Abstract
Focal atrial tachycardia (AT) is characterized by atrial activation starting at a small area (focus), from which it spreads out centrifugally. “Focal” implies that the site of origin cannot be mapped spatially beyond a single point or a few adjacent points with the resolution of a standard 4-mm-tip catheter. In contrast, macroreentrant AT is defined by activation that can be recorded over the entire tachycardia cycle length around a large central obstacle, which is generally several centimeters in diameter. Relatively small reentry circuits can resemble focal AT, especially if limited numbers of endocardial recordings are collected.
Available data suggest that a focal activation pattern can be caused by automaticity, triggered activity, or microreentry. Delineating the mechanism of focal AT, however, can be difficult, and the means of distinguishing focal AT mechanisms through pharmacological testing or electrophysiological (EP) study have limited sensitivity and specificity. In addition, there is a significant overlap in the EP characteristics of tachycardias with differing mechanisms.
When paroxysmal, AT frequently manifests with episodes of palpitations and heart racing that start and terminate abruptly. Incessant AT can precipitate cardiomyopathy in approximately one-third of patients. Pharmacological therapy is associated with limited efficacy in the treatment of focal AT. Catheter ablation is recommended in patients with recurrent symptomatic AT, especially when pharmacological therapy is unsuccessful, not tolerated, or not preferred.
Keywords
atrial tachycardia, focal tachycardia, microreentry, macroreentry, triggered activity, automaticity
Outline
Classification of Atrial Tachycardias, 305
Pathophysiology, 305
Incessant Atrial Tachycardias, 307
Anatomical Locations, 307
Pulmonary Vein Tachycardia, 308
Multifocal Atrial Tachycardia, 308
Sinus Node Reentrant Tachycardia, 309
Epidemiology, 309
Clinical Presentation, 309
Initial Evaluation, 309
Principles of Management, 309
Electrocardiographic Features, 311
P Wave Morphology, 311
QRS Morphology, 311
P/QRS Relationship, 311
Localization of the Tachycardia Site of Origin, 311
Electrophysiological Testing, 318
Baseline Observations During Sinus Rhythm, 318
Induction of Tachycardia, 318
Tachycardia Features, 320
Diagnostic Maneuvers During Tachycardia, 321
Diagnostic Maneuvers During Sinus Rhythm After Tachycardia Termination, 323
Exclusion of Other Arrhythmia Mechanisms, 324
Mapping, 324
Conventional Activation Mapping, 324
Pace Mapping, 328
Mapping Postpacing Intervals, 329
Electroanatomic Mapping, 330
Mapping Nonsustained Focal Atrial Tachycardia, 332
Ablation, 333
Target of Ablation, 333
Ablation Technique, 333
Ablation of Para-Hisian Atrial Tachycardias, 333
Endpoints of Ablation, 335
Outcome, 337
Classification of Atrial Tachycardias
Organized atrial tachycardias (ATs) are broadly categorized as either focal (originating from a small circumscribed area from which it spreads out centrifugally) or macroreentrant (continuous, uninterrupted activation wavefront rotating around a relatively large central obstacle).
Focal ATs can be caused by automatic, triggered, or microreentrant mechanisms. The mechanism of macroreentrant atrial tachycardia (MRAT) is reentrant activation around a large central obstacle, generally several centimeters in diameter, at least in one of its dimensions. The central obstacle can consist of normal anatomical structures (venous or valvular orifices) or abnormal structures (scars), and can be fixed, functional (anisotropic conduction block), or a combination of both. There is no single point of origin of activation, and atrial tissues outside the circuit are activated from various parts of the circuit ( Table 11.1 ).
| Focal atrial tachycardia |
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| Macroreentrant atrial tachycardia | Cavotricuspid isthmus-dependent right atrial macroreentry |
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| Noncavotricuspid isthmus-dependent right atrial macroreentry |
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| Left atrial macroreentry |
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Depending on whether the cavotricuspid isthmus (CTI) is critical to the reentry circuit, MRATs are divided into two groups: “CTI-dependent” or “non-CTI-dependent” MRAT. CTI-dependent MRATs include typical atrial flutter (AFL), lower loop reentry, and intra-isthmus reentry.
The term atrial flutter has traditionally been used to refer to a continuously undulating pattern on the ECG, without an isoelectric baseline in at least one lead, whatever the cycle length (CL). Typical AFL is reserved for a macroreentrant circuit with the activation wavefront rotating clockwise or counterclockwise around the tricuspid annulus and using the CTI as an essential part of the reentry circuit. Atypical AFL is only a descriptive term for an AT with an ECG pattern of continuous undulation of the atrial complex, different from that in typical AFL. However, the term “atypical AFL” introduces unnecessary confusion, and a mechanistic description of the AT circuit in relation to atrial anatomy is preferred (e.g., perimitral macroreentry, lesional right atrial [RA] macroreentry; see Table 11.1 ).
Importantly, classification of ATs based on the 12-lead electrocardiogram (ECG) has been abandoned. Now it is well recognized that the underlying mechanisms of AT, as defined by conventional and advanced mapping techniques, do not correlate well with ECG patterns. Neither the tachycardia rate nor the lack of isoelectric baseline between atrial deflections on the surface ECG is specific for any arrhythmia mechanism.
This chapter discusses focal AT. Typical AFL and MRAT are discussed in subsequent chapters.
Pathophysiology
Focal AT is characterized by atrial activation starting at a small area (focus), from which it spreads out centrifugally. “Focal” implies that the site of origin cannot be mapped spatially beyond a single point or a few adjacent points with the resolution of a standard 4-mm-tip catheter. In contrast, MRAT is defined by activation that can be recorded over the entire tachycardia cycle length (TCL) around a large central obstacle, which is generally several centimeters in diameter. Relatively small reentry circuits can resemble focal AT, especially if limited numbers of endocardial recordings are collected ( see Fig. 13.11 ). The term localized reentry has been used to refer to reentry in which the circuit is localized to a small area (covering a surface diameter of less than 3 cm) and does not have an easily identifiable central obstacle.
Available information suggests that a focal activation pattern can be caused by automaticity, triggered activity, or microreentry ( Table 11.2 ). Delineating the mechanism of focal AT, however, can be difficult, and the means of distinguishing focal AT mechanisms through pharmacological testing or electrophysiology (EP) study have limited sensitivity and specificity. In addition, there is a significant overlap in the EP characteristics of tachycardias with differing mechanisms. It is especially difficult to discriminate definitively between triggered activity and microreentry as a mechanism of focal AT; therefore some investigators have classified focal ATs as either automatic or nonautomatic. Furthermore, it is not clear that making such mechanistic distinctions among various types of focal ATs carries clinical significance, especially in the era of catheter ablation, although it is possible that such information could be useful in guiding drug therapy. In contrast, determination of the likely focal versus macroreentrant mechanism is critical for planning the mapping and ablation strategy.
| Automaticity | Triggered Activity | Microreentry | |
|---|---|---|---|
| Initiation |
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| Termination |
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| Response to AES |
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| Response to overdrive atrial pacing |
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| Response to adenosine |
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| Response to vagal maneuvers and adenosine |
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| Electrogram at site of origin |
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Not infrequently, two or more foci of AT can be found in the same patient. In these patients, the AT appears to have different EP characteristics from focal AT with a single focus, as it tends to involve the LA and has greater cardiovascular comorbidity, shorter CL, longer total activation time, and lower acute and long-term success rates of catheter ablation. The term multiple focal ATs needs to be distinguished from multifocal AT (MAT), which refers to the continuously shifting site of origin of the atrial impulse (see below).
Incessant Atrial Tachycardias
The term incessant is applied to an AT that is present for at least 50% of the time that a patient is monitored. Incessant AT frequently is automatic, but it can also be secondary to reentry or triggered activity. Incessant tachycardias occur in up to 25% of patients with focal AT. Foci arising from the atrial appendages and pulmonary veins (PVs) are frequently incessant (84% and 59%, respectively). Incessant ATs (regardless of the anatomical site of origin) can precipitate cardiomyopathy in approximately one-third of cases. Incessant tachycardias precipitating cardiomyopathy characteristically tend to have long atrial CLs as compared with ATs not associated with cardiomyopathy and hence may produce negligible symptoms and go unrecognized by the patient until symptoms related to cardiomyopathy develop.
Anatomical Locations
Focal ATs have a predilection for originating from certain anatomical regions of the atria ( Fig. 11.1 ). The RA is the site of origin for the majority (more than 60%) of focal ATs. Approximately two-thirds of RA ATs are distributed along the so-called ring of fire, extending from the superior aspect of the crista terminalis and down the long axis of the crista (“cristal tachycardias”), to the tricuspid annulus, coronary sinus (CS), and atrioventricular (AV) junction, with an apparent gradation in frequency from superior to inferior. This particular anatomical distribution of ATs may be related to the marked anisotropy characterizing the region of the crista terminalis. Such anisotropy, which is related to poor transverse cell-to-cell coupling, favors the development of microreentry by creating regions of slow conduction. Fractionated electrograms often seen at a successful AT ablation site can be markers of the requisite nonuniform anisotropic substrate. In addition, the normal sinus pacemaker complex is distributed along the long axis of the crista terminalis. The presence of automatic tissue, together with relative cellular uncoupling, may be a requirement for abnormal automaticity such that a normal atrium is prevented from electrotonically inhibiting abnormal phase 4 depolarization. Of note, the presence of structural heart disease increases the probability of RA location of the AT, but from sites outside the crista terminalis.
The PV ostia are the most common sites of origin of focal tachycardias within the LA; they account for approximately 67% of LA ATs and between 3% and 29% of all focal ATs. Other sites of tachycardia clustering include the CS os, mitral and tricuspid annuli, bases of right and left atrial appendages, para-Hisian region, and atrial septum. Focal ATs also can arise within the vein of Marshall, superior vena cava (SVC), or inferior vena cava (IVC). ATs have been described originating from the noncoronary aortic sinus of Valsalva. The distribution of AT foci can differ, depending on the patient population.
A recent report found that the majority of triggered-activity focal ATs originate along the crista terminalis and tricuspid and mitral annuli, whereas automatic ATs often originate from the right or left atrial appendage or PVs. Microreentrant ATs are frequently, but not always, related to previous ablation lines performed for AF or MRAT.
Pulmonary Vein Tachycardia
Arrhythmias originating from the PVs can have a critical role in the development of AF in susceptible individuals. Focal ATs arising from the PVs, however, appear to be a distinct clinical entity from the PV arrhythmias associated with AF. Patients with focal PV ATs do not seem to be at risk of AF in the long term; they resemble patients with focal ATs originating elsewhere with a localized isolated substrate that is successfully addressed with a focal ablative approach. Several potential explanations have been suggested for the different behavior. The underlying pathophysiological process in patients with AF is probably fundamentally different. It is a generalized process diffusely affecting the muscular sleeves in all four PVs, often with multiple PV foci originating distally (up to 2 to 4 cm) within the vein, compared with the focal nature of the process in patients with isolated PV tachycardia. In addition, the CLs of the PV ATs are longer (mean CL 340 milliseconds) than the reported CLs of PV tachycardia in AF patients (130 milliseconds). The CL of AT also tends to be irregular in patients with AF, but not in patients with PV AT. It is possible that foci with shorter CL and irregular activity may not conduct in a 1 : 1 fashion from the PV to the LA, with resulting fibrillatory conduction and AF. Furthermore, patients with AF tend to be older than those with PV AT and consequently more prone to more widespread atrial remodeling associated with age, hypertension, or other pathological processes.
Multifocal Atrial Tachycardia
MAT (also is known as chaotic AT) is usually caused by enhanced automaticity and is characterized by varying morphology of the P waves, suggesting that the pacemaker arises in different atrial locations ( Fig. 11.2 ). The shift in pacemaker focus is usually associated with different PR intervals (depending on its proximity to the atrioventricular node [AVN]) and varying R-R intervals. The ventricular rate is usually 100 to 130 beats/min but may be as low as 90 beats/min or as high as 250 beats/min. Some P waves can be aberrantly conducted, and some can be nonconducted, further contributing to the irregularity of the ventricular rate.
In general, the ECG diagnosis of MAT requires the following observations: (1) discrete P waves (in distinction to AF); (2) at least three distinctly different P wave morphologies in the same ECG lead (in distinction to focal and MRAT); (3) atrial rate faster than 90 to 100 beats/min (in distinction to wandering pacemaker); (4) absence of one dominant atrial pacemaker (in distinction to normal sinus rhythm [NSR] with frequent premature atrial complexes [PACs]); (5) P waves that are separated by isoelectric intervals (in distinction to AFL); and (6) varying PP, PR, and RR intervals.
MAT typically is associated with underlying pulmonary, cardiac, or metabolic disease. In particular, MAT is frequently observed in patients with chronic obstructive pulmonary disease (present in approximately 60% of patients with MAT) or congestive heart failure, especially those treated with theophylline, β-adrenergic agonists, or digoxin, or during a period with exacerbation of the underlying disorder, hypoxemia, or electrolyte imbalance (e.g., hypokalemia, hypomagnesemia, acidosis). MAT can also occur in patients following surgical procedures, especially those with postoperative complications such as respiratory compromise, sepsis, acute heart failure, pulmonary embolism, electrolyte abnormalities, or renal insufficiency. These patients also have higher incidence of other atrial arrhythmias, such as frequent PACs, AF, and AFL.
MAT does not usually precipitate hemodynamic compromise, and patient’s clinical symptoms are primarily related to the underlying illness rather than the tachycardia itself. Hence the management of MAT is mainly directed toward the treatment of the underlying disease, correction of electrolyte abnormalities, and withdrawal of offending drugs (e.g., theophylline, digoxin). IV magnesium can be helpful, even in patients with normal magnesium levels. Pharmacological therapy is associated with limited efficacy in suppressing the arrhythmia and controlling the ventricular rate during MAT. When MAT is symptomatic or leads to decompensation of underlying disease, beta-blockers and verapamil constitute the initial therapy, unless contraindicated because of the presence of bronchospasm or hypotension. Amiodarone can be useful in refractory cases. Electrical cardioversion is not effective and hence not recommended. Catheter ablation is not likely to be effective, given the underlying diffuse atrial abnormalities and severe comorbidities. Ablation of the AVN and pacemaker implantation for rate control is rarely indicated, and should be reserved to patients with severe symptoms related to the tachycardia and failed medical therapy.
Sinus Node Reentrant Tachycardia
Sinus node reentrant tachycardia was originally described as a tachycardia that could be induced and terminated by programmed electrical stimulation with a P wave morphology identical or similar to sinus P waves and TCLs of 350 to 550 milliseconds ( see Fig. 16.3 ). There have been some reports of endocardial ablation of sinus node reentrant tachycardias identified by these criteria. However, the precise identification of sinus node reentrant tachycardia remains elusive, and whether the reentry substrate is confined within the sinus node or involves perinodal atrial tissue is unknown, and whether it represents a category distinct from other intraatrial tachycardias is uncertain. More likely, sinus node reentrant tachycardia is a microreentrant focal ATs that happens to be arising along the crista terminalis, very close to the usual location of the sinus node. The arrhythmia typically presents as a paroxysmal tachycardia, and frequently as bursts of nonsustained AT, with P waves that are virtually identical to sinus P waves. Consistent with a reentry mechanism, this tachycardia is usually triggered and terminated abruptly by a PAC. The tachycardia can also be terminated by vagal maneuvers. In contrast to sinus tachycardia, sinus node reentrant tachycardia is characterized by abrupt onset and termination, and often has a longer PR interval than that observed during NSR (since the elevated adrenergic tone that drives the sinus node also accelerates AVN conduction).
Epidemiology
Focal atrial ectopy and nonsustained AT are frequently observed on Holter recordings and are seldom associated with symptoms. Sustained focal ATs are relatively infrequent; they are diagnosed in approximately 5% to 15% of patients referred for catheter ablation of supraventricular tachycardia (SVT). However, ATs comprise a progressively greater proportion of paroxysmal SVTs with increasing age, accounting for 23% in patients older than 70 years. Age-related changes in the atrial EP substrate, including cellular coupling and autonomic influences, likely contribute to the increased incidence of AT in older individuals. Men and women seem to be equally affected. In adults, focal ATs can occur in the absence of structural heart disease. Nevertheless, the incidence of associated structural heart disease is higher in patients with focal AT than those with other types of paroxysmal SVT. Among focal AT patients, those with multiple tachycardia foci are more likely to have underlying heart disease. The long-term prognosis in patients with focal AT is generally benign, except for those with incessant ATs, which can precipitate tachycardia-induced cardiomyopathy.
Clinical Presentation
Focal ATs can manifest as paroxysmal or incessant tachycardias. When paroxysmal, AT frequently manifests with episodes of palpitations and heart racing that start and terminate abruptly. Associated symptoms can include lightheadedness, dyspnea, chest discomfort, and weakness. Syncope is rare. Due to the higher prevalence of structural heart disease in this group of patients, symptoms of AT can be more severe than other types of paroxysmal SVTs. Decompensation of underlying heart failure or ischemic heart disease can be precipitated by episodes of AT.
Tachycardia-induced ventricular cardiomyopathy develops in 10% of patients with focal AT, but predominantly in those with incessant or, less commonly, frequently repetitive tachycardia. Incessant AT can precipitate cardiomyopathy in approximately one-third of patients, and frequently manifest with symptoms of congestive heart failure. In contrast to rapid paroxysmal ATs that are more likely to cause significant symptoms of palpitations and be diagnosed earlier in the clinical course, incessant ATs tend to have slower atrial and ventricular rates, and hence patients can remain asymptomatic until they present with decompensated heart failure secondary to tachycardia-induced cardiomyopathy. Elimination of the tachycardia results in normalization of LV function within a few months in the vast majority of patients.
AT can also manifest as a frequently repetitive tachycardia, with frequent episodes of AT interrupted by brief periods of NSR. The repetitive type can be tolerated well for years. It may cause symptoms only in cases of fast heart rates during phases of tachycardia, and it infrequently induces dilated cardiomyopathy.
Initial Evaluation
Clinical symptoms are not usually helpful in distinguishing paroxysmal focal AT from other forms of paroxysmal SVT. Documentation of the arrhythmia during spontaneous symptoms on ECG or ambulatory cardiac monitoring is important to establish the diagnosis. Holter or cardiac event monitoring (depending on the frequency of symptoms) is often adequate. Implantable loop recorders can be helpful in selected cases, with rare episodes associated with severe symptoms of hemodynamic instability (e.g., syncope).
The diagnosis of the incessant and frequently repetitive forms of AT usually can be readily made on ECG recordings based on P wave morphology and the frequent presence of AV block during the tachycardia on ECG recordings. An ECG pattern of AT with discrete P waves and isoelectric intervals is suggestive of a focal mechanism of the AT, but it does not rule out MRAT, especially in patients with complex structural heart disease, prior cardiac surgery for congenital heart disease, or previous AF catheter or surgical ablation. Not infrequently, the diagnosis of focal AT can be established with certainty only by an EP study.
Echocardiography is recommended to exclude or diagnose the presence of structural heart disease. Cardiac stress testing and other diagnostic studies are considered in patients at risk for coronary artery disease.
Invasive EP testing with subsequent catheter ablation can be used for diagnosis and therapy in cases with a clear history of paroxysmal regular palpitations. It can also be considered in patients with preexcitation or disabling symptoms without ECG documentation of an arrhythmia.
Principles of Management
Acute Management
The usual acute therapy for AT consists of IV beta-blockers, diltiazem, or verapamil ( Fig. 11.3 ). However, these drugs have modest efficacy (30% to 50%) in either terminating the focal AT or slowing the ventricular rate. Digoxin has not been well studied for focal AT. The response of focal AT to drug therapy is influenced, in part, by the underlying mechanism of the tachycardia. Automatic ATs are more likely to be terminated by beta-blockers, while the response of triggered AT is variable. On the other hand, the response of microreentrant AT can depend on the location of the microreentrant circuit, with those ATs arising from the perinodal region being most sensitive.
Vagal maneuvers and adenosine can be used for acute termination of AT. However, ATs can be terminated with vagal maneuvers only on rare occasions, and the response to adenosine is variable. While a significant proportion of triggered ATs will terminate with adenosine, persistence or transient suppression of the tachycardia (with possible transient AV block) is also a common response to adenosine, especially in automatic or microreentrant ATs.
For refractory cases, intravenous (IV) ibutilide, class IC drugs (e.g., flecainide, propafenone), or amiodarone can be considered. IV flecainide and propafenone are moderately effective; these agents are not available in the United States. The effectiveness of ibutilide for treatment of focal AT is unclear. IV amiodarone may be reasonable, especially in acute ill patients and those with decompensated heart failure. Electrical cardioversion can be considered for symptomatic patients with drug-resistant arrhythmia. Although electrical cardioversion seldom terminates automatic ATs, it can be successful for triggered and microreentrant ATs.
Chronic Management
Long-term therapeutic decisions should consider the severity of symptoms, impact on life style, effectiveness and tolerance of drug therapy, and the presence of concomitant structural heart disease, as well as patient preference ( Fig. 11.4 ).
Catheter Ablation
Catheter ablation is recommended in patients with recurrent symptomatic AT, especially when pharmacological therapy is unsuccessful, not tolerated, or not preferred. Catheter ablation is also recommended for incessant AT, even in asymptomatic patients, especially when tachycardia-induced cardiomyopathy has developed. In the latter group of patients, complete resolution of LV dysfunction has been observed following successful radiofrequency (RF) catheter ablation of the AT focus. Regardless of whether the arrhythmia is caused by abnormal automaticity, triggered activity, or microreentry, focal AT can be ablated by targeting the site of origin (focus) of the AT. Catheter ablation for focal AT carries a success rate of more than 90%, with a recurrence rate of 9%. The incidence of significant complications is relatively low (1% to 3%) in experienced centers.
Pharmacological Therapy
No large studies have been conducted to assess the effect of pharmacological treatment in patients with focal ATs, but both paroxysmal and especially incessant ATs are reported to be difficult to treat medically. Available data support a recommendation for initial therapy with calcium channel blockers or beta-blockers because these agents may prove to be effective and have low side-effect profiles. If these drugs are unsuccessful, then class IC agents (flecainide and propafenone) in combination with an AVN blocking agent, or class III agents (sotalol and amiodarone), may be considered; however, the potential benefit should be balanced by the potential risks of proarrhythmia and toxicity. Because ATs often occur in older patients and in the context of structural heart disease, class IC agents should be used only after cardiomyopathy and coronary artery disease have been excluded.
Electrocardiographic Features
P Wave Morphology
During AT, typically there are discrete P waves at rates of 130 to 240 beats/min, but possibly as slow as 100 beats/min or as fast as 300 beats/min. Antiarrhythmic drugs can slow the atrial rate without abolishing the AT. Classically, there are clearly defined isoelectric intervals between the P waves in all leads ( Fig. 11.5 ). However, in the presence of rapid atrial rates or broad P waves due to intraatrial conduction disturbances, there may be no isoelectric baseline. In these cases, the ECG shows an AFL pattern (continuous undulation without isoelectric baseline; Fig. 11.6 ). Nevertheless, one report demonstrated a high sensitivity (90%) and specificity (90%) of quantitative ECG indexes of shorter atrial activation and longer diastolic intervals in distinguishing focal from MRAT. This approach was effective in cases with and without 1 : 1 AV conduction and when the P or flutter waves overlay T waves.
P wave morphology depends on the anatomical location of the atrial focus, and it can be used to approximate the site of origin of the AT. However, the P wave can be partially masked by the preceding ST segment or T wave. Vagal maneuvers and adenosine infusion to provide transient AV block can be used to obtain a clear view of the P wave, assuming that the tachycardia does not terminate. The compensatory pause following a premature ventricular complex during the AT can also help delineate P wave morphology ( Fig. 11.7 ).
It has been suggested that the multilead body surface potential recording can be used to help localize the site of origin of the tachycardia. One report described a clinical application of ECG imaging (ECGI) as an adjunctive noninvasive technology to identify the site of origin of a focal AT accurately prior to catheter ablation ( eFig. 11.1 ).
Of note, P wave morphology at the onset of the tachycardia can help determine the mechanism of focal AT. Automatic ATs start 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. In comparison, intraatrial reentry or triggered-activity AT is usually initiated by a P wave from a PAC that generally differs in morphology from the P wave during the established arrhythmia ( Fig. 11.8 ).
QRS Morphology
QRS morphology during AT is usually the same as during NSR. However, functional aberration can occur at rapid atrial rates.
P/QRS Relationship
The AV relationship is usually 1 : 1 during ATs, but Wenckebach or 2 : 1 AV block ( Fig. 11.9 ) can occur at rapid rates, in the presence of AVN disease, or in the presence of drugs that slow AVN conduction. The presence of AV block during an SVT strongly suggests AT, excludes atrioventricular reentrant tachycardia (AVRT), and renders atrioventricular nodal reentrant tachycardia (AVNRT) unlikely.
ATs usually have a long RP interval; nonetheless, the RP interval can also be short, depending on the degree of AV conduction delay (i.e., PR interval prolongation) during the tachycardia.
Localization of the Tachycardia Site of Origin
P wave morphology on the 12-lead ECG during ATs is determined not only by the anatomical location of the AT focus but also by the subsequent activation pattern within the atrium of origin as well as the contralateral atrium. The activation sequence of the contralateral atrium is determined by the relative proximity of the source of activation to the insertion site of each of the preferential interatrial connections. These include Bachmann’s bundle, which connects the anterosuperior RA and LA, the interatrial connection located in the proximity of the CS os, the rim of the fossa ovalis, as well as small muscular bridges connecting the RA posterior wall with the LA posterior wall near the ostia of the right-sided PVs.
The ECG lead V 1 is the most useful in identifying the likely anatomical site of origin for focal AT. Lead V 1 is located to the right and anteriorly in relation to the atria (which should be considered anatomically as right anterior [RA] and left posterior [LA] structures). Thus, for example, tachycardias originating from the tricuspid annulus have negative P waves in lead V 1 because of the anterior and rightward location of this structure (i.e., activation travels away from lead V 1 ). The P wave in lead V 1 is universally positive for tachycardias originating from the PVs because of the posterior location of these structures (i.e., the impulse travels toward lead V 1 ).
In general, P waves identical to the sinus P wave are suggestive of sinus node reentrant tachycardia or perinodal AT. P wave vector in the inferior leads is indicative of the craniocaudal localization of AT origins. Foci in the superior aspect of the atria (such as superior PVs, atrial appendages, and superior crista terminalis) exhibit positive P waves in the inferior leads, whereas those originating from low atrial locations have negative P waves. ATs originating close to the interatrial septum exhibit P waves that are of shorter duration than the sinus P waves. Anterior RA or LA free wall or annular foci tend to have P waves with late precordial transition to an upright appearance. ATs originating from posterior atrial structures (such as the PVs or crista terminalis) usually have positive P waves in the anterior precordial leads.
Several algorithms ( Figs. 11.10 and 11.11 ) have been proposed for ECG localization of focal AT using P wave morphology. Importantly, while P wave morphology provides a useful guide to the localization of focal AT in patients without structural heart disease, activation patterns can be altered in patients with prior surgery or extensive atrial ablation or in those with significant structural heart disease, significantly rendering P wave morphology significantly less helpful.
Right Versus Left Atrial Tachycardias
Several features of P wave morphology can help distinguish RA from LA foci; leads aVL and V 1 are the most helpful for this purpose. In lead V 1 , a negative or biphasic (+/−) P wave predicts RA foci with 100% specificity and positive predictive value (sensitivity and negative predictive value in the range of 60% to 70%). Conversely, positive or biphasic (−/+) P waves in lead V 1 predict LA foci with 100% sensitivity and negative predictive value (specificity of 81% and positive predictive value of 76%).
In lead aVL, a positive or biphasic P wave predicts an RA focus with high accuracy (with the exception of right superior PV foci, whereby lead aVL can also exhibit positive P waves). Also, an isoelectric or negative P wave in lead I was 100% specific for an LA focus, but was only present in 50% of patients with LA foci.
The predictive value of P wave morphology for localizing the atrium of origin is more limited when the tachycardia foci arise from the interatrial septum. Those ATs are associated with variable P wave morphology and considerable overlap for tachycardias located on the left and right sides of the septum. As noted, P waves during ATs arising near the septum are generally narrower than those arising in the RA or LA free wall.
Right Atrial Tachycardias
Crista terminalis.
Cristal ATs (i.e., ATs arising from the crista terminalis) are characterized by right-to-left activation sequence, resulting in P waves that are positive and broad in leads I and II, positive in lead aVL, and biphasic in lead V 1 ( Fig. 11.12 ). A negative P wave in lead aVR predicts a cristal origin compared with anterior RA foci with a sensitivity of 100% and specificity of 93%. Biphasic (+/−) P waves in lead V 1 (or positive P waves in lead V 1 during both tachycardia and sinus rhythm), positive P waves in leads I and II, and negative P waves in lead aVR predict a cristal origin with 93% sensitivity, 95% specificity, 84% positive predictive value, and 98% negative predictive value.
High, middle, or low cristal locations can be identified by P wave polarity in the inferior leads. ATs originating from the lower crista terminalis exhibit P waves with isoelectric or biphasic patterns in the inferior leads (II, III, and aVF) and positive (but occasionally biphasic [−/+]) pattern in leads V 3 –V 6 ( eFig. 11.2 ).
Although there can be an overlap in tachycardia P wave morphology between superior crista (or SVC) foci and the right superior PV foci, due to the close anatomical proximity of these structures, these foci can be distinguished on the basis of changes to the P wave morphology in lead V 1 during tachycardia as compared with sinus P waves. In right superior PV AT, P waves in lead V 1 are invariably upright during tachycardia but can be either upright or biphasic (+/−) in sinus rhythm. When cristal AT has an upright P wave in lead V 1 (approximately 10%), it is invariably also upright during sinus rhythm. The combination of a biphasic or isoelectric P wave polarity in lead V 1 or a biphasic P wave polarity in lead aVL predicts an SVC focus.
Anterior septum.
In anteroseptal ATs (originating above the membranous septum), the P wave is biphasic or negative in lead V 1 . Because of relatively simultaneous biatrial activation, P wave duration is approximately 20 milliseconds narrower than the sinus P wave. Those ATs can mimic slow-fast AVNRT or orthodromic AVRT utilizing a superoparaseptal bypass tract (BT).
ATs originating in the para-Hisian region (apex of the triangle of Koch) typically exhibit narrow P waves that are consistently positive or isoelectric in leads I and aVL. In the inferior leads, the P wave is negative or biphasic (+/−) in the majority of cases, but can occasionally be positive or biphasic (−/+). In lead V 1 , the P wave is typically biphasic, with the dominant positive or negative component opposite to the pattern noted in the inferior leads. The negative inscription of P waves in the inferior leads is likely due to LA activation via CS interatrial connection, while positive P waves suggest activation of the LA via Bachmann’s bundle. In addition, para-Hisian ATs often exhibit a very characteristic narrow and biphasic (−/+) or triphasic (+/−/+) P wave morphology in the precordial leads, especially in V 4 to V 6 , and in the inferior leads ( eFig. 11.3 ). Importantly, given the complex anatomical relationship between both sides of the interatrial septum and the aortic root, a P wave morphology consistent with a para-Hisian or anteroseptal location does not accurately predict the successful ablation site (RA, aortomitral continuity, or noncoronary aortic sinus of Valsalva).
Midseptum.
Midseptal ATs (originating below the membranous septum and above the CS os) are associated with P waves that are biphasic or negative in lead V1 and negative in the inferior leads (see eFig. 11.3 ). Those ATs can mimic fast-intermediate AVNRT or orthodromic AVRT utilizing a midseptal BT.
Posterior septum.
In posteroseptal ATs (originating below and around the CS os), the P wave is positive or isoelectric-positive (but occasionally −/+ biphasic) in lead V 1 , exclusively negative in the inferior leads (II, III, and aVF), equally positive in leads aVL and aVR, and exclusively negative (but occasionally −/+ biphasic) in all four precordial leads (V 3 –V 6 ). The precordial transition to negativity is variable (see eFig. 11.3 ). P wave morphology in those ATs can mimic fast-slow AVNRT or orthodromic AVRT using a posteroseptal BT.
Tricuspid annulus.
A common feature of tricuspid annular ATs is the presence of an inverted P wave in leads V 1 and V 2 , with late precordial transition to an upright appearance (see eFig. 11.2 ). The nonseptal sites demonstrate negative P waves in lead V 1 , whereas inferolateral annular sites tend to have inverted P waves across the precordial leads, and superior sites closer to the septum show transition from negative in lead V 1 , through biphasic (−/+), to upright in the lateral precordial leads. In general, the polarity of leads II and III is deeply negative for an inferolateral annular location and low amplitude, positive, or biphasic for a superior location. In addition, tricuspid annular ATs typically have positive P waves in lead aVL and positive or isoelectric P waves in lead I.
In patients with ATs arising from the low RA, P waves that are either exclusively negative or have early negative components in precordial leads V 3 –V 6 indicate AT foci at the lower annular aspects of the RA such as the nonseptal tricuspid annulus (6 to 9 o’clock as viewed from the ventricle) and around the CS os, whereas positive P waves in V 3 –V 6 predict a low crista terminalis focus. To distinguish ATs of nonseptal tricuspid annular foci from CS os origins, P-wave morphology in leads I and V 1 can be of value. Positive P waves in lead I and negative P waves in lead V 1 suggest nonseptal tricuspid annular foci.
RA appendage.
Focal ATs originating from the RA appendage typically originate from the lateral base of the appendage but are also well described from an apical location. Because of their close anatomical proximity, these tachycardias are generally indistinguishable from superior tricuspid annular foci; they exhibit broad, negative, notched P waves in leads V 1 and V 2 and variable precordial transition to positive in lead V 6 . P waves in the inferior leads characteristically have low positive amplitudes (see eFig. 11.2 ).
Left Atrial Tachycardias
Pulmonary veins.
ATs arising from the PVs are characterized by entirely positive P waves in lead V 1 (in 100% of cases) and across the precordial leads, isoelectric or negative waves in lead aVL in 86%, and negative waves in lead aVR in 96%. Lead aVL can be biphasic or positive in right-sided PV ATs ( eFig. 11.4 ).
