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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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