Tomos Walters, MBBS, BMedSc, Jonathan M. Kalman, MBBS, PhD
A 55-year-old previously well woman presented with fatigue and progressively increasing exertional dyspnea. She appeared unwell, with clinical features of decompensated left ventricular (LV) failure. An ECG revealed long runs of a narrow complex long R-P tachycardia with a P-wave morphology similar to that of the occasional sinus beats observed (Figure 6-1). A transthoracic echocardiogram (TTE) revealed a dilated cardiomyopathy with an LV ejection fraction LVEF of 32%. Cardiac MRI demonstrated minimal myocardial fibrosis and coronary arteries were free of disease. Assessment in the electrophysiology laboratory confirmed a sustained tachycardia with a TCL of 460 msec, a VAAHV response to entrainment from the ventricular apex, and an earliest site of atrial activation in the region of the high crista terminalis (CT). Mapping identified the earliest atrial activation at this location, 20 msec ahead of the P wave. Ablation at this location resulted in speeding and termination of the tachycardia, which could subsequently not be induced with either atrial pacing or isoprenaline. Over 6 months there was no evidence of recurrent tachycardia. All clinical evidence of heart failure resolved, and repeat TTE demonstrated normalization of LV structure and function.
FIGURE 6-1 Patient TM. (A) Twelve-lead ECG showing recurrent bursts of FAT. Tachycardia P-wave morphology is similar to the sinus P-wave morphology. Biphasic (+/−) in V1, positive in lead I and negative in aVL indicates a CT origin. Positive morphology in the inferior leads indicates a position high on the CT. (B) Intracardiac electrograms EGMs. The earliest atrial signal is from the distal bipole of a catheter laid along the CT. (C) The upper left panel shows a coronal view of an anatomic specimen of the RA, with the CT running anterior to the SVC os and down the posterolateral right atrial wall before terminating anterior to the IVC. The lower left panel shows the electroanatomic map localizing the earliest site of activation during tachycardia to the superior CT, anteromedial to the SVC-RA junction. The panels on the right show LAO and RAO images of the catheter laid along the CT and of the ablation catheter at the time of successful termination of the tachycardia. (CT = crista terminalis; SVC = superior vena cava; IVC = inferior vena cava; FO = foramen ovale; CS os = coronary sinus os; RA = right atrium.) (D) The mapping catheter records an EGM 20 ms ahead of the P wave. Ablation at this location successfully terminated the tachycardia.
Focal atrial tachycardia (FAT) is a relatively uncommon form of supraventricular tachycardia (SVT) encountered in the electrophysiology laboratory in adults, accounting for no more than 15% of studies performed for management of SVT.1 While reports differ, FAT appears to be equally present in men and women and to be overrepresented in younger patients.2,3 The single most common location for FAT is the crista terminalis. Tachycardias arising from the CT show a particular preponderance in women and are relatively more likely to arise in older patients.
Patients may present with specific symptoms of variable severity that include palpitations, chest discomfort, dyspnea, fatigue, dizziness and syncope, with a first symptomatic event between the ages of 10 and 39 years in the majority.1 In a subset, the mode of presentation relates to the development of a tachycardia-mediated cardiomyopathy (TCM), reported in 10% in a single-center series of 345 patients with no preexisting structural heart disease.4
FAT is characterized by an identifiable focal origin with subsequent centrifugal atrial activation, with a mechanism based in any of abnormal automaticity, triggered activity, or microreentry.2,5 Precise definition of the electrophysiological mechanism of a given FAT may be difficult because of overlapping features and is of less relevance in the ablation era.
FAT has been thought to arise in structurally normal atria. There is, however, evidence from surgical specimens of myocardial inflammation, infiltration, or fibrosis in almost 50% of cases,6 which may be reflected in areas of low voltage and electrogram fractionation on electroanatomic maps.
FAT in the absence of significant structural heart disease is recognized to cluster in particular anatomic locations (Figure 6-2). Characteristic locations in the right atrium include the tricuspid annulus, the right perinodal region, the ostium of the coronary sinus, and the trabeculated right atrial appendage, with the most common site of origin along the long axis of the CT.7,8 In the largest published series, 73% were found to have their origin in the right atrium, with 43% clustered along the CT. Of these 47% were located in the superior portion, 47% in the mid portion, and 6% in the inferior portion.
FIGURE 6-2 (A) Clustering of 196 FATs in 186 consecutive patients undergoing catheter ablation. A coronal section through the heart at the atrioventricular junction, with the atrioventricular valves 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.). (B) A P-wave algorithm using the anterior precordial leads, lead aVL, the inferior leads, and any change in the V1 P wave between tachycardia and sinus rhythm. When tested prospectively, this algorithm correctly located the focus in 93% of cases.
In the absence of significant structural heart disease, the surface ECG P-wave morphology provides a noninvasive guide to the location of the tachycardia focus (Figures 6-2 and 6-3). Leads V1 and aVL are most useful in identifying a left or right atrial origin.8,9 A positive or biphasic (–/+) morphology in V1 is highly suggestive of a left atrial location, and either a negative or biphasic (+/–) morphology is strongly associated with a right atrial focus. A positive or biphasic P wave in aVL is associated with a right atrial location, with a positive predictive value of 83.3% and a negative predictive value of 84.6%. Predictive accuracy is most limited for foci in the midline, including those arising from the high CT.
FIGURE 6-3 Representative example of tachycardia P waves from common right atrial locations.
• Foci around the tricuspid annulus (TA) are identified by a negative P wave in V1, which may be bifid, and a positive or isoelectric P wave in aVL. As with foci on the CT, the morphology in the inferior leads depends on the relative superior-inferior positioning of the focus around the TA.
• The superior TA and the right atrial appendage (RAA) are anatomically very close and often have very similar P-wave morphologies.
• P waves arising from the perinodal region or interatrial septum are relatively narrow, with lead V1 being isoelectric or biphasic (–/+). The greatest diagnostic imprecision in interpretation of P-wave morphology is for midline tachycardias.
• For FAT arising from the coronary sinus (CS) ostium, lead V1 has an initial component that is either isoelectric or slightly inverted followed by a positive component (iso /+ or –/+). Moving across the precordium, the initial component becomes more negative, and the second component becomes isoelectric. Lead aVL is positive and the P waves are deeply negative in the inferior leads.
Kistler et al reported 62 FATs arising specifically from the CT.8 Lead V1 manifests a positive P wave in 25%, a biphasic (+/–) P wave in 67%, and a negative P wave in 7%. All had a negative morphology in lead aVR and a positive P wave in lead I, and 89% manifest a negative or isoelectric P wave in lead aVL. Tachycardias from the high and midportions of the CT typically manifest an upright inferior P wave.
There is a paucity of robust studies assessing the relative efficacy of the various pharmacologic management strategies. Class Ia, class Ic, and class III antiarrhythmic agents have been used to attempt chronic suppression of a tachycardia focus, but the reported success rates are disappointing. Quinidine and procainamide have demonstrated success in only 20% of cases, while flecainide and encainide have been reported successful in over 50%.10 Several small studies have demonstrated higher success rates with sotalol11 and with amiodarone, but the toxicity of these agents, in particular amiodarone, limits their applicability.
Over the past 20 years catheter ablation has evolved to become the cornerstone management technique, offering the potential for definitive cure with a low risk of major complications. Activation mapping with multipolar catheters, or more usually a 3-dimensional mapping system, is employed to localise the focus. The onset of the bipolar electrogram recorded at the site of successful ablation typically precedes the P-wave onset by >20 msec. Atrioventricular block or ventricular pacing may be required to fully reveal the P wave, the onset of which can then be defined in relation to activation at a stable endocardial reference such as a coronary sinus bipole. Recording a QS unipolar electrogram12 may aid in localizing a successful ablation site. Some studies have suggested that the signal at the successful site may be fractionated or multicomponent, but this has not been a consistent finding.7 Mapping of infrequent ectopy may be aided by the use of a non-contact mapping system, which can provide over 3000 virtual electrograms from a single beat.13
Catheter ablation of FAT in contemporary practice is highly successful. Although radiofrequency ablation is the standard approach, cryoablation is an alternative in the perinodal area. Series including both right and left atrial foci have reported success rates between 69% and 100%, with very low rates of major complications that may, depending on the site of ablation, include pericardial effusion and tamponade, phrenic nerve injury, sinoatrial and atrioventricular node injury, and pulmonary vein stenosis.3,14 Long-term recurrence rates are low, varying between 0% and 33%,15 with predictors of recurrence being a left atrial focus, older age, coexistent cardiac disease, and multiple foci.16 In patients with TCM, catheter ablation has been associated with a long-term drug-free success rate of 87%, and LV function typically returns to normal within 3 months.4
1. Rodriguez LM, de Chillou C, Schläpfer J, et al. Age at onset and gender of patients with different types of supraventricular tachycardias. Am J Cardiol. 1992;70(13):1213-1215.
2. Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90(3):1262-1278.
3. Kammeraad JAE, Balaji S, Oliver RP, et al. Nonautomatic focal atrial tachycardia: characterization and ablation of a poorly understood arrhythmia in 38 patients. Pacing Clin Electrophysiol. 2003;26(3):736-742.
4. Medi C, Kalman JM, Haqqani H, et al. Tachycardia-mediated cardiomyopathy secondary to focal atrial tachycardia: long-term outcome after catheter ablation. J Am Coll Cardiol. 2009;53(19):1791-1797.
5. Saoudi N, Cosío F, Waldo A, et al. A classification of atrial flutter and regular atrial tachycardia according to electrophysiological mechanisms and anatomical bases; a Statement from a Joint Expert Group from The Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Eur Heart J. 2001;22:1162-1182.
6. McGuire MA, Johnson DC, Nunn GR, Yung T, Uther JB and Ross DL. Surgical therapy for atrial tachycardia in adults. J Am Coll Cardiol. 1989;14(7):1777-1782.
7. Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ and Lesh MD. “Cristal Tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol. 1998;31(2):451-459.
8. Kistler PM, Roberts-Thomson KC, Haqqani HM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. 2006;48(5):1010-1017.
9. Tang CW, Scheinman MM, Van Hare GF, et al. Use of P wave configuration during atrial tachycardia to predict site of origin. J Am Coll Cardiol. 1995;26(5):1315-1324.
10. Kuck KH, Kunze KP, Schlüter M, Duckeck W. Encainide versus flecainide for chronic atrial and junctional ectopic tachycardia. Am J Cardiol. 1988;62(19):37L-44L.
11. Colloridi V, Perri C, Ventriglia F, Critelli G. Oral sotalol in pediatric atrial ectopic tachycardia. Am Heart J. 1992;123(1):254-256.
12. Tang K, Ma J, Zhang S, et al. Unipolar electrogram in identification of successful targets for radiofrequency catheter ablation of focal atrial tachycardia. Chin Med J. 2003;116(10):1455-1458.
13. Wieczorek M, Salili AR, Kaubisch S, Hoeltgen R. Catheter ablation of non-sustained focal right atrial tachycardia guided by virtual non-contact electrograms. Europace. 2011;13(6):876-882.
14. Anguera I, Brugada J, Roba M, et al. Outcomes after radio frequency catheter ablation of atrial tachycardia. Am J Cardiol. 2001;87(7):886-890.
15. Roberts-Thomson KC, Kistler PM, Kalman JM. Focal atrial tachycardia II: management. Pacing Clin Electrophysiol. 2006;29(7):769-778.
16. Chen SA, Tai CT, Chiang CE, Ding YA, Chang MS. Focal atrial tachycardia: reanalysis of the clinical and electrophysiologic characteristics and prediction of successful radiofrequency ablation. J Cardiovasc Electrophysiol. 1998;9(4):355-365.