(Circulation. 1996;93:2023-2032.)
© 1996 American Heart Association, Inc.
Articles |
Longitudinal Clinical and Electrophysiological Assessment of Patients With Symptomatic Wolff-Parkinson-White Syndrome and Atrioventricular Node Reentrant Tachycardia
From the Division of Cardiology, Department of Medicine, National Yang-Ming University, School of Medicine and Veterans General Hospital–Taipei (Taiwan), ROC.
Correspondence to Shih-Ann Chen, MD, Division of Cardiology, Department of Medicine, Veterans General Hospital–Taipei, 201 Sec 2 Shih-Pai Rd, Taipei, Taiwan, ROC.
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Abstract |
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Background Functional changes of the accessory AV pathways and dual AV node pathways are very important for patients with Wolff-Parkinson-White syndrome or AV node reentrant tachycardia who refuse to receive long-term medication or radiofrequency catheter ablation. However, no studies of serial clinical and electrophysiological characteristics in these patients have been performed.
Methods and Results One hundred thirteen patients with Wolff-Parkinson-White syndrome or AV node reentrant tachycardia were included in this study. The first and second follow-up electrophysiological studies were performed in years 5 and 10 after the baseline study, respectively. Conduction properties of the accessory pathways became poor over time. After a mean follow-up period of 9±1 years, antegrade ventricular preexcitation and retrograde accessory pathway conduction disappeared in 22.5% and 7.8% (P<.01), respectively; dual AV node pathway physiology persisted and retrograde fast pathway disappeared in 10.8% of the patients. Baseline conduction properties of the antegrade and retrograde accessory pathways and the retrograde fast pathway independently predicted late loss of conduction. Spontaneous disappearance of the original tachyarrhythmias occurred in 10.3% of all patients, and newly developed tachyarrhythmias in 15.2%. The incidence (38.5%) of newly developed atrial fibrillation was significantly higher in patients with manifest accessory pathways. Furthermore, symptom scores and attack frequency increased significantly over time in the patients with accessory pathways and AV node reentrant tachycardia.
Conclusions Disappearance of the original tachycardia and changing patterns of tachycardia, also with an increase in symptom scores and attack frequency, suggested that a detailed evaluation of these events is important and early intervention with radiofrequency ablation would be helpful.
Key Words: electrophysiology • Wolff-Parkinson-White syndrome • atrioventricular node • reentry • tachycardia
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Longitudinal assessment of the electrophysiological characteristics in patients with asymptomatic Wolff-Parkinson-White syndrome has been reported.1 However, no studies of serial clinical and electrophysiological characteristics in patients with symptomatic Wolff-Parkinson-White syndrome and AV node reentrant tachycardia have been performed. Knowledge about the functional changes of accessory AV pathways and dual AV node pathways is very important for patients who refused to receive long-term medication or radiofrequency catheter ablation.
Accessory AV pathways appear to occur during cardiogenesis, and it has been postulated that failure to lose accessory AV pathways during normal cardiac development accounts for their postnatal presence.2 3 4 Concealed accessory AV pathways could not be demonstrated on the ECG during sinus rhythm; they could be confirmed only by ventricular stimuli during electrophysiological study or occurrence of orthodromic tachycardia. Serial 12-lead surface ECGs in young patients with preexcitation usually demonstrated spontaneous disappearance of preexcitation in about one third to one half of patients during the long-term follow-up period.2 5 6 7 Serial changes of electrophysiological characteristics of the accessory AV pathway in the retrograde direction have never been described.
The genesis of dual AV node pathway physiology was not clear. The incidence of AV node reentrant tachycardia was lower in younger children and higher in older children and adults, suggesting that postnatal development of dual AV node pathway physiology would facilitate occurrence of this tachycardia.4 Serial changes of antegrade AV nodal conduction time could be estimated from the PR interval in 12-lead surface ECGs. However, the changes of dual AV node pathway physiology and retrograde fast pathway conduction properties could be demonstrated only by programmed electrical stimuli or occurrence of tachycardia. No studies of serial changes of clinical and electrophysiological characteristics in patients with AV node reentrant tachycardia have been performed.
Changes of the electrophysiological characteristics in patients with accessory AV pathway and dual AV node pathway physiology over time may alter the risk, pattern, and occurrence of symptomatic tachyarrhythmia and may influence decisions on treatment. To answer these questions, we assessed the serial changes of clinical and electrophysiological characteristics of the accessory pathway and dual AV node physiology in patients with symptomatic tachyarrhythmias.
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Methods |
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Between 1983 and 1985, 113 consecutive patients with Wolff-Parkinson-White syndrome or AV node reentrant tachycardia agreed to be enrolled in the study protocol to test serial changes of clinical and electrophysiological characteristics of accessory AV pathway and dual AV node pathway physiology. They had frequent attacks of supraventricular tachycardia before the baseline electrophysiological study (mean number of attacks, 2±1 per month). During the second follow-up electrophysiological studies, most of the patients were advised to receive radiofrequency ablation to cure these tachycardias.
Study Design
After the clinical evaluation and baseline
electrophysiological study, the patients
were advised to receive long-term regular medication according to
the results of electropharmacological tests if there was
hemodynamic compromise, high risk of sudden death, or
high frequency of supraventricular
tachycardia. Regular medication meant that patients
continued to take antiarrhythmic drugs regularly during the
follow-up period. Irregular medication meant that patients did not
take antiarrhythmic drugs regularly but rather only during the period
with frequent attacks of palpitation. A detailed review of clinical
events, physical checkup, 12-lead surface ECG, and use of
antiarrhythmic drugs was performed in the arrhythmia clinic
every 2 months. Patients went to the nearby emergency service for acute
treatment in the event of symptoms. If the patients had aggravation of
recurrent tachycardia, a change of antiarrhythmic drugs or
surgical ablation was recommended.
Considering the possibility of progressive changes of conduction properties, the first follow-up electrophysiological study was performed in year 5 and the second follow-up electrophysiological study in year 10 after the baseline study. If the patients had significant changes of ECG patterns, clinical symptoms, or new arrhythmias, the follow-up electrophysiological study was performed earlier.
Subjective perception of symptoms of paroxysmal supraventricular tachycardia was assessed by a semiquantitative questionnaire established in this laboratory.8 Each patient was asked to quantify each of the following symptoms on a score scale of 0, no symptoms; 1, mild; 2, moderate; and 3, severe: palpitation, asthenia (sensation of fatigue at rest), rest dyspnea, effort dyspnea, dizziness, chest oppression, blurred vision, and syncope (0, none; 1, presyncope; and 2, syncope). Patients were also asked to complete the symptom scores during each year.
Electrophysiological Study
The study protocol was approved by the Human Research
Committee in this institution. All patients were studied in the
postabsorptive, nonsedated state after written informed consent had
been obtained. As described previously, baseline
electrophysiological studies were performed
after antiarrhythmic drugs had been discontinued for at least 5
half-lives in all the patients (amiodarone discontinued for
1.5 months).9 10 The ECG and femoral arterial
pressure were monitored continuously throughout the procedures. In
brief, three multipolar catheters (interelectrode space, 2 mm for
Mansfield-Webster or 5 mm for USCI) were introduced via the femoral
veins and placed in the right atrium, His bundle area, and right
ventricle for recording and stimulation. The multipolar
catheter (USCI) or orthogonal electrode catheter (Mansfield-Webster)
used for coronary sinus recording was introduced
percutaneously into the jugular vein and placed in the
coronary sinus for recording and stimulation.
Intracardiac electrograms were simultaneously displayed
with surface ECG leads I, II, and V1 on a multichannel
oscilloscopic recorder (VR-13, Electronics for Medicine) and were
recorded at a paper speed of 100 to 150 mm/s at a filter frequency
setting of 30 to 500 Hz.
A programmed digital stimulator (DTU model 210 or 215, Bloom Associates, Ltd) was used to deliver electrical impulses of 2.0 ms at twice the late diastolic threshold. The standard protocols included (1) atrial and ventricular incremental pacing at cycle lengths ranging from just under that of sinus rhythm to the minimal cycle lengths maintaining atrioventricular and ventriculoatrial 1:1 conduction, respectively; (2) single and double atrial extrastimuli delivered during high right atrial pacing at one or two cycle lengths and during sinus rhythm; and (3) single and double ventricular extrastimuli delivered during right ventricular apical pacing at cycle lengths of 600 and 400 ms and during sinus rhythm.9 10 In patients with Wolff-Parkinson-White syndrome, left atrial stimulation was also performed. For the induction of atrial flutter/fibrillation, atrial burst pacing was performed if atrial extrastimuli could not induce flutter/fibrillation. Intravenous isoproterenol (1 to 4 µg/min) or atropine (0.02 to 0.04 mg/kg) was used to facilitate induction of tachyarrhythmias. The definitions of various arrhythmias were described previously,9 10 and these study protocols were identical in the three electrophysiological studies. Preexcitation that was found on the ECG and in electrophysiological testing at all times during the baseline and follow-up assessments was defined as persistent preexcitation.
Electropharmacological Study
The patients with pure supraventricular
reentrant tachycardia received electropharmacological study
after intravenous administration of verapamil
(0.15 mg/kg over a period of 2 minutes as a loading dose followed by
continuous infusion at 0.005
mg·kg-1·min-1);
if the patients still had sustained reentrant tachycardia
induced after verapamil, they received the study again
after administration of procainamide (10 mg/kg over a period of
30 minutes as a loading dose followed by continuous infusion at 50
µg·kg-1·min-1)
3 days later; if the patients still had sustained reentrant
tachycardia induced after procainamide, they took
an oral combination of verapamil and procainamide
or amiodarone in the follow-up period. The patients who had
reentrant tachycardia associated with atrial fibrillation
received the electropharmacological study after intravenous
administration of procainamide; if the patients still had
sustained atrial fibrillation with rapid ventricular
preexcitation after procainamide, they took oral
amiodarone in the follow-up period.
Statistical Analysis
All the data are expressed as mean±SD. ANOVA was used to
compare the numerical measurements of the
electrophysiological parameters
and symptom scores obtained in the serial studies. The
2 test with Yates' correction or Fisher's exact
test was used to assess the nonparametric data. The
variables with a value of P<.05 by ANOVA or
2 (Fisher exact) test were put into a Cox
proportional-hazards model. The Cox proportional-hazards model
was used to determine the potential predictors of newly developed
atrial fibrillation and spontaneous loss of these arrhythmogenic
substrates. Proportions of the patients without development of atrial
fibrillation or loss of the arrhythmogenic substrates were
analyzed by the Kaplan-Meier product-limit method, and
comparisons among different groups were performed with the log-rank
test.
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Results |
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After 4 patients who were lost to follow-up and 2 patients who underwent surgical ablation were excluded, 107 patients remained in this study. Patients' ages at the time of enrollment ranged from 11 to 71 years (mean, 45±16 years), and there were 67 male and 46 female patients. Twelve patients had associated cardiovascular diseases (6 hypertension, 1 coronary artery disease, 2 cardiomyopathy, 1 valvular heart disease, and 2 congenital heart disease). The mean follow-up period was 9±1 years (range, 8 to 10 years). None of the patients suffered sudden death.
Patients With Manifest Wolff-Parkinson-White
Syndrome
Clinical Characteristics
Before the baseline
electrophysiological study, all 43 patients
(33 male and 10 female) had AV reciprocating tachycardia,
associated with atrial fibrillation in 27 (62.8%, 23 male and 4
female). Among the 40 patients who completed the follow-up study,
38 (95%) continued to have AV reciprocating tachycardia. Five
of the 27 patients with atrial fibrillation had loss of preexcitation
during the follow-up period; 4 had disappearance of atrial
fibrillation after loss of preexcitation, and 1 still had atrial
fibrillation with conduction through the AV node and newly developed AV
node reentrant tachycardia. Furthermore, 5 (38.5%, 3 male and
2 female) of 13 patients who did not have atrial fibrillation before
the baseline study had newly developed atrial fibrillation with rapid
ventricular preexcitation (Figs 1
and 2). Age, sex, associated
cardiovascular disease, tachycardia cycle
length, effective refractory period of accessory pathways, wavelength,
conduction latency, and effective refractory period of the atrium were
similar between the patients with and without newly developed atrial
fibrillation; the Cox proportional-hazards model also showed that
none of these factors predicted new development of atrial fibrillation.
After the baseline electrophysiological
study, 30 patients (69.8%) received regular medication and 13 (30.2%)
received irregular medication; 24 patients took procainamide,
11 took verapamil, 6 took a combination of
procainamide and verapamil, and 2 took
amiodarone. In the year of the second follow-up study, 4
patients changed to take a combination of procainamide and
verapamil because of worsening symptoms with failure of the
initial drugs. Afterward, 2 patients received surgical ablation because
of drug failure (amiodarone) with severe symptoms, and 1
patient was lost to follow-up (at years 2, 3, and 5 after baseline
study, respectively). During years 8 and 9 after the baseline study, 2
patients (37 and 50 years old, respectively) who took
amiodarone to control tachyarrhythmias (antegrade
effective refractory periods were 200 and 210 ms, antegrade accessory
pathway 1:1 conduction cycle lengths were 220 and 230 ms, and shortest
RR intervals during atrial fibrillation with ventricular
preexcitation were 230 and 240 ms, respectively) had nonfatal cardiac
arrest due to atrial fibrillation with rapid ventricular
preexcitation and had successful resuscitation. The tachycardia
symptom scores increased significantly after year 6 of follow-up,
and attack frequency increased significantly after year 7 (Fig 3); they had successful radiofrequency ablation of
accessory pathways after the second follow-up study.
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Electrophysiological
Characteristics
The electrophysiological
parameters obtained in the baseline study were compared
with those obtained in the follow-up studies (Table 1). Significant changes of
electrophysiological parameters
were found only in the second follow-up study. The surface ECG
showed less preexcitation with increase of PR interval from 90±8 to
104±11 ms (P<.01) and decrease of QRS duration from 132±7
to 117±8 ms (P<.01). Because the tachycardia cycle
length is determined by the conduction properties of AV node and
retrograde accessory pathway, the two conduction routes were examined
to determine the correlation with tachycardia cycle length. The
change of orthodromic tachycardia cycle length correlated
positively with change of AV node Wenckebach block cycle length
(r=.8689, P=.0001); it did not correlate with
change of AV node effective refractory period (r=.29,
P=.816), effective refractory period (r=.07,
P=.6658), or minimal 1:1 conduction cycle length
(r=.18, P=.2796) of retrograde accessory pathway.
Changes of minimal 1:1 conduction cycle lengths of the antegrade and
retrograde accessory pathways showed positive correlation
(r=.5271, P=.0028). Changes of AV node conduction
properties did not correlate with those in the antegrade or retrograde
direction of accessory pathways. The change was more prominent in the
antegrade direction (Fig 4). The baseline and first
follow-up studies showed that 3 of 40 patients needed isoproterenol
to sustain tachycardia; the second follow-up study showed
that 2 patients had noninducible tachycardia and 2 of the other
38 patients needed isoproterenol to sustain tachycardia (Table 1).
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Nine patients had loss of antegrade preexcitation after follow-up
for 6±3 years (range, 4 to 8 years) (Fig 5). Only 1
patient (71 years old in the baseline study) with
catecholamine-sensitive orthodromic tachycardia
in the baseline and first follow-up studies had loss of retrograde
conduction in the second follow-up study, despite administration of
isoproterenol, atropine, and adenosine. The effective
refractory period and minimal 1:1 conduction cycle length of retrograde
accessory pathway of this patient were 400 and 510 ms, respectively.
The ages at the baseline study and at loss of preexcitation were 51±19
and 57±20 years, respectively. Furthermore, the 9 patients had longer
effective refractory periods (437±154 versus 265±52 ms;
P=.01) and longer minimal 1:1 conduction cycle lengths
(342±135 versus 282±49 ms; P=.006) of antegrade accessory
pathways during the baseline study than the patients who retained
persistent preexcitation. The mean age, sex, conduction properties of
the retrograde accessory pathways, shortest RR interval during atrial
fibrillation with ventricular preexcitation, location of
accessory pathways at enrollment, duration of follow-up, and
symptom scores were similar between them (Table 2). The
Cox proportional-hazards model showed that effective refractory
period (hazard ratio, 1.01; P=.0004) and minimal 1:1
conduction cycle length (hazard ratio, 1.01; P=.0009) of the
antegrade accessory pathway at the baseline study predicted loss of
preexcitation during the follow-up period.
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CL) and changes of AV node
Wenckebach block cycle length (
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Patients With Concealed Wolff-Parkinson-White
Syndrome
Clinical Characteristics
Among the 31 patients (15 male and 16 female) with AV
reentrant tachycardia, 1 male patient was associated with
atrial fibrillation. One patient was lost to follow-up at year 6
after the baseline study, and 1 patient had disappearance of this
tachycardia. Two patients (6.9%; 1 man and 1 woman, 59 and 43
years old, respectively) had newly developed atrial fibrillation during
the follow-up period (Figs 1
, 2, and 5); although the incidence
(6.9% versus 38.5%, P<.01) was significantly less than in
patients with manifest accessory pathways, none of the factors
analyzed could predict its occurrence. After the baseline
electrophysiological study, 22 patients
(68.3%) received regular medication and 9 (31.7%) received irregular
medication; 17 patients took procainamide, 8 took
verapamil, and 6 took a combination of procainamide
and verapamil. Three patients changed to take
amiodarone after year 7 of follow-up because of failure of
the combination of verapamil and procainamide. The
tachycardia symptom scores increased significantly after year 8
of follow-up, and significant increases of attack frequency
persisted after year 5 of follow-up in all the patients (Fig 3);
they had successful radiofrequency ablation of accessory pathways after
the second follow-up study.
Electrophysiological
Characteristics
Significant changes of
electrophysiological parameters
were found only in the second follow-up study (Table 1). The change
of tachycardia cycle length correlated with a change of AV node
Wenckebach block cycle length (r=.67, P<.001)
but was not correlated with AV node effective refractory period
(r=.07, P=.7384), minimal 1:1 conduction cycle
length (r=.27, P=.1658), or effective refractory
period (r=.19, P=.1347) of retrograde accessory
pathway. The changes of conduction properties of antegrade AV node and
retrograde accessory pathway did not show significant correlation.
The baseline and first follow-up studies showed that 3 patients
needed isoproterenol to facilitate induction of tachycardia.
The second follow-up study showed absence of retrograde accessory
pathway conduction in 3 patients; isoproterenol infusion could restore
retrograde conduction with appearance of orthodromic
tachycardia in 2 patients, and another patient had permanent
loss of retrograde conduction despite administration of isoproterenol
and atropine (Fig 5). The ages (22, 29, and 59 years), effective
refractory periods (300, 400, and 280 ms), and minimal 1:1 conduction
cycle lengths (300, 410, and 270 ms) of the 3 patients obtained in the
baseline study were similar to those in the other patients. The ages at
loss of retrograde conduction (without isoproterenol infusion) were 32,
39, and 66 years, respectively. The Cox proportional-hazards model
showed that effective refractory period (hazard ratio, 1.03;
P=.0122) and minimal 1:1 conduction cycle length (hazard
ratio, 1.03; P=.0204) of retrograde accessory pathway could
predict loss of retrograde accessory pathway conduction in the
follow-up period.
Patients With AV Node Reentrant
Tachycardia
Clinical Characteristics
Among the 39 patients (19 male and 20 female), 2 were lost to
follow-up at years 2 and 3 after the baseline study, respectively;
33 patients continued to have AV node reentrant tachycardia,
and 4 had disappearance of AV node reentrant tachycardia (loss
of retrograde VA conduction) with newly developed atrial
tachycardia (1 patient) or atrial fibrillation (3 patients,
8.1%, 2 male and 1 female). Although the incidence of atrial
fibrillation was significantly less than in patients with manifest
accessory pathways (8.1 versus 38.5%, P<.01), none of the
factors analyzed could predict its occurrence (Figs 1, 2, and 5). After the baseline electrophysiological
study, 22 patients (56.4%) received regular medication and 17 (43.6%)
received irregular medication; 20 patients took verapamil,
14 took procainamide, and 5 took a combination of
verapamil and procainamide. In the year of the
second follow-up study, 5 patients changed to take a combination of
verapamil and procainamide because of worsening
symptoms with failure of the initial drugs. The tachycardia
symptom scores increased significantly after year 9 of follow-up,
and significant increases of attack frequency persisted after year 7 of
follow-up in all the patients (Fig 3); they had successful
radiofrequency ablation of the slow AV node pathway after the second
follow-up study.
Electrophysiological
Characteristics
Significant changes of
electrophysiological parameters
were found only in the second follow-up study (Table 3). The average AV node reentrant tachycardia
cycle length increased from 325±27 to 353±29 ms (P<.001).
The change of tachycardia cycle length correlated with change
of slow pathway effective refractory period (r=.5274,
P=.0013) and AV node Wenckebach block cycle length
(r=.3684, P=.032); it did not correlate with AH
interval during sinus rhythm (r=.09, P=.6288),
effective refractory period of antegrade fast pathway
(r=.06, P=.7515), effective refractory period
(r=.15, P=.4046), or Wenckebach block cycle
length (r=.06, P=.7311) of retrograde VA
conduction. Furthermore, the changes of antegrade fast and slow pathway
effective refractory periods (r=.7434, P=.0001)
and Wenckebach block cycle length (r=.6871,
P=.0001) showed positive correlation. The changes of
conduction properties of the antegrade and retrograde directions did
not show significant correlation (effective refractory period,
r=.1563, P=.3849; Wenckebach block cycle length,
r=.0704, P=.697).
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The baseline and first follow-up studies showed that 5 of 37
patients needed isoproterenol to sustain tachycardia; the
second follow-up study showed that 4 of the 5 patients had
noninducibility of tachycardia and 7 of the other 33 patients
needed isoproterenol to sustain tachycardia. Loss of retrograde
VA conduction was found in 4 patients despite administration of
isoproterenol and atropine. The duration of follow-up was similar
between them (9±1 versus 9±1 years; P=.852). The 4
patients who lost retrograde conduction were older at enrollment (58,
59, 63, and 65 years, respectively; mean, 61±3 versus 43±14 years;
P<.001) and had longer effective refractory periods
(303±26 versus 258±29 ms; P=.006) and Wenckebach block
cycle lengths (375±19 versus 325±35 ms; P=.009) of
retrograde VA conduction during the baseline study than did the
patients who had persistent VA conduction (Table 4). The
ages at loss of retrograde VA conduction were 63, 65, 69, and 71 years,
respectively (mean, 67±4 years). The Cox proportional-hazards
model showed that retrograde VA Wenckebach block cycle length (hazard
ratio, 1.03; P=.0302) and effective refractory period
(hazard ratio, 1.05; P=.0163) at the initial study predicted
the loss of retrograde VA conduction during the follow-up
period.
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Overall Results
The overall results showed that 107 patients completed the
follow-up electrophysiological studies.
Eleven patients (10.3%) had spontaneous disappearance of the original
tachyarrhythmias (4 atrial fibrillation with
ventricular preexcitation, 3 AV reciprocating
tachycardia, and 4 AV node reentrant tachycardia), and
12 patients (11.2%) had newly developed tachyarrhythmias
(5 atrial fibrillation with ventricular preexcitation, 5
atrial fibrillation with AV node conduction, 1 atrial
tachycardia, and 1 AV node reentrant tachycardia).
Symptom scores and attack frequency increased in all three groups
during the follow-up period. All the patients who still had
symptomatic tachyarrhythmias agreed to receive
radiofrequency catheter ablation of arrhythmogenic substrates during
the second follow-up
electrophysiological study, and all had
successful results.
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Discussion |
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Major Findings
To the best of our knowledge, no similar study can be found in the literature. Both the antegrade and retrograde conduction properties of the accessory pathways became poor in the follow-up study, and poorer conduction properties of these pathways in the baseline studies were predictors of late loss of conduction through these pathways. It was interesting that 22.5% of the patients with ventricular preexcitation lost antegrade accessory pathway conduction, but most of the patients with accessory pathways conducting in the retrograde direction still retained their conduction properties. Antegrade dual AV node pathway physiology persisted in all the patients, but poorer conduction properties of the retrograde fast pathway also predicted late loss of conduction. Spontaneous disappearance of the original tachyarrhythmias occurred in 10.3% of patients, and newly developed tachyarrhythmias occurred in 15.2%; these incidences were significantly higher in the patients with manifest Wolff-Parkinson-White syndrome. Furthermore, the symptom scores and attack frequency also increased significantly during the follow-up period.
Wolff-Parkinson-White Syndrome
It is possible that the accessory pathway progressively loses
its ability to sustain rapid antegrade conduction with time. This
suggestion is supported by the spontaneous disappearance of
preexcitation and reciprocating tachycardia during the
first year of life, by the loss of preexcitation observed in adult
patients, and by the pathological observation of fibrosis in
patients with loss of anterograde conduction over accessory
pathways.1 3 5 6 7 11 12 13 14 15 16
Benson et al3 found spontaneous disappearance of preexcitation (30% of patients) and impairment of retrograde accessory pathway conduction properties in infants. They also observed that isoproterenol was used to facilitate induction of tachycardia in many more patients in the follow-up study. However, the predictors of these late changes were not demonstrated. Klein et al1 evaluated the serial changes of electrophysiological properties in patients with asymptomatic Wolff-Parkinson-White syndrome. They demonstrated progressive impairment of antegrade accessory pathway conduction properties with spontaneous loss of ventricular preexcitation in 31% of patients; furthermore, both advanced age and poor antegrade accessory pathway conduction properties at enrollment were independent predictors of late loss of ventricular preexcitation. However, serial changes of retrograde accessory pathway conduction properties were not reported. Krahn et al14 also showed that age affected the occurrence and persistence of preexcitation, and aging appeared to be associated with a reduction in the frequency of accessory pathway conduction in those patients with preexcitation at enrollment. The present study demonstrated similar findings in patients with symptomatic Wolff-Parkinson-White syndrome.
Disappearance of conduction and change of conduction properties were more prominent in the antegrade than the retrograde direction of accessory pathway. The mechanism of this discrepancy between antegrade and retrograde conduction was controversial. It is possible that the antegrade and retrograde accessory pathway conduction fibers were separately insulated but closely situated17 ; thus, most of the degeneration process did not occur simultaneously in the antegrade and retrograde directions. Furthermore, Leitch et al18 also demonstrated that antiarrhythmic drugs had a greater suppressive effect on the antegrade than on the retrograde accessory pathways. The "mismatch impedance" theory of De la Fuente et al19 might explain part of the findings. An insufficient input from the antegrade accessory pathway made it difficult to activate the ventricular mass to produce ventricular preexcitation due to a "mismatch impedance": for example, electrophysiological impedance due to the relatively small cable capacity of the accessory pathway with respect to the large ventricular muscle mass it must activate. In contrast, the input from the retrograde accessory pathway made it easy to activate the small atrial mass. Thus, most of the retrograde accessory pathways could retain conduction capacity.
The diminution of the accessory pathway conduction properties and reappearance of accessory pathway conduction after isoproterenol infusion implied the possibility of functional and morphological changes and also influenced decisions about the treatment of these patients. Follow-up study showed that these patients were responsive to ß-blockers. In addition, it is possible that the natural history of symptomatic patients was favorably altered through surgical or pharmacological treatment, thus also minimizing the incidence of sudden cardiac death in this cohort. However, almost all previous follow-up studies in patients with Wolff-Parkinson-White syndrome also included patients who were receiving medical treatment.2 5 6 7 12 14 15 It is not clear whether more patients with sudden death would be detected if the follow-up period were longer. The risk might decrease over time because more impairment of accessory pathway conduction properties would occur after a longer follow-up period; however, the progressive impairment of cardiac function over time leading to unstable hemodynamic conditions must be considered.
AV Node Reentrant Tachycardia
Electrophysiological study showed a
positive relation between the aging process and prolongation of the AH
interval, and the incidence of retrograde conduction through the normal
AV conduction axis was lower in the older patients.20 The
major cause of AV conduction impairment in older patients was natural
degeneration of the AV conduction axis. However, the changes of
electrophysiological characteristics of
dual AV node pathway and retrograde fast pathway were not clear. This
study showed no correlation between the changes of the antegrade and
retrograde conduction properties. This discrepancy might be due to
different electrophysiological
characteristics of the antegrade and retrograde AV conduction axis. The
findings from several studies support this hypothesis: a cellular
electrophysiological study showed a
slow-rising action potential in the antegrade propagation, but it
showed a more rapidly rising action potential in the retrograde
propagation21 ; a clinical
electrophysiological study showed a fixed
retrograde HA interval or less prolongation of HA interval compared
with change of antegrade AH interval during programmed stimulation from
the ventricle and atrium, respectively22 23 ; an
electropharmacological study also showed different effects of
antiarrhythmic drugs on the antegrade and retrograde AV conduction axes
(ß-blockers and calcium channel antagonists had more
prominent effects on antegrade conduction, whereas type IA drugs such
as quinidine and procainamide had more prominent effects on
retrograde conduction).24 25 26 27 28
The present study showed that prolongation of tachycardia cycle length over time depended on changes of antegrade slow pathway conduction properties, and this finding was similar to the results of a study by Bauernfeind et al.29 In the follow-up study, more patients needed isoproterenol to facilitate induction of tachycardia because of impairment of retrograde conduction properties over time. A previous study showed that AV node reentrant tachycardia was not easily inducible in the baseline study and needed isoproterenol to facilitate induction when retrograde conduction properties were poor.30
Changing Patterns of Tachyarrhythmias
Mechanisms of atrial fibrillation in patients with paroxysmal
supraventricular tachycardia are
controversial.31 32 33 34 35 36 37 38 39 The possible mechanisms include
hemodynamic deterioration during the
tachycardia, excessive atrial stretch, abnormalities of atrial
conduction and refractoriness (such as wavelength, atrial effective
refractory period, and dispersion of refractoriness), shorter
refractory period of antegrade accessory pathway, greater age, and
associated cardiovascular diseases.31 32 33 34 35 36 37
The present study showed that the patients with antegrade accessory
pathways had a significantly higher incidence of atrial fibrillation,
and 4 (80%) of 5 patients who had atrial fibrillation with
ventricular preexcitation had disappearance of atrial
fibrillation after loss of ventricular preexcitation. These
findings were compatible with previous reports that ablation of the
accessory pathways in patients with manifest Wolff-Parkinson-White
syndrome led to a significant reduction in the incidence of subsequent
atrial fibrillation,31 32 35 36 37 suggesting that the
antegrade accessory pathway is usually related to the spontaneous
occurrence of atrial fibrillation. Clair et al38 and Hamer
et al39 showed that the incidence of atrial fibrillation
in patients with supraventricular tachycardia
increased progressively during the follow-up period. The
present study also found that 10 (12.7%) of the 79 patients
without atrial fibrillation before baseline study had newly developed
atrial fibrillation. Although no factor was found to be predictive of
newly developed atrial fibrillation, the significantly higher incidence
of atrial fibrillation in the patients with manifest
Wolff-Parkinson-White syndrome than in patients with concealed
Wolff-Parkinson-White syndrome or AV node reentrant tachycardia
also suggested that antegrade accessory pathway was important in the
genesis of atrial fibrillation.
Occurrence of tachycardia due to reentry within the AV node has been reported in patients with accessory AV pathway.40 41 42 43 The present study also demonstrated a new appearance of AV node reentrant tachycardia after spontaneous disappearance of accessory pathway conduction. Although the incidence of double tachycardias (coexistent accessory pathway and AV node reentrant tachycardia) is not high and the treatment in this condition is controversial, a detailed diagnostic study before any intervention in patients with accessory pathways is important.42 43
Changes of Tachycardia Symptom Scores and
Frequency
Our laboratory demonstrated that conduction properties were
better in younger patients, but supraventricular
tachycardia was as easily induced in the elderly patients as in
the younger patients.9 44 Clair et al38
demonstrated that age was more important than other clinical
variables in predicting the symptomatic
recurrence of paroxysmal supraventricular
tachycardia and that young patients with paroxysmal
supraventricular tachycardia could expect to
experience more frequent tachycardias as they got older. More
frequent attacks of tachycardia, use of antiarrhythmic drugs,
and the aging process would cause impairment of cardiac function
associated with aggravation of symptoms during attacks of
tachycardia.45 46 47 48 49 These findings could support the
present results that the conduction properties of these
arrhythmogenic pathways became impaired over time, but the
tachycardia symptom scores and frequency increased
significantly over time.
Study Limitations
The present study included only a few children, who are
generally not evaluated by our service. Furthermore, no patients with
multiple accessory pathways were found in the present study; these
patients might affect the follow-up results. In the patients with
disappearance of conduction, the blocking sites (atrium–accessory
pathway or ventricle–accessory pathway interface; retrograde
ventricle–His bundle or His bundle–atrium interface) were not
clear because we did not record the accessory pathway potential or
the retrograde His bundle potential routinely. The transtelephonic
monitoring of ECG was not available in the initial 4 years of this
study, and these new tachyarrhythmias could be demonstrated
when the patients came to the emergency service; thus, the true
incidence of new tachyarrhythmias might be higher. The true
frequency of recurrent tachycardia during the follow-up
period had the same limitation; however, the symptom scores showed
progressive increases. Although these conclusions did not apply to the
occurrence of asymptomatic
supraventricular tachycardia, it is the
symptomatic tachycardias that are the focus of
patients' complaints and physicians' therapeutic interventions.
Conclusions
The considerable numbers of patients with disappearance of
the original tachycardia or changing patterns of
tachycardia, or with increases of symptom scores and attack
frequency, suggested that detailed evaluation of these events is
important for long-term management, and early intervention with
radiofrequency ablation would be helpful.
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Acknowledgments |
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This study was supported in part by grants from the National Science Council (NSC 84-2331-B010-018, 84-2331-B075-004), Taipei, Taiwan, ROC.
Received September 11, 1995; revision received November 9, 1995; accepted November 19, 1995.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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