atrial tachycardia_lecture

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Atrial Tachycardia Huang BienHsien Kuang Tien General Hospital Taichung Taiwan

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Page 1: Atrial tachycardia_lecture

Atrial Tachycardia

Huang Bien‐HsienKuang Tien General HospitalTaichungTaiwan

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(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500)

Atrial tachycardias (ATs) are an uncommon cause of supraventricular tachycardia (SVT):

Adults ‐ 5% of all SVTs subject to EP studiesPediatric 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

Atrial Tachycardia

Presenter
Presentation 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, 4th edition. 2004; pg. 500).
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Outline 

• Mechanism of atrial tachycadia• Locations of focal atrial tachycaria• Surface EKG of different sites of atrial tachycardia

• Mapping • New mapping technology (Introduction)• Ablation

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Focal Macroreentrant tachycardias.

Classification of Mechanisms

(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 500-501)

Presenter
Presentation Notes
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)
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Focal Atrial Tachycardia 

Focal AT exhibits activation spreading from a single focus either radially, circularly or centrifugally without an electrical activation spanning the tachycardia cycle length. 

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Mechanisms (Chen et al. Circulation 1994)

• Abnormal or enhanced automaticity• Triggered Activity (delayed afterdepolarization)•Microreentry

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Effects of Adenosine on Reentrant AT

Microreentrant AT (probably focal AT)

Macroreentrant AT

Reentrant circuit with zones of

conduction can

demonstrate adenosine sensitivity

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Classification of Atrial Tachycardia: Response to Adenosine

Termination No EffectTransient Suppression

FocalMacroreentrant Automatic AT

Intra-Atrial Reentry(Non-Decremental Tissue)Cristal

ATRepetitive

Monomorphic AT

Intra-Atrial Reentry(Decremental Tissue)

Markowitz, et al, JCE 1999; 10: 489

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Origins of Focal Atrial Tachyarrhythmias

Atrial Origin Venous Origin

RA LA SVC CS VOM PV

Cristal terminalisKoch's triangleAppendageAtrial septumBachmann's bundleTricuspid anulus

AppendageAtrial septumBachmann's bundleMitral anulus

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CT PathologyThe crista terminalis (CT) originates from the superior rim of the oval fossa (OF), swings in front of the orifice of the superior vena cava, continues downwards in the posterolateral wall, turns in beneath the orifice of the inferior vena cava (IVC) to ramify as a series of trabeculations in the inferior isthmus. 

CT

IVC

OF

CS

PM

ER

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CT Pathology

Sanchez-Quintana and Ho et al, Heart 2002

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Mapping and Ablation of Focal AT (I) 

ECG P wave polarity 

Body surface potential mapping of atrial

activation

Single catheter mapping with bipolar

recording ‐‐‐ earliest activation

Single catheter mapping with unipolar

recording ‐‐‐ QS pattern

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Mapping and Ablation of Focal AT (II) 

Double ring catheters mapping

Mechanical pressure by catheter tip

3‐D mapping using Carto or Ensite system

to find the earliest activation site

Intracardiac echocardiography to identify

the anatomic site

Angiography, 3‐D MRI, 3D‐CT to identify

the atrial – venous structure

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EKG characteristics of atrial tachycardia

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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.

Electrocardiographic Localization of Focal AT

(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 503)

InferolateralSuperolateral Annulus Septal

Presenter
Presentation Notes
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.
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Intracardiac EKG

If the earliest signal is recorded by the…

The origin of the AT is most likely the…

HIS EGM Anteroseptal RA

Proximal CS EGM Posteroseptal RA

Low or high RA EGM Somewhere in the RA

Distal CS EGM Lateral LA

HRA EGM Right superior pulmonary vein

Presenter
Presentation Notes
Intraatrial reentry tachycardia The earliest recorded EGM signal suggests the origin of the AT as in the Follows: If the earliest signal is recorded by the…The origin of the AT is most likely the… HIS EGManteroseptal RA Proximal CS EGMposteroseptal RA Low or high RA EGMsomewhere in the RA Distal CS EGMlateral LA HRA EGMright superior pulmonary vein
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SR AT AF

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C. Before Ablation D. After Ablation

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Surface ECG of repetitive nonsustained atrial tachycardia (AT) originating from the right superior pulmonary vein (PV). 

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Differential Diagnosis of AT During EP study

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Differential Diagnosis of AT

(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 505)

• Ventricular burst pacing can 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,

Presenter
Presentation Notes
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.
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(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 1061)

AT with a VAAV Pattern

Presenter
Presentation Notes
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.
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Prevalence and diagnostic value of Baseline observation

J Am Col Cardiol 2000; 36:574-82 – Morady et al.

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J Am Col Cardiol 2000; 36:574-82 – Morady et al.

Prevalence and diagnostic value of Tachycardia features

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Diagnostic value of Pacing Maneuvers During PSVT

J Am Col Cardiol 2000; 36:574-82 – Morady et al.

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Diagnostic value of Pacing Maneuvers During PSVT

J Am Col Cardiol 2000; 36:574-82 – Morady et al.

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New Mapping Technologies

(Zipes DP, Jalife J. Cardiac Electrophysiology: From cell to bedside, 4th edition. 2004; pg. 508)

• New mapping technologies such as basket catheters, electroanatomic mapping and non-contact mapping have helped to locate the site of the focus much quicker than the standard mapping techniques. Now with the advent of Spiral type catheters they also can be used to map the lower RA by the IVC, upper RA and SVC and CSos.

Presenter
Presentation Notes
New mapping technologies such as baslet catheters, electroanatomic mapping and non-contact mapping have helped to locate the site of the focus much quicker than the standard mapping techniques. Now with the advent of Spiral type catheters they also can be used to pap the lover RA by the IVC, upper RA and SVC and CSos.
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What is the benefit of 3‐D mapping in focal AT?

3‐D mapping really improves the knowledge and 

ablation results of focal AT?

Presenter
Presentation Notes
心房心肌病變是指廣泛性心房受質結構異常的現象, 由細胞病理學研究可得知, 心房心肌細胞有下列的變化: A substantial proportion of the atrial myocytes revealed marked changes in their cellular substructures, such as loss of myofibrils, accumulation of glycogen, changes in mitochondrial shape and size, fragmentation of SR, and dispersion of nuclear chromatin等等 有那些情形會造成心房心肌病變: 原因主要來自於 1.心臟衰竭等的本身心臟功能異常, 2.或是心搏過速造成心肌病變,Chronic atrial fibrillation造成electric and structural remodeling; 3. 以及一些inflammatory process; inflammatory caused oxidative damage and cause atrial fibrosis; and in animal models; therapies that reduce CRP levels as stating can decrease structure change in animal models. (Kumagai et al. Circulation research 2004)
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Surrounding tissue without anisotropic conduction

QS pattern

Hypothesis: Wavefront Propagation during AT

Wrap-around Effect (+)

Multi-component pattern

Wrap-around Effect (-)

Surrounding tissue with anisotropic conduction

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Single Focal AT

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• Key Locations– Identification of Focal Sites (if applicable) ‐Focal

– Identification of Anatomical Barriers (if applicable) ‐Macroreentrant

– Identification of Scar (if applicable) –Microreentrant (Focal)

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Focal Ablation

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

•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.

Presenter
Presentation Notes
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.