Color Atlas and Synopsis of Electrophysiology, 1st Ed.


Rod Passman, MD, MSCE



A 63-year-old man status post-mitral and tricuspid valve repair and biatrial maze procedure 4 years ago presents with palpitations. The patient denied any chest pain, presyncope, or syncope with these palpitations. An ECG (Figure 2-1) demonstrated atypical atrial flutter.


FIGURE 2-1 Presenting ECG showing atypical atrial flutter. Note organized P waves in lead V1 and the absence of the classic “sawtooth” pattern in the inferior leads.


• Post-maze atrial tachycardias occur more frequently in the right atrium.

• Most common mechanism is the persistence of electrical conduction through regions that were targeted for prior surgical ablation or the creation of a central anatomic barrier to conduction. In each of these mechanisms, a macroreentrant circuit is created that was maintained by protected anatomic boundaries.

• In some cases, the reentrant circuit involves a region of incompletely ablated tissue such as the musculature of the coronary sinus or the junction of the intercaval right atrial incision and the superior vena cava (Figure 2-2).


FIGURE 2-2 Intracardiac electrograms showing a right atrial flutter with narrow split potentials in the posterior right atrium near the superior aspect of the intercaval incision.

• The creation of surgical barriers may have allowed reentry to occur around a central obstacle that was functional (either the crista terminalis in the right atrium or Bachmann’s bundle in the left atrium).


• Cardioversion alone is unlikely to offer a long-term cure for atrial tachycardias that arise remote from the time of surgery.

• Antiarrhythmic therapy is a treatment option, though the long-term efficacy in this situation is unknown.

• Ablation has a high success rate for these arrhythmias; however, the identification of the critical sites for ablation often requires the use of an electroanatomic mapping system.

 Images An electroanatomic map was created to define the reentrant circuit (Figure 2-3). The entire cycle length of the tachycardia was present in the right atrium. Entrainment mapping was used to localize the critical isthmus of tissue that was targeted for catheter ablation.


FIGURE 2-3 A high-density geometry and activation map of the right atrium was created primarily using a duodeca catheter looped around the right atrium. This catheter was rotated around the chamber allowing for rapid mapping, collecting 10 activation points at a time. Internal/external interpolation controls how near to the geometry each timing point was collected to help ensure good contact. Reentry (versus standard) map display helps determine what percentage of the atrial flutter cycle length is present in the specific chamber and colors are evenly distributed along the cycle length. Low voltage identification (grey areas) help locate areas of scar/electrical barriers. Varying lesion colors displayed here help distinguish good ablation sites in very close proximity to sites associated with phrenic nerve capture.

 Images Optimal ablation sites were those with a postpacing interval within 20 ms of the tachycardia cycle length at which fractionated or narrowly split electrograms were recorded.

 Images Once a suitable ablation site was recorded, high-output pacing was performed to assess for phrenic nerve capture (yellow circles show sites of phrenic nerve capture).

 Images If phrenic nerve capture was absent, radiofrequency current was applied using a 4-millimeter irrigated catheter at a maximum power of 35 watts. The arrhythmia terminated at the site of radiofrequency ablation between the superior margin of the posterior intercaval incision (blue circles represent site of termination; brown circles represent additional ablation sites).

 Images The use of an electroanatomic mapping system was essential to create a virtual recreation of the atrial anatomy, mark anatomic sites of importance, and to guide catheter ablation lesions.


The St. Jude Medical EnSite NavX system is a 3-dimensional impedance-based mapping system that allows the user to nonfluoroscopically locate electrodes in the human body. The NavX system uses constant current over a set of six patches (anterior-posterior, side-to-side, cranial-caudal) (Figure 2-4) and Ohm’s law to create an impedance gradient across the thorax. When an electrode is placed inside this established impedance gradient, NavX measures the local impedance and calculates the position along that plane. This location is calculated along multiple axes to create a 3-dimensional navigation field. The NavX system can locate up to 132 electrodes simultaneously and updates electrode location approximately 204 times per second creating near real-time 3-D catheter visualization. The system can also save the coordinates of each electrode relative to a positional reference; as the electrodes move, additional data is stored, allowing the user to create a 3-D model of the endocardial surface. This model aids in reproducibly maneuvering to desired locations in the heart, to denote the locations of critical anatomic structures, and to mark sites of ablation or other sites of interest. The system is also capable of saving local bipolar and unipolar electrograms; this data can be used to create a variety of voltage and activation timing maps that can also assist in locating the optimal ablation location for various arrhythmias. Types of maps that can be created with EnSite NavX include:


FIGURE 2-4 Position of body surface patches used with the NavX system. The six-patch configuration is used to create electroanatomic gradients used to localize multiple electrodes in a 3-D space.

• Geometry

• Ablation points

• Voltage

• Propagation

• Activation

• Complex fractionated electrogram

• Dominant frequency

The St. Jude Medical EnSite Array offers a viable solution for complex or nonsustained arrhythmias. The Array is a balloon catheter constructed of a handmade wire mesh consisting of 64 individual electrodes and is the only noncontact mapping tool on the market (Figure 2-5). The balloon is filled with a heparinized saline and contrast mixture. Unlike traditional contact mapping techniques, noncontact mapping can display mapping data of an entire atrium from a single heartbeat without moving a roving catheter. The software processes unipolar electrograms to create both local activation time and voltage maps. These maps are displayed on a color-coded scale and can be viewed as either static or dynamic maps. Catheter movement is displayed in real time, and traditional contact data may also be collected with the Array.


FIGURE 2-5 EnSite Array. (A) 9-French, 110-cm body, open lumen with the balloon in low profile. (B) A 7.5-ml balloon inflated, stainless steel mesh. (C) Microscopic view of single microelectrodes on the balloon mesh.


• Define anatomy

• Tag location of critical anatomic landmarks

• Localize arrhythmia circuit with activation map

• Track ablation lesions

• Limit fluoroscopy



A 22-year-old woman with no significant past medical history presents to the emergency department (ED) with palpitations. The patient reports that the episodes began around age 18, occur 4 to 5 times per year, usually last several minutes, and have an abrupt onset and offset. In the ED, her ECG showed a narrow complex, short RP tachycardia at a rate of 180 beats per minute (Figure 2-6A and B). Adenosine terminated the tachycardia. The patient underwent an electrophysiologic study where she was found to have typical atrioventricular nodal reentry tachycardia (AVNRT) (Figure 2-6C). Since the target for ablation in AVNRT is the slow pathway, there is a risk for inadvertent heart block if lesions are delivered close to the compact AV node. A 3-D mapping system is helpful to provide a high-resolution detailed map of the cardiac anatomy including the location the coronary sinus os, which is a marker for location of the slow pathway and the atrioventricular node. Utilization of the “shadow” feature allowed for the display of the exact positioning of the catheter location where His potentials could be reliably recorded. With these important structures defined, coupled with electrogram information recorded at the site of catheter ablation, radiofrequency lesion can be safely delivered while minimizing the risk of injury to the AV node or coronary sinus (Figure 2-7). In addition, use of 3-D mapping allowed for a successful ablation while reducing fluoroscopy exposure in this young patient.



FIGURE 2-6 (A) ECG of AVNRT shows a narrow complex short RP tachycardia with P waves buried in the terminal portion of the QRS interval in (most easily seen in lead V1 (arrows). (B) ECG in sinus rhythm; note absence of P waves in the terminal portion of lead V1. (C) Intracardiac electrograms demonstrate long AH times and short (<70 msec) septal VA times consistent with typical AVNRT.


FIGURE 2-7 Three-dimensional map of right atrium. (Left: RAO view; Right: LAO view). The coronary sinus can be seen extending posterior and leftward (green), and the area of the His bundle is marked by the shadow of a catheter crossing the anteroseptal region of the tricuspid valve. Radiofrequency modification of the slow pathway was performed. The red circles represent sites of successful lesions with junction ectopic beats.



A 47-year-old woman with no significant past medical history complained of palpitations. She denied presyncope, syncope, chest pain, or dyspnea on exertion. Her ECG (Figure 2-8) showed frequent monomorphic PVCs, both isolated and in pairs, in a left bundle/inferior axis morphology. Her echo shows normal contractile function, and a Holter showed NSR with 43% monomorphic isolated PVCs and couplets and no NSVT. A stress test showed no ischemia. Her PVCs failed to decrease on β-adrenergic blockers, and the patient underwent EP study and ablation.


FIGURE 2-8 Baseline ECG showing PVCs.


• For asymptomatic individuals with normal ejection fraction and a PVC burden of <20%, no specific therapy is required.

• Treatment is necessary for symptomatic individuals or with those who have a reduced ejection fraction that is possibly tachycardia-mediated.

• β-Adrenergic blockers and verapamil may be used to suppress RVOT PVCs and are frequently used as first-line therapy.

• Antiarrhythmic drugs can also be considered.

• Radiofrequency ablation has a high success rate, low complication rate, and can avoid the need for long-term medical therapy in this often young and otherwise healthy patient population.

 Images Figure 2-9: Using EnSite NavX, a spiral catheter (“lasso” catheter) was used to map the PVCs in the RVOT. The earliest site was localized to the superior septal region just under the pulmonic valve (white region).


FIGURE 2-9 The EnSite system was used to collect 113 points from the 10 electrodes of a spiral catheter to simultaneously display local activation timing data and geometry. The use of multipolar catheters decreases the time spent collecting arrhythmia data. Any mapping catheter can be used to collect this data with the EnSite system. The use of standard activation timing map (versus reentrant) was used to display the earliest ventricular signal as white (then red through purple as signals get later). This area was then more closely evaluated as a potential ablation site, and successful ablation was performed in this region (brown lesions).

 Images Figure 2-10: Pace-mapping confirmed a 12/12 match with activation demonstrating local EGMs 31 msec prior to the onset of the PVC. Successful ablation was performed at that site.


FIGURE 2-10 Intracardiac EGM demonstrating onset of RVOT PVC 31 msec prior to surface QRS onset. Unipolar tracing demonstrates characteristic QS pattern.



The patient is a 64-year-old man with a history of hypertension, a permanent pacemaker for atrioventricular nodal dysfunction, and symptomatic paroxysmal atrial fibrillation who underwent wide area circumferential ablation 2 years ago. He presents with dyspnea on exertion and was found to be in atrial flutter (Figure 2-11).


FIGURE 2-11 Presenting ECG shows ventricular pacing with underlying atrial flutter.


• The development of left atrial tachycardias or atrial flutters occurs in 1% to 50% of patients.

• New onset left atrial flutters are more common following wide area circumfrential ablation using radiofrequency energy as opposed to pulmonary vein isolation alone or cryoballoon ablation.

• The risk of postablation left atrial flutters increases in patients with persistent AF, enlarged atria, or when linear lesions have been used.

• Left atrial flutters following ablation of AF are often due to macroreentrant circuits around the prior roof or mitral annular linear lesions.

• Nonreentrant focal arrhythmias can also occur around lesion edges.


• Left atrial flutters occurring within the 3-month blanking period following the index ablation may respond to cardioversion alone.

• Rate control is often problematic given the rapid ventricular rates associated with atrial flutter in general and the paradoxically faster rates seen with the slower atrial flutters often seen with diseased atrium.

• Response rates to antiarrhythmic therapy are thought to be low.

• Ablation remains a highly effective approach to these arrhythmias.

 Images EnSite NavX was used to create an activation map of the atrial flutter. Figure 2-12 shows an activation map of a left atrial flutter propagating over the left atrial roof. This map shows the full range of color from white to purple indicating that the full cycle length of the tachycardia (240 msec) is present in the left atrium. Entrainment mapping was used to confirm the location as part of the flutter circuit.


FIGURE 2-12 A 10-pole circular mapping catheter was used to create the left atrial geometry and activation map simultaneously. The use of a multipolar catheter allowed for the creation of maps with several hundrend data points in just a few minutes. Electrograms from a catheter in the coronoary sinus were used as a timing reference for the activation map. The propagation map shows the entire cycle length of the atrial flutter with “early” activation (white area) over the roof region closest to the right superior pulmonary vein. Analysis of the data shows where “early” activation (white area) penetrates “late” activation (purple) near the right superior pulmonary vein.

 Images Intracardiac electrograms from the anterior roof portion near the right superior pulmonary vein shows fractionated electrograms. Ablation at this site successfully terminated the tachycardia (Figure 2-13Aand B).



FIGURE 2-13 (A) IEGMs of left atrial flutter. Ablation catheter at anterior aspect of roof line by the right superior pulmonary vein shows fractionated electrograms (blue arrows). Onset of radiofrequency energy also pictured (red arrow). (B) Termination of atrial flutter at sight of breakthrough at prior ablation roof line.



A 56-year-old woman with hypertension and asthma developed intermittent palpitations. They generally occurred on a daily basis, and she describes episodes of waking up at night with her heart beating really fast. These episodes lasted about 10 minutes and occurred once per month. Her workup included an echocardiogram that showed normal left ventricular function and no evidence of structural heart disease. An event monitor documented paroxysms of supraventricular tachycardia (Figure 2-14).


FIGURE 2-14 Event monitor shows a long RP tachycardia at 160 beats per minute. Sinus rhythm with sinus arrhythmia is also pictured.


• ATs can be caused by automaticity, triggered activity, and microreentry.

• Three-quarters of ATs arise from the right atrium, the majority near the crista terminalis.

• Of those originating in the left atrium, the pulmonary veins are the most common site.


• Atrial tachycardia may be responsive to β-blockers and calcium channel blockers.

• Antiarrhythmic drugs may be used as second-line agents.

• Ablation of AT has a high success rate, but the inability to sustain the tachycardia may make ablation challenging. When the AT cannot be sustained, noncontact mapping with EnSite Array offers a viable treatment option.

 Images Figure 2-15: EnSite Array shows the sinus node and the earliest activation site (EA) along the superior aspect of the crista terminalis.


FIGURE 2-15 EnSite Array has the ability to produce a noncontact isochronal map based on the extrapolated unipolar data of a single beat. The isochronal map shows the timing activation for a sinus beat in the right atrium. Earliest activation (white) is shown high lateral in the region of the sinus node with activation spreading in a cranial-to-caudal direction.

 Images Figure 2-16 shows an isochronal activation of the atrial tachycardia.


FIGURE 2-16 The image shows an isochronal activation of the atrial tachycardia. This isochronal map shows earliest activation (white) in the high posterior lateral region of the right atrium with the activation continuing posterior and medial with the latest activation being anterior. This activation pattern is likely due to the crista terminalis blocking conduction in the anterior direction. Successful ablation was performed at the site of early activation.

 Images Figure 2-17 shows ablation catheter at the site of EA, which is 35 ms pre–p-wave. Ablation at this site rendered the AT noninducible.


FIGURE 2-17 Intracardiac electrograms show ablation catheter with early atrial activity. Catheter was located at superior aspect of crista terminalis at the site of the EA seen on EnSite Array.


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