Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Rakesh Latchamsetty, MD, and Fred Morady, MD


A 62-year-old man with a history of atrial fibrillation and atrial flutter had undergone one previous catheter ablation procedure consisting of pulmonary vein isolation and ablation of the cavotricuspid isthmus. Following this procedure, he had no further episodes of atrial fibrillation but presented several months later with persistent atrial tachycardia. He was taken to the electrophysiology lab for catheter ablation.

The patient presented to the laboratory in atrial tachycardia with 2:1 atrioventricular conduction (Figure 15-1). Upright P waves in V1 and earliest coronary sinus (CS) atrial activity in the distal CS indicated a left atrial source. Evaluation of the P waves during a period of extended atrioventricular block showed no isoelectric segment in several leads (Figure 15-2). This suggested a macroreentrant mechanism for the tachycardia. Detailed activation mapping was performed in the left atrium and confirmed a macroreentrant circuit revolving around the left pulmonary veins (Figure 15-3).


FIGURE 15-1 Twelve-lead ECG of patient’s atrial tachycardia on presentation to the laboratory. Deflections can be seen during the T waves in V1 suggesting 2:1 atrioventricular conduction.


FIGURE 15-2 Surface lead electrocardiogram capturing a period of extended atrioventricular block during the tachycardia. The lack of an isoelectric component in several leads suggests a macroreentrant mechanism for this atrial tachycardia.


FIGURE 15-3 Activation map in the left atrium revealed a macroreentrant tachycardia through the previously ablated left pulmonary vein antra. Two conduction gaps around the left pulmonary vein antra, one near the roof and the other at the crux, facilitated the reentrant circuit. Note the “early meets late” activation point where the purple and red colors abut. LIPV = left inferior pulmonary vein; LSPV = left superior pulmonary vein.

Rapid atrial pacing at a slightly faster cycle length than the tachycardia cycle length (TCL) was performed at sites believed to be within the macroreentrant circuit. Pacing at the crux of the left superior pulmonary vein (LSPV) and left inferior pulmonary vein demonstrated a postpacing interval (PPI) minus TCL of 20 ms (Figure 15-4). At the junction of the left atrial roof and the LSPV, a multicomponent atrial electrogram was identified that displayed both near-field and far-field components. Rapid atrial pacing at this location revealed a PPI-TCL of zeroms for the near-field component and a PPI-TCL of –20 ms for the far-field component (Figure 15-5). Ablation at this site resulted in termination of the tachycardia (Figure 15-6) and rendered it noninducible.


FIGURE 15-4 Rapid atrial pacing at the crux of the left superior and left inferior pulmonary veins revealed a postpacing interval (PPI) minus tachycardia cycle length (TCL) time of just 20 ms, indicating this location was at or very close to the tachycardia circuit. ABL = ablation; CS = coronary sinus; d = distal; p = proximal.


FIGURE 15-5 Rapid atrial pacing from the left atrial roof was performed during tachycardia. Note the multicomponent atrial electrogram at the distal ablation (ABL) catheter. The postpacing interval (PPI) to the initial component representing far-field atrial activity is actually 20 ms less than the tachycardia cycle length (TCL). The PPI to the second, or near-field component of the electrogram matches the TCL. CS = coronary sinus; d = distal; p = proximal.


FIGURE 15-6 Termination of the atrial tachycardia to sinus rhythm during ablation at the junction of the left atrial roof and left superior pulmonary vein. ABL = ablation; CS = coronary sinus; d = distal, p = proximal.


Classification of atrial tachycardia has evolved as diagnostic and therapeutic options for their management have evolved. Original classifications were based on mechanism (enhanced automaticity, triggered activity, and reentry) or appearance on surface ECG. More recently, atrial tachycardias have been classified as either focal or macroreentrant.1 A macroreentrant tachycardia naturally invokes reentry as a mechanism, whereas a focal atrial tachycardia can utilize any of the three primary tachycardia mechanisms: abnormal automaticity, triggered activity, or reentry.

The commonly accepted gold standard for distinguishing a focal versus macroreentrant tachycardia is the atrial activation pattern. As seen in our case study (Figure 15-3), activation mapping during a macroreentrant atrial tachycardia reveals a circuit with continuous atrial activity that encompasses at least 90% of the TCL and demonstrates an “early meets late” pattern at some point along the circuit.2 One should note that during mapping of a reentrant circuit, the terms “early” and “late” are arbitrary and depend on the fiducial point used as a reference for atrial timing. In contrast, electroanatomic mapping of a focal atrial tachycardia (Figure 15-7) shows centrifugal activation from a point source usually less than 2 cm in area.


FIGURE 15-7 Electroanatomic mapping during a focal atrial tachycardia reveals centrifugal atrial activation emanating from a single location.

For either mechanism, a detailed map during the tachycardia can identify targets for ablation. For a focal mechanism, the site of earliest atrial activity is targeted. For a macroreentrant circuit, electrical mapping is performed along the circuit to locate areas of slow conduction with a longer duration of fractionated electrograms, ideally at a narrow isthmus bounded by an anatomic obstacle or scar tissue (Figure 15-5). Successful sites for termination of the tachycardia frequently demonstrate an atrial electrogram duration that is >30% of the TCL.2 Ablation is typically performed across the slow area of conduction and extended linearly to an anatomic obstacle to provide a line of conduction block. Care must be taken to avoid any gaps in this line, as this can facilitate tachycardia recurrence.

Prior to electroanatomic mapping, several observations during tachycardia can provide clues to differentiate a focal versus macroreentrant mechanism. Cycle length variation >20 ms during the tachycardia is more often seen with a focal tachycardia than with reentrant circuits. A progressive reduction in cycle length at the onset of a tachycardia is suggestive of an automatic mechanism, as is a progressive lengthening of cycle length just before termination.3Tachycardia entrainment with rapid atrial pacing is used to identify a reentrant circuit, which can be a mechanism for either a microreentrant (focal) or macroreentrant tachycardia. Variability of the PPI when pacing at different cycle lengths at the same atrial location has been proposed as a sensitive and specific maneuver to differentiate between a focal and macroreentrant source, with a focal source showing greater PPI variability.4 Automatic sources are prone to overdrive suppression with increasing pacing rates, and microreentrant circuits are believed to be more subject to areas of decremental conduction—both resulting in longer PPIs with more rapid pacing. Decremental conduction may also explain why microreentrant circuits show more cycle length variation than macroreentrant circuits.5

P-wave morphology on ECG during a focal atrial tachycardia often displays an isoelectric component in all leads, whereas a macroreentrant tachycardia is expected to reveal continuous atrial activity. However, this finding is not always reliable.6 With very rapid tachycardia rates or in atria with significant conduction abnormalities (commonly seen in patients with prior ablation procedures), an isoelectric component may not be observed with a focal tachycardia. If distinct P waves are difficult to discern because of interference by the QRS complexes on ECG, ventricular pacing or administration of adenosine can often unveil several consecutive P waves for analysis.1 P wave duration >140 ms has also been shown to be a fairly sensitive and specific marker for a macroreentrant mechanism.7

The mechanism of tachycardia initiation and termination can help differentiate tachycardia mechanisms, although these are not entirely sensitive and specific findings. A focal automatic mechanism is more likely to be dependent on isoproterenol for induction and less likely to be induced by pacing.8 Automatic tachycardias are also more vulnerable to overdrive suppression by rapid atrial pacing. Triggered and reentrant atrial tachycardias are more likely to be induced with pacing. Triggered activity, in particular, maybe sensitive to specific pacing cycle lengths. Triggered activity is also more likely to be terminated with adenosine, propranolol, verapamil, and the Valsalva maneuver.8

Catheter ablation has become common for patients with atrial tachycardias resistant to medical therapy. Technological advances in electroanatomic mapping systems and ablation catheters have improved the ability to diagnose and ablate both focal tachycardias and macroreentrant circuits. Recent studies have reported high success rates for catheter ablation of atrial tachycardias.2,6 Novel mapping systems with automated electrogram analysis should continue to improve the efficiency and accuracy of such procedures.


1. Saoudi N, Cosio F, Waldo A, et al. Classification of atrial flutter and regular atrial tachycardia according to electrophysiologic mechanism and anatomic 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. J Cardiovasc Electrophysiol. 2001;12(7):852-866.

2. Yokokawa M, Latchamsetty R, Ghanbari H, et al. Characteristics of atrial tachycardia due to small vs large reentrant circuits after ablation of persistent atrial fibrillation. Heart Rhythm. 2013;10(4):469-476.

3. Goldreyer BN, Gallagher JJ, Damato AN. The electrophysiologic demonstration of atrial ectopic tachycardia in man. Am Heart J. 1973;85(2):205-215.

4. Colombowala IK, Massumi A, Rasekh A, et al. Variability in post-pacing intervals predicts global atrial activation pattern during tachycardia. J Cardiovasc Electrophysiol. 2008;19(2):142-147.

5. Veenhuyzen GD, Mitchell LB. Distinguishing focal from macroreentrant atrial tachycardias: has this job just become easier? J Cardiovasc Electrophysiol. 2008;19(2):148-149.

6. Wasmer K, Mönnig G, Bittner A, et al. Incidence, characteristics, and outcome of left atrial tachycardias after circumferential antral ablation of atrial fibrillation. Heart Rhythm. 2012;9(10):1660-1666.

7. Michaud GF, Tada H, Chough S, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing. J Am Coll Cardiol. 2001;38(4):1163-1167.

8. Chen SA, Chiang CE, Yang CJ, et al. Sustained atrial tachycardia in adult patients. Electrophysiological characteristics, pharmacological response, possible mechanisms, and effects of radiofrequency ablation. Circulation. 1994;90(3):1262-1278.