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Electrophysiologic properties of para-Hisian atrial tachycardia
Electrophysiologic properties of para-Hisian atrial tachycardia Sei Iwai, MD, FHRS,* Nitish Badhwar, MBBS, FHRS,† Steven M. Markowitz, MD, FHRS,* Bruce S. Stambler, MD, FHRS,‡ Edmund Keung, MD,† Randall J. Lee, MD, PhD,† Jeffrey H. Chung, MD,* Jeffrey E. Olgin, MD, FHRS,† Melvin M. Scheinman, MD, FHRS,† Bruce B. Lerman, MD, FHRS* From the *Department of Medicine, Division of Cardiology, Cornell University Medical Center, New York, New York, the † Division of Cardiology, University of California San Francisco Medical Center, San Francisco, California, and the ‡ Division of Cardiology, Case Western Reserve University School of Medicine, Cleveland, Ohio. BACKGROUND Focal atrial tachycardia (AT) originates from preferential sites, including the tricuspid and mitral annuli. AT arising from the atrioventricular annuli is initiated and terminated with programmed stimulation and is, in general, adenosine and verapamil sensitive. Para-Hisian AT arising from the apex of the triangle of Koch has been considered to be a distinct entity, characterized by unique electrophysiological properties. OBJECTIVE We sought to more fully delineate the electrophysiological and electrocardiographic properties of para-Hisian AT in a large series of patients. METHODS The study population consisted of 38 patients (63 ⫾ 15 years; 23 female) with AT from the para-Hisian region. The ATs were focal and originated from the anteroseptal tricuspid annulus, in close proximity to the His bundle recording. Proximity to the His bundle was confirmed by electrogram recordings, fluoroscopy, and centrifugal activation during three-dimensional mapping. RESULTS The mean AT cycle length was 421 ⫾ 69 ms. AT was associated with a distinct P-wave morphology that was significantly narrower than the P wave during sinus rhythm. Adenosine (5.0 ⫾ 1.5 mg) terminated AT in 34/35 patients. Intravenous
Introduction Recently, a classification system categorizing atrial tachycardias (ATs) as being either “focal” or “macroreentrant” has been proposed.1 The rationale of this classification is based on electrophysiological mechanism, as defined by entrainment and three-dimensional mapping, and has important implications regarding the strategy for ablation. The underlying mechanism of focal AT can be difficult to ascertain clinically but can be inferred from the mode of initiation and termination, response to entrainment, and specific pharmacological sensitivity. Focal ATs arise from preferential sites in the atria and most commonly originate from the crista terminalis, atrioventricular (AV) annuli, pulThe first two authors contributed equally to this paper. Address reprint requests and correspondence: Bruce B. Lerman, M.D., Division of Cardiology, Cornell University Medical Center, 525 East 68th Street, Starr 409, New York, New York 10021. E-mail address: blerman@ med.cornell.edu. (Received November 30, 2010; accepted March 6, 2011.)
verapamil terminated AT in three of three patients. Catheter ablation was attempted in 30 patients and was successful in 26 (87%). CONCLUSION The para-Hisian region is a source of focal AT, with properties consistent with AT arising circumferentially along the tricuspid and mitral annuli, and should be considered a subset of this broader group of “annular” ATs. The electropharmacologic findings in para-Hisian AT are mechanistically consistent with cyclic AMP-mediated triggered activity. KEYWORDS: Ablation; Adenosine; Arrhythmia; Atrial tachycardia; Mapping ABBREVIATIONS AMP ⫽ adenosine monophosphate; APC ⫽ atrial premature complex; AT ⫽ atrial tachycardia; AV ⫽ atrioventricular; AVNRT ⫽ atrioventricular nodal reentrant tachycardia; ECG ⫽ electrocardiographic; LV ⫽ left ventricular; NCC ⫽ noncoronary cusp; PPI ⫽ postpacing interval; RF ⫽ radiofrequency; TCL ⫽ tachycardia cycle length (Heart Rhythm 2011;8:1245–1253) © 2011 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
monary vein ostia, and coronary sinus ostium/musculature.2– 8 Less frequently, the atrial appendages and superior vena cava are identified as sites of AT origin.9,10 Threedimensional mapping systems may help in determining a reentrant mechanism by registration of electrical activity that spans 90%–100% of the tachycardia cycle length (TCL; head meets tail). In contrast, a focal origin of AT shows a centrifugal pattern of activation. The apex of the triangle of Koch, that is, the para-Hisian region, has been reported to be another distinct site of origin of AT, although its underlying arrhythmia mechanism has yet to be identified.11,12 The boundaries of the triangle of Koch include the tendon of Todaro, the septal leaflet of the tricuspid annulus, and the His bundle. It is unclear whether tachycardias from the apex of this region (i.e., near the His bundle) should be considered a separate entity given its signature origin or as part of the broader category of tachycardias arising from the AV annuli, which share identical electrophysiological properties. To
1547-5271/$ -see front matter © 2011 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
doi:10.1016/j.hrthm.2011.03.011
1246 clarify this distinction, we sought to fully characterize the pharmacological and electrophysiological properties of para-Hisian ATs. We have previously proposed that the effects of adenosine on AT can differentiate between focal and macroreentrant ATs.3,13 That is, in general, adenosine has no effect on macroreentrant circuits but can terminate or suppress focal ATs, depending on their underlying mechanism. In addition to its tissue-specific effects on supraventicular tissue mediated by IKACh,Ado, adenosine also has antiadrenergic effects, decreasing intracellular cyclic adenosine monophosphate (AMP).14 This results in inhibition of the L-type calcium current (ICa(L)) as well as the transient inward current (ITi).15 These effects are consistent with adenosine-mediated termination of tachycardia due to cyclic AMP-dependent triggered activity.
Methods Patient characteristics Thirty-eight consecutive patients (62 ⫾ 15 years; 23 females) who presented for invasive electrophysiological evaluation and catheter ablation of AT arising from the para-Hisian region comprise this series. This study was approved by the participating institutional review boards.
Noninvasive evaluation Patients underwent evaluation of cardiac structure, function, and ectopy burden. When possible, this included 24-hour Holter monitoring and/or inpatient telemetry. Presence of coronary artery disease was assessed as clinically indicated by stress testing and/or cardiac catheterization. Left ventricular (LV) systolic function was quantified by echocardiography, radionuclide ventriculography, and/or ventricular cineangiography. Structural heart disease was defined as the presence of coronary artery disease, an LV ejection fraction ⱕ 45%, and/or moderate/severe valvular disease.
Baseline electrophysiological study After giving informed written consent, patients underwent electrophysiological testing after an overnight fast. Patients were locally anesthetized (with 0.25% bupivacaine and/or lidocaine 1%) and sedated with intravenous midazolam and morphine/fentanyl. Quadripolar 6-Fr catheters were advanced to the His bundle position and right ventricular apex. Right atrial electrogram recordings were obtained with either a quadripolar catheter positioned in the high right atrium (RA) or a 7-Fr duodecapolar halo catheter positioned along the tricuspid annulus. A 6-Fr decapolar catheter was positioned in the coronary sinus to record left atrial activity along the mitral annulus. Bipolar intracardiac electrograms were filtered at 30 –500 Hz and recorded on optical disk. If mapping and/or ablation of the sinuses of Valsalva were required, access was obtained via transseptal atrial puncture or retrogradely via the aorta. The stimulation protocol included rapid atrial and ventricular pacing and introduction of atrial and ventricular extrastimuli at several basic drive cycle lengths. Stimuli were delivered as rectangular pulses of 2-ms duration at 4 times diastolic threshold. To facilitate induction of sus-
Heart Rhythm, Vol 8, No 8, August 2011 tained AT, when necessary, programmed stimulation was repeated after isoproterenol or dobutamine was infused to decrease the sinus cycle length by approximately 30%. Twenty patients underwent electroanatomic mapping using the Biosense CARTO system (Biosense-Webster, Diamond Bar, CA), with a reference locator pad (on the patient’s back) for spatial reference and a bipolar intracardiac electrogram (from the coronary sinus) used as temporal reference. A 7-Fr deflectable, 4-mm-tip quadripolar catheter (Biosense-Webster) was used for activation mapping and ablation in these patients. The remainder of the patients underwent activation mapping with either an alternative system (Real Time Position Mapping [RPM] System, EP Technologies, Boston Scientific, Natick, MA; or Ensite NavX, St. Jude Medical, St. Paul, MN) or solely using fluoroscopy.
P-wave analysis Surface 12-lead P-wave morphology was assessed as described in detail elsewhere.16 P waves were described as (1) positive (⫹), (2) negative (⫺), (3) biphasic (⫹/⫺ or ⫺/⫹) deflections from baseline, and (4) isoelectric (arbitrarily defined when there was no P-wave deflection from baseline of ⬎0.05 mV). The duration of the P wave was measured during tachycardia and sinus rhythm.
AT diagnosis AT was distinguished from other supraventricular tachycardias, including AV nodal reentry and AV reciprocating tachycardia, by standard electrophysiological criteria, as described in detail elsewhere.3 Criteria included (1) intracardiac atrial activation sequence during tachycardia different from that during sinus rhythm, (2) change in the A-A interval during tachycardia preceding any change in the V-V interval, (3) presence of AV conduction block or delay without affecting TCL, (4) dissociation of ventricular activity from the tachycardia, and/or (5) tachycardia initiation independent of a critical prolongation of the AH interval. In 16 patients, attempts to demonstrate manifest entrainment during tachycardia were made by pacing from the high right atrium and coronary sinus at progressively shorter cycle lengths, beginning 10 ms less than the TCL.
Definitions Focal AT was defined based on the following characteristics: (1) centrifugal atrial activation pattern, (2) dissociation of nearly the entire atria from the tachycardia with atrial extrastimuli, (3) early local atrial activation relative to the surface P wave, and/or (4) atrial activation map encompassing ⬍50% of TCL. Annular focal AT was identified when the above criteria were met, fluoroscopic and three-dimensional electroanatomic sites were consistent with an annular site, and an atrial and ventricular electrogram were present simultaneously at the site of successful ablation. A location was considered “para-Hisian” when either a His deflection was observed at the site of earliest atrial activation during tachycardia or the successful ablation site along the tricuspid annulus was within 1 cm of a site recording the His bundle potential.
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Focal AT consistent with triggered activity demonstrated reproducible initiation and termination with programmed stimulation as well as sensitivity to adenosine and verapamil. In contrast, diagnostic criteria for focal AT consistent with enhanced automaticity include the following characteristics: (1) spontaneous initiation and/or termination, (2) failure to initiate with programmed stimulation, and (3) demonstration of “warm-up” and/or “cool-down” phenomena. Criteria for focal AT due to microreentry include (1) the demonstration of entrainment and (2) fractionated electrograms at the origin of tachycardia.
Pharmacological testing Adenosine (Adenocard; Fujisawa, Deerfield, IL) was administered to 35 of the 38 patients during AT, as a rapid bolus through a central venous catheter, followed by a 10-mL flush of normal saline. The initial dose of adenosine was 3 to 6 mg, with the dose titrated incrementally by 3– 6 mg until AT terminated or was transiently suppressed or AV block occurred. Response of AT to adenosine was defined as sensitive, insensitive, or nonspecific (induction of atrial Table 1
fibrillation, another AT, or atrial premature complex [APC] before termination of tachycardia). Patients were excluded if termination was demonstrated solely due to an APC. Sensitivity was further subdivided into (1) termination or (2) transient suppression (associated with spontaneous reinitiation within 20 seconds). Verapamil (n ⫽ 3 patients) and diltiazem (n ⫽ 1 patient) were also infused to determine their effect on AT.
Catheter ablation Catheter ablation was performed using either radiofrequency (RF) or cryoablation. RF energy was applied using a 7-Fr 4-mm-tip ablation catheter with a target temperature of 60°C and maximal allowed power output of 50 W. RF energy was administered for up to 60 seconds per application and was terminated if significant chest discomfort, catheter movement, or impedance rise occurred. Cryoablation was peformed using a 4-mm-tip ablation catheter with a target temperature of ⫺80°C. Energy was applied for up to 4 minutes at each location.
Patient demographics and tachycardia characteristics
Patient no.
Age
Sex
Cardiac Hx
LVEF, %
AT CL, ms
AT initiation
Adenosine dose, mg/effect
Verapamil dose, mg/effect
Ablation attempted
Ablation success
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38
54 44 74 69 76 72 81 59 57 75 73 64 59 76 42 76 32 77 56 69 29 20 67 79 78 56 62 79 60 49 79 59 67 65 67 55 66 49
F F M F M F M M F F F M F F F F F M M F F F M F M F M F F M M F F M F M F M
NL HTN Ischemic CM; CABG NL CABG NL CABG Pulm HTN NL HTN Ischemic CM; HTN HTN NL HTN NL HTN NL CAD; CABG HTN HTN MVP NL CABG NL NL NL CAD HTN NL NL CABG NL NL HTN HTN HTN NL NL
NL NL 30 NL NL NL NL NL NL NL 40 NL NL NL NL NL NL 50 NL NL NL NL NL NL NL NL 50 NL NL NL NL NL NL NL NL NL NL NL
400 450 405 455 460 385 450 525 227 390 425 540 410 470 470 450 345 500 430 440 330 460 460 330 420 520 330 350 530 330 490 480 380 380 460 440 360 330
RAP; AES ⫹ ISO RAP; AES ⫹ DBA AES ⫹ ISO RAP; AES AES RAP; SP RAP SP; RAP/AES ⫹ ISO AES ⫹ ISO RAP RAP; AES RVP AES AES RAP AES RAP/AES ⫹ ISO Incessant RAP SP; AES; RAP AES AES RAP; SP; ISO AES ⫹ ISO ISO; RAP SP; AES AES ⫹ ISO SP; RAP; RVP SP RAP; AES ⫹ ISO RAP; AES ⫹ ISO RAP; SP RAP; SP RAP; AES RAP; SP RAP; ISO RAP; AES SP; RVP ⫹ ISO
6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 6/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 6/⫹ — 3/⫹ — 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ — 3/⫹ 6/⫹ 3/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 3/⫹ 3/⫹ 6/⫹ 3/⫹ 3/⫹
— 10/⫹ — 10/⫹ — — — — — 10/⫹ — — — — — — — — — — — — — — — — — — — — 7.5/⫹ (Diltiazem) — — — — — — —
Y N Y N N Y Y N Y Y Y Y Y Y N Y Y Y Y Y Y Y N Y N Y Y Y Y N Y Y Y Y Y Y Y Y
Y Y
Y Y Y N Y Y Y Y Y Y Y Y Y N Y Y Y Y Y Y N Y Y Y Y N Y Y
Note: AES: atrial extrastimuli; CABG: coronary artery bypass graft surgery; CAD: coronary artery disease; CL: cycle; CM: cardiomyopathy; DBA: dobutamine; HTN: hypertension; ISO: isoproterenol; LVEF: left ventricular ejection fraction; N: no; NL: normal; RAP: rapid atrial pacing; RVP: rapid ventricular pacing; SP: spontaneous; Y: yes; /⫹: termination of tachycardia; —: not given.
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Figure 1
Termination of para-Hisian AT with adenosine.
Statistics Results are presented as mean ⫾ standard deviation where appropriate. Comparison of P-wave duration in sinus rhythm and during AT was performed using the MannWhitney test. P⬍.05 was considered statistically significant.
Results Patient characteristics The baseline characteristics of the patients are listed in Table 1. The mean age was 62 ⫾ 15 years. Twenty-three of the 38 patients were female (60%). Structural heart disease was present in six (22%) patients. All six had ischemic heart disease; five had a history of coronary artery bypass surgery. Thirtyfour (89%) patients were taking antiarrhythmic agents or AV nodal blocking agents at the time of the procedure. These included -blockers (n ⫽ 25), calcium channel blockers (n ⫽ 13), and antiarrhythmic agents (flecainide ⫽ 4; sotalol ⫽ 2, propafenone ⫽ 1, amiodarone ⫽ 1).
Electrophysiological characteristics The mean TCL was 421 ⫾ 69 ms. In 37/38 cases, tachycardia was initiated with programmed stimulation. Thirty-five were initiated with atrial pacing (i.e., either rapid atrial pacing or atrial extrastimuli), two were initiated by rapid ventricular pacing (with V-A conduction), and one was incessant. Six patients required isoproterenol to initiate tachycardia, and AT was facilitated (i.e., became more easily inducible) with isoproterenol or dobutamine infusion in eight other patients. Dissociation of the ventricles was demonstrated during tachycardia in all cases. Other observations consistent with an AT included a V-A-A-V response to ventricular overdrive pacing, a varying V-A conduction time, and inability to dissociate the site of earliest atrial activation from the tachycardia. Entrainment was not demonstrated in any patient. Adenosine terminated sustained AT in 34/35 cases (Figure 1). In one patient, 3 mg did not terminate AT, and a higher dose was not given. The mean dose of adenosine in
the 24 patients in whom AT terminated was 5.0 ⫾ 1.5 mg. Adenosine was not given to three patients. Intravenous verapamil (10 mg) was administered during AT in three patients, resulting in termination of tachycardia in all three. Intravenous diltiazem (7.5 mg) was given to one patient, with prompt termination of the tachycardia. Dual AV nodal pathway physiology was noted in 17/38 patients (45%). Typical AV nodal reentrant tachycardia (AVNRT) was inducible in five patients. During AVNRT, the atria (including para-Hisian atrial tissue) and ventricles were dissociated from the tachycardia. AVNRT was ablated successfully in all five patients with RF energy applied in the region of the slow pathway. In addition, one patient was also inducible for an AT arising near the crista terminalis (which was also ablated), and two patients were noted to have a left AT, which was not ablated.
Electrocardiographic (ECG) characteristics The mean P-wave duration during AT was 77 ⫾ 18 ms, as compared with 107 ⫾ 17 ms during sinus rhythm (P⬍.0001), with an average shortening of the P wave of 30 ms during AT. The P-wave morphology during AT was distinctly different from the P wave during sinus rhythm (Figure 2). A 12-lead ECG during para-Hisian AT with discernible P waves was available in 35 patients (Table 2). The P waves were consistently positive or isoelectric in lead I and positive or biphasic with a terminal positive deflection in aVL. The inferior leads (II, III, aVF) were negative (or biphasic with a terminal negative deflection) in 20 patients and positive (or biphasic with a terminal positive deflection) in 15 patients. The polarity of the P wave in lead aVR was opposite to that observed in the inferior leads. The P-wave morphology in V1 was biphasic with the predominant component (positive or negative) being opposite to that noted in the inferior leads. Four patients (17, 34, 37, and 38) who underwent successful ablation in
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Figure 2 Representative P-waves morphologies during para-Hisian AT. The pair of 12-lead ECGs on the left side of the figure compares P-wave morphology during normal sinus rhythm (NSR) and AT in a patient with negative P waves in the inferior leads and a positive P wave in lead V1 during AT (short RP interval). The pair of 12-lead ECGs in the center panel compares P wave configuration during NSR and AT in a patient whose P waves are positive in the inferior leads and negative in lead V1 during AT. The tachycardia shown in the panel on the right side of the figure shows positive P waves in the inferior leads and a biphasic P wave (⫹/⫺) in lead V1.
noncoronary cusp had positive (or biphasic with a terminal positive deflection) P waves in the inferior leads.
Tachycardia mapping and catheter ablation Three-dimensional activation mapping was performed using the Biosense-CARTO system (20 cases), Real-time Position Management system (n ⫽ 4 cases), and/or Ensite Navx (n ⫽ 5 cases). The remainder of the procedures were performed using fluoroscopy alone. Activation mapping demonstrated a centrifugal activation pattern, consistent with a focal activation pattern. Figure 3 demonstrates a typical activation pattern as depicted by threedimensional electroanatomic mapping and intracardiac activation during AT. Catheter ablation was successful in 26/30 cases (87%). In four patients, mapping and ablation were performed in the noncoronary cusp (NCC) of the aortic valve.17,18 Figure 4 demonstrates intracardiac electrograms with the earliest activation in the NCC and the fluoroscopic site of successful ablation in the NCC. Figure 5 illustrates a simultaneous activation map of the right atrium and the left atrium during AT in another patient whose tachycardia was successfully ablated in the NCC. The map demonstrates earliest activation in the cusp with rapid spread to the left atrium and the right atrial septum that is adjacent to the cusp. The activation wavefront
spreads in a superoinferior manner in the left atrium with late activation of the coronary sinus and posteroinferior part of the left atrium. This explains positive P waves in leads II, III, and aVF during AT. Catheter ablation was not attempted in eight patients owing to patient preference in avoiding the potential risk of complete AV block or left heart catheterization. RF energy was applied in 22 patients, and cryoenergy was applied in eight patients. Two patients had transient 2:1 AV block that resolved during the procedure. Two other patients had a prolonged PR interval after ablation.
Discussion The principal findings in this study are that (1) the paraHisian region is a source of focal AT, with properties consistent with AT arising circumferentially along the tricuspid and mitral annuli, and should be considered a subset of this broader group of “annular” ATs; (2) ECG findings suggestive of a para-Hisian AT include narrowing of the P wave during AT and biphasic P waves in V1, with the dominant component having a polarity opposite to that observed in the inferior leads; and (3) the electropharmacologic findings in para-Hisian AT are mechanistically consistent with cyclic AMP-mediated triggered activity.
1250 Table 2
Heart Rhythm, Vol 8, No 8, August 2011 P-wave morphology during tachycardia: ECG leads
Patient
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
1 2 3 4 6 7 8 9 10 11 12 13 14 16 17* 18 19 20 21 22 23 25 26 27 28 29 30 31 32 33 34* 35 36 37* 38*
⫺/0 ⫹ ⫹ ⫹ 0/⫹ ⫹ ⫹ ⫹ 0 ⫹ ⫹ 0 0 ⫹ ⫹ ⫹ ⫹ ⫹ 0/⫹ 0 ⫹ ⫹ ⫹ 0 0 ⫹ ⫹ 0 ⫹ ⫹ ⫹ ⫺/⫹ 0 0 ⫹
⫹ ⫹/⫺ ⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺/⫹ ⫹ ⫺/⫹ ⫺/0 ⫺/0 ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫹ 0/⫺ 0/⫹ 0/⫹ ⫺ ⫺ ⫺/⫹ ⫹/⫺ ⫺/⫹ ⫺/0 ⫺ ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹/⫺ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫹/0 ⫺/0 ⫹ ⫹ ⫺ 0 ⫹ ⫺ ⫹/⫺ 0 ⫹ 0 ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫹ ⫹ ⫹ ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺
⫺/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ 0/⫹ ⫹ ⫹ ⫺/⫹ ⫹ ⫹ ⫹ 0 ⫹ 0 ⫹ ⫹ 0 0 0 ⫹ ⫹ ⫹ ⫹ ⫺/⫹ ⫹ ⫹ ⫹ ⫹ 0 ⫺/⫹ ⫹ ⫹ 0 ⫹ ⫹
⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/0 ⫺/0 ⫺/⫹ ⫹ ⫺/⫹ ⫺/0 ⫺ ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫺/0 0/⫹ 0/⫺ 0/⫺ 0/⫹ 0/⫹ ⫹/⫺ ⫺/⫹ ⫹/⫺ ⫹/⫺ ⫹/⫺ ⫹/⫺ ⫹ ⫺ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫹/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ 0/⫹ ⫺/⫹ ⫹/⫺ ⫺/⫹ 0/⫹ ⫺/⫹ 0/⫹ ⫺/⫹
0/⫹ 0/⫺ 0/⫺ 0/⫺ 0/⫹ 0 ⫹/⫺ ⫺/0 ⫺ ⫹/⫺ ⫹/0 ⫹/⫺ ⫹ ⫺ ⫺/⫹ ⫺ ⫺/⫹ ⫺/⫹ 0/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫺ ⫺/⫹ ⫺ ⫺ ⫹/⫺ ⫺/⫹ 0/⫹ ⫺ 0/⫹ ⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ 0 ⫺ ⫺/0 ⫺ ⫺ 0 0 ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺ ⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 0 ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 0 ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
Note: 0 ⫽ isoelectric; ⫺ ⫽ negative; ⫹ ⫽ positive; ⫹ / ⫺ ⫽ biphasic (positive then negative). *Patients with AT ablated from the coronary cusp. P-wave morphology was not discernable in patients 5, 15 and 24.
Focal AT Focal ATs have been reported to arise preferentially from distinct regions, including the crista terminalis and tricuspid and mitral annuli.2,3 Annular ATs are characterized by discrete electrograms, centrifugal spread, and sensitivity to adenosine. In general, this characteristic response of focal AT to adenosine is likely due to its abbreviation of action potential duration or its antiadrenergic properties.15 The apex of the triangle of Koch has been previously reported to be the source of a discrete form of AT.11,12 Although these initial cases were presumed to be due to reentry, the underlying mechanism had not been definitively characterized.
Specialized AV ring tissues Atrial tissue surrounding the tricuspid and mitral valve annuli is specialized and distinct from other atrial myocytes. Periannular cells are similar to atrial cells histologically but may resemble nodal cells electrophysiologically. They lack connexin-43 but stain for caveolin-3, a marker of cardiac myocytes, and HCN4, the major iso-
form of If (funny channel).19 Furthermore, the AV rings have been shown to take their origin from inferior extensions of the AV node.20 The clinical significance of these findings is not yet elucidated, but since the tricuspid and mitral annuli are reported loci of triggered activity as well as automaticity, these unique properties may play a potential role in arrhythmogenicity of this region and may explain their common electrophysiologic properties.21–23
Para-Hisian ATs Early reports of ATs from the apex of the triangle of Koch suggested reentry as the underlying mechanism.11,12 Importantly, however, while the tachycardias were not consistent with abnormal automaticity, diagnostic maneuvers did not specifically exclude triggered activity as a potential mechanism, and entrainment was never demonstrated. More recently, a small series of verapamil-sensitive ATs arising from the vicinity of the AV node has been reported.24 Based primarily on observation that the postpacing interval (PPI) at the site of earliest atrial activation was equivalent to the TCL, the inves-
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Figure 4 Surface leads and intracardiac electrograms during AT. The earliest site of activation is in the NCC of the aortic valve. The lower half of the figure is a fluoroscopic image (left anterior oblique projection) demonstrating catheter position at the site of successful ablation. Abbreviations are as in Figure 3.
Figure 3 Activation during para-Hisian tachycardia. Three-dimensional electroanatomic map of right atrial activation pattern during tachycardia. There is a centrifugal atrial activation pattern with the earliest site of activation in close proximity to His bundle. The lower half of the figure shows intracardiac tracings during tachycardia. Shown are surface leads 1, aVF, V1, and V6 and intracardiac electrograms from the high right atrium (HRA), His bundle (HB), proximal coronary sinus (CSp),, distal coronary sinus (CSd), right ventricular apex (RVA), proximal ablation electrogram (ABLp), and distal ablation electrogram (ABLd).
tigators concluded that the arrhythmia was consistent with a reentrant circuit. However, a short PPI-TCL interval does not mechanistically differentiate between focal arrhythmias due to microreentry and triggered activity.25,26 Independent of the focal mechanism, pacing at the exit site of the tachycardia will result in resetting of tachycardia and a nearly equivalent PPI and TCL, reflecting the close proximity of the pacing electrode and the arrhythmogenic focus/circuit. Other observations during tachycardia are also consistent with a focal, nonreentrant rhythm, including the absence of fractionated potentials, typically seen in microreentry, and the inability to map ⱖ50% of the TCL.27
Accessing para-Hisian ATs from the NCC In four patients, the earliest site of atrial activation was found in the NCC of the aortic valve. Prior series have
reported successful ablation of AT from this region. Embryologic studies in mice have traced the specialized conduction system around the aortic root and AV canal in early stages and found marked regression in later stages.28 It has been postulated that the persistence of conduction system tissue in this region may be responsible for this form of AT. However, considering that the NCC is anatomically contiguous to the His bundle region and that earliest right atrial activation in these patients occurs near the His bundle, it is likely that series reporting NCC ATs and those reporting para-Hisian ATs are describing patients with the same entity, that is, para-Hisian AT.
ECG predictors Previous studies have used the surface P-wave morphology during AT to predict the site of origin of tachycardia.16 P-wave morphology is largely determined by the direction of septal and left atrial activation; hence, the morphology may vary among patients with the same AT, depending on the dominant route of left atrial activation.29 Compared with sinus rhythm, all patients with para-Hisian AT had a narrower P wave during tachycardia. The P waves were consistently positive or isoelectric in leads I and aVL. The P-wave morphology in the inferior leads showed two distinct patterns. It was negative or biphasic with terminal negativity in the majority of patients, whereas positive or biphasic P waves and terminal positivity were observed in the remainder. Lead V1 was biphasic with the dominant positive or negative
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Figure 5 A: Simultaneous left atrial (LA) right atrial (RA) three-dimensional electroanatomical activation map during tachycardia. The map shows a focal activation pattern originating from the NCC (arrow pointing to the red dot). The posteroinferior part of the LA and coronary sinus (CS) show late activation. B: Propagation map of the LA and RA during tachycardia. The upper panel shows the right anterior oblique view followed by the posteroanterior view in the lower panel. The map shows rapid spread of activation to the septal regions of the LA and RA. LA activation proceeds in a superoinferior direction with late activation of the posteroinferior LA and CS, consistent with the presence of positive P waves in leads 11, 111, and aVF.
component opposite to the pattern noted in the inferior leads. It is likely that patients with negative P waves in the inferior leads have activation of the left atrium via the posteroinferior input from the coronary sinus and those with positive P waves in the inferior leads have activation of the left atrium via Bachmann’s bundle.30 All patients with para-Hisian AT who required successful ablation at the NCC showed a positive (or biphasic with terminal positivity) P-wave morphology in the inferior leads. This is explained by the superoinferior activation of the left atrium during AT as noted in Figure 5. These characteristic ECG findings were also noted in recent reports of AT requiring ablation in the NCC.17,18
However, these findings are not specific and therefore does not distinguish between AT successfully ablated from the NCC and that ablated from the para-Hisian region.
Limitations Although this is the largest series of patients with paraHisian AT, this study only included those patients in whom sustained tachycardia or long runs of nonsustained tachycardia could be consistently induced and anatomic localization could be confirmed. Patients with brief nonsustained AT or isolated atrial ectopy were not included, and thus it is possible that mechanisms other than triggered activity could
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Para-Hisian AT
also be responsible for arrhythmias arising from the paraHisian region.
1253
12.
Clinical implications The location (annulus) and identical electropharmacologic responses of para-Hisian ATs suggest that paraHisian ATs are mechanistically due to triggered activity and represent a subset of atrial annular (tricuspid) tachycardias, differentiated only by their proximity to the His bundle. The tachycardia is associated with a distinctive surface P-wave morphology. Catheter ablation of this form of AT is safe and effective; however, in some cases, access to this region is facilitated by mapping and ablating from the NCC of the aortic valve.
References 1. Saoudi N, Cosio 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. 2. Kalman JM, Olgin JE, Karch MR, Hamdan M, Lee RJ, Lesh MD. “Cristal tachycardias”: origin of right atrial tachycardias from the crista terminalis identified by intracardiac echocardiography. J Am Coll Cardiol 1998;31:451– 459. 3. Iwai S, Markowitz SM, Stein KM, et al. Response to adenosine differentiates focal from macroreentrant atrial tachycardia: validation using three-dimensional electroanatomic mapping. Circulation 2002;106:2793–2799. 4. Kistler PM, Sanders P, Hussin A, et al. Focal atrial tachycardia arising from the mitral annulus: electrocardiographic and electrophysiologic characterization. J Am Coll Cardiol 2003;41:2212–2219. 5. Morton JB, Sanders P, Das A, Vohra JK, Sparks PB, Kalman JM. Focal atrial tachycardia arising from the tricuspid annulus: electrophysiologic and electrocardiographic characteristics. J Cardiovasc Electrophysiol 2001;12:653– 659. 6. Kistler PM, Sanders P, Fynn SP, et al. Electrophysiological and electrocardiographic characteristics of focal atrial tachycardia originating from the pulmonary veins: acute and long-term outcomes of radiofrequency ablation. Circulation 2003;108:1968–1975. 7. 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. 8. Badhwar N, Kalman JM, Sparks PB, et al. Atrial tachycardia arising from the coronary sinus musculature: electrophysiological characteristics and long-term outcomes of radiofrequency ablation. J Am Coll Cardiol 2005;46:1921–1930. 9. Roberts-Thomson KC, Kistler PM, Haqqani HM, et al. Focal atrial tachycardias arising from the right atrial appendage: electrocardiographic and electrophysiologic characteristics and radiofrequency ablation. J Cardiovasc Electrophysiol 2007;18:367–372. 10. Dong J, Schreieck J, Ndrepepa G, Schmitt C. Ectopic tachycardia originating from the superior vena cava. J Cardiovasc Electrophysiol 2002;13:620 – 624. 11. Iesaka Y, Takahashi A, Goya M, et al. Adenosine-sensitive atrial reentrant
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tachycardia originating from the atrioventricular nodal transitional area. J Cardiovasc Electrophysiol 1997;8:854 – 864. Lai LP, Lin JL, Chen TF, Ko WC, Lien WP. Clinical, electrophysiological characteristics, and radiofrequency catheter ablation of atrial tachycardia near the apex of Koch’s triangle. Pacing Clin Electrophysiol 1998;21:367–374. Markowitz SM, Stein KM, Mittal S, Slotwiner DJ, Lerman BB. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol 1999;10:489 –502. Belardinelli L, Isenberg G. Isolated atrial myocytes: adenosine and acetylcholine increase potassium conductance. Am J Physiol 1983;244:H734 –737. Lerman BB, Belardinelli L. Cardiac electrophysiology of adenosine. Basic and clinical concepts. Circulation 1991;83:1499 –1509. 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;26:1315–1324. Ouyang F, Ma J, Ho SY, et al. Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation. J Am Coll Cardiol 2006;48:122–131. Das S, Neuzil P, Albert CM, et al. Catheter ablation of peri-AV nodal atrial tachycardia from the noncoronary cusp of the aortic valve. J Cardiovasc Electrophysiol 2008;19:231–237. McGuire MA, de Bakker JM, Vermeulen JT, et al. Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics. Circulation 1996;94:571–577. Yanni J, Boyett MR, Anderson RH, Dobrzynski H. The extent of the specialized atrioventricular ring tissues. Heart Rhythm 2009;6:672– 680. Wit AL, Fenoglio JJ, Jr., Hordof AJ, Reemtsma K. Ultrastructure and transmembrane potentials of cardiac muscle in the human anterior mitral valve leaflet. Circulation 1979;59:1284 –1292. Anumonwo JM, Delmar M, Jalife J. Electrophysiology of single heart cells from the rabbit tricuspid valve. J Physiol 1990;425:145–167. Bassett AL, Fenoglio JJ, Jr., Wit AL, Myerburg RJ, Gelband H. Electrophysiologic and ultrastructural characteristics of the canine tricuspid valve. Am J Physiol 1976;230:1366 –1373. Yamabe H, Tanaka Y, Morihisa K, et al. Analysis of the anatomical tachycardia circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of the atrioventricular node. Circ Arrhythm Electrophysiol; 2010:3:54 – 62. Ideker RE, Rogers JM, Fast V, Li L, Kay GN, Pogwizd SM. Can mapping differentiate microreentry from a focus in the ventricle? Heart Rhythm 2009;6:1666–1669. Mohamed U, Skanes AC, Gula LJ, et al. A novel pacing maneuver to localize focal atrial tachycardia. J Cardiovasc Electrophysiol 2007;18:1– 6. Markowitz SM, Nemirovksy D, Stein KM, et al. Adenosine-insensitive focal atrial tachycardia: evidence for de novo micro-re-entry in the human atrium. J Am Coll Cardiol 2007;49:1324 –1333. Jongbloed MR, Schalij MJ, Poelmann RE, et al. Embryonic conduction tissue: a spatial correlation with adult arrhythmogenic areas. J Cardiovasc Electrophysiol 2004;15:349 –355. Okumura K, Plumb VJ, Page PL, Waldo AL. Atrial activation sequence during atrial flutter in the canine pericarditis model and its effects on the polarity of the flutter wave in the electrocardiogram. J Am Coll Cardiol 1991;17:509 –518. Waldo AL, Maclean AH, Karp RB, Kouchoukos NT, James TN. Sequence of retrograde atrial activation of the human heart. Correlation with P wave polarity. Br Heart J 1977;39:634 – 640.
Introduction Recently, a classification system categorizing atrial tachycardias (ATs) as being either “focal” or “macroreentrant” has been proposed.1 The rationale of this classification is based on electrophysiological mechanism, as defined by entrainment and three-dimensional mapping, and has important implications regarding the strategy for ablation. The underlying mechanism of focal AT can be difficult to ascertain clinically but can be inferred from the mode of initiation and termination, response to entrainment, and specific pharmacological sensitivity. Focal ATs arise from preferential sites in the atria and most commonly originate from the crista terminalis, atrioventricular (AV) annuli, pulThe first two authors contributed equally to this paper. Address reprint requests and correspondence: Bruce B. Lerman, M.D., Division of Cardiology, Cornell University Medical Center, 525 East 68th Street, Starr 409, New York, New York 10021. E-mail address: blerman@ med.cornell.edu. (Received November 30, 2010; accepted March 6, 2011.)
verapamil terminated AT in three of three patients. Catheter ablation was attempted in 30 patients and was successful in 26 (87%). CONCLUSION The para-Hisian region is a source of focal AT, with properties consistent with AT arising circumferentially along the tricuspid and mitral annuli, and should be considered a subset of this broader group of “annular” ATs. The electropharmacologic findings in para-Hisian AT are mechanistically consistent with cyclic AMP-mediated triggered activity. KEYWORDS: Ablation; Adenosine; Arrhythmia; Atrial tachycardia; Mapping ABBREVIATIONS AMP ⫽ adenosine monophosphate; APC ⫽ atrial premature complex; AT ⫽ atrial tachycardia; AV ⫽ atrioventricular; AVNRT ⫽ atrioventricular nodal reentrant tachycardia; ECG ⫽ electrocardiographic; LV ⫽ left ventricular; NCC ⫽ noncoronary cusp; PPI ⫽ postpacing interval; RF ⫽ radiofrequency; TCL ⫽ tachycardia cycle length (Heart Rhythm 2011;8:1245–1253) © 2011 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
monary vein ostia, and coronary sinus ostium/musculature.2– 8 Less frequently, the atrial appendages and superior vena cava are identified as sites of AT origin.9,10 Threedimensional mapping systems may help in determining a reentrant mechanism by registration of electrical activity that spans 90%–100% of the tachycardia cycle length (TCL; head meets tail). In contrast, a focal origin of AT shows a centrifugal pattern of activation. The apex of the triangle of Koch, that is, the para-Hisian region, has been reported to be another distinct site of origin of AT, although its underlying arrhythmia mechanism has yet to be identified.11,12 The boundaries of the triangle of Koch include the tendon of Todaro, the septal leaflet of the tricuspid annulus, and the His bundle. It is unclear whether tachycardias from the apex of this region (i.e., near the His bundle) should be considered a separate entity given its signature origin or as part of the broader category of tachycardias arising from the AV annuli, which share identical electrophysiological properties. To
1547-5271/$ -see front matter © 2011 Published by Elsevier Inc. on behalf of Heart Rhythm Society.
doi:10.1016/j.hrthm.2011.03.011
1246 clarify this distinction, we sought to fully characterize the pharmacological and electrophysiological properties of para-Hisian ATs. We have previously proposed that the effects of adenosine on AT can differentiate between focal and macroreentrant ATs.3,13 That is, in general, adenosine has no effect on macroreentrant circuits but can terminate or suppress focal ATs, depending on their underlying mechanism. In addition to its tissue-specific effects on supraventicular tissue mediated by IKACh,Ado, adenosine also has antiadrenergic effects, decreasing intracellular cyclic adenosine monophosphate (AMP).14 This results in inhibition of the L-type calcium current (ICa(L)) as well as the transient inward current (ITi).15 These effects are consistent with adenosine-mediated termination of tachycardia due to cyclic AMP-dependent triggered activity.
Methods Patient characteristics Thirty-eight consecutive patients (62 ⫾ 15 years; 23 females) who presented for invasive electrophysiological evaluation and catheter ablation of AT arising from the para-Hisian region comprise this series. This study was approved by the participating institutional review boards.
Noninvasive evaluation Patients underwent evaluation of cardiac structure, function, and ectopy burden. When possible, this included 24-hour Holter monitoring and/or inpatient telemetry. Presence of coronary artery disease was assessed as clinically indicated by stress testing and/or cardiac catheterization. Left ventricular (LV) systolic function was quantified by echocardiography, radionuclide ventriculography, and/or ventricular cineangiography. Structural heart disease was defined as the presence of coronary artery disease, an LV ejection fraction ⱕ 45%, and/or moderate/severe valvular disease.
Baseline electrophysiological study After giving informed written consent, patients underwent electrophysiological testing after an overnight fast. Patients were locally anesthetized (with 0.25% bupivacaine and/or lidocaine 1%) and sedated with intravenous midazolam and morphine/fentanyl. Quadripolar 6-Fr catheters were advanced to the His bundle position and right ventricular apex. Right atrial electrogram recordings were obtained with either a quadripolar catheter positioned in the high right atrium (RA) or a 7-Fr duodecapolar halo catheter positioned along the tricuspid annulus. A 6-Fr decapolar catheter was positioned in the coronary sinus to record left atrial activity along the mitral annulus. Bipolar intracardiac electrograms were filtered at 30 –500 Hz and recorded on optical disk. If mapping and/or ablation of the sinuses of Valsalva were required, access was obtained via transseptal atrial puncture or retrogradely via the aorta. The stimulation protocol included rapid atrial and ventricular pacing and introduction of atrial and ventricular extrastimuli at several basic drive cycle lengths. Stimuli were delivered as rectangular pulses of 2-ms duration at 4 times diastolic threshold. To facilitate induction of sus-
Heart Rhythm, Vol 8, No 8, August 2011 tained AT, when necessary, programmed stimulation was repeated after isoproterenol or dobutamine was infused to decrease the sinus cycle length by approximately 30%. Twenty patients underwent electroanatomic mapping using the Biosense CARTO system (Biosense-Webster, Diamond Bar, CA), with a reference locator pad (on the patient’s back) for spatial reference and a bipolar intracardiac electrogram (from the coronary sinus) used as temporal reference. A 7-Fr deflectable, 4-mm-tip quadripolar catheter (Biosense-Webster) was used for activation mapping and ablation in these patients. The remainder of the patients underwent activation mapping with either an alternative system (Real Time Position Mapping [RPM] System, EP Technologies, Boston Scientific, Natick, MA; or Ensite NavX, St. Jude Medical, St. Paul, MN) or solely using fluoroscopy.
P-wave analysis Surface 12-lead P-wave morphology was assessed as described in detail elsewhere.16 P waves were described as (1) positive (⫹), (2) negative (⫺), (3) biphasic (⫹/⫺ or ⫺/⫹) deflections from baseline, and (4) isoelectric (arbitrarily defined when there was no P-wave deflection from baseline of ⬎0.05 mV). The duration of the P wave was measured during tachycardia and sinus rhythm.
AT diagnosis AT was distinguished from other supraventricular tachycardias, including AV nodal reentry and AV reciprocating tachycardia, by standard electrophysiological criteria, as described in detail elsewhere.3 Criteria included (1) intracardiac atrial activation sequence during tachycardia different from that during sinus rhythm, (2) change in the A-A interval during tachycardia preceding any change in the V-V interval, (3) presence of AV conduction block or delay without affecting TCL, (4) dissociation of ventricular activity from the tachycardia, and/or (5) tachycardia initiation independent of a critical prolongation of the AH interval. In 16 patients, attempts to demonstrate manifest entrainment during tachycardia were made by pacing from the high right atrium and coronary sinus at progressively shorter cycle lengths, beginning 10 ms less than the TCL.
Definitions Focal AT was defined based on the following characteristics: (1) centrifugal atrial activation pattern, (2) dissociation of nearly the entire atria from the tachycardia with atrial extrastimuli, (3) early local atrial activation relative to the surface P wave, and/or (4) atrial activation map encompassing ⬍50% of TCL. Annular focal AT was identified when the above criteria were met, fluoroscopic and three-dimensional electroanatomic sites were consistent with an annular site, and an atrial and ventricular electrogram were present simultaneously at the site of successful ablation. A location was considered “para-Hisian” when either a His deflection was observed at the site of earliest atrial activation during tachycardia or the successful ablation site along the tricuspid annulus was within 1 cm of a site recording the His bundle potential.
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Focal AT consistent with triggered activity demonstrated reproducible initiation and termination with programmed stimulation as well as sensitivity to adenosine and verapamil. In contrast, diagnostic criteria for focal AT consistent with enhanced automaticity include the following characteristics: (1) spontaneous initiation and/or termination, (2) failure to initiate with programmed stimulation, and (3) demonstration of “warm-up” and/or “cool-down” phenomena. Criteria for focal AT due to microreentry include (1) the demonstration of entrainment and (2) fractionated electrograms at the origin of tachycardia.
Pharmacological testing Adenosine (Adenocard; Fujisawa, Deerfield, IL) was administered to 35 of the 38 patients during AT, as a rapid bolus through a central venous catheter, followed by a 10-mL flush of normal saline. The initial dose of adenosine was 3 to 6 mg, with the dose titrated incrementally by 3– 6 mg until AT terminated or was transiently suppressed or AV block occurred. Response of AT to adenosine was defined as sensitive, insensitive, or nonspecific (induction of atrial Table 1
fibrillation, another AT, or atrial premature complex [APC] before termination of tachycardia). Patients were excluded if termination was demonstrated solely due to an APC. Sensitivity was further subdivided into (1) termination or (2) transient suppression (associated with spontaneous reinitiation within 20 seconds). Verapamil (n ⫽ 3 patients) and diltiazem (n ⫽ 1 patient) were also infused to determine their effect on AT.
Catheter ablation Catheter ablation was performed using either radiofrequency (RF) or cryoablation. RF energy was applied using a 7-Fr 4-mm-tip ablation catheter with a target temperature of 60°C and maximal allowed power output of 50 W. RF energy was administered for up to 60 seconds per application and was terminated if significant chest discomfort, catheter movement, or impedance rise occurred. Cryoablation was peformed using a 4-mm-tip ablation catheter with a target temperature of ⫺80°C. Energy was applied for up to 4 minutes at each location.
Patient demographics and tachycardia characteristics
Patient no.
Age
Sex
Cardiac Hx
LVEF, %
AT CL, ms
AT initiation
Adenosine dose, mg/effect
Verapamil dose, mg/effect
Ablation attempted
Ablation success
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38
54 44 74 69 76 72 81 59 57 75 73 64 59 76 42 76 32 77 56 69 29 20 67 79 78 56 62 79 60 49 79 59 67 65 67 55 66 49
F F M F M F M M F F F M F F F F F M M F F F M F M F M F F M M F F M F M F M
NL HTN Ischemic CM; CABG NL CABG NL CABG Pulm HTN NL HTN Ischemic CM; HTN HTN NL HTN NL HTN NL CAD; CABG HTN HTN MVP NL CABG NL NL NL CAD HTN NL NL CABG NL NL HTN HTN HTN NL NL
NL NL 30 NL NL NL NL NL NL NL 40 NL NL NL NL NL NL 50 NL NL NL NL NL NL NL NL 50 NL NL NL NL NL NL NL NL NL NL NL
400 450 405 455 460 385 450 525 227 390 425 540 410 470 470 450 345 500 430 440 330 460 460 330 420 520 330 350 530 330 490 480 380 380 460 440 360 330
RAP; AES ⫹ ISO RAP; AES ⫹ DBA AES ⫹ ISO RAP; AES AES RAP; SP RAP SP; RAP/AES ⫹ ISO AES ⫹ ISO RAP RAP; AES RVP AES AES RAP AES RAP/AES ⫹ ISO Incessant RAP SP; AES; RAP AES AES RAP; SP; ISO AES ⫹ ISO ISO; RAP SP; AES AES ⫹ ISO SP; RAP; RVP SP RAP; AES ⫹ ISO RAP; AES ⫹ ISO RAP; SP RAP; SP RAP; AES RAP; SP RAP; ISO RAP; AES SP; RVP ⫹ ISO
6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 6/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 6/⫹ — 3/⫹ — 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ 6/⫹ — 3/⫹ 6/⫹ 3/⫹ 3/⫹ 6/⫹ 3/⫹ 6/⫹ 3/⫹ 3/⫹ 3/⫹ 6/⫹ 3/⫹ 3/⫹
— 10/⫹ — 10/⫹ — — — — — 10/⫹ — — — — — — — — — — — — — — — — — — — — 7.5/⫹ (Diltiazem) — — — — — — —
Y N Y N N Y Y N Y Y Y Y Y Y N Y Y Y Y Y Y Y N Y N Y Y Y Y N Y Y Y Y Y Y Y Y
Y Y
Y Y Y N Y Y Y Y Y Y Y Y Y N Y Y Y Y Y Y N Y Y Y Y N Y Y
Note: AES: atrial extrastimuli; CABG: coronary artery bypass graft surgery; CAD: coronary artery disease; CL: cycle; CM: cardiomyopathy; DBA: dobutamine; HTN: hypertension; ISO: isoproterenol; LVEF: left ventricular ejection fraction; N: no; NL: normal; RAP: rapid atrial pacing; RVP: rapid ventricular pacing; SP: spontaneous; Y: yes; /⫹: termination of tachycardia; —: not given.
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Figure 1
Termination of para-Hisian AT with adenosine.
Statistics Results are presented as mean ⫾ standard deviation where appropriate. Comparison of P-wave duration in sinus rhythm and during AT was performed using the MannWhitney test. P⬍.05 was considered statistically significant.
Results Patient characteristics The baseline characteristics of the patients are listed in Table 1. The mean age was 62 ⫾ 15 years. Twenty-three of the 38 patients were female (60%). Structural heart disease was present in six (22%) patients. All six had ischemic heart disease; five had a history of coronary artery bypass surgery. Thirtyfour (89%) patients were taking antiarrhythmic agents or AV nodal blocking agents at the time of the procedure. These included -blockers (n ⫽ 25), calcium channel blockers (n ⫽ 13), and antiarrhythmic agents (flecainide ⫽ 4; sotalol ⫽ 2, propafenone ⫽ 1, amiodarone ⫽ 1).
Electrophysiological characteristics The mean TCL was 421 ⫾ 69 ms. In 37/38 cases, tachycardia was initiated with programmed stimulation. Thirty-five were initiated with atrial pacing (i.e., either rapid atrial pacing or atrial extrastimuli), two were initiated by rapid ventricular pacing (with V-A conduction), and one was incessant. Six patients required isoproterenol to initiate tachycardia, and AT was facilitated (i.e., became more easily inducible) with isoproterenol or dobutamine infusion in eight other patients. Dissociation of the ventricles was demonstrated during tachycardia in all cases. Other observations consistent with an AT included a V-A-A-V response to ventricular overdrive pacing, a varying V-A conduction time, and inability to dissociate the site of earliest atrial activation from the tachycardia. Entrainment was not demonstrated in any patient. Adenosine terminated sustained AT in 34/35 cases (Figure 1). In one patient, 3 mg did not terminate AT, and a higher dose was not given. The mean dose of adenosine in
the 24 patients in whom AT terminated was 5.0 ⫾ 1.5 mg. Adenosine was not given to three patients. Intravenous verapamil (10 mg) was administered during AT in three patients, resulting in termination of tachycardia in all three. Intravenous diltiazem (7.5 mg) was given to one patient, with prompt termination of the tachycardia. Dual AV nodal pathway physiology was noted in 17/38 patients (45%). Typical AV nodal reentrant tachycardia (AVNRT) was inducible in five patients. During AVNRT, the atria (including para-Hisian atrial tissue) and ventricles were dissociated from the tachycardia. AVNRT was ablated successfully in all five patients with RF energy applied in the region of the slow pathway. In addition, one patient was also inducible for an AT arising near the crista terminalis (which was also ablated), and two patients were noted to have a left AT, which was not ablated.
Electrocardiographic (ECG) characteristics The mean P-wave duration during AT was 77 ⫾ 18 ms, as compared with 107 ⫾ 17 ms during sinus rhythm (P⬍.0001), with an average shortening of the P wave of 30 ms during AT. The P-wave morphology during AT was distinctly different from the P wave during sinus rhythm (Figure 2). A 12-lead ECG during para-Hisian AT with discernible P waves was available in 35 patients (Table 2). The P waves were consistently positive or isoelectric in lead I and positive or biphasic with a terminal positive deflection in aVL. The inferior leads (II, III, aVF) were negative (or biphasic with a terminal negative deflection) in 20 patients and positive (or biphasic with a terminal positive deflection) in 15 patients. The polarity of the P wave in lead aVR was opposite to that observed in the inferior leads. The P-wave morphology in V1 was biphasic with the predominant component (positive or negative) being opposite to that noted in the inferior leads. Four patients (17, 34, 37, and 38) who underwent successful ablation in
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Figure 2 Representative P-waves morphologies during para-Hisian AT. The pair of 12-lead ECGs on the left side of the figure compares P-wave morphology during normal sinus rhythm (NSR) and AT in a patient with negative P waves in the inferior leads and a positive P wave in lead V1 during AT (short RP interval). The pair of 12-lead ECGs in the center panel compares P wave configuration during NSR and AT in a patient whose P waves are positive in the inferior leads and negative in lead V1 during AT. The tachycardia shown in the panel on the right side of the figure shows positive P waves in the inferior leads and a biphasic P wave (⫹/⫺) in lead V1.
noncoronary cusp had positive (or biphasic with a terminal positive deflection) P waves in the inferior leads.
Tachycardia mapping and catheter ablation Three-dimensional activation mapping was performed using the Biosense-CARTO system (20 cases), Real-time Position Management system (n ⫽ 4 cases), and/or Ensite Navx (n ⫽ 5 cases). The remainder of the procedures were performed using fluoroscopy alone. Activation mapping demonstrated a centrifugal activation pattern, consistent with a focal activation pattern. Figure 3 demonstrates a typical activation pattern as depicted by threedimensional electroanatomic mapping and intracardiac activation during AT. Catheter ablation was successful in 26/30 cases (87%). In four patients, mapping and ablation were performed in the noncoronary cusp (NCC) of the aortic valve.17,18 Figure 4 demonstrates intracardiac electrograms with the earliest activation in the NCC and the fluoroscopic site of successful ablation in the NCC. Figure 5 illustrates a simultaneous activation map of the right atrium and the left atrium during AT in another patient whose tachycardia was successfully ablated in the NCC. The map demonstrates earliest activation in the cusp with rapid spread to the left atrium and the right atrial septum that is adjacent to the cusp. The activation wavefront
spreads in a superoinferior manner in the left atrium with late activation of the coronary sinus and posteroinferior part of the left atrium. This explains positive P waves in leads II, III, and aVF during AT. Catheter ablation was not attempted in eight patients owing to patient preference in avoiding the potential risk of complete AV block or left heart catheterization. RF energy was applied in 22 patients, and cryoenergy was applied in eight patients. Two patients had transient 2:1 AV block that resolved during the procedure. Two other patients had a prolonged PR interval after ablation.
Discussion The principal findings in this study are that (1) the paraHisian region is a source of focal AT, with properties consistent with AT arising circumferentially along the tricuspid and mitral annuli, and should be considered a subset of this broader group of “annular” ATs; (2) ECG findings suggestive of a para-Hisian AT include narrowing of the P wave during AT and biphasic P waves in V1, with the dominant component having a polarity opposite to that observed in the inferior leads; and (3) the electropharmacologic findings in para-Hisian AT are mechanistically consistent with cyclic AMP-mediated triggered activity.
1250 Table 2
Heart Rhythm, Vol 8, No 8, August 2011 P-wave morphology during tachycardia: ECG leads
Patient
I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
1 2 3 4 6 7 8 9 10 11 12 13 14 16 17* 18 19 20 21 22 23 25 26 27 28 29 30 31 32 33 34* 35 36 37* 38*
⫺/0 ⫹ ⫹ ⫹ 0/⫹ ⫹ ⫹ ⫹ 0 ⫹ ⫹ 0 0 ⫹ ⫹ ⫹ ⫹ ⫹ 0/⫹ 0 ⫹ ⫹ ⫹ 0 0 ⫹ ⫹ 0 ⫹ ⫹ ⫹ ⫺/⫹ 0 0 ⫹
⫹ ⫹/⫺ ⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺/⫹ ⫹ ⫺/⫹ ⫺/0 ⫺/0 ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫹ 0/⫺ 0/⫹ 0/⫹ ⫺ ⫺ ⫺/⫹ ⫹/⫺ ⫺/⫹ ⫺/0 ⫺ ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹/⫺ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫹/0 ⫺/0 ⫹ ⫹ ⫺ 0 ⫹ ⫺ ⫹/⫺ 0 ⫹ 0 ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫹ ⫹ ⫹ ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺
⫺/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ 0/⫹ ⫹ ⫹ ⫺/⫹ ⫹ ⫹ ⫹ 0 ⫹ 0 ⫹ ⫹ 0 0 0 ⫹ ⫹ ⫹ ⫹ ⫺/⫹ ⫹ ⫹ ⫹ ⫹ 0 ⫺/⫹ ⫹ ⫹ 0 ⫹ ⫹
⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/0 ⫺/0 ⫺/⫹ ⫹ ⫺/⫹ ⫺/0 ⫺ ⫹ ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ ⫹ ⫹ ⫺ ⫺ ⫺/⫹ ⫹
⫺/0 0/⫹ 0/⫺ 0/⫺ 0/⫹ 0/⫹ ⫹/⫺ ⫺/⫹ ⫹/⫺ ⫹/⫺ ⫹/⫺ ⫹/⫺ ⫹ ⫺ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫹/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ 0/⫹ ⫺/⫹ ⫹/⫺ ⫺/⫹ 0/⫹ ⫺/⫹ 0/⫹ ⫺/⫹
0/⫹ 0/⫺ 0/⫺ 0/⫺ 0/⫹ 0 ⫹/⫺ ⫺/0 ⫺ ⫹/⫺ ⫹/0 ⫹/⫺ ⫹ ⫺ ⫺/⫹ ⫺ ⫺/⫹ ⫺/⫹ 0/⫹ 0/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺/⫹ ⫺ ⫺ ⫺/⫹ ⫺ ⫺ ⫹/⫺ ⫺/⫹ 0/⫹ ⫺ 0/⫹ ⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ 0 ⫺ ⫺/0 ⫺ ⫺ 0 0 ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺ ⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 ⫺ ⫹ ⫹ ⫺ ⫹ ⫺/⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 0 ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
0/⫹ 0/⫺ 0/⫹ 0/⫹ ⫺/⫹ ⫺/0 ⫺ ⫹/0 ⫺ ⫺/0 ⫺/0 0 0 ⫹ ⫹ ⫺ ⫹ ⫹ ⫺ ⫺ ⫹ ⫺ ⫺ ⫺ ⫺ ⫺ ⫹ ⫺ ⫺ 0 ⫹ ⫺ ⫺ ⫺/⫹ 0/⫹
Note: 0 ⫽ isoelectric; ⫺ ⫽ negative; ⫹ ⫽ positive; ⫹ / ⫺ ⫽ biphasic (positive then negative). *Patients with AT ablated from the coronary cusp. P-wave morphology was not discernable in patients 5, 15 and 24.
Focal AT Focal ATs have been reported to arise preferentially from distinct regions, including the crista terminalis and tricuspid and mitral annuli.2,3 Annular ATs are characterized by discrete electrograms, centrifugal spread, and sensitivity to adenosine. In general, this characteristic response of focal AT to adenosine is likely due to its abbreviation of action potential duration or its antiadrenergic properties.15 The apex of the triangle of Koch has been previously reported to be the source of a discrete form of AT.11,12 Although these initial cases were presumed to be due to reentry, the underlying mechanism had not been definitively characterized.
Specialized AV ring tissues Atrial tissue surrounding the tricuspid and mitral valve annuli is specialized and distinct from other atrial myocytes. Periannular cells are similar to atrial cells histologically but may resemble nodal cells electrophysiologically. They lack connexin-43 but stain for caveolin-3, a marker of cardiac myocytes, and HCN4, the major iso-
form of If (funny channel).19 Furthermore, the AV rings have been shown to take their origin from inferior extensions of the AV node.20 The clinical significance of these findings is not yet elucidated, but since the tricuspid and mitral annuli are reported loci of triggered activity as well as automaticity, these unique properties may play a potential role in arrhythmogenicity of this region and may explain their common electrophysiologic properties.21–23
Para-Hisian ATs Early reports of ATs from the apex of the triangle of Koch suggested reentry as the underlying mechanism.11,12 Importantly, however, while the tachycardias were not consistent with abnormal automaticity, diagnostic maneuvers did not specifically exclude triggered activity as a potential mechanism, and entrainment was never demonstrated. More recently, a small series of verapamil-sensitive ATs arising from the vicinity of the AV node has been reported.24 Based primarily on observation that the postpacing interval (PPI) at the site of earliest atrial activation was equivalent to the TCL, the inves-
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Para-Hisian AT
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Figure 4 Surface leads and intracardiac electrograms during AT. The earliest site of activation is in the NCC of the aortic valve. The lower half of the figure is a fluoroscopic image (left anterior oblique projection) demonstrating catheter position at the site of successful ablation. Abbreviations are as in Figure 3.
Figure 3 Activation during para-Hisian tachycardia. Three-dimensional electroanatomic map of right atrial activation pattern during tachycardia. There is a centrifugal atrial activation pattern with the earliest site of activation in close proximity to His bundle. The lower half of the figure shows intracardiac tracings during tachycardia. Shown are surface leads 1, aVF, V1, and V6 and intracardiac electrograms from the high right atrium (HRA), His bundle (HB), proximal coronary sinus (CSp),, distal coronary sinus (CSd), right ventricular apex (RVA), proximal ablation electrogram (ABLp), and distal ablation electrogram (ABLd).
tigators concluded that the arrhythmia was consistent with a reentrant circuit. However, a short PPI-TCL interval does not mechanistically differentiate between focal arrhythmias due to microreentry and triggered activity.25,26 Independent of the focal mechanism, pacing at the exit site of the tachycardia will result in resetting of tachycardia and a nearly equivalent PPI and TCL, reflecting the close proximity of the pacing electrode and the arrhythmogenic focus/circuit. Other observations during tachycardia are also consistent with a focal, nonreentrant rhythm, including the absence of fractionated potentials, typically seen in microreentry, and the inability to map ⱖ50% of the TCL.27
Accessing para-Hisian ATs from the NCC In four patients, the earliest site of atrial activation was found in the NCC of the aortic valve. Prior series have
reported successful ablation of AT from this region. Embryologic studies in mice have traced the specialized conduction system around the aortic root and AV canal in early stages and found marked regression in later stages.28 It has been postulated that the persistence of conduction system tissue in this region may be responsible for this form of AT. However, considering that the NCC is anatomically contiguous to the His bundle region and that earliest right atrial activation in these patients occurs near the His bundle, it is likely that series reporting NCC ATs and those reporting para-Hisian ATs are describing patients with the same entity, that is, para-Hisian AT.
ECG predictors Previous studies have used the surface P-wave morphology during AT to predict the site of origin of tachycardia.16 P-wave morphology is largely determined by the direction of septal and left atrial activation; hence, the morphology may vary among patients with the same AT, depending on the dominant route of left atrial activation.29 Compared with sinus rhythm, all patients with para-Hisian AT had a narrower P wave during tachycardia. The P waves were consistently positive or isoelectric in leads I and aVL. The P-wave morphology in the inferior leads showed two distinct patterns. It was negative or biphasic with terminal negativity in the majority of patients, whereas positive or biphasic P waves and terminal positivity were observed in the remainder. Lead V1 was biphasic with the dominant positive or negative
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Figure 5 A: Simultaneous left atrial (LA) right atrial (RA) three-dimensional electroanatomical activation map during tachycardia. The map shows a focal activation pattern originating from the NCC (arrow pointing to the red dot). The posteroinferior part of the LA and coronary sinus (CS) show late activation. B: Propagation map of the LA and RA during tachycardia. The upper panel shows the right anterior oblique view followed by the posteroanterior view in the lower panel. The map shows rapid spread of activation to the septal regions of the LA and RA. LA activation proceeds in a superoinferior direction with late activation of the posteroinferior LA and CS, consistent with the presence of positive P waves in leads 11, 111, and aVF.
component opposite to the pattern noted in the inferior leads. It is likely that patients with negative P waves in the inferior leads have activation of the left atrium via the posteroinferior input from the coronary sinus and those with positive P waves in the inferior leads have activation of the left atrium via Bachmann’s bundle.30 All patients with para-Hisian AT who required successful ablation at the NCC showed a positive (or biphasic with terminal positivity) P-wave morphology in the inferior leads. This is explained by the superoinferior activation of the left atrium during AT as noted in Figure 5. These characteristic ECG findings were also noted in recent reports of AT requiring ablation in the NCC.17,18
However, these findings are not specific and therefore does not distinguish between AT successfully ablated from the NCC and that ablated from the para-Hisian region.
Limitations Although this is the largest series of patients with paraHisian AT, this study only included those patients in whom sustained tachycardia or long runs of nonsustained tachycardia could be consistently induced and anatomic localization could be confirmed. Patients with brief nonsustained AT or isolated atrial ectopy were not included, and thus it is possible that mechanisms other than triggered activity could
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Para-Hisian AT
also be responsible for arrhythmias arising from the paraHisian region.
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12.
Clinical implications The location (annulus) and identical electropharmacologic responses of para-Hisian ATs suggest that paraHisian ATs are mechanistically due to triggered activity and represent a subset of atrial annular (tricuspid) tachycardias, differentiated only by their proximity to the His bundle. The tachycardia is associated with a distinctive surface P-wave morphology. Catheter ablation of this form of AT is safe and effective; however, in some cases, access to this region is facilitated by mapping and ablating from the NCC of the aortic valve.
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