Ebook Electrocardiography of arrhythmias - A comprehensive review: Part 2

(BQ) Part 2 book Electrocardiography of arrhythmias - A comprehensive review presents the following contents: Atrial tachycardia, atrial flutter, atrial fibrillation, atrial fibrillation, ventricular tachycardia in structural heart disease, ventricular tachycardia in the absence of structural heart disease,...

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ATRIAL TACHYCARDIA

Atrial tachycardia (AT) is defined as a regular atrial rhythm

originating from the atrium at 100 bpm to 240 bpm The

presence of an atrial rate above 100 bpm with three

differ-ent P wave morphologies signifies differdiffer-ent foci of atrial

depolarization and is called a multifocal atrial tachycardia

(MAT) Previous classifications of AT had been based

exclu-sively on the routine electrocardiogram (ECG) with a

con-stant rate and an isoelectric line between the two consecutive

P waves Atrial flutter (AFL) is typically a reentrant

arrhyth-mia defined as having a pattern of regular tachycardia with

a rate above 240 bpm without an isoelectric baseline

between deflections The typical (cavotricuspid dependent)

AFL usually shows sawtooth pattern in inferior ECG leads

ATs can also have a reentrant mechanism, usually seen

around a scar in the atrium The ECG pattern can mimic

an atypical (noncavotricuspid dependent) AFL However,

neither rate nor lack of isoelectric baseline is specific for

any tachycardia mechanism A rapid AT in a scarred atrium

can mimic AFL, and, on the other hand, a typical AFL can

show distinct isoelectric intervals between flutter waves, in

diseased atria, or in the presence of antiarrhythmic drug

therapy Therefore it becomes a matter of semantics to

define an AT or an atypical AFL AT can result from a focal

mechanism such as abnormal automaticity or triggered

activity Unlike prior definitions stating that focal ATs have

a constant rate, a focal AT can show a significant cycle

length (>15%) variation, more than that seen in a reentrant

AT, and can also occur in diseased atria Table 7-1 shows

the classification of AT/AFL Focal automatic ATs occur

mostly in children and young adults Focal automatic ATs

begin with a P wave identical to the P wave during the

arrhythmia, and the rate generally increases gradually

(warms up) over the first few seconds Automatic ATs are

catecholamine sensitive and cannot be induced or

termi-nated by programmed electrical stimulation (PES) ATs

resulting from triggered activity can arise anywhere in the

atria but most commonly originate from the crista

termi-nalis, tricuspid annulus, and mitral annulus These ATs can

be induced and terminated with PES The majority of focal

ATs caused by triggered activity are adenosine sensitive

Rarely, a microreentrant AT can appear to be focal in origin

during mapping, but its reentrant mechanism can be

elu-cidated after a careful electrophysiology study including

entrainment Macroreentrant AT and AFL are discussed in detail in Chapter 8

The location of the focal source of an AT is determined by

P wave morphology and vector on 12-lead ECG ( Figures 7-1 and 7-2 ) Focal AT can arise anywhere in the atrium, pulmonary veins (PVs), and venae cavae ( Figures 7-3 through 7-9 ) Focal ATs usually have discrete P waves at rates of 110 to 240 bpm, but AT/AFL arising from PVs can

be as fast as 300 bpm Antiarrhythmic drugs can slow the AT/AFL rate by decreasing the conduction velocity or increasing the refractory period of the reentrant circuit, and an isoelectric line between two P waves can be seen Shorter atrial activation with a shorter P wave duration and longer diastolic intervals on the ECG distinguishes a focal from a macroreentrant AT with 90% sensitivity and specificity Careful analysis of the 12-lead ECG and rhythm strips as well as vagal maneuvers and drug interventions (adenosine and atrioventricular [AV] nodal blockers) help in determining the mechanism of an AT An electrophysiology study is helpful in determining the focus of

an AT or the isthmus of a reentrant AT ( Figures 7-10 through 7-18 ).

P AND QRS RELATIONSHIP DURING ATRIAL TACHYCARDIA

1 ATs usually have a long R-P′ tachycardia but can have

a short R-P′ tachycardia in the presence of significant first-degree heart block at baseline or in the presence

of dual AV nodal physiology with AV conduction via the slow pathway.

2 The atrial to ventricular relationship depends on the ability of the AV node conduction during tachycardia

It is usually 1 : 1 conduction during ATs; however, Wenckebach pattern or 2 : 1 AV block can occur The presence of AV block during supraventricular tachycardia strongly suggests AT and excludes an AV reentrant tachycardia Rarely, an AV nodal reentrant tachycardia with lower common pathway block or His-Purkinje

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CHAPTER 7 AtriAl tAchycArdiA

188

disease may show AV block and variable relation of P

waves with QRS.

3 Termination of a supraventricular tachycardia without

a following QRS practically rules out an AT.

EFFECT OF DRUG THERAPY ON ATRIAL

TACHYCARDIA AND ATRIAL FLUTTER

With AV nodal disease or AV nodal drug therapy, 4 : 1 or

variable AV block is seen In the presence of antiarrhythmic

drug therapy, the cycle length of AFL can prolong or atrial

fibrillation can organize to a relatively slower flutter that

allows the AV node to conduct 1 : 1, resulting in a rapid

ventricular response and increased risk for life-threatening

ventricular arrhythmia Adenosine can terminate focal ATs

resulting from triggered activity.

LOCALIZATION OF FOCAL ATRIAL

TACHYCARDIAS

Several algorithms have been proposed for ECG

localiza-tion of focal AT using the P wave morphology and axis on

a 12-lead ECG (see Figures 7-1 and 7-2 ) However,

some-times P wave morphology can be difficult to determine on

account of the partial masking by ST segment/T wave

Simple vagal maneuvers or intravenous adenosine

admini-stration during 12-lead ECG rhythm strip recording can

separate the P wave from T wave Alternatively, a post–

premature ventricular contraction compensatory pause can

separate the P wave from the T wave and delineate P wave

morphology ECG lead V1 is the most useful in identifying

the likely anatomic site of origin for a focal AT The right atrium (RA) is an anterior structure, and the left atrium (LA) is a posterior structure The lead V1 is located to the right and anteriorly in relation to the atria Therefore P wave morphology in lead V1 plays a vital role in determining the origin of focal ATs A right AT originating from the tricuspid annulus or crista terminalis has negative P waves in lead V1 because the atrial activation travels away from lead V1.1,2

P waves in lead V1 are positive for ATs originating from the PVs because of the posterior location in the chest In general, negative P waves in the anterior precordial leads suggest an anterior RA or LA free wall location Negative P waves in the inferior leads suggest a low (inferior) atrial origin One study showed that ATs originating from PVs are significantly faster (mean cycle lengths: 289 ± 45 ms and

280 ± 48 ms in patients without and with PV ablation for atrial fibrillation, respectively) compared with left ATs (mean cycle lengths: 392 ± 106 ms and 407 ± 87 ms, patients without and with PV ablation for atrial fibrillation, respectively).3 P waves in focal PV ATs usually have longer duration (≥110 ms) A prior catheter ablation of atrial fibrillation

or reentrant AT, maze procedure, and surgery for tal heart disease can affect the localization of the AT/AFL focus or circuit.

congeni-RIGHT ATRIAL TACHYCARDIA

A negative or biphasic (positive, then negative) P wave in lead V1 has a 100% specificity and positive predictive value for ATs arising from the RA ( Figures 7-19 through 7-30 ; see also Figures 7-9 through 7-18 ) P waves during ATs arising near the septum are generally narrower than those

TABLE 7-1 Classification of atrial tachycardia and atrial flutter

blocker

shows an area of continuous or mid-diastolic potential

Macroreentrant

lower-loop reentrydouble-loop reentryintra-isthmus reentry

Noncavotricuspid isthmus dependent

Upper-loop reentry (see chapter 8)lesional (incision related)

Scar related (congenital heart disease, cardiac surgery, cardiomyopathy)

PES

AFL, Atrial flutter; AT, atrial tachycardia; PAC, premature atrial complex; PES, programmed electrical stimulation; PVC, premature ventricular complex.

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CHAPTER 7 AtriAl tAchycArdiA 189

arising in the RA or LA free wall because of a relatively

rapid activation from the midline to both atria, whereas

the impulse from ATs with a right or left lateral atrial origin

has to travel a longer distance to excite the whole

contra-lateral atria.

SINUS NODE REENTRY TACHYCARDIA

Sinus node reentry is defined as a reentrant tachycardia

involving the sinus node and perinodal tissue that is

induced and terminated with PES and is adenosine

sensi-tive However, there has not been recent confirmation of

this entity in the literature It is possible that sinus node

reentry tachycardia may represent a high cristal AT

origi-nating near the sinus node that is adenosine sensitive if the

mechanism of the tachycardia is triggered activity

Alter-natively, it is an AT owing to microreentry in tissue near

the sinus node or perinodal region (superior crista

termi-nalis) that is responsive to adenosine because of

involve-ment of sinus nodal tissue The P wave morphology during

the tachycardia is identical to that seen during sinus

rhythm.

INAPPROPRIATE SINUS TACHYCARDIA

Inappropriate sinus tachycardia (see Figure 7-12 ) is defined

as a persistent increase in the resting sinus rate (usually

>80-90 bpm) unrelated to, or out of proportion with, the

level of physical, emotional, pathologic, or pharmacologic

stress, or an exaggerated heart rate response to minimal

exertion or a change in body posture It occurs in a

dispro-portionately high number among health care professionals

The tachycardia originates at the superior part of the sinus

node and is refractory to medical therapy During

electro-physiology study it is mapped at the sinus node at the

supe-rior part of the crista terminalis.

CRISTAL ATRIAL TACHYCARDIA

In cristal AT (see Figures 7-4 and 7-18 through 7-22 ), P

waves are biphasic in lead V1 and negative in lead aVR The

presence of negative P waves in aVR identifies cristal ATs

with 100% sensitivity and 93% specificity P waves are

posi-tive and broad in leads I and II, as well as posiposi-tive in lead

aVL, owing to right-to-left activation High, mid, or low

cristal ATs can be identified according to the P wave

polar-ity in the inferior leads.

TRICUSPID ANNULAR AND LATERAL RIGHT

Tricuspid annular and lateral right ATs (see Figures 7-4 and

7-22 through 7-26 ) have negative P waves in lead V1 The

P wave polarity in inferior leads helps to differentiate the

inferior from the superior location of the AT ATs

originat-ing from superior sites closer to the interatrial septum have

transition from negative in lead V1 through biphasic to

upright in the lateral precordial leads An anteroinferior AT

usually has inverted P waves across the precordial leads and

HIGH SEPTAL ATRIAL TACHYCARDIA

High septal ATs with a relatively long P-R interval can mimic slow-fast AVNRT or orthodromic AVRT with superoparaseptal accessory pathways.

MIDSEPTAL ATRIAL TACHYCARDIA

Midseptal ATs can mimic fast-intermediate AVNRT or orthodromic AVRT with midseptal accessory pathway.

POSTEROSEPTAL ATRIAL TACHYCARDIA

Posteroseptal ATs have P waves positive in lead V1, negative

in the inferior leads, and positive in leads aVL and aVR These ATs can mimic fast-slow AVNRT or orthodromic AVRT using a posteroseptal accessory pathway or persistent form of junctional reciprocating tachycardia.

Anteroseptal and midseptal right ATs have a biphasic

or negative P wave morphology in lead V1 The tion of a negative or biphasic P wave in V1 and a positive

combina-or biphasic P wave in all infericombina-or leads favcombina-ors an tal AT, whereas the presence of a negative or biphasic P wave in V1 and a negative P wave in at least two of the three inferior leads favors a midseptal AT The presence of a positive P wave in V1 and a negative P wave in all three inferior leads favors a posteroseptal AT The electrophysiology study

anterosep-is critical for differentiating these tachycardias from cal AV node reentry or a septal accessory pathway In several series, 27% to 35% of patients had ATs originating from this region.

atypi-AORTIC CUSP

Atrial musculature has not been demonstrated to extend into the aortic coronary cusps of the sinus of Valsalva ( Figure 7-32 ; see also Figure 7-7 ) However, the origin of focal ATs can be mapped from the aortic sinus of Valsalva because of its close relation with right and left atrial

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190

myocardium behind the thin aortic wall at the level of the

sinotubular junction Most of the ATs reported are from

the noncoronary cusp but rarely can arise from the left or

the right coronary cusp P wave morphology in ATs

origi-nating from the noncoronary cusp of the aorta is

negative-positive in leads V1 and V2, predominantly upright or

biphasic in inferior leads and lead aVL, and negative in

aVR.4 The precordial leads are negative-positive in V1 and

V2, negative-positive or positive in leads V3-V5, and

posi-tive in lead V6.

LEFT ATRIAL TACHYCARDIA

Left-sided ATs can arise anywhere from the LA, but PVs

and the mitral valve annulus are the main sources A

posi-tive or biphasic (negaposi-tive, then posiposi-tive) P wave in lead V1

is associated with a 100% sensitivity and negative predictive

value for ATs originating in the LA ( Figures 7-33 through

7-42 ; see also Figures 7-8 and 7-9 ).

ATRIAL TACHYCARDIAS ARISING FROM MITRAL

ANNULAR AND LEFT ATRIAL APPENDAGE

Mitral annular ATs mostly originate from the superior

aspect of the mitral annulus in close proximity to the

aorto-mitral continuity P waves of AT originating from this area

have an initial narrow negative deflection followed by a

positive deflection in lead V1, negative/isoelectric in lead

aVL, negative in leads I, and isoelectric or slightly positive

in the inferior leads The positivity of the P wave becomes

progressively less from V1 through V6 ATs originating

from anterolateral mitral annulus and LA appendage have

P wave positive in lead V1 and inferior leads (lead III >II),

and negative in lateral leads (I and aVL) with a deeply

nega-tive P wave in lead I ATs arising from coronary sinus or

posterior mitral annulus have bifid-positive P waves in leads

V1, aVL, and negative P waves in the inferior leads ( Figures

7-43 and 7-44 ; see also Figures 7-36 through 7-42 ).

ATRIAL TACHYCARDIAS ARISING FROM

PULMONARY VEINS

ATs arising from PVs ( Table 7-2 ; see also Figures 7-8, 7-9,

7-37 through 7-40 ) are characterized by entirely positive P

waves in lead V1 in 100%, isoelectric or negative in lead aVL

in 86%, and negative in lead aVR in 96% of cases ATs

origi-nating from the superior PVs have larger amplitude P waves

in the inferior leads than those in ATs arising from the

inferior PVs P wave morphology and polarity of ATs

originating from right superior PVs can mimic ATs from the superior region of RA, except that it is positive in V1

It is unlike negative P waves in lead V1 in right ATs or a biphasic (positive-negative) P wave in ATs originating from posterior RA P wave morphology generally is of greater accuracy in distinguishing right-sided from left-sided PVs

in contrast to superior from inferior PVs ATs arising from inferior PVs generally show lesser amplitude (or negative P waves in inferior leads) than ATs arising from superior PVs.

Teh AW, Kistler PM, Kalman JM Using the 12-lead ECG to local-atrial tachycardia J Cardiovasc Electrophysiol 2009;20:706-709;

Zhou YF, Wang Y, Zeng YJ, et al Electrophysiologic characteris-from non-coronary sinuses of valsalva in the aorta J Interv Card

Electrophysiol 2010;28:147-151.

5 Kistler PM, Fynn SP, Haqqani H, et al Focal atrial tachycardia from the ostium of the coronary sinus: electrocardiographic and electrophysiological characterization and radiofrequency

ablation J Am Coll Cardiol 2005;45:1488-1493.

TABLE 7-2 Right superior pulmonary vein atrial tachycardias versus left superior pulmonary vein atrial tachycardias

P WAVE RIGHT SUPERIOR PV AT LEFT SUPERIOR PV AT

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>50 mcV

– or 0 P in aVL+ P in V1

+ P in

II, III,aVF

– P in

II, III,aVF

– or –/+

P in >3leadsV2–V6

+ P inV5, V6;

CSbody

TARAA

LPVLAA

CTRPVRPVTA

CS osLS

Neg in allinf leads

Sinus rhythm

P wave

Iso

Bifid in IIand/or V1

PosNeg

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192

FIGURE 7-3 ▶ A schematic representation of the anatomic distribution of focal atrial tachycardias.1 The atrioventricular valvular annuli have

been removed CS, coronary sinus; CT, crista terminalis; LA, left atrium; LAA, left atrial appendage; MA, mitral annulus; PV, pulmonary vein;

RA, right atrium; RAA, right atrial appendage; TA, tricuspid annulus

FIGURE 7-4 ▶ Representative examples of the tachycardia P wave from left atrial sites.1 CS os, Coronary sinus ostium; CT, crista terminalis;

RAA, right atrial appendage; TA, tricuspid annulus

IIIIIIAVRAVLAVFV1V2V3V4V5V6

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FIGURE 7-5 ▶ Representative examples of the P wave morphology during atrial tachycardia for septal and midline foci.2 Cs os, Coronary sinus

ostium

Septal and perionodal foci

FIGURE 7-6 ▶ Atrial tachycardia originating from coronary sinus The P wave morphology from three patients is presented The characteristic

findings were as follows: a deeply inverted P wave in the inferior leads with 4 of 13 patients having a secondary upright component (B and C) Lead V1 was inverted (B and C) or isoelectric (A) then upright Leads aVL and aVR were positive in all 13 patients in case series.5

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194

FIGURE 7-7 ▶ Atrial tachycardia arising from the noncoronary aortic cusp Noncoronary and, to some extent, left aortic cusp are in close

relation with atrial myocardium (A), whereas right and left coronary cusps are in close relationship with ventricular myocardium (B) Atrial and

ventricular tachycardias can be mapped from these coronary cusps, depending on the relationship of muscular bands (atrial or ventricle)

Examples of P wave morphology in three patients with noncoronary cusp atrial tachycardia are shown in C AO, Aortic root; L, left coronary

cusp; MV, mitral valve; N, noncoronary cusp; PV, pulmonary valve; R, right coronary cusp; TV, tricuspid valves

IIIIIIaVRaVLaVFV1V2V3V4V5V6

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FIGURE 7-8 ▶ The P waves in sinus rhythm and atrial ectopy from the high crista and right superior pulmonary vein Foci at the right superior pulmonary vein show a change in configuration in lead V1 from biphasic in sinus rhythm to upright during tachycardia, a change not observed for right-sided tachycardias.1 CT, Crista terminalis; RSPV, right superior pulmonary vein

FIGURE 7-9 ▶ Representative examples of the tachycardia P wave from left atrial sites.1 CS, Coronary sinus; LAA, left atrial appendage;

LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein

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FIGURE 7-10 ▶ Focal atrial tachycardia (AT): The frequent bursts of AT suggest a focal source

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FIGURE 7-11 ▶ Automatic atrial tachycardia (AT) Automatic ATs (focal) may present in repetitive bursts with acceleration and deceleration of

tachycardia rate (warm-up and cool-down phenomenon) Cycle length variation greater than 15% suggests a focal source of the AT Negative

P waves in lead aVL and positive P wave in lead V1 suggest a left atrial source P wave duration greater than 80 ms and P wave voltage greater than 0.1 mV suggest a left superior pulmonary vein focus This focal AT was mapped at the posterior left superior pulmonary vein

A

B

Superior vena cava

Right superiorpulmonary veinRightatrium

Right inferiorpulmonary veinInferior vena cava

C

Left atrium

Left inferiorpulmonary veinLeft superior pulmonary vein

AT focus

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198

FIGURE 7-12 ▶ Resting ECG of a 47-year-old woman without any structural heart disease, anxiety, or thyroid disorder ECG shows sinus tachycardia at 117 bpm Her baseline heart rate fluctuated between 85 and 120 bpm, and the heart rate increased disproportionately with minimal exertion She was very symptomatic with this heart rate Partial success was achieved with catheter ablation of the upper part of the sinus node

FIGURE 7-13 ▶ A, ECG depicts atrial tachycardia (AT) with 2:1 atrioventricular (AV) block

A

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B

C

B, AT reinitiates (red arrow) after spontaneous termination during AV nodal–blocking drug therapy, and later showed

type I second-degree AV block (Wenckebach pattern) with termination after the nonconducted P waves (blue arrow) AT also terminates and

reinitiates C, Morphology of sinus P waves Negative P waves in leads V1 and aVR suggest a cristal source of the AT Negative P waves and

positive P waves in inferior leads suggest an inferolateral source and cristal source, respectively However, the P waves are negative-positive,

which suggests the origin between the two areas AT was mapped at the low lateral right atrium D, Diagram showing the focus of AT at the

lower right lateral atrium and possible activation pattern of the right atrium AAo, Ascending aorta; CS/ThV, coronary sinus/Thebesian valve; CT, crista terminalis; CTI, cavotricuspid isthmus; ER/EV, eustachian ridge/eustachian valve; IVC, inferior vena cava; OF, foramen ovale; RAA, right atrial appendage; RCA, right coronary artery; RV, right ventricle; STV, septal tricuspid valve leaflet; SVC, superior vena cava; TT, tendon of Todaro

FIGURE 7-13, cont’d ▶

SVC

AAoRAA

RA

RCA

RVCT

CT

STV

IVCER/EV

D

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200

FIGURE 7-14 ▶ A, Intracardiac ECG shows earliest activation of the focal AT was in the high right atrium B, AT terminated (arrow) with

intravenous adenosine, which is one of the characteristics of focal ATs resulting from triggered mechanism The reentrant and automatic focal

ATs do not terminate with adenosine CS, Coronary sinus; His D, distal His; His M, middle His; His P, proximal His

A

B

CS distal

CS protimal RV

HRA V6 V1 II I

His D His M His P

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FIGURE 7-15 ▶ Persistent atrial tachycardia (AT) in a patient after cardiac surgery Reentrant mechanism of the tachycardia was demonstrated

in the electrophysiology laboratory during entrainment mapping (A) AT circuit was mapped around the atriotomy scar in the lateral right

atrium (B) CT, Crista terminalis; IVC, inferior vena cava; SVC, superior vena cava; TA, tricuspid annulus

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202

FIGURE 7-16 ▶ Paroxysmal rapid atrial cardia (AT) with wide and narrow QRS com-plexes Rapid AT is associated with intermittent right bundle branch block aberrancy (Ashman phenomenon)

tachy-FIGURE 7-17 ▶ Atrial tachycardia (AT) with wide and narrow QRS complexes AT initially con-ducts antidromically via the parahisian accessory pathway (wide QRS complexes) but later blocks, and conduction to the ventricle is entirely via the atrioventricular node

FIGURE 7-18 ▶ Rapid atrial tachycardia (AT) in

a 6-month-old child with sepsis and a structurally normal heart AT rate is 300 bpm, which was associated with a left atrial thrombus Usually, a left atrial thrombus is seen in patients with atrial fibrillation and atrial flutter; however, rapid AT can also result in left atrial thrombus

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FIGURE 7-19 ▶ Focal atrial tachycardia (AT) presenting as wide

complex tachycardia (WCT) A, Patient presented with a WCT with a

right bundle branch block (RBBB) morphology QRS complexes during the WCT have a typical RBBB morphology, suggesting aberrancy Pres-ence of upright P waves in inferior leads practically rules out a ventricu-

lar tachycardia with 1 : 1 retrograde conduction B, During intravenous

diltiazem therapy, AT with 2 : 1 atrioventricular block was demonstrated

C, Morphology of P waves during the sinus rhythm P waves during AT

are negative in leads V1 and aVR and positive in the inferior leads AT

was focal and was mapped at the high crista terminalis region (D)

Inferior vena cava

Superior vena cava

Right atrium

AT focusRight inferior pulmonary vein

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suggest a high septal source AT was mapped at the paraseptal area above the proximal His bundle (D) AAo, Ascending aorta; AVN,

atrioven-tricular node; CS/ThV, coronary sinus/Thebesian valve; CT, crista terminalis; CTI, cavotricuspid isthmus; ER/EV, eustachian ridge/eustachian valve;

IVC, inferior vena cava; OF, fossa ovalis; RAA, right atrial appendage; RCA, right coronary artery; RV, right ventricle; SI, inferior septum; STV, septal

tricuspid valve; SVC, superior vena cava; TT, tendon of Todaro

A

B

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STV

IVCER/EV

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206

FIGURE 7-21 ▶ High cristal tachycardia Focal atrial tachycardia (AT) with positive P waves in lead I, and inferior leads suggests a high right

atrial source (A) Negative P waves in lead V1 suggest right atrial source Negative P waves suggest a cristal rather than lateral or tricuspid

annular source Focal AT was mapped at the high cristal area (B) AAo, Ascending aorta; AVN, atrioventricular node; CS/ThV, coronary sinus/

Thebesian valve; CT, crista terminalis; CTI, cavotricuspid isthmus; ER/EV, eustachian ridge/eustachian valve; IVC, inferior vena cava; OF, fossa ovalis;

RAA, right atrial appendage; RCA, right coronary artery; RV, right ventricle; SI, inferior septum; STV, septal tricuspid valve; SVC, superior vena cava;

CT

OFTTSTV

IVCER/EV

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FIGURE 7-22 ▶ Midcristal atrial tachycardia (AT) ECG reveals positive P waves in lead I and inferior leads (A) However, P wave amplitude in inferior lead is less than that in sinus rhythm or compared with sinus tachycardia (B) or a high cristal AT (see Figure 7-21) This suggests the focus of AT in the midcristal region Tachycardia was mapped in this region 2 cm below the superior vena cava (C)

A

B

C

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208

FIGURE 7-23 ▶ Low cristal atrial tachycardia (AT) ECG depicts positive P waves in lead I and negative in the inferior leads (A) This suggests

the focus of AT in the midcristal region Negative P waves in lead V1 and aVR suggest cristal or posterior focus of AT Negative P waves in inferior

leads suggest inferior focus in the right atrium The focus of the AT was mapped at the low crista terminalis (B)

A

B

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FIGURE 7-24 ▶ Focal atrial tachycardia (AT) originating from the inferior lateral right atrial atrium The AT has negative P waves in lead V1 and

positive P waves in lead aVR, which suggest a relatively anterior or annular focus of AT in the right atrium A, Negative P waves in inferior leads suggest inferior focus in the right atrium B, AT focus was mapped at the low lateral right atrium

A

B

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210

FIGURE 7-25 ▶ Atrial tachycardia (AT) originating from the low

lateral tricuspid annulus AT (A) slowed following antiarrhythmic therapy (B) C, P wave morphology during sinus rhythm in the same

patient The AT has negative P waves in lead V1 and positive P waves

in lead aVR, which suggest a relatively anterior or annular focus of AT

in the right atrium Negative P waves in the inferior leads suggest an inferior focus in the right atrium Negative P waves in leads V3 to V6 (≥3 precordial leads) suggest an annular focus AT focus was mapped

at the low lateral tricuspid annulus (D) AV, Atrioventricular

Left atrial appendage Left superior and

inferior pulmonaryveins

Left atriumRight superior andinferior pulmonaryvein ostium

Coronary sinusInferior vena cava

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FIGURE 7-26 ▶ Focal atrial tachycardia (AT) in an 18-year-old woman with postpartum cardiomyopathy AT has negative P waves in lead V1

and positive P waves in lead aVR, which suggest a relatively anterior or annular focus of AT in the right atrium (A) Negative P waves in inferior

leads suggest an inferior focus in the right atrium Negative P waves in leads V3 to V6 (≥3 precordial leads) suggest an annular focus AT shows type I second-degree atrioventricular block AT focus was mapped at the low lateral tricuspid annulus Tachycardia originated from the infero-

lateral tricuspid annulus (B)

A

B

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212

FIGURE 7-27 ▶ Focal atrial tachycardia (AT) originating from the inferior tricuspid annulus AT has isoelectric P waves in lead V1 and positive

P waves in lead aVR, which suggest a relatively anterior or annular focus of AT in the right atrium (A) Negative P waves in inferior leads suggest

an inferior focus in the right atrium Negative P waves in leads V3 to V6 (≥3 precordial leads) suggest an annular focus at the low lateral tricuspid

annulus Narrower P waves in AT than P waves in the sinus rhythm (B) suggest the AT focus is close to the septum Tachycardia originated from the inferior tricuspid annulus close to the septum (C)

A

B

C

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FIGURE 7-28 ▶ Focal atrial tachycardia (AT) originating at the ostium of the coronary sinus A, AT has negative P waves in lead V1 and positive

P waves in lead aVR, which suggest a relatively anterior or annular focus of AT in the right atrium Negative P waves in inferior leads suggest

inferior focus in the right atrium Positive P waves in leads V5 and V6 suggest a septal focus B, Patient also had wandering atrial pacemaker

with predominant inferior right atrial rhythm with occasional sinus P wave (arrows) C, AT focus was mapped at the low septum at the coronary

sinus ostium

A

B

C

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FIGURE 7-30 ▶ Focal atrial tachycardia (AT) from midposterior right atrium in a 52-year-old woman with nonischemic cardiomyopathy

A, ECG depicts initial negative P waves in leads V1 and aVR along with positive P waves in lead I that suggest a right atrial origin of the AT Positive P waves in leads V2 to V6 suggest the AT focus is closer to septal location ECG in sinus rhythm (B) shows left atrial enlargement and

poor progression of R wave in precordial leads AT was mapped to the posterior right atrium close to the septum and medial to the crista

terminalis (C)

A

B

C

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216

FIGURE 7-31 ▶ Right atrial tachycardia (AT) near the tricuspid annulus

in a 20-year-old patient with mesocardia, double outlet ventricle with hypolastic right ventricle, and severe pulmonary stenosis Patient developed ATs of multiple morphologies of both focal and reentrant

nature A, AT was a focal originating from the anterolateral right atrium

B, Reentrant AT originating from the same area (C)

A

B

AortaLeft atrium

Left ventricle

Rightventricle

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A

B

C

FIGURE 7-32 ▶ Parahisian atrial tachycardia (AT) P waves in AT (A) are most likely positive in lead V1 and negative in lead aVL, which suggests

a left atrial source However, owing to T wave and P wave fusion, the P wave amplitude and vector cannot be ascertained Furthermore, the predictive value of P wave morphology for localizing the atrium of origin a septal AT is more limited because of variation of activation pattern

of both atria B, Sinus P waves C, Focal AT was mapped to the parahisian area, just anterior and proximal to the His bundle

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FIGURE 7-33 ▶ Atrial tachycardia (AT ) originating from the noncoronary cusp A, P wave morphology is negative-positive in lead V1 and

biphasic in inferior leads and lead aVL B, AT focus was mapped at the noncoronary cusp of sinus of Valsalva C, The activation pattern of atrial

impulse during AT from the origin L, Left coronary cusp; MV, mitral valve; N, noncoronary cusp; R, right coronary cusp; TV, tricuspid valves

Pulmonar

y

valveAorticvalve

Bicuspidvalve

Left coronary

artery

Right coronaryartery

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A

B

C

FIGURE 7-34 ▶ Atrial tachycardia (AT)–induced cardiomyopathy in an 80-year-old patient P waves during AT (A) are narrow and positive in

leads V1, aVR, and aVL, suggesting septal origin P waves are biphasic in leads II and III, suggesting a lower septal site of origin However, AT was mapped to the left upper septum (parahisian area) During catheter ablation near the site of the AT focus, transient PR prolongation was noted, suggesting a left septal extension of fast atrioventricular nodal pathway Tachycardia was ablated successfully just caudal to the site where transient P-R prolongation was observed Patient also had rate-related left bundle branch block aberrancy with right axis deviation ECG

during sinus rhythm (B) shows poor progression of R wave and a left axis deviation Site of successful catheter ablation is shown in C

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220

FIGURE 7-35 ▶ Adenosine-sensitive focal atrial tachycardia (AT) P waves are positive-negative in lead V1 and positive in leads I and AVR,

suggesting a left atrial focus A, P waves are positive in lead aVL and negative in inferior leads, suggesting AT focus in the inferior left atrium

P waves are relatively narrow, suggesting its source is close to the midline B, AT focus was mapped at the inferolateral mitral annulus

A

B

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222

FIGURE 7-37 ▶ Rapid irregular focal atrial tachycardia (AT) P wave is positive in leads V1 and aVL and inferior leads and negative in leads aVR

and aVL (A) This focal AT was mapped to the posterosuperior left atrium close to the ostium of the right superior pulmonary vein (B)

A

B

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FIGURE 7-38 ▶ Focal automatic atrial tachycardia (AT) A, P waves are upright in lead V1 and inferior leads (red arrow) and negative in lead

aVL P wave amplitude in lead II is greater than 0.1 mV The tachycardia later changes to irregular rhythm (atrial flutter/atrial fibrillation) B, AT

focus was mapped at the superomedial aspect of the left superior pulmonary vein roof

A

B

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224

FIGURE 7-39 ▶ Focal atrial tachycardia (AT) in patient with history of mitral valve surgery A, P waves are positive-negative in lead V1,

iso-electric in lead I, and negative in lead aVL, suggesting a left atrial origin Positive P waves in the inferior leads suggest an anterior focus in the

left atrium B, AT was mapped to the superomedial mitral annulus

A

B

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FIGURE 7-40 ▶ Focal atrial tachycardia (AT) in patient with history of catheter ablation of atrial fibrillation A, P waves are better delineated

after the monomorphic premature ventricular contraction P waves are positive in lead V1 and isoelectric in lead aVL, suggesting left atrial focus

of the AT P waves are isoelctric in all the limb leads P wave pattern can vary after a catheter ablation or maze procedure for atrial fibrillation

B, Focal AT was mapped to the right inferior pulmonary vein

A

B

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226

FIGURE 7-41 ▶ Focal atrial tachycardia (AT) and atrial flutter in a patient with

a history of catheter ablation of atrial fibrillation Tachycardia is rapid and

irregu-lar with a mild variation in P wave morphology (A and B) P waves are positive

in leads V1 and aVL and lead II Negative P waves in leads aVL and aVR suggest

a close to midline focus of the AT P wave amplitude greater than 50 µV in lead

I and greater than 1 mV in lead II suggests a right superior pulmonary vein origin

of the tachycardia C, Tachycardia was mapped to the superior aspect of the

right superior pulmonary vein

A

B

C

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