Catheter Ablation
Content
Catheter Ablation
Overview
Background
Radiofrequency (RF) catheter ablation (RFCA) has revolutionized treatment
for tachyarrhythmias and has become first-line therapy for some tachycardias.
Although developed in the 1980s and widely applied in the 1990s, formalized
guidelines for its use in clinical practice were not developed until some years
later.[1, 2, 3, 4]
Catheters were first used for intracardiac recording and stimulation in the late
1960s, but surgical treatment for refractory tachyarrhythmias was the
mainstay of nonpharmacologic therapy until it was superseded by catheter
ablation. The initial energy source used was direct current (DC) from a
standard external defibrillator. A shock was delivered between the distal
catheter electrode and a cutaneous surface electrode; however, this highvoltage discharge was difficult to control and could cause extensive tissue
damage.
RF energy, a low-voltage, high-frequency form of electrical energy familiar to
physicians from its use in surgery (eg, electrocautery), quickly supplanted DC
ablation. The relative safety of RF energy has contributed to the widespread
adoption of catheter ablation as a therapeutic modality.
RF energy produces small, homogeneous, necrotic lesions by heating tissue.
Lesion size is influenced, in part, by the length of the distal ablation electrode
and the type of catheter (standard vs saline-cooled). With typical power
settings and good catheter contact pressure with cardiac tissue, lesions are
minimally about 5-7 mm in diameter and 3-5 mm in depth.
Future directions
A curative procedure for atrial fibrillation (AF) is a major goal in clinical cardiac
electrophysiology. Success has been achieved in patients with paroxysmal
lone AF by eliminating conduction from the pulmonary veins to the left atrium,
as many of these episodes are triggered by rapid electrical activity arising
from tissue near the pulmonary vein ostia or from muscle sleeves surrounding
the proximal veins. Other forms of AF may require some degree of substrate
ablation (eg, linear transmural lesions in the left atrium).
Techniques are evolving to address the challenge of a catheter-based cure for
all forms of AF. Three-dimensional electroanatomic maps, overlaid on
magnetic resonance imaging (MRI) or computed tomography (CT) scans of
the left atrium, can facilitate navigation of the catheter and mapping of the
arrhythmogenic substrate. Intracardiac echocardiography may also help in
avoiding collateral damage to the pulmonary veins or esophagus, ensuring
adequate endocardial contact, and monitoring for complications (eg,
pericardial effusion and thrombus development).
Alternative energy sources are being investigated in the ablation of AF (eg,
balloon-based technologies using cryoablation,[5] ultrasound, and laser). In
addition, robotic catheter navigation is now available to deliver RFCA.
Research is also focused on developing better methods and tools for catheter
ablation of ventricular tachycardia (VT), and even ventricular fibrillation (VF),
in patients with structural heart disease. Epicardial electrophysiology via
subxiphoid pericardial puncture is a relatively new frontier; some
tachyarrhythmia substrates (especially VT in nonischemic cardiomyopathy)
cannot be reached from the endocardium.
Indications
There are three class I indications for catheter ablation. The first is
symptomatic supraventricular tachycardia (SVT) due to atrioventricular (AV)
nodal reentrant tachycardia (AVNRT), Wolff-Parkinson-White (WPW)
syndrome, unifocal atrial tachycardia, or atrial flutter (especially common right
atrial forms). For these conditions, catheter ablation is first-line therapy if that
is the patient’s preference.
The second indication is AF with lifestyle-impairing symptoms and inefficacy or
intolerance of at least one antiarrhythmic agent.[6, 3] Both left atrial ablation for
restoration of sinus rhythm and AV junction ablation for rate control are class I
indications, depending on the circumstance.
The third indication is symptomatic VT.[7] Catheter ablation is first-line therapy
in idiopathic VT if that is the patient’s preference. In structural heart disease,
catheter ablation is generally performed for drug inefficacy or intolerance or as
adjunctive therapy in patients with an implantable cardioverterdefibrillator (ICD) who are experiencing frequent ICD discharges.
Uncommon indications for catheter ablation include the following:
Symptomatic drug-refractory (inefficacy or intolerance) idiopathic sinus
tachycardia
Lifestyle-impairing ectopic beats
Symptomatic junctional ectopic tachycardia
RFCA has been applied to most clinical tachycardias, even to polymorphic VT
and VF in preliminary studies. Success rates are highest in patients with
common forms of SVT, namely AVNRT and orthodromic reciprocating
tachycardia (ORT).
Contraindications
Few absolute contraindications to RFCA exist. Left atrial ablation and ablation
for persistent atrial flutter should not be performed in the presence of known
atrial thrombus. Similarly, mobile left ventricular thrombus would be a
contraindication to left ventricular ablation.
Mechanical prosthetic heart valves are generally not crossed with ablation
catheters. Women of reproductive age should not be exposed to fluoroscopy if
any possibility exists that they are pregnant.
Outcomes
Atrial fibrillation
RFCA of the AV junction results in excellent rate control, relieves palpitations,
and improves functional capacity. However, patients who undergo this
procedure require permanent pacemaker implantation to manage the resulting
AV block and require warfarin therapy to prevent stroke because the AF itself
is not affected. AV nodal modification is less therapeutic than AV junction
ablation and may result in late heart block.
Single-procedure success rates for curing AF with RFCA are as high as 80%
for paroxysmal AF in the absence of structural heart disease and may be as
low as 50% or less in patients with persistent AF in the presence of structural
heart disease and left atrial enlargement.[8] Repeat procedures are typically
needed in at least 25% of patients and result in an increase in these success
rates.
Success rates for AF ablation have historically been based on patient
symptoms and periodic electrocardiographic (ECG) monitoring. Success rates
are lower if intensive ambulatory monitoring to detect asymptomatic AF
recurrence is used, such as daily monitoring for a month with an auto-
triggering event monitor. Some patients require the use of previously
ineffective antiarrhythmic drugs to maintain success.
Supraventricular tachyarrhythmias
The common forms of SVT (eg, AVNRT, SVT associated with WPW
syndrome) are usually curable with a single procedure; the success rate is
typically 90-95%. Cure rates for unifocal atrial tachycardia and common right
atrial flutter are somewhat lower but still approach 90%. Recurrent
tachyarrhythmias typically occur in the first few months after ablation and may
be amenable to cure with a second procedure.
AVNRT is usually amenable to cure with a slow pathway ablation near the
inferior atrial septum, where the risk of heart block is 1-2% with RF energy. In
those uncommon cases where RF ablation near the compact AV node is
required (eg, fast pathway ablation for AVNRT or an accessory pathway in a
para-Hisian location), the risk of heart block may approach 5% or a little
higher.
In a number of centers, catheter-based cryoablation, rather than RFCA, is
used near the compact AV node to minimize the risk of heart block. With
cryoablation, heart block is generally reversible with prompt rewarming.
However, cryoablation appears to be slightly less effective than RF as an
energy source, especially for deep accessory pathways.
Ventricular tachyarrhythmias
Idiopathic VT is curable (success rate, ~80%), provided that it is readily
inducible during the electrophysiologic study. The most common location for
these VTs is the right ventricular outflow tract. Because these VTs are usually
not reentrant in nature, a significant percentage are not inducible. Some
cannot be ablated because of their deep septal location or their epicardial
location near a coronary artery.
Of patients with VT associated with structural heart disease, half to two thirds
can obtain palliation with catheter ablation. Extensive scarring in these
ventricles may limit the efficacy of the relatively small lesions made by RFCA,
and multiple VT circuits may also contribute to this moderate success rate. In
practice, many of these patients have implantable cardioverter-defibrillators
(ICDs), and catheter ablation is used as adjunctive therapy for frequent device
activations.
For patients with structural heart disease and stable VT, the potential benefit
of catheter ablation before implantation of an ICD was demonstrated in the
Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) study.
[9]
This prospective, randomized, controlled international trial in 104 patients
found that time to recurrence of VT or VF was longer in the ablation group
(median, 18.6 months) than in the control group (5.9 months). At 2 years,
estimates for survival free from VT or VF were 47% in the ablation group and
29% in the control group.
Periprocedural Care
Preprocedural planning
The preprocedural evaluation always includes a thorough history and physical
examination, as well as a review of electrocardiograms (ECGs; 12-lead, if
available) obtained during the tachycardia and in sinus rhythm. At a minimum,
preprocedural blood work typically includes a complete blood count and an
assessment of renal function and electrolyte levels.
An echocardiogram is frequently obtained to exclude structural heart disease.
Other tests that are indicated in specific situations include exercise testing
with or without cardiac imaging (especially for exercise-induced
tachyarrhythmias), and cardiac catheterization.
The patient should fast overnight before the procedure. Cardiac medications
with electrophysiologic effects (eg, beta blockers, calcium channel blockers,
digoxin, and class I and III antiarrhythmic drugs) are often tapered or
discontinued before the procedure. Warfarin may or may not be held prior to
the procedure. For example, performing left atrial ablation for atrial fibrillation
on warfarin may reduce thromboembolic complications.[10]
Patient preparation
Catheter ablation typically requires that the patient be under conscious
sedation with intravenous tranquilizers and narcotics. General anesthesia is
used in children and selected adults.
Monitoring and follow-up
After generic supraventricular tachcardia (SVT) ablation or idiopathic
ventricular tachycardia (VT) ablation, some physicians empirically treat
patients with 4 weeks of aspirin therapy with the aim of potentially reducing
the risk of thromboembolic sequelae.
Anticoagulation with warfarin or one of the newer agents is typically employed
for at least 1 month after ablation for patients presenting in persistent atrial
flutter and for 3 months after left atrial ablation for patients with AF.
Echocardiography is not routinely performed unless a complication (eg,
pericardial effusion) may have occurred. Postprocedural electrophysiologic
testing is not routinely performed unless recurrent tachyarrhythmias are
suspected.
Technique
Approach considerations
Typically, two to five electrode catheters are percutaneously inserted via the
femoral or internal jugular veins and are positioned within the left heart, the
right heart, or both. Multiple catheters are needed to induce and map various
tachyarrhythmias before radiofrequency (RF) catheter ablation (RFCA).
Cannulation of the coronary sinus is helpful to map left-sided accessory
pathways or evaluate other left-sided tachyarrhythmia substrates.
For left-heart catheterization, one of the following two approaches may be
taken:
Transseptal catheterization via the interatrial septum
Retrograde catheterization across the aortic valve
The latter is typically reserved for ventricular tachycardia (VT) ablations or
accessory pathway ablations.
Anticoagulation with intravenous (IV) heparin is used to reduce the risk of
periprocedural thromboembolism.
Atrial fibrillation
RFCA of the atrioventricular (AV) junction is the simplest catheter ablation
procedure performed in patients with atrial fibrillation (AF). AV nodal
modification is less effective and is not frequently performed except in an
attempt to avoid pacemaker implantation. Both of these approaches are used
to achieve good rate control in AF, but unlike ablation techniques in atrial
tissue, neither one restores normal sinus rhythm. In addition, AV junction
ablation mandates permanent pacemaker implantation.
Catheter ablation of atrial tissue to cure AF continues to evolve. The
procedure is technically demanding and is both more risky and less
successful than AV junction ablation. Nevertheless, the observation of
Haissaguerre[11] and others that pulmonary vein foci can trigger AF has
stimulated much additional research, and there is considerable scientific
excitement that this common tachyarrhythmia may be amenable to a curative
catheter procedure.
For catheter ablation of atrial tissue for AF, the most commonly used
technique is a wide circumferential ablation around the pulmonary veins (see
the image below). The goal is to electrically isolate rapid electrical activity
arising from inside the veins, or adjacent to the pulmonary vein ostia, from the
rest of the left atrium.
Electroanatomic map of posterior
left atrium, illustrating pulmonary veins: right superior pulmonary vein (RSPV), right
inferior pulmonary vein (RIPV), left superior pulmonary vein (LSPV), and left inferior
pulmonary vein (LIPV). Red circles represent actual discrete radiofrequency (RF)
applications, predominantly delivered in circumferential pattern around the pulmonary
veins. This ablation strategy can isolate pulmonary vein foci that initiate atrial fibrillation
(AF) or alter substrate of left atrium to inhibit fibrillatory activity due to reentry. Image
courtesy of American College of Cardiology Foundation.
No consensus exists on the optimal left atrial ablation technique, beyond
robust pulmonary vein isolation, nor is there a consensus on what constitutes
a clinically successful procedure. Nevertheless, evidence is accruing that
catheter ablation for AF is more effective than antiarrhythmic drug therapy,
especially for patients in whom antiarrhythmic pharmacotherapy has already
failed. Guidelines for the management of AF list catheter ablation as a
reasonable strategy for selected patients with lone, paroxysmal AF even in the
absence of attempted antiarrhythmic drug therapy.[10]
The complete surgical Maze procedure (incisions in both atria with or without
transmural RF lesions) is still the most effective technique for potentially
curing AF in all comers, regardless of chronicity or whether structural heart
disease is present. The best success rates with left atrial catheter ablation are
in patients with paroxysmal AF and hearts that are not too structurally
abnormal.
Atrial flutter
Atrial flutter is most commonly due to a large reentrant circuit in the right
atrium, involving an isthmus of tissue between the tricuspid valve annulus and
the inferior vena cava. Most commonly, reentry proceeds counterclockwise up
the atrial septum and down the lateral wall of the right atrium, inscribing
inverted (ie, "sawtooth") flutter waves in the inferior leads and upright P waves
in V1 (see the images below).
Schema of common variety of atrial flutter.
Reentry circuit is confined to right atrium and circulates as counterclockwise
macroreentrant circuit proceeding superiorly over atrial septum and inferiorly over lateral
atrial wall. Wave front circulates through narrow isthmus of tissue between tricuspid
valve annulus and inferior vena cava. Linear ablation across this isthmus (cavotricuspid
isthmus) cures this common form of atrial flutter.
Typical counterclockwise atrial
flutter (most common form of atrial flutter in patients who have not had prior ablation).
Cardinal features are perfectly regular atrial rhythm with inverted P waves inferiorly that
have positive overshoot, upright P waves in V1, and inverted P waves in V6.
Clockwise reentry using this same circuit can also occur, giving upright P
waves inferiorly and inverted P waves in V1. Linear ablation of the
cavotricuspid isthmus cures these common forms of atrial flutter. (See the
video below.)
Three-dimensional electroanatomic map of cavotricuspid isthmus flutter. Colors
progress from red to purple and represent relative conduction time in right atrium (early
to late). Ablation line (red dots) has been created from tricuspid annulus to inferior vena
cava. This interrupts flutter circuit.
Non–isthmus-dependent flutters can occur elsewhere in the right atrium, as
well as in the left atrium. Left atrial flutters are uncommon, may be difficult to
ablate, and generally require a three-dimensional mapping system to facilitate
the procedure.
Atrioventricular nodal reentrant tachycardia
In the common form of AV nodal reentrant tachycardia (AVNRT), the inferior
atrionodal input to the AV node serves as the anterograde limb (ie, the slow
pathway) of the reentry circuit, and the superior atrionodal input serves as the
retrograde limb (ie, the fast pathway). Typically, AVNRT can be cured by
targeting the slow pathway near the inferior tricuspid valve annulus at the level
of the coronary sinus os or somewhat higher.
The risk of iatrogenic heart block with ablation in this region is quite low (12%) when RF energy is used and close to zero when cryoablation is
performed. Targeting the slow pathway is safer than targeting the fast
pathway, which is located closer to the compact AV node. (See the images
below.)
Diagrammatic schema of typical
type of atrioventricular (AV) nodal reentrant tachycardia (AVNRT). Slow pathway
(dashed arrow) is usual anterograde limb of reentry circuit and usual ablation target
area (shaded). Fast pathway (solid arrow) is usual retrograde limb of reentry circuit and
commonly activates atria simultaneously with ventricular activation, producing typical
ECG finding of AVNRT shown below. P wave is not visible, because it is buried in QRS
complex. Infrequently, reentry circuit is reversed, with anterograde conduction over fast
pathway and retrograde conduction over slow pathway, producing atypical ECG finding
of AVNRT shown in lower rhythm strip of figure (ie, long R-P tachycardia, in which
interval between QRS complex and retrograde P wave is longer than subsequent P-R
interval, and P wave is in second half of R-R interval). Fast pathway is close to compact
AV node, and ablation in this area is avoided if possible because of risk of iatrogenic
heart block.
Pseudo S waves inferiorly are
retrograde P waves. This short interval (no isoelectric baseline) between QRS complex
and retrograde P wave is highly specific for atrioventricular (AV) nodal reentrant
tachycardia (AVNRT). Pseudo R wave in V1 may also be observed but is not seen here.
In many instances, retrograde P wave occurs during QRS activation and is not
observed; this "no-P-wave" tachycardia also suggests AVNRT.
Sinus rhythm in same patient with
atrioventricular (AV) nodal reentrant tachycardia (AVNRT) as in preceding ECG. Note
that pseudo S waves are no longer visible.
Orthodromic reciprocating tachycardia
In orthodromic reciprocating tachycardia (ORT), the AV node serves as the
anterograde limb, and an accessory AV connection (typically called an
accessory pathway) serves as the retrograde limb (see the images below).
Schema of orthodromic
reciprocating tachycardia (ORT). Atrioventricular (AV) node serves as anterograde limb,
whereas accessory pathway (AV connection) serves as retrograde limb.
Supraventricular tachycardia
(SVT) in patient with orthodromic reciprocating tachycardia (ORT) due to concealed
pathway. Note retrograde P wave, seen best in lead V2, separated from QRS complex
by isoelectric baseline. This pattern of "short R-P tachycardia" (in which interval
between QRS complex and retrograde P wave is shorter than subsequent P-R interval
and P wave is in first half of R-R interval) suggests SVT incorporating accessory
pathway.
If an accessory pathway only conducts retrograde, it is termed a concealed
accessory pathway because it is not identifiable on an electrocardiogram
(ECG) in sinus rhythm (compare with Wolff-Parkinson-White [WPW] syndrome
below). Typically, ORT can be cured by targeting the accessory pathway as it
crosses the mitral or tricuspid valve annulus.
Wolff-Parkinson-White syndrome
Whereas ORT uses an accessory pathway in the retrograde direction, WPW
syndrome by definition indicates an accessory pathway capable of
anterograde conduction and is manifest by preexcitation (delta waves) on the
sinus rhythm ECG.
AF in WPW syndrome may result in life-threateningly fast anterograde
conduction over the accessory pathway, manifested by an irregular widecomplex (preexcited) tachycardia that can sometimes degenerate to
ventricular fibrillation (VF). AF in WPW syndrome may be triggered by ORT.
Ablation of the accessory pathway cures WPW syndrome, eliminating ORT, as
well as AF, in the majority of patients.
Unifocal atrial tachycardia
Unifocal atrial tachycardia, which can arise from either atrium or the
noncoronary cusp of the aorta, is somewhat more challenging to ablate than
the more common forms of generic supraventricular tachycardia (SVT). For
those tachycardias originating from the left atrium, transseptal catheterization
via a patent foramen ovale or transseptal puncture is usually required.
Ventricular tachycardia
Idiopathic VT most commonly arises from the right ventricular outflow tract
and less commonly originates in the inferoseptal left ventricle about two thirds
of the way toward the apex from the base of the left ventricle. These forms of
VT are amenable to catheter ablation, though success rates are somewhat
lower than those for the common forms of SVT.
VT in structural heart disease is also amenable to ablation. Some form of
three-dimensional electroanatomic mapping is employed for these complex
ablations to identify the scar that contributes to the anatomic substrate for
reentry. Intracardiac echocardiography during the procedure and
preprocedural imaging with magnetic resonance imaging (MRI) or computed
tomography (CT) are also used in some instances. Anatomy from
such imaging can be integrated with the electroanatomic map if
necessary. Some VT substrates, especially VT in nonischemic
cardiomyopathy, are not reachable from the endocardium. In these instances,
percutaneous epicardial mapping and ablation are necessary.
Complications
The radiation risk from catheter ablation is low, but it may exceed the risk from
common radiologic procedures. The average risk of genetic defects has been
computed at 1 case per million births. The average risk of fatal malignancies
ranges from 0.3 to 2.3 deaths per 1000 cases for every 60 minutes of
fluoroscopy.[12] Many ablation procedures require less than 60 minutes of
fluoroscopy.
Major complications occur in approximately 3% of patients who undergo
ablation procedures, including thromboembolism in fewer than 1% (higher in
some AF ablation series) and death in 0.1-0.2% of all procedures. The
incidence of cardiac complications varies according to the site and type of
ablation. Cardiac complications include the following:
High-grade AV block
Cardiac tamponade (highest in AF ablation, up to 6%)
Coronary artery spasm/thrombosis
Pericarditis
Valve trauma
Vascular complications, which occur in approximately 2-4% of procedures,
include the following:
Retroperitoneal bleeding
Hematoma
Vascular injury
Transient ischemic attack/stroke
Hypotension
Thromboembolism or air embolism
Pulmonary complications include the following:
Pulmonary hypertension, with or without hemoptysis (secondary to
pulmonary vein stenosis)
Pneumothorax
Miscellaneous complications include the following:
Left atrial–esophageal fistula
Acute pyloric spasm/gastric hypomotility
Phrenic nerve paralysis
Radiation- or electricity-induced skin damage
Infection at access site
Inappropriate sinus tachycardia
Proarrhythmia
Overview
Background
Radiofrequency (RF) catheter ablation (RFCA) has revolutionized treatment
for tachyarrhythmias and has become first-line therapy for some tachycardias.
Although developed in the 1980s and widely applied in the 1990s, formalized
guidelines for its use in clinical practice were not developed until some years
later.[1, 2, 3, 4]
Catheters were first used for intracardiac recording and stimulation in the late
1960s, but surgical treatment for refractory tachyarrhythmias was the
mainstay of nonpharmacologic therapy until it was superseded by catheter
ablation. The initial energy source used was direct current (DC) from a
standard external defibrillator. A shock was delivered between the distal
catheter electrode and a cutaneous surface electrode; however, this highvoltage discharge was difficult to control and could cause extensive tissue
damage.
RF energy, a low-voltage, high-frequency form of electrical energy familiar to
physicians from its use in surgery (eg, electrocautery), quickly supplanted DC
ablation. The relative safety of RF energy has contributed to the widespread
adoption of catheter ablation as a therapeutic modality.
RF energy produces small, homogeneous, necrotic lesions by heating tissue.
Lesion size is influenced, in part, by the length of the distal ablation electrode
and the type of catheter (standard vs saline-cooled). With typical power
settings and good catheter contact pressure with cardiac tissue, lesions are
minimally about 5-7 mm in diameter and 3-5 mm in depth.
Future directions
A curative procedure for atrial fibrillation (AF) is a major goal in clinical cardiac
electrophysiology. Success has been achieved in patients with paroxysmal
lone AF by eliminating conduction from the pulmonary veins to the left atrium,
as many of these episodes are triggered by rapid electrical activity arising
from tissue near the pulmonary vein ostia or from muscle sleeves surrounding
the proximal veins. Other forms of AF may require some degree of substrate
ablation (eg, linear transmural lesions in the left atrium).
Techniques are evolving to address the challenge of a catheter-based cure for
all forms of AF. Three-dimensional electroanatomic maps, overlaid on
magnetic resonance imaging (MRI) or computed tomography (CT) scans of
the left atrium, can facilitate navigation of the catheter and mapping of the
arrhythmogenic substrate. Intracardiac echocardiography may also help in
avoiding collateral damage to the pulmonary veins or esophagus, ensuring
adequate endocardial contact, and monitoring for complications (eg,
pericardial effusion and thrombus development).
Alternative energy sources are being investigated in the ablation of AF (eg,
balloon-based technologies using cryoablation,[5] ultrasound, and laser). In
addition, robotic catheter navigation is now available to deliver RFCA.
Research is also focused on developing better methods and tools for catheter
ablation of ventricular tachycardia (VT), and even ventricular fibrillation (VF),
in patients with structural heart disease. Epicardial electrophysiology via
subxiphoid pericardial puncture is a relatively new frontier; some
tachyarrhythmia substrates (especially VT in nonischemic cardiomyopathy)
cannot be reached from the endocardium.
Indications
There are three class I indications for catheter ablation. The first is
symptomatic supraventricular tachycardia (SVT) due to atrioventricular (AV)
nodal reentrant tachycardia (AVNRT), Wolff-Parkinson-White (WPW)
syndrome, unifocal atrial tachycardia, or atrial flutter (especially common right
atrial forms). For these conditions, catheter ablation is first-line therapy if that
is the patient’s preference.
The second indication is AF with lifestyle-impairing symptoms and inefficacy or
intolerance of at least one antiarrhythmic agent.[6, 3] Both left atrial ablation for
restoration of sinus rhythm and AV junction ablation for rate control are class I
indications, depending on the circumstance.
The third indication is symptomatic VT.[7] Catheter ablation is first-line therapy
in idiopathic VT if that is the patient’s preference. In structural heart disease,
catheter ablation is generally performed for drug inefficacy or intolerance or as
adjunctive therapy in patients with an implantable cardioverterdefibrillator (ICD) who are experiencing frequent ICD discharges.
Uncommon indications for catheter ablation include the following:
Symptomatic drug-refractory (inefficacy or intolerance) idiopathic sinus
tachycardia
Lifestyle-impairing ectopic beats
Symptomatic junctional ectopic tachycardia
RFCA has been applied to most clinical tachycardias, even to polymorphic VT
and VF in preliminary studies. Success rates are highest in patients with
common forms of SVT, namely AVNRT and orthodromic reciprocating
tachycardia (ORT).
Contraindications
Few absolute contraindications to RFCA exist. Left atrial ablation and ablation
for persistent atrial flutter should not be performed in the presence of known
atrial thrombus. Similarly, mobile left ventricular thrombus would be a
contraindication to left ventricular ablation.
Mechanical prosthetic heart valves are generally not crossed with ablation
catheters. Women of reproductive age should not be exposed to fluoroscopy if
any possibility exists that they are pregnant.
Outcomes
Atrial fibrillation
RFCA of the AV junction results in excellent rate control, relieves palpitations,
and improves functional capacity. However, patients who undergo this
procedure require permanent pacemaker implantation to manage the resulting
AV block and require warfarin therapy to prevent stroke because the AF itself
is not affected. AV nodal modification is less therapeutic than AV junction
ablation and may result in late heart block.
Single-procedure success rates for curing AF with RFCA are as high as 80%
for paroxysmal AF in the absence of structural heart disease and may be as
low as 50% or less in patients with persistent AF in the presence of structural
heart disease and left atrial enlargement.[8] Repeat procedures are typically
needed in at least 25% of patients and result in an increase in these success
rates.
Success rates for AF ablation have historically been based on patient
symptoms and periodic electrocardiographic (ECG) monitoring. Success rates
are lower if intensive ambulatory monitoring to detect asymptomatic AF
recurrence is used, such as daily monitoring for a month with an auto-
triggering event monitor. Some patients require the use of previously
ineffective antiarrhythmic drugs to maintain success.
Supraventricular tachyarrhythmias
The common forms of SVT (eg, AVNRT, SVT associated with WPW
syndrome) are usually curable with a single procedure; the success rate is
typically 90-95%. Cure rates for unifocal atrial tachycardia and common right
atrial flutter are somewhat lower but still approach 90%. Recurrent
tachyarrhythmias typically occur in the first few months after ablation and may
be amenable to cure with a second procedure.
AVNRT is usually amenable to cure with a slow pathway ablation near the
inferior atrial septum, where the risk of heart block is 1-2% with RF energy. In
those uncommon cases where RF ablation near the compact AV node is
required (eg, fast pathway ablation for AVNRT or an accessory pathway in a
para-Hisian location), the risk of heart block may approach 5% or a little
higher.
In a number of centers, catheter-based cryoablation, rather than RFCA, is
used near the compact AV node to minimize the risk of heart block. With
cryoablation, heart block is generally reversible with prompt rewarming.
However, cryoablation appears to be slightly less effective than RF as an
energy source, especially for deep accessory pathways.
Ventricular tachyarrhythmias
Idiopathic VT is curable (success rate, ~80%), provided that it is readily
inducible during the electrophysiologic study. The most common location for
these VTs is the right ventricular outflow tract. Because these VTs are usually
not reentrant in nature, a significant percentage are not inducible. Some
cannot be ablated because of their deep septal location or their epicardial
location near a coronary artery.
Of patients with VT associated with structural heart disease, half to two thirds
can obtain palliation with catheter ablation. Extensive scarring in these
ventricles may limit the efficacy of the relatively small lesions made by RFCA,
and multiple VT circuits may also contribute to this moderate success rate. In
practice, many of these patients have implantable cardioverter-defibrillators
(ICDs), and catheter ablation is used as adjunctive therapy for frequent device
activations.
For patients with structural heart disease and stable VT, the potential benefit
of catheter ablation before implantation of an ICD was demonstrated in the
Ventricular Tachycardia Ablation in Coronary Heart Disease (VTACH) study.
[9]
This prospective, randomized, controlled international trial in 104 patients
found that time to recurrence of VT or VF was longer in the ablation group
(median, 18.6 months) than in the control group (5.9 months). At 2 years,
estimates for survival free from VT or VF were 47% in the ablation group and
29% in the control group.
Periprocedural Care
Preprocedural planning
The preprocedural evaluation always includes a thorough history and physical
examination, as well as a review of electrocardiograms (ECGs; 12-lead, if
available) obtained during the tachycardia and in sinus rhythm. At a minimum,
preprocedural blood work typically includes a complete blood count and an
assessment of renal function and electrolyte levels.
An echocardiogram is frequently obtained to exclude structural heart disease.
Other tests that are indicated in specific situations include exercise testing
with or without cardiac imaging (especially for exercise-induced
tachyarrhythmias), and cardiac catheterization.
The patient should fast overnight before the procedure. Cardiac medications
with electrophysiologic effects (eg, beta blockers, calcium channel blockers,
digoxin, and class I and III antiarrhythmic drugs) are often tapered or
discontinued before the procedure. Warfarin may or may not be held prior to
the procedure. For example, performing left atrial ablation for atrial fibrillation
on warfarin may reduce thromboembolic complications.[10]
Patient preparation
Catheter ablation typically requires that the patient be under conscious
sedation with intravenous tranquilizers and narcotics. General anesthesia is
used in children and selected adults.
Monitoring and follow-up
After generic supraventricular tachcardia (SVT) ablation or idiopathic
ventricular tachycardia (VT) ablation, some physicians empirically treat
patients with 4 weeks of aspirin therapy with the aim of potentially reducing
the risk of thromboembolic sequelae.
Anticoagulation with warfarin or one of the newer agents is typically employed
for at least 1 month after ablation for patients presenting in persistent atrial
flutter and for 3 months after left atrial ablation for patients with AF.
Echocardiography is not routinely performed unless a complication (eg,
pericardial effusion) may have occurred. Postprocedural electrophysiologic
testing is not routinely performed unless recurrent tachyarrhythmias are
suspected.
Technique
Approach considerations
Typically, two to five electrode catheters are percutaneously inserted via the
femoral or internal jugular veins and are positioned within the left heart, the
right heart, or both. Multiple catheters are needed to induce and map various
tachyarrhythmias before radiofrequency (RF) catheter ablation (RFCA).
Cannulation of the coronary sinus is helpful to map left-sided accessory
pathways or evaluate other left-sided tachyarrhythmia substrates.
For left-heart catheterization, one of the following two approaches may be
taken:
Transseptal catheterization via the interatrial septum
Retrograde catheterization across the aortic valve
The latter is typically reserved for ventricular tachycardia (VT) ablations or
accessory pathway ablations.
Anticoagulation with intravenous (IV) heparin is used to reduce the risk of
periprocedural thromboembolism.
Atrial fibrillation
RFCA of the atrioventricular (AV) junction is the simplest catheter ablation
procedure performed in patients with atrial fibrillation (AF). AV nodal
modification is less effective and is not frequently performed except in an
attempt to avoid pacemaker implantation. Both of these approaches are used
to achieve good rate control in AF, but unlike ablation techniques in atrial
tissue, neither one restores normal sinus rhythm. In addition, AV junction
ablation mandates permanent pacemaker implantation.
Catheter ablation of atrial tissue to cure AF continues to evolve. The
procedure is technically demanding and is both more risky and less
successful than AV junction ablation. Nevertheless, the observation of
Haissaguerre[11] and others that pulmonary vein foci can trigger AF has
stimulated much additional research, and there is considerable scientific
excitement that this common tachyarrhythmia may be amenable to a curative
catheter procedure.
For catheter ablation of atrial tissue for AF, the most commonly used
technique is a wide circumferential ablation around the pulmonary veins (see
the image below). The goal is to electrically isolate rapid electrical activity
arising from inside the veins, or adjacent to the pulmonary vein ostia, from the
rest of the left atrium.
Electroanatomic map of posterior
left atrium, illustrating pulmonary veins: right superior pulmonary vein (RSPV), right
inferior pulmonary vein (RIPV), left superior pulmonary vein (LSPV), and left inferior
pulmonary vein (LIPV). Red circles represent actual discrete radiofrequency (RF)
applications, predominantly delivered in circumferential pattern around the pulmonary
veins. This ablation strategy can isolate pulmonary vein foci that initiate atrial fibrillation
(AF) or alter substrate of left atrium to inhibit fibrillatory activity due to reentry. Image
courtesy of American College of Cardiology Foundation.
No consensus exists on the optimal left atrial ablation technique, beyond
robust pulmonary vein isolation, nor is there a consensus on what constitutes
a clinically successful procedure. Nevertheless, evidence is accruing that
catheter ablation for AF is more effective than antiarrhythmic drug therapy,
especially for patients in whom antiarrhythmic pharmacotherapy has already
failed. Guidelines for the management of AF list catheter ablation as a
reasonable strategy for selected patients with lone, paroxysmal AF even in the
absence of attempted antiarrhythmic drug therapy.[10]
The complete surgical Maze procedure (incisions in both atria with or without
transmural RF lesions) is still the most effective technique for potentially
curing AF in all comers, regardless of chronicity or whether structural heart
disease is present. The best success rates with left atrial catheter ablation are
in patients with paroxysmal AF and hearts that are not too structurally
abnormal.
Atrial flutter
Atrial flutter is most commonly due to a large reentrant circuit in the right
atrium, involving an isthmus of tissue between the tricuspid valve annulus and
the inferior vena cava. Most commonly, reentry proceeds counterclockwise up
the atrial septum and down the lateral wall of the right atrium, inscribing
inverted (ie, "sawtooth") flutter waves in the inferior leads and upright P waves
in V1 (see the images below).
Schema of common variety of atrial flutter.
Reentry circuit is confined to right atrium and circulates as counterclockwise
macroreentrant circuit proceeding superiorly over atrial septum and inferiorly over lateral
atrial wall. Wave front circulates through narrow isthmus of tissue between tricuspid
valve annulus and inferior vena cava. Linear ablation across this isthmus (cavotricuspid
isthmus) cures this common form of atrial flutter.
Typical counterclockwise atrial
flutter (most common form of atrial flutter in patients who have not had prior ablation).
Cardinal features are perfectly regular atrial rhythm with inverted P waves inferiorly that
have positive overshoot, upright P waves in V1, and inverted P waves in V6.
Clockwise reentry using this same circuit can also occur, giving upright P
waves inferiorly and inverted P waves in V1. Linear ablation of the
cavotricuspid isthmus cures these common forms of atrial flutter. (See the
video below.)
Three-dimensional electroanatomic map of cavotricuspid isthmus flutter. Colors
progress from red to purple and represent relative conduction time in right atrium (early
to late). Ablation line (red dots) has been created from tricuspid annulus to inferior vena
cava. This interrupts flutter circuit.
Non–isthmus-dependent flutters can occur elsewhere in the right atrium, as
well as in the left atrium. Left atrial flutters are uncommon, may be difficult to
ablate, and generally require a three-dimensional mapping system to facilitate
the procedure.
Atrioventricular nodal reentrant tachycardia
In the common form of AV nodal reentrant tachycardia (AVNRT), the inferior
atrionodal input to the AV node serves as the anterograde limb (ie, the slow
pathway) of the reentry circuit, and the superior atrionodal input serves as the
retrograde limb (ie, the fast pathway). Typically, AVNRT can be cured by
targeting the slow pathway near the inferior tricuspid valve annulus at the level
of the coronary sinus os or somewhat higher.
The risk of iatrogenic heart block with ablation in this region is quite low (12%) when RF energy is used and close to zero when cryoablation is
performed. Targeting the slow pathway is safer than targeting the fast
pathway, which is located closer to the compact AV node. (See the images
below.)
Diagrammatic schema of typical
type of atrioventricular (AV) nodal reentrant tachycardia (AVNRT). Slow pathway
(dashed arrow) is usual anterograde limb of reentry circuit and usual ablation target
area (shaded). Fast pathway (solid arrow) is usual retrograde limb of reentry circuit and
commonly activates atria simultaneously with ventricular activation, producing typical
ECG finding of AVNRT shown below. P wave is not visible, because it is buried in QRS
complex. Infrequently, reentry circuit is reversed, with anterograde conduction over fast
pathway and retrograde conduction over slow pathway, producing atypical ECG finding
of AVNRT shown in lower rhythm strip of figure (ie, long R-P tachycardia, in which
interval between QRS complex and retrograde P wave is longer than subsequent P-R
interval, and P wave is in second half of R-R interval). Fast pathway is close to compact
AV node, and ablation in this area is avoided if possible because of risk of iatrogenic
heart block.
Pseudo S waves inferiorly are
retrograde P waves. This short interval (no isoelectric baseline) between QRS complex
and retrograde P wave is highly specific for atrioventricular (AV) nodal reentrant
tachycardia (AVNRT). Pseudo R wave in V1 may also be observed but is not seen here.
In many instances, retrograde P wave occurs during QRS activation and is not
observed; this "no-P-wave" tachycardia also suggests AVNRT.
Sinus rhythm in same patient with
atrioventricular (AV) nodal reentrant tachycardia (AVNRT) as in preceding ECG. Note
that pseudo S waves are no longer visible.
Orthodromic reciprocating tachycardia
In orthodromic reciprocating tachycardia (ORT), the AV node serves as the
anterograde limb, and an accessory AV connection (typically called an
accessory pathway) serves as the retrograde limb (see the images below).
Schema of orthodromic
reciprocating tachycardia (ORT). Atrioventricular (AV) node serves as anterograde limb,
whereas accessory pathway (AV connection) serves as retrograde limb.
Supraventricular tachycardia
(SVT) in patient with orthodromic reciprocating tachycardia (ORT) due to concealed
pathway. Note retrograde P wave, seen best in lead V2, separated from QRS complex
by isoelectric baseline. This pattern of "short R-P tachycardia" (in which interval
between QRS complex and retrograde P wave is shorter than subsequent P-R interval
and P wave is in first half of R-R interval) suggests SVT incorporating accessory
pathway.
If an accessory pathway only conducts retrograde, it is termed a concealed
accessory pathway because it is not identifiable on an electrocardiogram
(ECG) in sinus rhythm (compare with Wolff-Parkinson-White [WPW] syndrome
below). Typically, ORT can be cured by targeting the accessory pathway as it
crosses the mitral or tricuspid valve annulus.
Wolff-Parkinson-White syndrome
Whereas ORT uses an accessory pathway in the retrograde direction, WPW
syndrome by definition indicates an accessory pathway capable of
anterograde conduction and is manifest by preexcitation (delta waves) on the
sinus rhythm ECG.
AF in WPW syndrome may result in life-threateningly fast anterograde
conduction over the accessory pathway, manifested by an irregular widecomplex (preexcited) tachycardia that can sometimes degenerate to
ventricular fibrillation (VF). AF in WPW syndrome may be triggered by ORT.
Ablation of the accessory pathway cures WPW syndrome, eliminating ORT, as
well as AF, in the majority of patients.
Unifocal atrial tachycardia
Unifocal atrial tachycardia, which can arise from either atrium or the
noncoronary cusp of the aorta, is somewhat more challenging to ablate than
the more common forms of generic supraventricular tachycardia (SVT). For
those tachycardias originating from the left atrium, transseptal catheterization
via a patent foramen ovale or transseptal puncture is usually required.
Ventricular tachycardia
Idiopathic VT most commonly arises from the right ventricular outflow tract
and less commonly originates in the inferoseptal left ventricle about two thirds
of the way toward the apex from the base of the left ventricle. These forms of
VT are amenable to catheter ablation, though success rates are somewhat
lower than those for the common forms of SVT.
VT in structural heart disease is also amenable to ablation. Some form of
three-dimensional electroanatomic mapping is employed for these complex
ablations to identify the scar that contributes to the anatomic substrate for
reentry. Intracardiac echocardiography during the procedure and
preprocedural imaging with magnetic resonance imaging (MRI) or computed
tomography (CT) are also used in some instances. Anatomy from
such imaging can be integrated with the electroanatomic map if
necessary. Some VT substrates, especially VT in nonischemic
cardiomyopathy, are not reachable from the endocardium. In these instances,
percutaneous epicardial mapping and ablation are necessary.
Complications
The radiation risk from catheter ablation is low, but it may exceed the risk from
common radiologic procedures. The average risk of genetic defects has been
computed at 1 case per million births. The average risk of fatal malignancies
ranges from 0.3 to 2.3 deaths per 1000 cases for every 60 minutes of
fluoroscopy.[12] Many ablation procedures require less than 60 minutes of
fluoroscopy.
Major complications occur in approximately 3% of patients who undergo
ablation procedures, including thromboembolism in fewer than 1% (higher in
some AF ablation series) and death in 0.1-0.2% of all procedures. The
incidence of cardiac complications varies according to the site and type of
ablation. Cardiac complications include the following:
High-grade AV block
Cardiac tamponade (highest in AF ablation, up to 6%)
Coronary artery spasm/thrombosis
Pericarditis
Valve trauma
Vascular complications, which occur in approximately 2-4% of procedures,
include the following:
Retroperitoneal bleeding
Hematoma
Vascular injury
Transient ischemic attack/stroke
Hypotension
Thromboembolism or air embolism
Pulmonary complications include the following:
Pulmonary hypertension, with or without hemoptysis (secondary to
pulmonary vein stenosis)
Pneumothorax
Miscellaneous complications include the following:
Left atrial–esophageal fistula
Acute pyloric spasm/gastric hypomotility
Phrenic nerve paralysis
Radiation- or electricity-induced skin damage
Infection at access site
Inappropriate sinus tachycardia
Proarrhythmia
