Biatrial Tachycardia
2016; Lippincott Williams & Wilkins; Volume: 9; Issue: 5 Linguagem: Inglês
10.1161/circep.115.003175
ISSN1941-3149
AutoresJames E. Ip, Jim W. Cheung, Christopher F. Liu, George Thomas, Steven M. Markowitz, Bruce B. Lerman,
Tópico(s)Cardiac electrophysiology and arrhythmias
ResumoHomeCirculation: Arrhythmia and ElectrophysiologyVol. 9, No. 5Biatrial Tachycardia Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBBiatrial TachycardiaDistinguishing Between Active and Passive Activation James E. Ip, MD, Jim W. Cheung, MD, Christopher F. Liu, MD, George Thomas, MD, Steven M. Markowitz, MD and Bruce B. Lerman, MD James E. IpJames E. Ip From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. , Jim W. CheungJim W. Cheung From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. , Christopher F. LiuChristopher F. Liu From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. , George ThomasGeorge Thomas From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. , Steven M. MarkowitzSteven M. Markowitz From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. and Bruce B. LermanBruce B. Lerman From the Department of Medicine, Division of Cardiology, Cornell University Medical Center & New York Presbyterian Hospital, NY. Originally published6 May 2016https://doi.org/10.1161/CIRCEP.115.003175Circulation: Arrhythmia and Electrophysiology. 2016;9IntroductionThe approach to successful ablation of arrhythmias is based on elucidating the underlying mechanism and relative dimensions of the tachycardia circuit. Activation mapping readily distinguishes macroreentry from focal arrhythmias, the latter of which have centrifugal spread. When macroreentrant atrial tachycardia is suspected, entrainment maneuvers with atrial overdrive pacing at various anatomic sites help differentiate right-sided from left-sided circuits. Based on the difference between the postpacing interval (PPI) and tachycardia cycle length (TCL), the proximity of the pacing site to the reentrant circuit can be assessed.1 However, even in a reentrant tachycardia, a short PPI–TCL interval (< 30 ms) may not always reliably identify whether the pacing site is within the tachycardia circuit, particularly when widely disparate locations seem to be "in the circuit". In these cases, it is important to return to the fundamental principles of entrainment and to recognize the subtle changes in antidromic and orthodromic wavefronts in response to overdrive pacing that help to correctly identify the tachycardia circuit.See Editor's Perspective by Asirvatham and StevensonCase PresentationA 57-year-old man with a history of hypertension, hyperlipidemia, coronary artery disease, rheumatic heart disease, and 5 previous surgeries for mechanical aortic and mitral valve replacements and coronary artery bypass grafting presented with 6 months of worsening dyspnea on exertion that correlated with the onset of persistent atrial tachycardia (Figure 1). In the electrophysiology laboratory, the patient's clinical atrial TCL was 360 ms. Diagnostic catheters were placed to encircle the tricuspid annulus within the coronary sinus (CS) and at the superior margin of the tricuspid annulus to record the His bundle (Figure 2A). Entrainment mapping demonstrated a short PPI–TCL from the cavotricuspid isthmus (CTI; Figure 2B), the proximal CS (Figure 2C), and the superior tricuspid annulus (Figure 2D). Entrainment from the distal CS also showed a PPI–TCL of 0 ms (Figure 2E). Based on the activation sequence during tachycardia and standard entrainment responses that showed a PPI–TCL <30 ms at widely disparate locations in the right atria (RA) and left atria (LA), the circuit of the tachycardia remained indeterminate.Download figureDownload PowerPointFigure 1. Twelve-lead ECG of atrial tachycardia.Download figureDownload PowerPointFigure 2. Entrainment mapping during tachycardia. A, Catheter positions of intracardiac catheters in left anterior oblique projection. B, Surface leads 1, aVF, and V1 are shown, as well as intracardiac recordings from the right atrium (RA), His bundle (His), and coronary sinus (CS) during overdrive atrial pacing from multiple right and left atrial locations. A entrainment mapping from the cavotricuspid isthmus (CTI). The PPI–TCL was 0 ms. C, Entrainment mapping from the proximal CS. The PPI–TCL was 0 ms. D, Entrainment mapping from the superior tricuspid annulus. The PPI–TCL was 18 ms. E, Entrainment mapping from the distal CS. The PPI–TCL was 0 ms. CSd indicates distal coronary sinus catheter; CSp, proximal coronary sinus; d, distal; p, proximal; PL, posterolateral; PS, posteroseptal; PPI, postpacing interval; RA (PL), posterolateral right atrial catheter; RA (PS), posteroseptal right atrial catheter; and TCL, tachycardia cycle length.DiscussionTypical atrial flutter is a right atrial macroreentant tachycardia that funnels the activation wavefront through the CTI.2 It is diagnosed by activation mapping, demonstrating counterclockwise propagation of reentry around the tricuspid annulus and by entrainment mapping. During entrainment mapping, the return cycle length after cessation of overdrive atrial pacing is typically short (PPI–TCL 50 ms) from locations distant from the circuit, such as the distal CS. In our case, not only were short PPI–TCL intervals measured from the proximal CS and 2 locations in the RA, but the distal CS also showed a PPI–TCL of 0 ms during multiple atrial overdrive pacing sequences, an unexpected finding with typical atrial flutter. A short PPI–TCL from the distal CS is typically seen with left-sided circuits, particularly mitral annular flutter or roof-dependent flutter.1 However, such tachycardias are not expected to also have short PPI–TCL from the lateral RA.One hallmark of entrainment is the observation of fusion (collision of the antidromic pacing wavefront with the orthodromically conducted tachycardia beat) with concurrent reset (the orthodromically conducted pacing beat advances the TCL to the pacing cycle length).3 Because the typical atrial flutter circuit is confined to the RA and the left atrium is passively activated, CS activation proceeds in a proximal to distal direction. Overdrive pacing from the distal CS during atrial flutter typically results in an antidromic wavefront that activates the CS eccentrically (distal to proximal sequence) and a long PPI–TCL interval after cessation of pacing because the pacing site is remote from the tachycardia circuit (Figure 3).Download figureDownload PowerPointFigure 3. A, Usual response to entrainment from the distal coronary sinus (CS) during typical atrial flutter (not from patient presented in this study). Overdrive pacing results in fixed fusion along the CS and a long postpacing interval (PPI)–tachycardia cycle length (TCL) of 95 ms. B, Schematic showing entrainment of typical counterclockwise flutter circuit. Entrainment from distal CS leads to long postpacing interval with antidromic activation (blue arrow) of the coronary sinus (distal to proximal) during pacing and orthodromic activation of the coronary sinus (proximal to distal) after cessation of pacing (green arrow). Orange bar represents collision of antidromic (blue arrow) and orthodromic (red arrow) wavefronts during entrainment. CSd indicates distal coronary sinus catheter; CSp, proximal coronary sinus; d, distal; MA, mitral annulus; p, proximal; and TA, tricuspid annulus.In the case presented, results from entrainment mapping from the proximal CS, superior tricuspid annulus, and CTI were consistent with typical RA flutter, but the interpretation of the circuit topology was confounded by a short PPI–TCL interval from the distal CS. Therefore, based on our findings, the differential diagnosis includes biatrial tachycardia with dual loop reentry (figure-of-8) around the tricuspid and mitral annuli, biatrial tachycardia with single loop reentry around the tricuspid and mitral annuli, or RA flutter with the left atrium participating as a passive bystander during entrainment. Additional observations during tachycardia as well as overdrive pacing from the distal and proximal CS serve to elucidate the mechanism.Because CS activation during tachycardia is concentric (proximal to distal), biatrial dual loop reentry with figure-of-8 activation around the annuli is excluded (counterclockwise around the tricuspid annulus and clockwise along the mitral annulus). Close analysis of the electrograms during overdrive pacing from the distal CS during tachycardia (Figure 4A) reveals 2 critical observations. The first is that CS activation during overdrive pacing from the distal CS is a fusion of orthodromic and antidromic wave fronts. Typically, CS activation during entrainment of atrial flutter from the distal CS is purely eccentric (distal to proximal) because the antidromic pacing wavefront (n-beat) captures the CS before the orthodromic wavefront from the immediately preceding beat (n−1 beat) does (Figure 3A and 3B). After cessation of pacing, there is a long PPI, and the resumption of tachycardia is associated with concentric activation of the CS from the orthodromic wavefront.Download figureDownload PowerPointFigure 4. A, Entrainment from distal coronary sinus (CS). Asterisk shows last entrained beat (CS(p)). Note the simultaneous activation during pacing along the coronary sinus because of collision of wavefronts from the antidromic (blue arrow) and orthodromic (red arrow) directions. Tachycardia resumes after cessation of pacing (green arrow). See text for discussion. B, Schematic showing how entrainment from distal CS can lead to short postpacing interval (PPI–TCL <30 ms) in the case of biatrial tachycardia with the left atrium participating in a large circuit (single loop reentry). Because of scar (grey rectangle) along the septum, activation during CS pacing proceeds over Bachmann's bundle. Entrainment from the distal CS leads to an antidromic wavefront (blue arrow) with fused activation within the coronary sinus that continues in an orthodromic direction after cessation of pacing (green arrow). Orange bar represents collision of antidromic (blue arrow) and orthodromic (red arrow) wavefronts during entrainment. C, Schematic showing how entrainment from distal CS can lead to a short postpacing interval (PPI–TCL <30 ms) in the case of right atrial flutter with left atrial bystander participation. Delayed activation along the septum because of scar (greyrectangle) leads to fused activation (collision of antidromic wavefront [blue arrow] and orthodromic wavefront [superimposed blue and red arrows] from the previous beat) in the coronary sinus, which continues in an orthodromic direction after cessation of pacing (green arrow). In addition, the antidromic wavefront from distal CS pacing (blue arrow) collides with the orthodromic wavefront from the active circuit (red arrow) within the anterior atrial septum. The delayed descending activation time along the septum (a, blue dashed line) must be equivalent to the activation time around the tricuspid annulus (b, red solid line) in this scenario. Also, activation of the active circuit is longitudinally dissociated from the antidromic wavefront because of a protected channel through the scar (black bars). See text for detailed discussion. BB indicates Bachmann's bundle; CSd, distal coronary sinus catheter; CSp, proximal coronary sinus; d, distal; p, proximal; PPI, postpacing interval; and TCL, tachycardia cycle length.The second observation is that the last entrained beat at the most proximal CS electrogram does not originate from the immediate beat after the pacing stimulus but from the following beat (Figure 4A, asterisk) because that electrogram is accelerated to the pacing cycle length (320 ms). In order for this phenomenon to occur, there has to be delayed interatrial conduction and prolonged refractoriness within the CS. Prolonged conduction to the anteroseptum (detected by the His catheter and proximal poles of the RA catheter) allows the pacing impulse, via retrograde conduction over Bachmann's bundle, to orthodromically activate the CTI and the proximal CS electrogram during the last captured beat (labeled with asterisk). After the cessation of pacing, only the proximal CS electrogram of the next beat is accelerated to the pacing rate and the remaining electrograms are not captured at the pacing rate because the tachycardia resumes (green arrow). Careful inspection of the CS electrograms reveals that during overdrive pacing from the distal CS, the antidromic wavefront (blue arrow) fuses with the orthodromic wavefront (red arrow) in the region of the proximal CS. Orthodromic activation resumes after cessation of pacing (green arrow) and results in a PPI equal to the TCL. Such a scenario can occur in biatrial tachycardia when both atria participate in a single loop reentry circuit (Figure 4B) or in RA flutter with the left atrium participating as a bystander with delayed septal activation (Figure 4C). In the latter case, for the PPI to equal the TCL, the activation time from pacing the distal CS to Bachmann's bundle to the proximal CS and back to the distal CS has to be equivalent to the activation time of the reentrant circuit around the tricuspid annulus. Moreover, this scenario requires the presence of longitudinal dissociation along the septum in the form of a protected channel, which would obviate collision of the antidromic and orthodromic wavefronts, which would otherwise terminate tachycardia. Although such a scenario is unlikely, definitive differentiation between active and passive activation of the left atrium can be made by the presence or absence of biatrial linking during entrainment from the proximal CS during tachycardia.In the case of biatrial flutter with active participation of the left atrium, the distal CS should be linked to the RA, that is, the activation interval between the left and RA are fixed during tachycardia and during entrainment. This is a similar concept to the maneuver used to determine whether a supraventricular tachycardia is dependent on a fixed ventricular-to-atrial relationship (ventriculoatrial linking).4 The ventriculoatrial interval of the return cycle after atrial overdrive pacing during supraventricular tachycardia is expected to be within 10 ms of the ventriculoatrial interval during tachycardia in the case of orthodromic reciprocating tachycardia because the timing of atrial activation is dependent on ventricular activation. Similarly, it is informative to compare the interval between distal CS atrial activation (CSd-A) and septal atrial activation (as recorded on the His bundle electrogram [His-A]) during tachycardia and entrainment when pacing from the proximal CS. In the case of active LA participation (single loop reentry), the CSd-A and the His-A are activated in series during tachycardia and should show the same sequential relationship during proximal CS entrainment. Furthermore, because they are linked, the CSd-A to His-A interval during proximal CS overdrive pacing should be similar to that during tachycardia. In contrast, in RA flutter with passive LA participation, the distal CS and right anteroseptum are activated in parallel. Therefore, although the CS and right anteroseptum are also activated in parallel during CS overdrive pacing, the CSd-A to His-A interval will differ slightly between pacing and tachycardia because the sites are activated independently and are not linked. As shown in Figure 2C, the CSd-A to His-A activation sequence and timing are identical during entrainment and tachycardia (red bars, 135 ms), suggesting that the tachycardia mechanism is a counterclockwise reentry around both tricuspid and mitral annuli with the left atrium participating in a large circuit (single loop reentry). A summary of these observations/maneuvers is shown in Table.Table. Summary of Observations and Maneuvers to Diagnose Biatrial TachycardiaObservations/ManeuversTypical Atrial FlutterBiatrial Tachycardia With Active LA Participation in Figure-of-8 Dual Loop ReentryBiatrial Tachycardia With LA as BystanderBiatrial Tachycardia With Active LA Participation in Single Loop ReentryEntrainment from CTI and CSp showing PPI–TCL <30 msYesYesYesYesEntrainment from dCS showing PPI–TCL 1≈1>1CSd indicates distal coronary sinus; CSp, proximal coronary sinus; CTI, cavotricuspid isthmus; His, His bundle; LA, left atria; PPI, postpacing interval; SVT, supraventricular tachycardia; and TCL, tachycardia cycle length.A continuous line of radiofrequency ablation lesions extended across the CTI terminated tachycardia (Figure 5A), confirming the diagnosis of biatrial tachycardia with a single reentrant loop around both annuli. Although dual loop reentry with simultaneous activation around the tricuspid and mitral annuli in a figure-of-8 fashion is excluded based on concentric activation of the CS, such a tachycardia would be expected to continue around the mitral annulus, despite ablation along the CTI because the common critical isthmus would likely be along the septum. After termination of tachycardia, biatrial conduction intervals during proximal CS pacing provided further evidence that the biatrial tachycardia was single loop reentry with active LA participation rather than RA flutter with bystander LA participation (Figures 2C and 5B). In the former scenario, the CSd-A and His-A are activated in series during tachycardia and in parallel during proximal CS pacing in sinus rhythm. Therefore, the CSd-A to His-A interval should be greater during tachycardia than during proximal CS pacing. In contrast, in RA flutter with passive LA participation, the CSd-A and His-A are activated in parallel during both tachycardia and proximal CS pacing. Therefore, the CSd-A to His-A interval in tachycardia would be similar to CSd-A to His-A interval during proximal CS pacing. As shown in Figure 5B, the CSd-A to His-A interval is much shorter during pacing proximal CS in sinus rhythm (14 ms) compared with that during tachycardia (135 ms; Figure 2C), thus confirming the diagnosis of single loop reentry. Although pacing was performed at a longer cycle length (500 ms) than the tachycardia (360 ms), it is unlikely that this accounted for the large differential in activation time between the CSd-A and His-A (Figure 5B). However, it is important to recognize this potential limitation and to avoid any misinterpretation of this maneuver by pacing at the same cycle length as the tachycardia.Download figureDownload PowerPointFigure 5. A, Termination of tachycardia during ablation along the cavotricuspid isthmus. B, Pacing proximal coronary sinus (CS) during sinus rhythm shows a much shorter activation interval between the distal CS and right anteroseptum (His-A) because of parallel activation (14 ms) compared with serial activation during tachycardia (135 ms; Figure 2C). C, Pacing the high right atrium revealed eccentric activation along the CS with significant interatrial delay. D, Schematic showing mechanism of eccentric activation of the coronary sinus (distal → proximal) is because of presence of septal scar (grey rectangle) and preferential activation of the left atrium over Bachman's bundle. Blue bars represent areas of conduction block. CSd indicates distal coronary sinus catheter; CSp, proximal coronary sinus; d, distal; and p, proximal.After termination of tachycardia, no arrhythmias were inducible with programmed stimulation. Pacing the high RA showed eccentric activation along the CS with significant interatrial delay (Figure 5C). During subsequent mapping, significant scar was observed along the right posterior atrial septum as evidenced by the absence of electrograms along the posteroseptal poles of the RA catheter (Figure 2B through 2E). Pacing from the high RA is delayed or blocked in the low septum, leading to preferential conduction over Bachmann's bundle, resulting in distal to proximal activation of the CS (Figure 5D). This scar was likely the result of this patient's 5 previous cardiac surgeries involving right and left atriotomies and provided the myopathic substrate for the electrophysiological phenomenona and macroreentant biatrial tachycardia observed in our case.To our knowledge, this is the first reported case of biatrial reentrant tachycardia involving both tricuspid and mitral annuli and a single circuit. Although there has been a recent report of tachycardias involving the left atria and RA after linear ablation from the anterior mitral annulus to the right superior pulmonary veins or to a roof line,5 these tachycardias were not CTI-dependent.Although the PPI–TCL is considered a critical interval for determining whether a pacing site is within a reentrant circuit, there are occasionally exceptions to the rule. For example, a long PPI–TCL can be observed with entrainment of typical atrial flutter from the CTI. This may occur if the pacing cycle length is significantly shorter than the TCL and produces rate-dependent slowing of conduction or alterations of conduction pathways. Furthermore, despite a pacing cycle length within 20 ms of the TCL, 18% of patients can have a misleadingly pronged PPI–TCL because of local pacing latency.6 A PPI that is shorter than the TCL (negative PPI–TCL) after cessation of overdrive pacing can also be observed and be misleading.5 This can occur because of erroneous measurement (ie, determining PPI when multiple local electrograms are present on the bipolar signal) or pacing that results in capture of far-field tissue across a conduction barrier adjacent to the pacing site, for example, Eustachian ridge.7Returning to the first principles of entrainment and being attentive to the subtle changes in antidromic and orthodromic wavefronts in response to overdrive pacing, as well as to comparisons of conduction intervals during pacing (Table), are essential in elucidating the critical components of a macroreentant circuit.DisclosuresNone.FootnotesCorrespondence to James E. Ip, MD, Division of Cardiology, Cornell University Medical Center, New York Presbyterian Hospital, 525 East 68th St, Starr 4, New York, NY 10021. E-mail [email protected]References1. Miyazaki H, Stevenson WG, Stephenson K, Soejima K, Epstein LM. Entrainment mapping for rapid distinction of left and right atrial tachycardias.Heart Rhythm. 2006; 3:516–523. doi: 10.1016/j.hrthm.2006.01.014.CrossrefMedlineGoogle Scholar2. Asirvatham SJ. Correlative anatomy and electrophysiology for the interventional electrophysiologist: right atrial flutter.J Cardiovasc Electrophysiol. 2009; 20:113–122. doi: 10.1111/j.1540-8167.2008.01344.x.CrossrefMedlineGoogle Scholar3. Waldo AL, MacLean WA, Karp RB, Kouchoukos NT, James TN. Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery.Circulation. 1977; 56:737–745.LinkGoogle Scholar4. Knight BP, Ebinger M, Oral H, Kim MH, Sticherling C, Pelosi F, Michaud GF, Strickberger SA, Morady F. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia.J Am Coll Cardiol. 2000; 36:574–582.CrossrefMedlineGoogle Scholar5. Mikhaylov EN, Mitrofanova LB, Vander MA, Tatarskiy RB, Kamenev AV, Abramov ML, Szili-Torok T, Lebedev DS. Biatrial tachycardia following linear anterior wall ablation for the perimitral reentry: incidence and electrophysiological evaluations.J Cardiovasc Electrophysiol. 2015; 26:28–35. doi: 10.1111/jce.12543.CrossrefMedlineGoogle Scholar6. Vollmann D, Stevenson WG, Lüthje L, Sohns C, John RM, Zabel M, Michaud GF. Misleading long post-pacing interval after entrainment of typical atrial flutter from the cavotricuspid isthmus.J Am Coll Cardiol. 2012; 59:819–824. doi: 10.1016/j.jacc.2011.11.023.CrossrefMedlineGoogle Scholar7. Kaneko Y, Nakajima T, Irie T, Kato T, Iijima T, Kurabayashi M. Putative mechanism of a postpacing interval paradoxically shorter than the tachycardia cycle length.J Cardiovasc Electrophysiol. 2012; 23:666–668. doi: 10.1111/j.1540-8167.2011.02147.x.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kanter R and Hanfland R (2021) Biatrial reentrant tachycardia after surgery for congenital heart disease: Completing the circle with Mines on our mind, Heart Rhythm, 10.1016/j.hrthm.2021.07.037, 18:11, (1842-1843), Online publication date: 1-Nov-2021. Moore J, Bowman H, Gallotti R and Shannon K (2021) Mechanisms and outcomes of catheter ablation for biatrial tachycardia in adults with congenital heart disease, Heart Rhythm, 10.1016/j.hrthm.2021.06.1193, 18:11, (1833-1841), Online publication date: 1-Nov-2021. Arai T, Hojo R, Tokioka S, Kitamura T and Fukamizu S (2021) Treatment strategy and endpoint of catheter ablation for bi‐atrial tachycardia after substrate modification ablation in a low voltage zone of the left atrial anterior wall: Long‐term results, Journal of Arrhythmia, 10.1002/joa3.12558, 37:4, (1007-1014), Online publication date: 1-Aug-2021. Sagawa Y, Yamauchi Y, Okishige K, Sasano T, Sommer P, Ang R, Iliodromitis K, Tindale A and Thomson R (2021) Utility of coherent and ripple mapping for post-mitral valve plasty biatrial macro-re-entrant tachycardia: a case report, European Heart Journal - Case Reports, 10.1093/ehjcr/ytaa547, 5:2, Online publication date: 4-Feb-2021. Gracia E and Fan R (2018) Biatrial flutter circuit involving an anomalous insertion of the Bachmann bundle into the superior vena cava, HeartRhythm Case Reports, 10.1016/j.hrcr.2018.04.014, 4:8, (353-355), Online publication date: 1-Aug-2018. Kitamura T, Martin R, Denis A, Takigawa M, Duparc A, Rollin A, Frontera A, Thompson N, Massoullié G, Cheniti G, Wolf M, Vlachos K, Martin C, Al Jefairi N, Duchateau J, Klotz N, Pambrun T, Sacher F, Cochet H, Hocini M, Haïssaguerre M, Maury P, Jaïs P and Derval N (2018) Characteristics of Single-Loop Macroreentrant Biatrial Tachycardia Diagnosed by Ultrahigh-Resolution Mapping System, Circulation: Arrhythmia and Electrophysiology, 11:2, Online publication date: 1-Feb-2018.Asirvatham S and Stevenson W (2016) Mapping Reentry, Circulation: Arrhythmia and Electrophysiology, 9:5, (e003609), Online publication date: 1-May-2016. May 2016Vol 9, Issue 5 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCEP.115.003175PMID: 27153876 Manuscript receivedMay 18, 2015Manuscript acceptedJuly 10, 2015Originally publishedMay 6, 2016 Keywordscardiac arrhythmiasbiatrial tachycardiaatrial fluttersupraventricular tachycardiaentrainmentPDF download Advertisement SubjectsElectrophysiologyValvular Heart Disease
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