Pulmonary vein (PV) isolation can be performed at different levels in the ostium. Initially, segmental isolation, targeting individual strands of atrial myocardial tissue in PV ostia, was performed using the combination of a circular mapping catheter and a standard ablation catheter.1 In most centres, clinical success rates were moderate. Soon, however, it was recognized that wider encircling improved success and reduced complications.2 Additional ablation lines and substrate modification may further increase success, but may also create a substrate for left atrial flutters.3–5 The creation of a long continuous ablation line around a PV antrum using a single ablation electrode is technically challenging. Kistler et al. described a prospective randomized study to investigate the contribution of image integration to catheter ablation of atrial fibrillation.6 The value of Cartomerge® was investigated on the basis of an incomplete Carto map. It is highly remarkable that even then, image integration did not affect the quality of the procedure. The study suggests that an anatomically correct geometry does not facilitate the creation of continuous transmural lesions. Such geometry definitively helps to outline the desired course of the ablation lines, but apparently it does not improve the continuity of that line. Use it if you like it, but don't expect any miracles. The ablation procedure was performed using an irrigated ablation electrode to create the long ablation lines around both pairs of PV ostia.6 Wall contact during ablation, precise catheter manipulation, and the delivery of sufficient radiofrequency (RF) power are the most important determinants of successful electrical isolation. While irrigated catheters are highly advisable to reduce the risk of blood clot formation during RF ablation, electrode cooling greatly eliminates the electrode temperature increase as feedback for tissue contact. This may have been the reason for the investigators using a remarkable irrigation protocol: the flow rate was maintained at 2 mL/min unless the 50°C target temperature was reached with <20 W. One should remember that a flow rate of 2 mL/min may only be sufficient to keep the irrigation holes open, not to prevent blood clot formation on the heated tissue surface.7 Even with standard non-irrigated electrodes, detection of wall contact and lesion formation on the basis of electrode temperature response remains difficult. A high electrode temperature increase at low power may be caused not only by intimate electrode–tissue contact, but also by low blood flow. Local electrogram characteristics and amplitude, impedance drop during ablation, fluoroscopic imaging, and intracardiac echocardiography (ICE) are alternative ways to judge wall contact, but they all have important limitations or add significant complexity. A combination of these methods and 3D mapping systems are used in most labs, but even then, multiple acute gaps in the lines are more the rule than the exception. Moreover, a large number of patients experience a recurrence after a first procedure because of resumed conduction through the antrum lines despite the fact that the observation time after isolation often is lengthened by additional ablations.8 Persistent continuity of ablation lines should be our main goal for future developments. A 30 W/50°C setting was originally used for segmental PV isolation where myocardial sleeves may be relatively thin. To prevent collateral damage, one should always try to limit RF power, but with low power it may sometimes be very difficult to achieve complete electrical isolation of the PV antrum that includes sections with thicker myocardium and the appendix ridge where catheter stability is a major challenge.9 Kistler et al. used an electrogram amplitude <0.1 mV or amplitude reduction >80% as endpoint during ablation.10 Reduction of the local unipolar electrogram clearly is an indicator for lesion formation. Often, however, electrograms <0.1 mV still can be found inside the PV ostia and some of these can be proven to be true local activations. Conversely, an electrogram >0.1 mV within PVs can be a remote signal from the bulk of the left or right atrium, left atrial appendage, or superior caval vein. The latter signals, very misleadingly, sometimes also show decremental properties with atrial extrastimuli. Consequently, a simple amplitude criterion is not sufficient to declare PVs electrically silent. If the goal is complete electrical isolation then one should meticulously investigate the origin of all electrograms distal from the ablation line and continue the search for leaks until all local signals have disappeared. Adenosine may reveal latent leaks, but mapping of those leaks can be very difficult.11 Kistler et al. speculate that image fusion in NavX could result in more reduction in fluoroscopy time than with Carto. With NavX, an accurate geometry can be created in 15 min, with only a few minutes of fluoroscopy. With image fusion, only these few minutes are at stake and it is unlikely that image fusion will reduce fluoroscopy time more than Cartomerge®. Reduction in radiation exposure, however, always remains a valid argument to investigate new technologies. Many electrophysiology (EP) labs are equipped with fluoroscopy systems that were originally designed to visualize tiny arteries and stents. EP procedures, however, do not require that image quality; we mainly have to see the contrasting catheters. Fluoroscopy systems in EP labs can therefore use extra primary beam filtration and lower pulse rates. In addition, one is obliged to use standard measures such as lower body-protecting lead flaps and an upper body-protecting glass screen. With a badge on the collar above the apron, the total annual dose of all operators performing catheter ablation procedures in a single EP lab can then stay below 5 mSv. Any team with a significantly higher total operator badge dose for catheter ablation procedures alone should seek advice from the fluoroscopy system manufacturer. Most modern systems have three different dose rate settings that are individually programmable by the manufacturer. Both electrophysiologists and interventional cardiologists can then be satisfied when they have to share the lab, and often operator and patient dose rates can be reduced by a factor of 5 or more without any impact on the quality of EP procedures. As a method for reducing fluoroscopy exposure, the application of advanced technologies, such as ICE, robotic or magnetic catheter navigation, image integration, and even 3D mapping systems alone, only makes sense when basic measures such as optimized fluoroscopy settings have been put in operation. Conflict of interest: F.H.M.W. is a consultant for St Jude Medical.
In the differential diagnosis of supraventricular tachycardia, pacing maneuvers or observation rarely provide a diagnosis when used individually.1 The introduction of transcatheter therapy for cardiac arrhythmia transforms electrophysiology from an exclusive, scholarly, almost Talmudic, field to an interventional goal-oriented field where successful elimination of the arrhythmia by “burning” often serves as “proof” of the arrhythmia mechanism (Learning by Burning). In a series of papers by Callans et al.2–4 published in this Journal, the term “learning while burning” was coined, emphasizing that in contrast to the goal oriented approach, ablation procedure is indeed a powerful tool for understanding the interplay between anatomical substrate and the pathophysiology of clinical arrhythmia. The authors in the present Journal article5 put a new twist on that concept by utilizing junctional beats induced during ablation procedure of AV nodal slow pathway modification to gain a new insight to the differential diagnosis of atrioventricular node reentry tachycardia (AVNRT) versus junctional tachycardia (JT). The authors should be applauded for a meticulous execution of the study protocol and a rigorous validation of their findings that showed convincingly that the mean H-A during JT is shorter than the mean H-A during AVNRT and that the mean delta H-A (defined as retrograde H-A during ventricular pacing minus H-A during tachycardia) is negative during AVNRT, as opposed to positive during JT. In the study design, both AVNRT and JT were induced in each patient. When these measurements were compared on an individual basis (meaning that every patient's measurements during AVNRT were compared with his or her own measurements during JT controlling for variability between patients), these findings hold true in most patients (see Figs. 2 and 3). How can we explain these finding based on our present knowledge about the electrophysiological properties of these arrhythmias? AVNRT is the most common cause of supraventricular tachycardia in patients referred for electrophysiological study (EPS).1 The “common,”“typical,”“slow-fast” type is present in over 80% of all cases of AVNRT.6 In a simplistic model, AVNRT results from reentry involving two anatomically distinct AV node structures7,8 (i.e., “slow” and “fast” pathways). In “slow-fast” AVNRT, the reentry circuit consists of anterograde conduction through the slow pathway and retrograde conduction by the fast pathway with the earliest retrograde atrial activation in the “fast pathway region” at the apex of the triangle of Koch, recorded on the His-bundle electrogram from the right septum.9,10 Unfortunately, life is not that simple: the three-dimensional anatomy and cytoarchitecture of the AV junction is complex11,12 and the exact location of the atrionodal connections and slow and fast pathways are still controversial. Although several elegant models based on functional characteristics of different areas of the compact AV node and surrounding structures were proposed to explain dual-AV node physiology, the sheer bulk of the literature on the subject and the ongoing debate attest that none of them is proven.13,14 In as many as 40% of the patients with AVNRT, there are multiple AV nodal pathways.15 Even in patients with typical AVNRT, recording with close-spaced electrodes in the His, coronary sinus (CS), and the slow-pathway areas has shown that there is heterogeneity of the retrograde fast pathway conduction pattern.16 Recording of the His bundle potential from the right and left sides of the septum has shown that the earliest retrograde atrial activation during AVNRT is most often recorded on the left side of the septum.17 Thus, it is not surprising that there is a considerable variability in H-A intervals in patients with typical AVNRT, making it difficult at times to differentiate between typical AVNRT and other arrhythmias (including JT) based on H-A interval alone. According to the slow-fast pathway model, the retrograde atrial activation sequence during right ventricular pacing at the tachycardia cycle length, immediately after typical AVNRT, propagates retogradely from the His bundle through the lower common pathway to the fast pathway, and should be similar to the activation sequence during typical AVNRT. Retrograde H-A interval during ventricular pacing (H-Ap; measured from the end of the most proximal His potential to earliest A) is the sum of retrograde conduction time of the lower common pathway and the retrograde fast pathway. The H-A of typical AVNRT (H-At) according to this model is retrograde conduction time of the fast pathway minus anterograde conduction time of the lower common pathway. The difference between H-Ap and H-At (so called delta H-A) equals retrograde plus anterograde conduction time of the lower common pathway13 (assuming that the retrograde fast pathway conduction time is identical during pacing and AVNRT). A positive delta HA suggests that a lower common pathway is present. A negative delta HA, which, in fact, was found in the present study5 and by others,18 cannot be explained by this simple model. Although there are several explanations for this phenomenon, including difference in conduction velocity, activation path,19 and a combination thereof,13 a negative delta HA probably reflects a very short or an absent lower common pathway. Automatic JT as described by Coumel20 is a rare arrhythmia seen mainly in the pediatric population21 and postcardiac surgery21,22 and very rarely in adults.23 In the few cases studied, abnormal automaticity within or in close proximity to the His bundle was found.24–26 JT is frequently seen during radio frequency ablation using the AV node modification by slow pathway approach. In fact, the presence of JT is associated with successful slow pathway ablation.27,28 The pathophysiology of JT during ablation is thought to be enhanced automaticity due to heating of the tissue29,30 or local release of norepinephrine.31 Studies in pig and rabbit heart models have shown that heating in a discrete area located in the middle of the triangle of Koch that was located in close proximity to the compact AV node induced JT. In that area, no slow pathway potential was seen and it was distant from the site of earliest retrograde atrial activation. There was a large variation between individual animals regarding the location of these sites.30 In canine blood-perfused atrioventricular node preparations, JT was induced by heating anterior to the CS os with the earliest retrograde atrial activation site at the His-potential recording site or in the middle of Koch's triangle. After interruption of the posterior input to the AV node, atrial activation during JT spread from the low posterior to the high anterior septum.29 In humans, VA block during junctional ectopy is a harbinger of AV block in patients undergoing RF ablation of the slow pathway,27 suggesting that the retrograde atrial activation during JT may involve the His area or the common lower pathway. However, in that same paper, the authors observed that “VA conduction should be expected during the junctional ectopy that accompanies slow pathway ablation, even when there is poor VA conduction during baseline ventricular pacing,” and that the AV block was proximal to the His.27 These astute observations suggest that the site of VA conduction during JT is proximal to site of VA block during ventricular pacing. Wagshal et al.32 reported that higher temperature lesions simultaneously abolish all slow pathway activity as well as the focus of JT, which suggests that the JT source is located or triggered by slow pathway tissue. In a study by Lee et al.,33 atrial activation sequences were assessed by comparing H-A interval (measured at the high right atrium) during various forms of AVNRT and JT induced by ablation. In 27 patients with slow-fast AVNRT, H-A during JT was shorter than during AVNRT: 58 ± 24 msec compared with 68 ± 21 msec, respectively (P < 0.01). In the present study,5 a similar trend in mean H-A interval was observed: 35 msec versus 54 msec during JT and AVNRT, respectively. These findings call into question the concept that JT seen during RF ablation originates or has an exit point near the His area as described in the rare “de novo” automatic JT.24 Obviously, if a junctional beat originates near the His, distally to a common pathway, the H-A interval during JT will be longer than H-A interval during AVNRT that has a more proximal turn-around point to the fast pathway. In that situation, one would expect near-zero delta H-A in JT and positive delta H-A in AVNRT—in contrast to the finding of present5 and other33 studies. Studies in animal models and high resolution mapping in humans have demonstrated several mechanisms that can account for the shorter H-A interval during JT compared with AVNRT: changes in activation sequences that may cause direct activation of the atria, compact AV node,29 anisotropic spread from one more AV nodal transitional zone,34 fibers connecting to the fast pathway,35 or fibers connecting the slow pathway ablation area directly to the fast pathway in a more proximal location.33 Local heating may cause an increase in conduction velocity due to a direct effect30 or adrenergic stimulation. A recent study in a canine complete AV block model has shown that the application of RF energy caused a shift from the distal portion of the AV junctional area to a more proximal one. This enhanced junctional automaticity was suppressed by esmolol but not affected by atropine.31 In conclusion, differential diagnosis of a short RP tachycardia can be challenging. The paper by Srivathsan et al.5 adds a valuable new technique regarding the diagnosis of JT versus AVNRT, as well as provides insight into the electrophysiological mechanism of this fascinating and elusive arrhythmia. Further research is needed to ascertain whether these findings can be extended to the clinical forms of JT. Acknowledgment: The author would like to thank Dr. Shaul Atar for critical review of the manuscript.