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Atrial Tachycardia
       蔡佳醍醫師
     台大醫院心臟內科
1
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
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
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)
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)
Focal Atrial Tachycardias




6
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)
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)
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)
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)
MOST COMMON SITES
      Right Atrium
       – Right Atrial Appendage
       – Coronary Sinus Ostium
       – Crista Terminalis


      Left Atrium
       – Pulmonary Vein Ostia
       – Left Atrial Appendage

11
12
Focal Atrial Tachycardia - Right
            Atrial Appendage
                          Right Atrial
                          Appendage




13                        AP View
Focal Atrial Tachycardia – Coronary
                 Sinus Ostium

                            LAO VIEW



                          Tricuspid Valve




       Effective Site

14                       CS Os     LAO View
Focal Atrial Tachycardia – Left Sided
         Focus (RA Septum is Early)
                            PA VIEW OF
                            RA


                             SEPTUM




       HIS



      CS OS

15                                PA View
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.
Focal AT Sites




  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
Electrocardiographic Localization of Right 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. II]:2431-2439
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
Representative Focal AT 12-Lead ECGs




 A: A CT-AT that originated from segment 1. B: A CT-AT that originated from segment 2.
  20
(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
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)
21
Representative Focal AT 12-Lead ECGs




 A: A TA-AT that originated from segment 1. B: A TA-AT that originated from segment 3. C:
 A Sep-AT that originated from near the apex of Koch’s triangle, showing narrow P waves
 with an initial large negative and a late small positive component in leads II, III and aVF.
 22
(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
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)
23
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)
24
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)
25
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)
26
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).
1. When AV block occurs, a bypass tract can be ruled out (AV block
   also observed in AV node reentry).
2. Adenosine may also terminate AT.
3. 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)
27
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)
28
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.



29
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
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.
 30
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1061)
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)
31
DD septal AP from atypical AVNRT




32
Mechanisms of Macroreentrant AT




33
Macroreentrant Atrial Tachycardia




                                                                    LIPV




     Macroreentrant AT originating near the LIPV and propagating
34
     around the Mitral valve.
     (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 502)
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)
35
Entrainment: Fusion
      This is a demonstration of pacing with fusion.




36
Entrainment: Progressive Fusion




37              14. Waldo A. JCE. 1997;8:341.
Concealed Entrainment
                This is a demonstration of concealed entrainment.




     Concealed Entrainment
38
Concealed Entrainment
     PPI :Post pacing interval         FCL: Flutter cycle length




                   15. Lesh et al. JCE Vol.7,No 4, April 1996
39
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
40
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




41
Entrainment Mapping




     8. Olgin, et. al., Journal of Cardiovascular Electrophysiology,
42   Vol.7, No.11, Nov 96.
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
43
Double Potentials (con’t)




44
Double Potentials at CT during AFL




45
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)
46
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.
 47
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1066)
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.




 48
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
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.




 49
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
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.




 50
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
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.

 51
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
Atrial Tachycardia
                               CARTO Sucks

     Crista Terminalis
                         SVC




                                        TV


                IVC

52                               RAO View
Left Atrial Tachycardia




53
Left Atrial Tachycardia




54
Focal Atrial Tachycardias Ablation Sites




   This shows the ablation sites in a large group of AT ablation cases.


 55
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1063)
Mapping and Ablation Techniques:
           Macroreentrant AT (I)
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.


 56
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
Mapping and Ablation Techniques:
           Macroreentrant AT (II)
• 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.




 57
(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)

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Atrial Tachycardia Mechanisms and Localization

  • 1. Atrial Tachycardia 蔡佳醍醫師 台大醫院心臟內科 1
  • 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
  • 12. 12
  • 13. Focal Atrial Tachycardia - Right Atrial Appendage Right Atrial Appendage 13 AP View
  • 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 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 Right 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. II]:2431-2439
  • 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. Representative Focal AT 12-Lead ECGs A: A CT-AT that originated from segment 1. B: A CT-AT that originated from segment 2. 20 (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
  • 21. 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) 21
  • 22. Representative Focal AT 12-Lead ECGs A: A TA-AT that originated from segment 1. B: A TA-AT that originated from segment 3. C: A Sep-AT that originated from near the apex of Koch’s triangle, showing narrow P waves with an initial large negative and a late small positive component in leads II, III and aVF. 22 (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
  • 23. 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) 23
  • 24. 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) 24
  • 25. 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) 25
  • 26. 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) 26
  • 27. 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). 1. When AV block occurs, a bypass tract can be ruled out (AV block also observed in AV node reentry). 2. Adenosine may also terminate AT. 3. 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) 27
  • 28. 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) 28
  • 29. 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. 29 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)
  • 30. 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. 30 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1061)
  • 31. 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) 31
  • 32. DD septal AP from atypical AVNRT 32
  • 34. Macroreentrant Atrial Tachycardia LIPV Macroreentrant AT originating near the LIPV and propagating 34 around the Mitral valve. (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 502)
  • 35. 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) 35
  • 36. Entrainment: Fusion This is a demonstration of pacing with fusion. 36
  • 37. Entrainment: Progressive Fusion 37 14. Waldo A. JCE. 1997;8:341.
  • 38. Concealed Entrainment This is a demonstration of concealed entrainment. Concealed Entrainment 38
  • 39. Concealed Entrainment PPI :Post pacing interval FCL: Flutter cycle length 15. Lesh et al. JCE Vol.7,No 4, April 1996 39
  • 40. 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 40
  • 41. 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 41
  • 42. Entrainment Mapping 8. Olgin, et. al., Journal of Cardiovascular Electrophysiology, 42 Vol.7, No.11, Nov 96.
  • 43. 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 43
  • 45. Double Potentials at CT during AFL 45
  • 46. 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) 46
  • 47. 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. 47 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1066)
  • 48. 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. 48 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
  • 49. 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. 49 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
  • 50. 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. 50 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
  • 51. 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. 51 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
  • 52. Atrial Tachycardia CARTO Sucks Crista Terminalis SVC TV IVC 52 RAO View
  • 55. Focal Atrial Tachycardias Ablation Sites This shows the ablation sites in a large group of AT ablation cases. 55 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1063)
  • 56. Mapping and Ablation Techniques: Macroreentrant AT (I) 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. 56 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)
  • 57. Mapping and Ablation Techniques: Macroreentrant AT (II) • 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. 57 (Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1062-1063)