Chapter 16 Supraventricular Arrhythmiasjunctional tachycardia, there is commonly one-to-
one AV association.
Treatment should be directed at the underlying
condition (Table 16.4).
AV re-entrant tachycardia
Accessory pathways are muscle fi bers that connect
the atrium with the ventricle. Pathways that are
capable of antegrade conduction to the ventricle are
termed “manifest” and are present in 0.15–0.25% of
the general population. Other pathways conduct
retrogradely only and are known as “concealed”.
Approximately 95% of the arrhythmias in patients
with the Wolff–Parkinson–White (WPW) syndrome
are manifest as “orthodromic” tachycardias (ante-
grade conduction over the normal AV node–His
axis and retrograde over the accessory pathway).
About 5% involve “antidromic” tachycardia with
antegrade conduction over the pathway and retro-
grade over the node. A less common form of tachy-
cardia is labeled PJRT and involves retrograde
conduction over a decremental pathway in the pos-
teroseptal region.
The most feared rhythm occurring in patients
with WPW is atrial fi brillation, occurring over a
pathway with short refractory period capable of
rapid conduction to the ventricle. This arrhythmia
is potentially life-threatening. Risk factors include
shortest preexcited RR interval during atrial fi brilla-
tion of <250 ms, multiple pathways, history of rapid
tachycardia and Ebstein’s anomaly.
Acute treatment
Emergency therapy for those with orthodromic
tachycardia involves use of carotid massage and/or
adenosine. Agents that block atrioventricular (AV)
nodal conduction (i.e. IV Ca++ channel blockers or
beta-blockers may be effective). Treatment for those
with rapid preexcited atrial fi brillation include IV
procainamide or ibutilide, if the patient is stable and
emergency direct-current shock if the patient has
hemodynamic instability.
Long-term therapy
Long-term drug therapy has been increasingly
replaced by catheter ablation of the pathways. The
most effective drug regimen is use of a combination
of a Class 1 C agent (propafenone or fl ecainide) and
a beta-blocker agent. Catheter ablation is successful
in approximately 95% of cases and is associated with
signifi cant adverse effects in 1.8–4% including a
0.08–0.13% risk of death (see Table 16.5).
Since publication of the guidelines a prospective
study designed to assess the effi cacy of an experi-
mental Class II agent (azimilide) for patients with
various supraventricular arrhythmias has been pub-
lished [24]. The study contained 56 patients with
PSVT and they found no signifi cant difference in the
time to recurrence of symptoms between treated
patients (18 days) vs. the placebo group (35 days).
The authors concluded that the 125 mg daily dose
of azimilide did not confer a benefi cial effect com-
pared with placebo treatment.
Recent advances include refi nement of ablative
techniques to allow for ablation of anteroseptal
accessory pathways that could not be ablated via a
right or left sided approach. The pathway could be
ablated from the noncoronary cusp of the aortic
valve [25]. Other newer ablative techniques involve
use of navigational systems to allow for more precise
mapping [26], use of cryoablation for pathways
close to the His bundle [27], or the introduction of
epicardial approaches for pathway ablation [28].Treatment of asymptomatic subjects
The treatment of asymptomatic patients with acces-
sory pathways remains controversial. Given the very
low incidence of sudden death as the primary
arrhythmia event and the very low positive predic-
tive value of invasive studies, it is felt that routine
ablation of these pathways are not warranted. The
decision to ablate the pathway(s) in those with high-
risk occupations (i.e. pilots) should be made on
individual considerations.Focal atrial tachycardias
Focal atrial tachycardias (FAT) are identifi ed in the
laboratory by radial spread of activation from a dis-
crete focus. These tachycardias do not occur ran-
domly throughout the atria, but have several sites of
predilection. In the right atrium favored sites include
the crista terminalis, peri-annular region, septum
and the os of the coronary sinus. In the left atrium
sites of predilection include the pulmonary veins,
mitral annulus and appendage. The mechanism of
atrial tachycardia may be due to triggered rhythms,
abnormal automaticity or micro re-entry. Even in
the laboratory setting it is often diffi cult to