CHAPTER 6

Ventricular Preexcitation

HISTORICAL PERSPECTIVE In the normal heart , there are no muscular connect ions between the atr ia and

ventr ic les. In 1893, Kent descr ibed the rare occurrence of such connect ions, but

wrongly assumed that they represented pathways of normal conduct ion.1 Mines

suggested in 1914 that th is accessory atr ioventr icu lar (AV) connect ion (Bundle of

Kent ) might cause tachyarrhythmias. In 1930, Wol f f and White in Boston and

Park inson in London reported thei r combined ser ies of 11 pat ients wi th b izarre

ventr icu lar complexes and short PR intervals.2 Then, in 1944, Segers int roduced the

t r iad of shor t PR interval , preexci tat ion of the ventr ic les character ized by a pro longed

upstroke of the QRS complex (del ta wave) , and tachyarrhythmia that character ize the

Wolf f–Park inson–White (WPW ) syndrome .

CLINICAL PERSPECTIVE Ventr icu lar preexci tat ion refers to a congeni ta l cardiac abnormal i ty in which a par t of

the ventr icu lar myocardium receives e lectr ica l act ivat ion f rom the atr ia before the

arr iva l of an impulse v ia the normal AV conduct ion system (Fig. 6.1) . AV myocardia l

bundles commonly exis t dur ing fetal l i fe , but then d isappear by the t ime of b i r th.3

When even a s ingle myocardia l connect ion pers is ts , there is the potent ia l for

ventr icu lar preexci tat ion. In some indiv iduals, ev idence of preexci tat ion may not

appear unt i l la te in l i fe , whi le in others wi th l i fe long evidence of ventr icular

preexci tat ion on the e lectrocardiogram (ECG), the WPW syndrome may not occur unt i l

la te in l i fe . Conversely, in fants wi th the WPW syndrome may outgrow any or a l l

ev idence of th is abnormal i ty wi th in a few years.4

Figure 6.1. Schemat ic i l lust rat ion of the anatomic re lat ionship between the normal AV

conduct ion system and the accessory AV conduct ion pathway provided by the Bundle of Kent .

The sol id bar represents the nonconduct ing st ructures ( inc luding the coronary ar ter ies and

veins, valves, and f ibrous and fat ty connect ive t issue) that prevent conduct ion of e lectr ica l

impulses f rom the atr ia l myocardium to the ventr icu lar myocardium. (AVN , AV node; HB , His

bundle; RBB , r ight bundle branch; KB , Kent bundle; LBB , le f t bundle branch.)

F igure 6.2 i l lust rates the contrast between the a l terat ion of the PR and QRS intervals

that resul ts f rom bundle-branch block (BBB) and f rom ventr icu lar preexc i tat ion. Right

or le f t BBB (F ig. 6.2A) does not a l ter the PR interval , but pro longs the QRS complex

by delaying act ivat ion of one of the ventr ic les. Ventr icu lar preexci tat ion (F ig. 6.2B)

shortens the PR interval and produces a “del ta wave” in the in i t ia l par t of the QRS

complex. The tota l t ime f rom the beginning of the P wave to the end of the QRS

complex remains the same as in the normal condi t ion because conduct ion v ia the

abnormal pathway does not in ter fere wi th conduct ion v ia the normal AV conduct ion

system. Therefore, before the ent i re ventr icu lar myocardium can be act ivated by

progression of the preexci tat ion wave f ront , e lectr ica l impulses f rom the normal

conduct ing system arr ive to act ivate the remainder of the ventr icu lar myocardium.

Figure 6.2. The two types of a l tered or “aberrant” conduct ion f rom the atr ia to the ventr ic les.

The dashed l ine in A represents late act ivat ion of the ventr ic le served by the b locked bundle

branch, and the dashed l ine in B represents the ear ly act ivat ion of the ventr ic le connected wi th

the atr ia v ia an accessory muscle bundle.

F igure 6.3A i l lust rates the normal cardiac anatomy that permits AV conduct ion only v ia

the AV node ( the open channel at the crest of the interventr icu lar septum). Thus, there

is normal ly delay in the act ivat ion of the ventr icular myorcardium (PR segment) , as

noted in the ECG recording shown in the f igure. When the congeni ta l abnormal i ty

responsib le for the WPW syndrome is present (F ig. 6.3B) the ventr icu lar myocard ium

is act ivated f rom two sources: (a) v ia the preexci tat ion pathway ( the open channel

between the r ight at r ium and r ight ventr ic le) ; and (b) v ia the normal AV conduct ion

pathway. The resul tant abnormal QRS complex ( termed a fus ion beat ) is composed of

the abnormal preexci tat ion wave and normal mid- and terminal QRS waveforms.

Figure 6.3. Relat ionship between an anatomic Bundle of Kent and physio logic preexci tat ion of

the ventr icu lar myocardium ( top) , and the typical ECG changes of ventr icu lar preexci tat ion

(bottom) . Normal condi t ion is presented (A) for contrast wi th the abnormal condi t ion (B) .

(Modi f ied f rom Wagner GS, Waugh RA, Ramo BW. Cardiac arrhythmias. New York: Churchi l l

L iv ingstone, 1983:13.)

The ECG of an indiv idual wi th ventr icu lar preexc i tat ion is abnormal in several ways:

1. In the presence of a normal s inus rhythm, the PR interval is abnormal ly short and

the durat ion of the QRS complex is abnormal ly pro longed. Ventr icu lar preexci tat ion

produces a prolonged upstroke of the QRS complex, which has been termed a del ta

wave (Fig. 6.4) .

Figure 6.4. Twelve- lead ECG of an 18-year-o ld woman wi th a h is tory of f requent episodes of

“heart f lu t ter ing” (A) and a 34-year-o ld man wi thout cardiac symptoms (B) . Arrows ind icate the

posi t ive del ta waves in many leads and the negat ive del ta waves in leads I I , I I I , and aVF in A

and in lead V1 in B .

2 . In the presence of an atr ia l tachyarrhythmia, such as atr ia l f lu t ter / f ibr i l la t ion

(Chapter 15, “Reentrant Atr ia l Tachycardias—The Atr ia l F lut ter /F ibr i l la t ion Spectrum”) ,

the ventr icu lar rate a lso becomes rapid. The ventr ic les are no longer “protected” by

the s lowly conduct ing AV node (F ig. 6.5) .

Figure 6.5. Twelve- lead ECG recording and lead I I rhythm str ip of a 24-year-o ld woman wi th

ventr icu lar preexci tat ion dur ing atr ia l f ibr i l la t ion. The i r regular i t ies of both the ventr icu lar rate

and QRS-complex morphology are apparent , especia l ly on the 10-s lead I I rhythm str ip at the

bot tom.

3. The abnormal AV muscular connect ion completes a c i rcui t by provid ing a pathway

for e lectr ical react ivat ion of the at r ia f rom the ventr ic les. This c i rcui t prov ides a

cont inuous loop for the e lectr ica l act ivat ing current , which may resul t in a s ingle

premature beat or a pro longed, regular , rapid atr ia l and ventr icu lar rate cal led a

tachyarrhythmia (F ig. 6.6) . In F igure 6.6B, an atr ia l premature beat has occurred

which sends a wave of depolar izat ion through the atr ia and toward the Bundle of Kent .

Because th is beat or ig inated in such c lose proximi ty to the Bundle of Kent , the bundle

has not had suf f ic ient t ime to repolar ize. As a resul t , the premature wave of

depolar izat ion cannot cont inue through th is accessory AV conduct ion pathway to

preexci te the ventr ic les. However, the premature wave is able to progress to the

ventr ic les v ia the normal AV conduct ion pathway in the AV node and interventr icu lar

septum. This depolar izat ion wave then t ravels through the ventr ic les, and s ince i t does

not col l ide wi th an opposing wave (as occurs wi th ventr icu lar preexci tat ion in F igure

6.6A), i t reenters the at r ium through the Bundle of Kent , creat ing a ret rograde atr ia l

exci tat ion (F ig. 6C).

Figure 6.6. The schemat ic d iagram from Figure 6.3 is reproduced wi th the normal example

omit ted. Typical ventr icu lar preexci ta t ion appears again in A . In B , the x ind icates the s i te of

or ig in of the atr ia l premature beat and the st ippl ing in the ventr icu lar myocardium indicates

pers is tent ref ractor iness as a resul t of the previous exci tat ion. In C , the completed c i rc le

inc ludes the r ight at r ium, AV node, His bundle, RBB, r ight ventr ic le, and Bundle of Kent .

(Modi f ied f rom Wagner GS, Waugh RA, Ramo BW. Cardiac arrhythmias. New York: Churchi l l

L iv ingstone, 1983:13.)

The inf luence of ventr icular preexci ta t ion on the ventr icu lar rate dur ing atr ia l

f lu t ter / f ibr i l la t ion and on tachyarrhythmias induced by an accessory pathway is

d iscussed in Chapter 15 ( “Reentrant Atr ia l Tachycardias—The Atr ia l F lut ter /F ibr i l la t ion

Spectrum”) and Chapter 16 ( “Reentrant Junct ional Tachyarrhythmias”) , respect ive ly.

The combinat ion of a PR interval of durat ion <0.12 s, a del ta wave at the beginning of

the QRS complex, and a rapid, regular tachyarrhythmia has been termed the Wol f f–

Park inson–White (WPW) syndrome. The PR interval is short because the descending

e lectr ica l impulse bypasses the normal AV-nodal conduct ion delay. The del ta wave is

produced by s low int ramyocardia l conduct ion that resul ts when the descending

impulse, instead of being del ivered to the ventr icu lar myocardium via the normal

conduct ion system, is del ivered d i rect ly into the ventr icu lar myocardium via an

abnormal or “anomalous” muscle bundle. The durat ion of the QRS complex is

pro longed because i t begins “ too ear ly, ” in contrast to the s i tuat ions presented in

Chapter 4 ( “Chamber Enlargement”) and Chapter 5 ( “ Int raventr icu lar Conduct ion

Abnormal i t ies”) , in which the durat ion of the QRS complex is pro longed because i t

ends too late. The ventr ic les are act ivated successively rather than s imul taneously:

the preexci ted ventr ic le is act ivated v ia the Bundle of Kent , and the other ventr ic le is

then act ivated v ia the normal AV node and His-Purk in je system (F ig. 6.3) .

Var ious terms have been appl ied to the abnormal anatomic st ructure and resul t ing

abnormal e lectrophysio logic funct ion respons ib le for the WPW syndrome (Table 6.1) .

Table 6.1. Structure and Funct ion Terms

ELECTROCARDIOGRAPHIC DIAGNOSIS OF VENTRICULAR PREEXCITATION Typical ly, wi th ventr icu lar preexci tat ion, the PR interval is less than 0.12 s in durat ion

and the QRS complex is greater than 0.10 s. However, the PR interval is not a lways

abnormal ly short (F ig. 6.7A) and the QRS complex is not a lways abnormal ly pro longed

(F ig. 6.7B). Conduct ion through the Bundle of Kent may be re lat ive ly s low, or the

Bundle of Kent may d i rect ly enter the His bundle. Among almost 600 pat ients wi th

documented ventr icu lar preexci tat ion, 25% had PR intervals of 0.12 s or longer and

25% had a QRS-complex durat ion of 0.10 s or shorter .5

Figure 6.7. Twelve- lead ECGs f rom a 57-year-o ld man wi thout card iac-re lated symptoms (A)

and a 41-year-o ld woman wi th recurrent episodes of weakness and who sensed a rapid heart

rate (B) . Arrows in A ind icate abnormal ly s low onset of the QRS complex fo l lowing a normal

PR interval (0.16 s) and arrows in B indicate an abnormal ly short PR interval preceding a QRS

complex of normal durat ion (0.08 s) .

When ventr icu lar preexc i tat ion is suspected in a pat ient wi th tachyarrhythmias but no

ECG evidence preexci ta t ion, the fo l lowing d iagnost ic procedures may be helpfu l :

• Pace the atr ia e lectronical ly at increasingly rapid rates to induce conduct ion

v ia any exis t ing accessory pathway.

• Produce vagal nerve st imulat ion to impair normal conduct ion through the AV

node so as to induce conduct ion v ia any exist ing accessory pathway.

• In fuse d igoxin int ravenously for the same purpose as in Procedure 2.

Ventr icu lar preexci tat ion may mimic a number of other cardiac abnormal i t ies. When

there is a wide, posi t ive QRS complex in leads V1 and V2, i t may s imulate r ight

bundle-branch block (RBBB), r ight-ventr icu lar hypert rophy (RVH), or a poster ior

myocardia l in farct ion. When there is a wide, negat ive QRS complex in lead V1 or V2,

preexci tat ion may be mistaken for le f t bundle-branch block (LBBB) (Fig. 6.8A) or le f t -

ventr icu lar hypert rophy (LVH). A negat ive del ta wave, producing Q waves in the

appropr iate leads, may imi tate anter ior , la teral , or in fer ior in farct ion. As wi l l be

d iscussed in Chapter 10 ( “Myocardia l In farct ion”) , the prominent Q waves in leads aVF

and V1 in F igure 6.8B could be mistaken for in fer ior or anter ior in farct ion,

respect ively. Simi lar ly, the deep, wide Q wave in lead aVF and broad in i t ia l R wave in

lead V1 in Figure 6.8C could be mistaken for in fer ior or poster ior in farct ion,

respect ive ly.

Figure 6.8. Twelve- lead ECGs f rom a 40-year-o ld woman admit ted to a hospi ta l emergency

department for symptoms of d izz iness (A) , a 46-year-o ld woman admit ted to a coronary care

uni t wi th chest pain but no c l in ical conf i rmat ion of a myocardia l in farct ion (B) , and a 31-year-

o ld male medical res ident wi thout cardiac symptoms but an incorrect d iagnosis of myocardia l

in farct ion by computer ized interpretat ion of a rout ine ECG (C) . Arrows in A ind icate del ta

waves producing QRS complexes mimicking LBBB, and arrows in B and C ind icate del ta waves

producing QRS complexes mimicking myocardia l in farct ion.

ELECTROCARDIOGRAPHIC LOCALIZATION OF THE PATHWAY OF VENTRICULAR PREEXCITATION Many at tempts have been made to determine the myocardia l locat ion of ventr icu lar

preexci tat ion according to the d i rect ion of the del ta waves in the var ious ECG leads.

Rosenbaum and col leagues6 div ided pat ients into two groups (Group A and Group B)

on the basis of the d i rect ion of the “main def lect ion of the QRS complex” in

t ransverse-plane leads V1 and V2 (Table 6.2) .

Table 6.2. Relat ionship Between Pathway Locat ion and ECG Changes

Other c lassi f icat ion systems consider the d i rect ion only of the abnormal del ta wave in

at tempt ing to bet ter local ize the pathway of ventr icu lar preexci tat ion. Since curat ive

surgical and catheter ablat ion techniques for e l iminat ing i t have become avai lable,

more precise local izat ion of the accessory pathway is c l in ica l ly important ,7 and many

addi t ional ECG cr i ter ia have therefore been proposed for achieving th is . However,

precise local izat ion of an accessory AV pathway is made di f f icu l t by several factors,

inc luding minor degrees of preexci tat ion, the presence of more than one accessory

pathway, d is tor t ions of the QRS complex caused by super imposed myocardia l

in farct ion, or ventr icu lar hypert rophy. Nevertheless, Mi ls te in and his associates8

devised the a lgor i thm presented in Figure 6.9 that enabled them to correct ly ident i fy

the locat ion of 90% of more than 140 accessory pathways.

Figure 6.9. Mi ls te in 's a lgor i thm for local izat ion of accessory pathways. Note: For purposes of

th is schema, LBBB indicates a posi t ive QRS complex in lead I wi th a durat ion of at least 0.09 s

and wi th rS complexes in leads V1 and V2. (RAS , r ight anterosepta l ; LL , le f t la tera l ; PS ,

posterosepta l ; RL , r ight la tera l . ) (Modi f ied f rom Mi ls tein S, Sharma AD, Guiraudon GM, et a l .

An a lgor i thm for the e lectrocardiographic local izat ion of accessory pathways in the Wol f f -

Park inson-Whi te syndrome. Pacing Cl in Electrophysio l 1987;10:555–563.)

Al though accessory pathways may be found anywhere in the connect ive t issue

between the atr ia and ventr ic les, near ly a l l are found in three general locat ions (F ig.

6.10) , as fo l lows

Figure 6.10. Schemat ic v iew ( f rom above) of a cross-sect ion of the heart at the junct ion

between the atr ia and the ventr ic les. The ventr icular out f low aort ic and pulmonary va lves are

located anter ior ly, and the ventr icu lar in f low mit ra l (b icuspid) and t r icuspid valves are located

poster ior ly. The three general locat ions of Bundles of Kent are: 1 , LA-LV f ree wal l ; 2 , poster ior

septa l ; and 3 , the r ight anteroseptal and r ight la teral locat ions of Mi ls te in and col leagues

combined as RA-RV f ree wal l . (Modi f ied f rom Tonkin AM, Wagner GS, Gal lagher JJ, et a l .

In i t ia l forces of ventr icu lar depolar izat ion in the Wol f f -Park inson-Whi te syndrome. Analys is

based upon local izat ion of the accessory pathway by ep icard ia l mapping. Circulat ion

1975;52:1031.)

• Lef t la tera l ly, between the lef t -at r ia l and lef t -ventr icu lar f ree wal ls (50%).

• Poster ior ly, between the atr ia l and ventr icu lar septa (30%).

• Right la tera l ly or anter ior ly, between the r ight at r ia l and r ight ventr icu lar f ree

wal ls (20%).

Tonkin and associates presented a s imple method for local iz ing accessory pathways to

one of the foregoing areas on the basis of the d i rect ion of the del ta wave (Table 6.3) .9

They considered a point 20 ms af ter the onset of the del ta wave in the QRS complex

as thei r reference.

Table 6.3. Considerat ion of Del ta Wave at QRS Onset + 0.02 s

ABLATION OF ACCESSORY PATHWAYS Figure 6.11A and Figure 6.12A i l lust rate the typ ical ECG appearances of preexci tat ion

of the r ight ventr icu lar f ree wal l and the interventr icu lar septum, respect ive ly.

Successfu l ablat ion of the accessory pathways (F ig. 6.11B and Fig. 6.12B) revealed

the under lying presence of normal QRS complexes.

Figure 6.11. Ser ia l 12- lead ECGs f rom a 44-year-o ld woman wi th a h is tory of recurrent

symptoms of d izz iness and shortness of breath just before (A) and 1 week af ter (B) catheter-

induced radio- f requency ablat ion of her Bundle of Kent . Arrows ind icate del ta waves in A and a

normal appearance of the QRS complex in B .

Figure 6.12. Ser ia l 12- lead ECGs f rom a 28-year-o ld woman wi th recurrent episodes of rapid

heart beat 1 day before (A) and 1 day af ter (B) catheter- induced radio- f requency ablat ion of

her Bundle of Kent . Arrows ind icate del ta waves in A and a normal appearance of the QRS

complex in B .

GLOSSARY Bundle of Kent:

a congeni ta l abnormal i ty in which a bundle of myocardia l f ibers connects the atr ia and

the ventr ic les.

Delta wave:

a s lowing of the in i t ia l aspect of the QRS complex caused by premature exci tat ion

(preexci tat ion) of the ventr ic les v ia a Bundle of Kent .

Fusion beat:

act ivat ion of the ventr ic les by two di f ferent wave f ronts, resul t ing in an abnormal

appearance of the QRS complexes on the ECG.

Preexcitat ion:

premature act ivat ion of the ventr icu lar myocardium via an abnormal AV pathway cal led

a Bundle of Kent .

Tachyarrhythmia: an abnormal cardiac rhythm wi th a ventr icu lar rate ≥100 beats/min.

Woff–Parkinson–White syndrome:

the c l in ical combinat ion of a short PR interval , an increased durat ion of the QRS

complex caused by an in i t ia l s low def lect ion (del ta wave), and supraventr icu lar

tachyarrhythmias.

REFERENCES 1. Kent AFS. Researches on the st ructure and funct ion of the mammal ian heart . J

Physio l 1893;14:233.

2. Wol f f L. Syndrome of shor t P-R interval wi th abnormal QRS complexes and

paroxysmal tachycardia (Wol f f -Park inson-Whi te syndrome). Circulat ion 1954;10:282.

3. Becker AE, Anderson RH, Durrer D, et a l . The anatomical substrates of Wol f f -

Park inson-Whi te syndrome. Circulat ion 1978;57:870–879.

4. Giard ina ACV, Ehlers KH, Engle MA. Wol f f -Park inson-Whi te syndrome in in fants and

chi ldren: a long term fo l low up study. Br Heart J 1972;34:839–846.

5. Goudevenos JA, Katsouras CS, Graeklas G, et a l . Ventr icu lar pre-exci tat ion in the

general populat ion: a study on the mode of presentat ion and c l in ical course. Heart

2000;83:29–34.

6. Rosenbaum FF, Hecht HH, Wi lson FN, et a l . Potent ia l var iat ions of thorax and

esophagus in anomalous atr ioventr icu lar exci tat ion (Wol f f -Park inson-Whi te syndrome).

Am Heart J 1945;29:281–326.

7. Gal lagher JJ, Gi lber t M, Svenson RH, et a l. Wol f f -Park inson-Whi te syndrome: the

problem, evaluat ion, and surgical correct ion. Circulat ion 1975;51:767–785.

8. Mi ls te in S, Sharma AD, Guiraudon GM, et a l . An a lgor i thm for the

e lectrocardiographic local izat ion of accessory pathways in the Wol l f -Park inson-Whi te

syndrome. Pace 1987;10:555–563.

9. Tonkin AM, Wagner GS, Gal lagher JJ, et a l . In i t ia l forces of ventr icu lar

depolar izat ion in the Wol f f -Park inson-White syndrome: analys is based upon

local izat ion of the accessory pathway by epicard ia l mapping. Circulat ion

1975;52:1030–1036.

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