2. Atrial Tachycardia
Atrial tachycardias (ATs) are an uncommon cause of
supraventricular tachycardia (SVT):
Adults - 5% of all SVTs subject to EP studies
Pediatric patients:
10-15% of the SVTs in pediatric patients without
congenital heart defects (CHD)
More in those who have undergone a surgical correction
of their CHD
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500)
2
3. Atrial Tachycardias
Locations:
Tachycardia originating in
atrial muscle at a site(s)
other than the sinus node or
the AV node.
Mechanisms:
Abnormal automaticity,
trigger activities, or reentry
3
4. Mechanisms based on Ablation
Focal AT: activation spreading from a single
focus either radially, circularly or centrifugally
without an electrical activation spanning the
tachycardia cycle length.
4
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)
5. Classification of Mechanisms
Macroreentrant : reentry occurring over fairly large
well-defined circuits that span the entire tachycardia
cycle length(>70%). Also the earliest and latest atrial
activations are in close proximity.
The various patterns are:
Single loop (like typical atrial flutter)
Figure of eight (made up of two loops)
Reentry through narrow channels adjacent to scar,
anatomic barriers (i.e. tricuspid annulus)
5
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)
7. Focal Atrial Tachycardias
• Focal atrial tachycardia has three mechanisms:
automaticity, triggered activity and microreentry.
• Automatic atrial tachycardia is identified by the presence
of the following characteristics:
• AT can be initiated by an isoproterenol infusion
• PES cannot initiate or terminate the AT
• AT can be gradually suppressed with overdrive pacing, but
then resumes with a gradual increase in the atrial rate
• AT is terminated by propranolol
• AT episodes have a “warm up” and/or “cool down
phenomenon
• AT cannot be terminated by adenosine
7
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)
8. Focal Atrial Tachycardias
Triggered activity is identified by the presence of the following
characteristics:
• AT can be initiated with rapid atrial pacing
•No entrainment is observed, but overdrive suppression or
termination occurs
• Delayed afterdepolarizations can be recorded near the origin
using a monophasic action potential catheter before the AT
onset, but not at sites remote from the tachycardia
• AT terminated by adenosine, propranolol, verapamil,
, Valsava maneuvers and carotid sinus pressure
8
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)
9. Focal Atrial Tachycardias
Microreentry is identified by the presence of the
following characteristics:
• AT can be reproducibly initiated and terminated by
atrial pacing and extrastimuli
• No delayed afterdepolarizations can be recorded using
a monophasic action potential catheter
• Manifest and concealed entrainment observed while
pacing during the tachycardia
9
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)
10. Focal Atrial Tachycardia
∗ ∗
Focal AT in a post-open heart patient with the focus originating in
the right atrial free wall with centrifugal spread of the activation.
10
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 502)
11. MOST COMMON SITES
Right Atrium
– Right Atrial Appendage
– Coronary Sinus Ostium
– Crista Terminalis
Left Atrium
– Pulmonary Vein Ostia
– Left Atrial Appendage
11
14. Focal Atrial Tachycardia – Coronary
Sinus Ostium
LAO VIEW
Tricuspid Valve
Effective Site
14 CS Os LAO View
15. Focal Atrial Tachycardia – Left Sided
Focus (RA Septum is Early)
PA VIEW OF
RA
SEPTUM
HIS
CS OS
15 PA View
16. Electrocardiographic Localization of Focal AT
• Focal atrial tachycardia is characterized by P waves separated by an isoelectric interval in
all ECG leads.
• The P-wave can often be obscured by the T wave or QRS complexes during the
16tachycardia.
17. Focal AT Sites at RA
17
(Tada H, et al. Simple Electrocardiographic Critera for Identifying the Site of Origin of Focal Right Atrial Tachycardia. PACE 1998;21[Pt.
II]:2431-2439
18. Electrocardiographic Localization of Focal AT
Short-PR
18
(Tada H, et al. Simple Electrocardiographic Critera for Identifying the Site of Origin of Focal Right Atrial Tachycardia. PACE 1998;21[Pt.
19. AT Arising from the Crista Terminalis
• The CT is a common site for ATs (as much as 75% of right
ATs).
• CT demonstrates marked anisotropy due to poor transverse cell
to cell coupling. This may create slow conduction and thus
microreentry. Also the CT contains a cluster of cells with
automaticity.
• If superolateral, they will have positive P-waves in leads, II, III
and aVF. If inferolateral, they will have negative P-waves in
leads, II, III and aVF.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 504)
19
20. AT Arising from the AV Annulus
• ATs arising for the tricuspid annulus are relatively uncommon,
accounting for only about 13% of right atrial ATs. The P-wave
will be negative in the precordial and inferior leads.
• ATs may also arise form the mitral valve annulus. In that case the
P-waves are negative in aVL and positive in V1.
• The demonstration of cells with AV nodal EP properties
lacking connexin43 near the annulus, the mechanism is believed
to be microreentry involving these nodal-like cells.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 504)
20
21. AT Arising from the CSos Musculature
• Focal ATs of up to 12% of right ATs occur in the area around the
CSos, outside or just inside the os.
• In very rare cases, AT can occur from deep in the CS and arises
from the CS musculature. These cannot usually be ablated from
the left atrial endocardium and need to be ablated from within
the CS.
• A negative P-wave in V6 is often seen in ATs originating from
the CSos.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 504)
21
22. AT Arising from the Atrial Septum
•These ATs are sensitive to lower doses of adenosine than ATs arising
from the crista terminalis. These also more often require the use of
isoproterenol to induce than right atrial free wall ATs.
•In up to 10% of ATs in the right atrium can arise from the apex of
Koch’s triangle (para-hisian). These are adenosine sensitive and can
be induced with isoproterenol. These can usually be ablated without
damage to the AV node.
•The P-wave duration for these ATs is on average 20 msec shorter
during AT than sinus rhythm.
•In these patients it is important to map both the right and left atria. In
patients with a left-sided origin, the P-waves can be either positive or
negative in V1, so it is misleading. Up to 40% of patients with the
earliest activation recorded in Koch’s triangle have a left atrial focus.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 504)
22
23. Sinus Node Reentrant Tachycardia
•Sinus Node Reentrant Tachycardias are presumed to be
due to microreentry in the tissue near the sinus node or the
perinodal region (superior crista terminalis). The P-Wave
morphology is identical to that during sinus rhythm.
•Focal ATs may also arise from the superior vena cava
(SVC). Those ATs arising from around the SVC may
conduct to the right atrium (RA).
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
23
24. Inappropriate Sinus Tachycardia
• The hallmark feature of inappropriate sinus tachycardia (IST) is
a consistently elevated resting heart rate and exaggerated heart
rate response to low levels of physical activity.
•Some patients may have primary autonomic abnormalities,
including postural orthostatic tachycardia syndrome. Others may
have primary abnormalities of the sinus node.
• These patients show a blunted response to adenosine (0.1 to
0.15 mg/kg) with less of a sinus cycle length prolongation than
age- matched controls. Thus structural abnormalities of the
sinus node are the cause of IST in those patients.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
24
25. ECG Differential Diagnosis of AT
• ATs, especially septal ATs, need to be differentiated from
concealed septal bypass tracts, AV node reentry (fast-slow
atypical AVNRT).
2. When AV block occurs, a bypass tract can be ruled out (AV block
also observed in AV node reentry).
3. Adenosine may also terminate AT.
4. Only AT patients experienced oscillations in the atrial cycle
length.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
25
26. ECG Differential Diagnosis of AT
• Burst pacing from the right ventricle for 3-6 beats during
the tachycardia at a cycle length faster than the
tachycardia results in:1) tachycardia termination; 2)
entrainment of the tachycardia; 3) dissociation of the
ventricle from the tachycardia.
• If the ventricles are dissociated from the tachycardia, a
bypass tract is excluded.
• If burst RV pacing reproducibly terminates the
tachycardia, without conduction to the atrium, AT is
excluded.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
26
27. RV overdrive pacing to DD septal AT from septal
AP or atypical AVNRT
• Ventricular burst pacing can also be performed for longer
periods of time at a rate just slightly faster than the tachycardia
cycle length.
• If the atrial activation sequence during pacing is different than
that during tachycardia, an AT is present.
• When pacing is stopped, and the ECG sequence following the
last paced ventricular beat demonstrates a V-A-A-V response,
an AT is present.
27
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
28. AT with a VAAV Pattern
Immediately after the last paced ventricular beat (S), atrial tachycardia
with a variable degree of atrioventricular (AV) block is demonstrated,
with a typical VAAV pattern.
28
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1061)
29. RA overdrive pacing to DD septal AT from septal
AP or atypical AVNRT
• Overdrive right atrial pacing during the tachycardia at a
cycle length slightly faster than the tachycardia cycle
length can cause termination or tachycardia continuation
upon cessation of pacing.
• VA interval measured from the onset of the surface QRS
on the first postpacing ventricular beat to the onset of the
atrial electrogram on the His catheter of the return cycle.
• If the VA interval is within 10 msec of the VA interval
during the tachycardia, the tachycardia is due to AVNRT
or a bypass tract. If the AV interval is variable or
different, AT is present.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505-508)
29
32. Macroreentrant Atrial Tachycardia
LIPV
Macroreentrant AT originating near the LIPV and propagating
32
around the Mitral valve.
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 502)
33. Specific Types of Macroreentrant AT
• Sites of macroreentrant ATs:
• Right atrium
• Left atrium
• Biatrial
• Left atrial septum
• Right pulmonary veins (single loop and figure of eight)
• Between 2 areas of low voltage or around one such area
• Left atrial flutters
• Reentry involving the CS and its musculature
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 509-510)
33
35. Concealed Entrainment
This is a demonstration of concealed entrainment.
Concealed Entrainment
35
36. Concealed Entrainment
PPI :Post pacing interval FCL: Flutter cycle length
15. Lesh et al. JCE Vol.7,No 4, April 1996
36
37. Post Pacing Interval (PPI) in
Entrainment with Fusion
Return cycle length= (Time from pacing site)x2 +TCL
The reentry circuit = Tachycardia cycle length (TCL)
PLUS
Time from pacing site to the circuit
PLUS
Time from circuit to the pacing site
=Return Cycle Length
= pacing site
37
38. PPI in Concealed Entrainment
If the pacing occurred inside of the tachycardia circuit, the
time it takes for the tachycardia to resume will be the
tachycardia cycle length only, since there is no distance out
side of the circuit to add time.
Return cycle length= (Time from pacing site)x2 +TCL
= pacing site
38
39. Entrainment Mapping
8. Olgin, et. al., Journal of Cardiovascular Electrophysiology,
39 Vol.7, No.11, Nov 96.
40. Double Potentials
Double potentials are indicative of a line
of block
Lines of block are either fixed or
functional
– Atriotomy sites and the eustachian ridge
are examples of fixed lines of block
– Evidence exists that block in region of
crista terminalis during atrial flutter is a
form of functional conduction block
40
43. Ablation of Atrial Tachycardia
Key Locations
– Identification of Focal Sites (if applicable) -
Focal
– Identification of Anatomical Barriers (if
applicable) - Macroreentrant
– Identification of Scar (if applicable) –
Microreentrant (Focal)
43
44. Mapping and Ablation Techniques: Focal AT
Once a focal mechanism has been determined, the site is
targeted by detailed atrial endocardial mapping during
the AT or ectopic beats. A knowledge of the most
common sites and the P-wave morphology can facilitate
the mapping and ablation.
•Leads aVL and V1 are helpful to distinguish right from
left atrial foci (isoelectric or - aVL/+V1 = left; + or
biphasic aVL/- or biphasic V1 = right).
•Positive P waves in the inferior leads suggests a superior
or anteripr focus, and biphasic or negative indicates
posterior or inferior.
•A negative P-wave in aVR = a right atrial focus.
44
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1066)
45. Mapping and Ablation Techniques: Focal AT
Endocardial Activation Mapping:
• Use HRA, His, CS catheters to regionalize the AT origin
based on the activation pattern.
• Next the ablation catheter is inserted and moved to find
the site of earliest activation relative to the onset of the
surface P-wave or onset of activation at the CSos or HRA
which is in a known fixed relationship to the P-wave onset
during AT.
45
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
46. Mapping and Ablation Techniques: Focal AT
Endocardial Activation Mapping:
• Fractionated or prepotentials (spikes) are also successful
ablation sites, but the specificity and sensitivity is low.
• Intermittent mechanical block of the AT with catheter
manipulation is also a good indicator of a successful site,
but care must be taken to avoid loss of conduction for
hours.
46
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
47. Focal Ablation
Focal Ablation:
•Acceleration of the tachycardia before termination is an
excellent sign.
•Also rapid termination of the tachycardia within 10
seconds of starting the RF delivery is also a good sign.
•Successful focal ablation is verified by failure to
reinduce the AT before and during an isoproterenol
infusion.
47
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
48. Focal Ablation (Cont.)
Focal Ablation:
•Ablation at the atrial septum or Koch’s triangle can cause
AV block. However, the presence of a His potential is
not a contraindication for ablation. The energy needs to
be titrated in such cases, by starting with 10 Watts and
increase with 5-10 Watt increments to a maximum of 40
Watts with continuous AV conduction monitoring to
prevent AV block.
•If the earliest site is the para-hisian area, right PV ectopy
or LA origin need to be ruled out.
•If the earliest site is the superior crista, right PV ectopy
also need to be ruled out. Another unusual potential site
is the SVC.
48
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
52. Focal Atrial Tachycardias Ablation Sites
This shows the ablation sites in a large group of AT ablation cases.
52
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1063)
53. Mapping and Ablation Techniques:
Macroreentrant AT
Conventional methods include activation and entrainment mapping to
identify the obstacles and boundaries of the reentrant circuits, and the
critical isthmus within the reentrant circuit that becomes the target of
the ablation.
• The entire circuit can be mapped with the earliest and latest
activations being adjacent (head meets tail).
• Striking changes in signal amplitude, timing or both with very
slight shifts in the catheter position indicate anatomic barriers to
conduction.
• A combination of diastolic potentials and concealed entrainment
pacing with the post-pacing interval within 20 msec of the TCL
identifies a “protected isthmus” within the reentrant circuit.
53
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
54. Mapping and Ablation Techniques:
Macroreentrant AT (Cont.)
• Macroreentrant AT can arise from upper loop reentry in the right
atrium due to a conduction gap in the crista terminalis (CT). Lower
turn-around points are located at the conduction gaps in the CT. RF
linear ablation of the conduction gap (narrowest part of the
reentrant circuit) effectively abolishes the right free wall AT.
• Left atrial reentrant substrates are mostly at the posterior wall, the
PV ostium or base of the appendage. Left atrial marcroreentrant
AT is highly variable of 1-3 loops rotating around the mitral
annulus, PVs and zone of block or a silent area.
• 3D mapping is usually needed in LA macroreentrant AT.
54
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
55. Case 1
A 58 year old lady was referred to us due to
frequent episodes of palpitation refractory to
Propafenone and Amiodarone.
An EP study had been performed 6 month prior to
referral in another center and ablation was not tried
because of presumed para-hisian atrial tachycardia .
Another EP study was performed. The diagnostic
catheters were placed in High RA, His, RV apex,
Coronary Sinus and Tricuspid Ring (halo).
The arrhythmia was induced by isopreterenol
infusion.
55
56. Earliest A at para-hisian site in initial tracing
56
57. Before ablation at the parahisian sites, other
potential sites should be considered because
of the risk of AV block.
Entrainment mapping at TV-IVC isthmus
rule out typical AFL.
Although CS showed concentric, LA
mapping was still performed. LA mapping,
including the right PVs, did not reveal earlier
site than the His area.
57
59. Discussion
Due to the close contact of the right and left
aortic cusps with ventricles, arrhythmias
originating from these cusps present with
PVC's or VT.
Non- coronary cusp of the aorta with its
posterior orientation is in the vicinity of the
right atrium and ectopic pulses from here
conduct to atrial chambers resulting in PAC's
or AT.
59
60. Case 2
•A 34 y/o woman presented with intermittent palpitation for 3
weeks.
•UCG revealed no structural heart.
•ECG revealed intermittent atrial tachycardia or paroxysmal
atrial fibrillation
60
61. Earliest A at the upper crista terminalis (SVC not earliest)
61
63. Case 3
A 28 y/o woman had suffered from
palpitation and shortness of breath for one
week.
She went to ER where ECG showed PSVT.
IV verapamil was administered; however,
ECG showed PSVT turned to cardiac
standstill.
Prolonged CPR did not result in ROSC, and
ECMO was instituted.
63
64. She was then transferred to NTUH.
SVT recurred immediately at arrival at
NTUH ER.
Variable AV conduction was noted. AT was
confirmed.
HRA AT was favored since the A sequence
mimicked sinus tachycardia in 12-lead EKG.
UCG revealed LVEF 26%.
64
65. EPS revealed mid cirsta terminalis AT.
After ablation, no more tachycardia was
inducible (patient was in ECMO with high
dose dopamine; no isoproterenol was
administer to induce tachycardia).
Two weeks later before discharge, UCG
revealed LVEF 53%.
65
Editor's Notes
Atrial tachycardias (ATs) are an uncommon cause of supraventricular tachycardia (SVT) and only account for 5% of all SVTs that adults undergo EP studies for. ATs are more common in pediatric patients and account for 10-15% of the SVTs in pediatric patients without congenital heart defects (CHD) and more in those who have undergone a surgical correction of their CHD (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4 th edition. 2004; pg. 500).
Atrial tachycardias are classified as tachycardia that arises from the atrium with a regular atrial rate. These can be further classified into focal or macroreentrant tachycardias . This classification leaves out some atrial tachycardias such as innapropriate sinus node tachycardia and sinus node reentry, but it does cover most ATs. Focal atrial tachycardia exhibits activation spreading from a single focus either radially, circularly or centrifugally without an electrical activation spanning the tachycardia cycle length (right atrial activation is considerably shorter than the tachycardia cycle length). Macroreentrant atrial tachycardia (typical atrial flutter, lower loop reentry, double loop reentry, left atrial macroreentrant tachycardias, scar-related atrial tachycardia, reverse typical atrial flutter and right atrial free wall macroreentry) are due to reentry occurring over fairly large well-defined circuits that span the entire tachycardia cycle length ( > 70%). Also the earliest and latest atrial activations are in close proximity. The various patterns are: Single loop (like typical atrial flutter) Figure of eight (made up of two loops) Reentry through narrow channels adjacent to scar, anatomic barriers (i.e. tricuspid annulus)
Atrial tachycardias are classified as tachycardia that arises from the atrium with a regular atrial rate. These can be further classified into focal or macroreentrant tachycardias . This classification leaves out some atrial tachycardias such as innapropriate sinus node tachycardia and sinus node reentry, but it does cover most ATs. Focal atrial tachycardia exhibits activation spreading from a single focus either radially, circularly or centrifugally without an electrical activation spanning the tachycardia cycle length (right atrial activation is considerably shorter than the tachycardia cycle length). Macroreentrant atrial tachycardia (typical atrial flutter, lower loop reentry, double loop reentry, left atrial macroreentrant tachycardias, scar-related atrial tachycardia, reverse typical atrial flutter and right atrial free wall macroreentry) are due to reentry occurring over fairly large well-defined circuits that span the entire tachycardia cycle length ( > 70%). Also the earliest and latest atrial activations are in close proximity. The various patterns are: Single loop (like typical atrial flutter) Figure of eight (made up of two loops) Reentry through narrow channels adjacent to scar, anatomic barriers (i.e. tricuspid annulus)
Focal atrial tachycardia has three mechanisms: automaticity, triggered activity and microreentry. Automatic atrial tachycardia is identified by the presence of the following characteristics: AT can be initiated by an isoproterenol infusion PES cannot initiate or terminate the AT AT can be gradually suppressed with overdrive pacing, but then resumes with a gradual increase in the atrial rate AT is terminated by propranolol AT episodes have a “warm up” and/or “cool down phenomenon AT cannot be terminated by adenosine, but transiently slows or suppresses AT especially when the TA can be induced with isoproterenol
Focal atrial tachycardia has three mechanisms: automaticity, triggered activity and microreentry. Automatic atrial tachycardia is identified by the presence of the following characteristics: AT can be initiated by an isoproterenol infusion PES cannot initiate or terminate the AT AT can be gradually suppressed with overdrive pacing, but then resumes with a gradual increase in the atrial rate AT is terminated by propranolol AT episodes have a “warm up” and/or “cool down phenomenon AT cannot be terminated by adenosine, but transiently slows or suppresses AT especially when the TA can be induced with isoproterenol
Triggered activity is identified by the presence of the following characteristics: AT can be initiated with rapid atrial pacing or atrial exstrastimuli dependant on reaching a certain range of pacing cycle lengths No entrainment is observed, but overdrive suppression or termination occurs Delayed afterdepolarizations can be recorded near the origin using a monophasic action potential catheter before the AT onset, but not at sites remote form the tachycardia AT terminated by adenosine Rarely requires isoproterenol to induce the AT AT terminated by dipyridamole, propranolol, verapamil, edrophonium, Valsava maneuvers and carotid sinus pressure
Focal atrial tachycardia has three mechanisms: automaticity, triggered activity and microreentry. Automatic atrial tachycardia is identified by the presence of the following characteristics: AT can be initiated by an isoproterenol infusion PES cannot initiate or terminate the AT At can be gradually supressed with overdrive pacing, but then resumes with a gradual increase in the atrial rate At is terminated by propranolol AT episodes have a “warm up” and/or “cool down phenomenon AT cannot be terminated by adenosine, but transiently slows or suppresses AT especially when the TA could be induced with isoproterenol Triggered activity is identified by the presence of the following characteristics: AT can be initiated with rapid atrial pacing or atrial exstrastimuli dependant on reaching a certain range of pacing cycle lengths No entrainment is observed, but overdrive suppression or termination occurs Delayed afterdepolarizations can be recorded near the origin using a monophasic action potential catheter before the AT onset, but not at sites remote form the tachycardia AT terminated by adenosine Rarely requires isoproterenol to induce the AT AT terminated by dipyridamole, propranolol, verapamil, edrophonium, Valsava maneuvers and carotid sinus pressure Microreentry is identified by the presence of the following characteristics: AT can be reproducibly initiated and terminated by atrial pacing and extrastimuli No delayed afterdepolarizations can be recorded using a monophasic action potential catheter Manifest and concealed entrainment observed while pacing during the tachycardia AT frequently terminated by verapamil and adenosine, but adenosine usually has no effect The interval between the initiating premature beat and first beat of the AT are inversely related
Focal AT in a post-open heart patient with the focus originating in the right atrial free wall with centrifugal spread of the activation.
Focal atrial tachycardia is characterized by P waves separated by an isoelectric interval in all ECG leads. There are various algorithms available that look at P-wave morphology. These are useful, but the P-wave can often be obscured by the T wave or QRS complexes during the tachycardia. This figure shows one algorithm. The P=wave configuration in leads aVL and V1 are most helpful for differentiating right from left atrial AT. A positive or biphasic P-wave in aVL predicted a right atrial focus and a positive P-wave in V1 predicted a left atrial focus. However, this algorithm can incorrectly predict right superior pulmonary vein (RSPV) AT foci (positive P-wave in aVL instead of the suspected negative P-wave), probably due to the close proximity of the RSPV to the high lateral right atrium. In those patients, during sinus rhythm and AT, there was a change in the P-wave morphology in V1 from biphasic to a positive P-wave for RSPV foci. Also a negative P-wave in aVR identified AT on the crista terminalis. In the LAO view, a positive P-wave in the inferior leads differentiated superolateral AT from inferolateral AT. Any AT with an inferomedial or inferolateral foci, the P-wave is negative in at least one of the inferior leads. Negative P-waves in V5 and V6 identified inferomedial ATs. For ATs from Koch’s triangle, theP-wave duration in the inferior leads was shorter than during sinus rhythm. A positive and relatively flat P-wave in lead aVL and a positive P-wave in lead I of greater than 50 µVindicates a foci of right PV origin. A notched P-wave in lead II is predictive of a left PV origin. Also a lead III/II amplitude ratio of ≥ 0.8 and a duration of positivity in lead V1 (>80 msec) is predictive for left PV origins. Left PV foci are characterized by low amplitude , flat P-waves in lead I, negative polarity in lead aVL, similar amplitudes in both leads III and II and a longer duration of positivity in lead V1. Superior PVs are distinguished from inferior PVs by the P-wave amplitude in lead II being greater than 100 µV for superior PVs. Abbreviations in the figure: +, positive P waves; -, negative P waves; 0, isoelectric P waves; +/-, biphasic P waves; Pdur, P-wave duration; LSPV, left superior pulmonary vein; LIPV left inferior pulmonary vein; RSPV, right superior pulmonary vein; RIPV, right inferior pulmonary vein; SVT, supraventricular tachycardia; SR, sinus rhythm.
Right atrium in the LAO view (45°) and location of each focus of AT. The right atrium was subdivided with a vertical line drawn down the middle of the SVC and IVC (L SVC-IVC) and a horizontal line at the level of the His bundle (L His).
Algorithm to predict the focus of right AT on the basis of the P wave configuration on the 12-lead ECG. A negative P wave in lead aVR usually indicates a crista terminalis focus. In ATs with a tricuspid annulus or septal focus, negative P waves in leads V3 and V6 indicate the focus is in segment 3. In ATs arising from segment 3, a ratio of the P wave duration in the inferior leads during AT divided by that during sinus rhythm of < 0,85 indicates that the focus of the AT is near the apex of Koch’s triangle. The P wave configuration in the inferior leads is useful to distinguish a superior from an inferior origin in any type of AT.
ICE can be helpful in determining the close proximity of an AT to the crista terminalis (CT). The CT is a common site for ATs (as much as 75% of right ATs). The reason is possibly that the CT demonstrates marked anisotropy due to poor transverse cell to cell coupling. This may create slow conduction and thus microreentry. Also the CT contains a cluster of cells with automaticity. CT ATs will have differing P-waves depending on if they arise from the superior or inferior portion of the CT. If superolateral, they will have positive P-waves in leads, II, III and aVF. If inferolateral, they will have negative P-waves in leads, II, III and aVF.
ATs arising for the tricuspid annulus are relatively uncommon, accounting for only about 13% of right atrial ATs. The P-wave will be negative in the precordial and inferior leads. ATs may also arise form the mitral valve annulus. In that case the P-waves are negative in aVL and positive in V1. The annular ATs are easily terminated with adenosine (less than half the dose for AVNRT). Due to the sensitivity to adenosine and the demonstration of cells with AV nodal EP properties lacking connexin43 near the annulus, the mechanism is believed to be microreentry involving these nodal-like cells.
Focal ATs of up to 12% of right ATs occur in the area around the CSos, outside or just inside the os. In very rare cases, AT can occur from deep in the CS and arises from the CS musculature. These cannot usually be ablated from the left atrial endocardium and need to be ablated from within the CS. A negative P-wave in V6 is often seen in ATs originating from the CSos.
Focal ATs occurring in the septum include ATs originating from the anterior septum, mid-septum, posterior septum and Koch’s triangle. Up to 27-35% of ATs can be these ATs. In up to 10% of ATs in the right atrium can arise from the apex of Koch’s triangle. These ATs are sensitive to lower doses of adenosine than ATs arising from the crista terminalis. These also more often require the use of isoproterenol to induce than right atrial free wall ATs. Anteroseptal and midseptal right ATs have a biphasic or negative P-wave in lead V1. An anteroseptal AT has a biphasic or negative P-wave in V1 and a positive or biphasic P-wave in all the inferior leads. A midseptal AT has a negative or biphasic P-wave in V1 and negative P wave in at leads two of the three inferior leads. A posteroseptal At has a positive P-wave in V1 and negative P-wave in all three inferior leads. In up to 10% of ATs in the right atrium can arise from the apex of Koch’s triangle. These are adenosine sensitive and can be induced with isoproterenol. These can usually be ablated without damage to the AV node. The P-wave duration for thee ATs is on average 20 msec shorter during AT than sinus rhythm. In these patients it is important to map both the right and left atria, because conduction can occur very fast through Bachmann’s bundle resulting in early right-sided breakthrough. In patients with a left- sided origin, the P-waves can be either positive or negative in V1, so it is misleading. Up to 40% of patients with the earliest activation recorded in Koch’s triangle have a left atrial focus.
Sinus Node Reentrant Tachycardias are presumed to be due to microreentry in the tissue near the sinus node or the perinodal region (superior crista terminalis). The P-Wave morphology is identical to that during sinus rhythm. Focal ATs may also arise from the superior vena cava (SVC). Those ATs arising form around the SVC may conduct to the right atrium (RA). There are also reports of fibrillatory activity in the SVC with exit block to the RA making the rhythm masquerade as a focal You can also have a conduction delay occur between the SVC and RA which can initiate an AT.
The hallmark feature of inappropriate sinus tachycardia (IST) is a consistently elevated resting heart rate and exaggerated heart rate response to low levels of physical activity. Some patients have an elevated intrinsic heart rate and others an exaggerated response to isoproterenol. The ECG characteristics are an identical P-wave as that during sinus rhythm Some patients may hav primary autonomic abnormalities, including postural orthostatic tachycardia syndrome. Others may have primary abnormalities of the sinus node. These patients show a blunted response to adenosine (0.1 to 0.15 mg/kg) with less of a sinus cycle length prolongation than age- matched controls. This same blunted response occurs after pharmacologic autonomic blockade as well. Thus structural abnormalities of the sinus node are the cause of IST in those patients.
ATs, especially septal ATs, need to be differentiated from concealed septal bypass tracts, AV node reentry and other rare arrhythmias. The most useful ECG or EP finding is AV block. When AV block occurs, a bypass tract can be ruled out. Adenosine (6 to 18mg boluses) is useful for AT, however, there was no correlation between the response to adenosine and the location of the AT focus. Also termination or suppression of the AT occurs in more than half the patients, but it is not helpful for differentiating automatic ATs from triggered ATs or reentrant ATs. AV block after adenosine only occurs in patients with AT, but occurs in less than 30% of patients. Also only AT patients experienced oscillations in the atrial cycle length before adenosine.
Burst pacing (or single or double extrastimuli) from the right ventricle for 3- 6 beats during the tachycardia at a cycle length much faster than the tachycardia results in tachycardia termination, entrainment of the tachycardia, or dissociation of the ventricle from the tachycardia. If the ventricles are dissociated from the tachycardia, a bypass tract is excluded. If burst pacing reproducibly terminates the tachycardia, without conduction to the atrium, AT is excluded. Ventricular burst pacing can also be performed for longer periods of time at a rate just slightly faster than the tachycardia cycle length, and when the atrial activation is accelerated to the pacing rate, indicating 1:1 ventriculoatrial conduction, and if the atrial activation sequence during pacing is different than that during tachycardia, then either an AT or a bystander accessory pathway (AP) is present. If the atrial activation sequence is identical, and when pacing is stopped, and the ECG sequence following the last paced ventricular beat demonstrates a V-A-A-V response (last atrial complex accelerated to the pacing rate followed by another complex before the next ventricular complex), an AT is present. A “pseudo” V-A-A-V response can be seen with a slowly conducting septal AP or the slow slow type AVNRT.
Burst pacing (or single or double extrastimuli) from the right ventricle for 3- 6 beats during the tachycardia at a cycle length much faster than the tachycardia results in tachycardia termination, entrainment of the tachycardia, or dissociation of the ventricle from the tachycardia. If the ventricles are dissociated from the tachycardia, a bypass tract is excluded. If burst pacing reproducibly terminates the tachycardia, without conduction to the atrium, AT is excluded. Ventricular burst pacing can also be performed for longer periods of time at a rate just slightly faster than the tachycardia cycle length, and when the atrial activation is accelerated to the pacing rate, indicating 1:1 ventriculoatrial conduction, and if the atrial activation sequence during pacing is different than that during tachycardia, then either an AT or a bystander accessory pathway (AP) is present. If the atrial activation sequence is identical, and when pacing is stopped, and the ECG sequence following the last paced ventricular beat demonstrates a V-A-A-V response (last atrial complex accelerated to the pacing rate followed by another complex before the next ventricular complex), an AT is present. A “pseudo” V-A-A-V response can be seen with a slowly conducting septal AP or the slow slow type AVNRT.
Immediately after the last paced ventricular beat (S), atrial tachycardia with a variable degree of atrioventricular (AV) block is demonstrated, with a typical VAAV pattern.
Overdrive right atrial pacing during the tachycardia at a cycle length slightly faster than the tachycardia cycle length can cause termination or tachycardia continuation upon cessation of pacing. If the VA interval is within 10 msec of the VA interval during the tachycardia, then the tachycardia is due to AVNRT or a bypass tract. If the VA interval is variable or different, then AT is present. Another maneuver is atrial overdrive pacing during the tachycardia at the longest cycle length that results in AV block. The last paced AH interval upon cessation of pacing is evaluated. If termination of the tachycardia is associated with a relatively short AH interval compared with the AH intervals that resulted in continuation of the tachycardia, then the tachycardia is considered to be AV nodal dependent and cannot be AT. Another maneuver is to compare the AH interval during tachycardia and during atrial pacing from the high right atrium at or near the tachycardia cycle length. If the AH interval during atrial pacing is more than 40 msec longer than the AH interval during the tachycardia, atypical AVNRT is likely. The AH intervals during atrial pacing and the tachycardia will be within 20 msec if an AT or concealed AP is present. Change in the AA interval preceding a change in the VV interval indicates AT.
Macroreentrant tachycardias can be divided into those that are isthmus dependent (conducting between the tricuspid annulus and IVC) and those that are non-isthmus dependent. The majority are isthmus dependent (atrial flutter, lower loop reentry, double wave reentry, macroreentrant AT in the right atrial free wall, and macroreentrant AT in the right or left atria related to previous surgical scars. The non-isthmus dependent macroreentrant ATs are related usually to an area of scar form usually an incision. The mechanisms are usually reentry due to areas of slow conduction or areas of scar. When a protective zone of slow conduction exists, reentry can from. These are usually associated with post-surgical scar from previous incisions. By locating the critical isthmuses in which slow conduction passes through two areas of scar, the AT can be cured by ablating across that sithmus.
Macroreentrant AT originating near the LIPV and propagating around the Mitral valve.
Sites of macroreentrant ATs: Right atrium Left atrium Biatrial Left atrial septum Right pulmonary veins (single loop and figure of eight) Between two areas of low voltage or around one area of low voltage Left atrial flutters Reentry involving the CS and its musculature
If entrainment occurs outside the circuit, the ECG will be a combination of the tachycardia morphology and what the morphology would look like when pacing in normal sinus rhythm (fusion).
This is a demonstration of pacing with concealed entrainment. If entrainment occurs within the circuit, the ECG morphology remains constant (concealed entrainment). The upper diagram shows the tachycardia morphology The diagram below it shows the same morphology only accelerated to the pacing cycle length
TA 1-20 : 20 pole electrode catheter TA1,2 at low anterolateral right atrium (7:30 o'clock) Pacing from 7:00 o'clock at 200 msec CL results in entrainment (first 3 beats) and the morphology at the recording site during pacing capture (transient entrainment) and during spontaneous atrial flutter is unchanged, indicating that activation of this site occurs the same way during pacing as it does during spontaneous atrial flutter confirming you are pacing in the circuit. Also the PPI = TCL confirms this as well.
*Another factor to observe in entrainment is the time it takes for the tachycardia to resume after pacing is stopped. This is know as the Return Cycle Length, or the Post Pacing Interval (PPI). *It is imperative to note that this time measurement applies to the recordings made from the same electrodes that were used for pacing . *If the pacing occurred outside of the tachycardia circuit, the time it takes for the tachycardia to resume will be longer than if it were inside the circuit. Return cycle length= (Time from pacing site)x2 +TCL
If the pacing occurred inside of the tachycardia circuit, the time it takes for the tachycardia to resume will be the tachycardia cycle length only, since there is no distance out side of the circuit to add time.
This graphic shows the results of entrainment pacing used to map a tachycardia circuit. All of the sites captured the atrium and sped the heart rate to the pacing rate. Only the spots on the baseline of the graph (2,4,6,8, and all of the clock numbers) were identified as within the tachycardia circuit since the return cycle length was the same as the tachycardia cycle length. Note that only sites 4,6,8, and 6:00 also show concealed entrainment, meaning that this part of the circuit is “protected”.
Example A: when an impulse travels along a line of block, single potentials will be recorded at the electrode located on the line (as indicated by the circles). Example B: When the impulse travels in a perpendicular path toward the line of block, double or split potentials will be recorded due to the time delay as the impulse wraps around the region.
This slide illustrates the double potential at the block site (CT)during AFL. Please point to 1. The far field and the near field components 2. The slop of the far field components are stiffer then the near field component , which indicate almost simultaneous conduction , while the near field component indicate sequential activation. 3. RA 9 electrogram is from the most proximal pair of the duo deca 4. The duo deca catheter is on the anterior side of the CT
Once a focal mechanism has been determined, the site is targeted by detailed atrial endocardial mapping during the AT or ectopic beats. A knowledge of the most common sites and the P-wave morphology can facilitate the mapping and ablation. P-wave Polarity: The P-waves may be buried in the T wave or QRS and thus premature ventricular extrastimuli to advance the ventricular timing or cause AV block, or the use of adenosine or carotid massage can help discern the P-waves. Then by analyzing the P-wave, a general idea of the site can be determined. Leads aVL and V1 are helpful to distinguish right from left atrial foci (isoelectric or - aVL/+V1 = left; + or biphasic aVL/- or biphasic V1 = right). Positive P waves in the inferior leads suggests a superior or anteripr focus, and biphasic or negative indicates posterior or inferior. A negative P-wave in aVR = a right atrial focus; negative polarity in the precordial and inferior leads = inferoanterior tricuspid annulus; combination of a negative P- wave in V6, poitive inV1 and negative in all 3 inferior leads = posteroseptal AT around or below the CSos; positive P-wave in V1 forATs around the AV node = left side of interatrial septum; and almost identical P-waves during AT and sinus rhythm = high crista terminalis or sinus nodal AT.
Endocardial Activation Mapping: To begin HRA, His and CS catheters are used to regionalize the AT origin based on the activation pattern. Next the ablation catheter is inserted and moved to find the site of the earliest activation relative to the onset of the surface P-wave or onset of the activation at the CSos or HRA which is in a known fixed relationship to the P-wave onset during the AT. This however, is time consuming and difficult. Thus various catheter such as Duo-Decapolar or basket catheters can be used, but still lack enough detail. The “two catheter technique” in which two catheters are moved around and one is left in place as a reference and the other moved to find a site with earlier activation than the first catheter. If the earliest site is the superior crista, right PV ectopy need to be ruled out. Another unusual potential site is the SVC. Once the earliest activation site is found, unipolar recording to locate a QS pattern with a rapid intrinsic slope indicates the origin site.
Endocardial Activation Mapping: Fractionated or prepotentials (spikes) are also successful ablation sites, but the specificity and sensitivity is low. Intermittent mechanical block of the AT with catheter manipulation is also a good indicator of a successful site, but care must be taken to avoid loss of conduction for hours. Paced activation sequence mapping in which the ablation catheter is used to pace at the presumed site and see if the activation sequence and P-wave morphology matches that of the AT. However the spatial resolution of this method is about 1.7cm. New mapping systems such as ESI and CARTO are also helpful. ESI may be better, because CARTO requires sustained arrhythmias to complete the mapping whereas ESI Ensite can map the AT in one beat.
Focal Ablation: Once the site is identified 25 to 30Watts of RF energy are delivered for 30-60 seconds Acceleration of the tachycardia before termination is an excellent sign. Also rapid termination of the tachycardia within 10 seconds of starting the RF delivery is also a good sign. Successful focal ablation is verified by failure to reinduce the AT before and during an isoproterenol infusion. For inappropriate sinus tachycardia ablation is begun at the superior aspect of the crista terminalis and then drug down to the inferior aspect until the heart rate decreases by 25- 35% during an isoproterenol infusion or atropine bolus. This is associated withmany complications such sinoatrial junction stenosis, superior vena cava syndrome, sinus node dysfunction and phrenic nerve damage.
Focal Ablation: Ablation at the atrial septum or Koch’s triangle can cause AV block. However, the presence of a His potential is not a contraindication for ablation. The energy needs to be titrated in such cases, by starting with 10 Watts and increase with 5-10 Watt increments to a maximum of 40 Watts while continuousl;y monitoring the AV conduction to prevent AV block. For annular ablation, you should finf a small A wave and large V wave (A less than ½ V). High frequency spike potentials preceding the atrial activation and P wave is searched for for PV origin tachycardias. However limiting the power to 30 Watts and temp to 50-55 °C is recommended to avoid thromus and PV stenosis. The success rate for AT ablation is about 93%. The older the age the greater chance for multiple sites and the chance for recurrence.
This shows the ablation sites in a large group of AT ablation cases.
Conventional methods include activation and entrainment mapping to identify the obstacles and boundaries of the reentrant circuits, and the critical isthmus within the reentrant circuit that becomes the target of the ablation. The entire circuit can be mapped with the earliest and latest activations being adjacent. The areas of scar or obstacles can be determined by areas of low voltage, fractionated electrograms or absence of electrical activity. Striking changes in signal amplitude, timing or both with very slight shifts in the catheter position indicate anatomic barriers to conduction. A combination of diastolic potentials and concealed entrainment pacing with the post-pacing interval within 20 msec of the TCL identifies a “protected isthmus” within the reentrant circuit.
Macroreentrant AT can arise from upper loop reentry in the right atrium due to a conduction gap in the crista terminalis (CT). The circuit goes clockwise or counter-clockwise around the central obstacle (CT, area of functional block and SVC). Lower turn-around points are located at the conduction gaps in the CT. It is possible that slow anisotropic conduction across the CT further predisposes lesions in that area to serve as substrates for intra-atrial reentrant tachycardia. RF linear ablation of the conduction gap (narrowest part of the reentrant circuit) effectively abolishes the right free wall AT. Left anatomic substrates are wide areas with electrical silence ( <0.05 mV) and are mostly at the posterior wall or zone of block (double potentials separated by an isoelectric interval ≥50 msec) usually anchored at the PV ostium or base of the appendage. Left atrial marcroreentrant AT is highly variable of 1-3 loops rotating around the mitral annulus, PVs and zone of block or a silent area. Also the area between the left atrial septum and right PVs is an area of genesis of left atrial macroreentrant AT. Use of an 8mm or irrigation catheter can assist i ablating these arrhythmias.
