three episodes, and 8 in twoepisodes. The average heart rates for the entiremonitoring time exceeded 100 beats/min in bothpatients. In these two patients the symptoms coin-cided with some of the episodes of AV block. Sev-enteen episodes (two of which resulted in syn-cope) occurred between 9:10 AM and 10 PM. Fiveepisodes (one associated with syncope) took placebetween 6;02 AM and 6:20 AM, all while the patientwas awake.

Because of these findings, the patients wereinitially referred for invasive electrophysiologicalevaluation. Gonventionally performed studieswere interpreted as normal. Consequently, tilttests were done using the technique previouslydescribed in our departments^ Patient 1 devel-oped syncope without isoproterenol 8.5 minutesafter having been tilted at an 80" angle. Blood pres-sure started to decline before sinus rate decreased

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MALIGNANT - CASE 1 (TWO EPISODES)

-—K—*JL—-A—'JL

PR ISO 200 230

PP 640 720 760

BJ.—.—J—.—X~^—X—U-i^

Figure 2. Recorded from the first Group II patient. A. The top strip was recorded at paper speed(12.5 m/s). The bottom strip (simultaneously recorded monitoring leads corresponding to themiddle portion of the previous strip) show.<i a sudden Wenckebach episode with prolongation ofPR and PP intervals before a run of 2:1 AV block, which is interrupted (or terminated) by anescape beat. B. Another episode (from the same patient) depicting a similar mode of initiationbut terminating in six blocked P waves. The entire episode can perhaps be categorized as aparoxysmal or advanced second degree AV block, atypical, because these episodes do notusually show PR prolongation prior to the first blocked P wave.

> 20 beats.^'' During symptoms, sinus rate was 70beats/min, one P wave was blocked, and the bloodpressure fell to 84/60 mm Hg. After 4 pig of iso-proterenol, patient 2 had symptoms with a bloodpressure of 78/46 mm Hg and a sinus rate of 100beats/min.

Discussion

Group I

These episodes, as well as those of apparentMobitz type II AV block, fulfilled the characteris-tics of what is usually considered as benign vagal-induced WP, an entity well defined morphologi-cally from surface, and intracardiac, recordings.and mechanistically, when occurring sponta-neously or reproduced iatrogenically by carotid

sinus massage.̂ ** 12,14,25 28 interestingly, suddenWP was called "subtle Wenckebach" hy Lange

Several studies found them to be an expres-sion of abrupt surges of enhanced vagal tone ex-erted predominantly on the AV node (causing de-lay in conduction, and/or block of a P wave) whilebeing less intense on the sinus node where theywere manifested by sinoatrial slowing.^""^^ Whenreproduced by carotid sinus massage, Zaman etal/^ observed that the vagal effects depended onvarious factors: moment ofthe cycle at which themassage was begun, basic sinus rate, inevitablevariations in intensity and speed of massage, se-lectivity (sidedness) of vagal influences at a givenmoment, background sympathetic activity, andintrinsic vagal sensitivity of the sinus and AV

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MALIGNANT - CASE 2

•-M-JJU4A4''*-4.^^'HLM^W''HU-JL^^

B

A: 3 CONTINUOUS STRIPS (AT HALF PAPER SPEED)B: CENTER PART OF A (AT USUAL PAPER SPEED)C: IS CONTINUOUS WITH A

Figure 3. From the second Group II patient. A. Note that the rate is slower (top strip), thenaccelerates in the middle strip before slightly decelerating with an increase in the PH intervals(end of middle and beginning of the bottom strip), B. Shows five consecutively blocked P waves.The entire episode can be categorized as an atypical form of paroxysmal or advanced seconddegree block, C is continuous with A.

nodes in given patients. Thus, if electrophysiolog-ical studies are to be performed in these cases,they should include a methodology requiring aslowing of rates, not the conventional approach,which would most likely yield negative re-sults."'^^ The importance of these factors wasshown in the experimental studies of Moore andSpear^^ using plunge electrodes. They demon-strated how vagal stimulation with 100-secondtrains of impulses, performed with constant atrial(paced) rates at preselected moments of the cycle,produced a variety of AV nodal conduction pat-terns including typical or atypical WP and evenMobitz II conduction disturbances (block of a Pwave with constant PP intervals not preceded hyPR prolongation).^^ Not surprisingly, the expres-sions of vagally mediated AV nodal hlock are partof a spectrum that includes episodes of suddenWP (Fig. lA) as well as episodes of apparent Mob-itz II block in which the PP intervals decrease but

there is no detectable change in the PR interval atthe body surface in the heat before the blocked Pwave (Fig. lB).^"'^^ The patients had bizarre symp-toms not related to the episodes of AV block.

Group II

These episodes were, as previously stated,categorized as sudden only because of their modeof initiation since 16 terminated in more than one(2,3,5, and 6) consecutively blocked P waves [Figs.2 and 3). Thus, according to the criteria used, allthe episodes could also be classified as paroxys-mal, or advanced second degree, AV block.̂ •̂ •̂ **"̂ ^These episodes were also different from those inGroup I because both mean sinus cycle lengthsprior to the beginning of PR and PP prolongationand cycle lengths at the moment of initiation weresignificantly shorter (Table I). No episodes wererecorded froni 10 PM to 6 AM. Some episodes led to

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pauses > 3 seconds and, even, syncope. Moreover,the mean 24-hour rates were higher than 100beats/min (600 ms).

The neurocardiogenic nature of the syncope(rather than its being the result of structural heartdisease) was supported by the negative invasiveelectrophysiological findings, and more impor-tant, by the positive tilt test and the fact that bothpatients have remained free of symptoms, for 19and 25 months, respectively, after administrationof oral propranolol without pacemaker implanta-tion.''""^^ That the exact electrocardiographicchanges during the natural state and the test werenot the same is not surprising since such lack ofcorrelation has been noted before.̂ '̂̂ ^"^^ Unfor-tunately, as stated by Sutton and Petersen,^^ asubstantial series of Holter recordings of heartrate behavior during clinical vasovagal syncopehas not yet been published, and there is no suchseries comparing naturally occurring symptomswith tilt-induced syncope in the same subjects.The study of Takase et al.'"^ dealt only with dif-ferences in heart rate variability but the patientswere asymptomatic when the Holters were per-formed.

AV Block in Patients with NeurocardiogenicSyncope

The literature regarding this association islimited and rather unclear. For example, Jaeger etal.'^ reported having seen "many patients (num-bers not given)" referred for pacemaker implanta-tion on the basis of Holter recordings of high de-gree AV block that were ultimately found to besecondary to vasovagal syncope. Foleno et al.'^noted the occurrence of intermittent complete, orparoxysmal AV block in 1 of 12 patients tilted be-cause of syncope. Breignole et al.'"* observed AVblock in 4 (patients 7,8,9, and 13) EPS negative pa-tients of 25 consecutive patients referred for eval-uation of unexplained syncope. In the study ofFitzpatrick and Sutton"*" there were 40 patientswith vasovagal syncope during tilt testing, 12 ofwhom had atrioventricular block or junctionalbradycardia with sinus arrest. Also, in another ar-ticle by Jaeger and coworkers,^^ they mention thatmarked bradycardia and AV nodal block duringneurocardiogenic syncope may represent "accen-

tuated antagonism" of sympathetic activity by asudden vagal discharge (again, the number of pa-tients was not mentioned). In some of the previ-ously mentioned studies pacemakers were usedwith varying degrees of success. The role of per-manent cardiac pacing has been recently dis-cussed by Daubert et al.^'' in a book, as well as inpart II of a recent symposium on neurocardiogenicsyncope recently published in PACE."*̂

Reasons for the Coexistence with,and Emergence from, Fast Sinus Ratesof Malignant Episodes

Because there were no apparent reasons forthe fast resting sinus rate and for their dispropor-tionate increases witb minimal stresses, it can bespeculated that these patients could have had acoexistent sinus node abnormality, namely inap-propriate sinus tachycardia with intermittent sud-den, but not maintained, bursts of enhanced vagal

For example, Bauernfeind et al.̂ "* reported anunusual response to intravenous phenylephrinein 2 of 7 patients with "chronic" persistent sinustachycardia, namely, a minimally, or lesser thanexpected (that is, inappropriate according to thedosage) sinoatrial slowing coexisting with type 1AV nodal block. Trohman et al.̂ ^ performed tilttests and radionuclear studies in 4 patients withinappropriate sinus tachycardia. Neurocardio-genic syncope preceded by an increase (in the al-ready faster-than-normal) sinus rates was pro-voked in 2 (50%) of 4 of patients with priorsyncopal episodes.^^ Moreover, in a study per-formed in our department, 1 of 10 patients withthis entity manifested WPs at rates > 90beats/min."*^

However, Grubb and Kosinski^^ have cau-tioned not to label as inappropriate sinus tachy-cardia the (third) response pattern that they sawduring positive tilt, which was called postural or-thostatic tachycardia syndrome. These patientshave a different symptomatology than those withtrue inappropriate sinus tachycardia.'*^

Site of AV Block

The apparent mechanism, the narrow QRScomplexes, and some electrophysiological studies

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suggest that block occurred at the AV nodallevel.^"'ii'^«-^° Furthermore, WPs that led to syn-cope were included because their mode of initia-tion was the requirement for entry in this study. Infact, according to whose nomenclature is ac-cepted, the entire number of episodes could beclassified as paroxysmal AV block or advancedAV block."'̂ '̂ **'̂ ^ It should be stressed that the cor-responding definitions of the latter, though in-cluding the abruptness and repetitiveness of theblock and the possible changes in atrial rate, makeno mention of the behavior of the PR intervalsprior to the blocked P waves.'*-̂ -̂ "-̂ ^ In contrast,Zipes^ shows a tracing (Zipes' Fig. 1) of what hecalls "transient" AV nodal block (attributed to ex-cessive vagal stimulation) where the PR interval isprolonged prior to block of 10 consecutive Pwaves (as in our Figs. 2 and 3). Although mostepisodes of paroxysmal AV block are infra-Hisianthere are some reports (corroborated by His bun-dle recordings) where, with narrow QRS com-plexes, the conduction disturbance has been lo-calized to the AV node and attributed tohyper-responsiveness of this structure to vagal re-flexes.^^•'̂ •''̂ "^° Two patients with symptomaticspontaneous AV nodal (vagal) block reported byStrassberg et al.*^ (corroborated by and repro-duced during His bundle studies) had some de-

gree of sinus node slowing, but no PR prolonga-tion, prior to the occurrence of AV block.

Limitations

Although, most likely, the block occurred atthe AV nodal level, this could not be definitelyproven in absence of His bundle recordings. Thatthe two patients with syncope had inappropriatesinus tachycardia was also inferred since none ofthe studies required to confirm this diagnosiswere performed.

Clinical Implications

This study suggests that in addition to the be-nign, vagal-induced, sudden WP there is a variantthat, having the same mode of initiation, can ter-minate as paroxysmal or advanced, AV block. Thesymptomatic episodes are not due to structuralconducting system disease but, rather, constitutean infrequent electrocardiographic manifestationofthe neurocardiogenic syncope.

Addendum: While this article was in press, threepublications in Circulation demonstrated that adenosine canproduce findings similar to those of our Group I (1997;96:1201, 1997; 96:3921. and 1996: 96:47).

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1588 August 1998 PACE. Vol. 21