Unifying Algorithm for Mechanistic Diagnosis of Atrial Tachycardia

Abstract

Background-No existing criteria unequivocally differentiate focal atrial tachycardia (AT) caused by microreentry, triggered activity, or enhanced automaticity. Although macroreentrant AT is readily diagnosed based on entrainment criteria, the smaller circuit dimension associated with microreentrant AT makes it challenging to validate the presence of reset with fusion. An algorithm was, therefore, developed that is independent of entrainment but which reliably identifies specific mechanisms of focal AT. Methods and Results-Fifty-nine patients with AT underwent adenosine testing after mapping of tacycardia. Ten ATs had nonfocal activation, with ≥90% of tachycardia cycle length identified with electroanatomical mapping, findings consistent with macroreenty. All ATs were insensitive to adenosine. Forty-nine patients had focal AT with centrifugal activation. In 32/49 (67%) ATs, electrograms were nonfractionated, and <50% of tachycardia cycle length could be mapped. Based on programmed stimulation, 26/32 (81%) of these ATs were classified as due to triggered activity and 6/32 (19%) as due to enhanced automaticity. Adenosine terminated 100% of triggered ATs and transiently slowed or suppressed 100% of automatic ATs. The remaining 17 focal ATs had localized fractionated electrograms (≥35% of tachycardia cycle length) at the site of successful ablation and were classified as microreentrant. Adenosine had no effect in these ATs. The response to adenosine accurately differentiated all subtypes of focal AT, P<0.05. Conclusions-Adenosine-sensitivity (termination or transient slowing/suppression) in response to adenosine was 100% sensitive and specific for identifying focal AT mechanisms due to triggered activity or automaticity, respectively. Absence of adenosine effect on focal AT identifies tachycardia due to microreentry. Methods Study PopulationWe studied 59 consecutive patients who presented for invasive electrophysiological evaluation and catheter ablation of AT and received adenosine during tachycardia. The presence of structural heart disease was based on a diagnosis of cardiomyopathy, valvular disease, coronary artery disease (> 60% stenosis), or prior myocardial infarction. All procedures were performed after informed consent was obtained for a study approved by the Institutional Review Board of Weill Cornell Medical College. Baseline Electrophysiology StudyAll patients underwent electrophysiology study in a postabsorptive state. Antiarrhythmic drugs were held for 5 half-lives before the study. Quadripolar catheters were positioned at 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 or a 7-Fr duodecapolar catheter positioned along the tricuspid annulus. A 6-Fr decapolar catheter was positioned in the coronary sinus to record left atrial and left ventricular activity. In selected patients, a 5-spline mapping catheter configured as radial spokes was deployed (PentaRay Nav; Biosense-Webster, Dia...

Approach to catheter ablation of left atrial flutters

“…However, normal electrograms are identified at the origin in the majority of focal ATs . Focal and reentrant ATs demonstrate differential responses to adenosine, which can be used to investigate tachycardia mechanism . Adenosine terminates ATs due to triggered activity and transiently suppresses automatic ATs.…”

“…The mechanisms that give to focal tachycardias in the atrium are triggered activity and automaticity. 5 It has been proposed that some focal tachycardias arise from areas of cellular uncoupling, which explains the presence of complex electrograms at the origin of selected focal ATs. 6 However, normal electrograms are identified at the origin in the majority of focal ATs.…”

Entrainment mapping: Theoretical considerations and practical implementation

“…A focal activation pattern alone does not allow for differentiation of the mechanism–a focal tachycardia can be caused by triggered activity or automaticity, or localized (micro) re‐entry. The differentiation between these mechanisms can be challenging . If entrainment cannot be demonstrated with assessment of fusion, concealed entrainment may still be occurring, and not easily distinguished from overdrive suppression of an automatic tachycardia.…”

“…The differentiation between these mechanisms can be challenging. 23 If entrainment cannot be demonstrated with assessment of fusion, concealed entrainment may still be occurring, and not easily distinguished from overdrive suppression of an automatic tachycardia. Their response to atrial overdrive pacing (the more appropriate term in this case) can result in resetting with a PPI equivalent, and the PPI will still be shortest close to the AT focus, although it is longer than the TCL.…”

Adenosine and Atrial Tachycardia

“…4,5 In this issue of the Journal, Dr Lerman and his colleagues present their experience with adenosine in delineating the mechanism of AT in a large series of patients. 6 Among the 59 patients, approximately one third had undergone a prior procedure for either AF or AT. The criteria for macroreentry included accounting for >90% of the tachycardia cycle length (CL) and documenting intersection of early and late areas on 3-dimensional (3D) mapping.…”