We are facing a new challenge: will imaging be the resolutive tool or will new mapping catheters and mapping system together with mathematical simulation solve this rebus? Clinical imaging will always remain attractive, particularly for elective cases and may add decisive information to best plan an ablation strategy: it represents a great tool in the hands of the electrophysiologist; however, as electrophysiologists, the imaging we should pursue is electrical – the depiction of the entire reentry circuit remains the sole proof of the target to ablate.

There is emerging evidence that a keen understanding of atrial myofiber architecture is paramount to characterizing and treating atrial arrhythmias. Heterogeneity in the three dimensional anatomic structure of the atrium has previously been shown to create distinct endocardial and epicardial activation patterns during tachycardia in a canine model (1). In the clinical setting, the epicardial atrial architecture and its contribution to arrhythmias have been less well explored until recently. There has been a renewed interest in and appreciation of epicardial and interatrial connections, particularly in the treatment of left atrial arrhythmias refractory to traditional endocardial ablation.The vein of Marshall has been postulated to harbor epicardial connections between the coronary sinus (CS) and the left atrium (LA), sustaining peri-mitral flutters refractory to endocardial ablation (2,3). Conduction across the intercaval bundle, which connects the right atrium to the right superior pulmonary vein, has been reported to render isolation of the RSPV challenging requiring ablation at the carina or from the RA (4,5). Similarly, the Bachmann bundle, the main pathway of interatrial connection, has been shown to be critical for maintenance of biatrial flutters (6,7). More recently, conduction across the subepicardial septopulmonary bundle has been implicated in the maintenance roof dependent flutter despite isolation of the endocardial posterior wall (8). In contrast, the role of epicardial connections in sustaining right atrial arrhythmias has been less well described.In this edition of the Journal, Chaumont et al. describe five patients who underwent electrophysiology study for typical atrial flutter, who had persistent arrhythmia despite achieving a line of block along the endocardial aspect of cavotricuspid isthmus (CTI) (9). Using entrainment and activation mapping during tachycardia, they identified atrial tissue critical to the arrhythmia circuit in the middle cardiac vein in four patients, and in close proximity to the CS ostium in one patient. Ablation at these locations restored sinus rhythm. Electroanatomic mapping was not available for most of these cases. Rather than a limitation, this absence allowed an amazing demonstration “old school” deductive electrophysiology.The authors should be commended for this series of cases which demonstrate connections that sustain atrial flutter by bypassing the endocardially blocked CTI. This study elucidates the complex, layered physiology underpinning atrial flutter, considered among the simpler of arrhythmias we treat in the electrophysiology laboratory. The strength of the study is the elegant intracardiac electrograms for each case which allowed the authors to infer the mechanism of refractory arrhythmia and eliminate it by targeting critical areas guided by EGMs within the coronary venous system. Prior studies of atrial fibrillation have suggested that epicardial-endocardial breakthrough maybe an important mechanism in maintenance of persistent AF (10). It appears that a similar mechanism maybe responsible for maintaining typical flutter refractory to endocardial CTI ablation.Based on their findings, the authors propose a CS to low right atrium (RA) epicardial connection in the first four patients, and an RA to RA epicardial connection in one patient critical to the tachycardia circuit. Anatomically, however, it is unclear whether discrete connections akin to accessory pathways exist between these regions of interest to explain the observed findings. It is more likely that the atrial flutter circuit encompasses the entire thickness of the atrium, and owing to fiber orientation across the two layers, there are regions where the endocardial and epicardial surfaces communicate with each other. At these locations we appreciate the epicardial component of persistent flutter once the endocardium is ablated and line of block is achieved but tachycardia continues uninterrupted. This concept is illustrated in Figure 1, which demonstrates a case of persistent mitral annular flutter refractory to endocardial mitral annular line. Epicardial conduction necessary for maintaining tachycardia was observed after endocardial ablation, and ablation from the coronary sinus slowed and terminated the tachycardia.The advent of high resolution 3-dimensional mapping systems has allowed characterization of atrial activation patterns in detail during tachycardia. Pathik et al investigated epicardial-endocardial breakthrough in activation mapping of right atrial macro-reentry tachycardia in 26 patients (11). They defined breakthrough as the presence of focal endocardial activation with radial spread unaccounted for by an endocardial wavefront, with same timing on every tachycardia cycle. Epicardial-endocardial breakthrough was observed in over 50% of the patients, with majority at the posterior RA, and one each at cavotricuspid isthmus postablation, RA septum, and the inferolateral RA. In four patients, areas of breakthrough were within the tachycardia circuit, and in one patient the breakthrough region was critical for arrhythmia maintenance. In all cases, breakthrough sites were adjacent to endocardial slowing or line of block—as mentioned above this finding is not entirely surprising, given that endocardial block is necessary to observe epicardial breakthrough while activation mapping.A detailed morphologic and histologic study of the inferior right atrial isthmus by Cabrera et al may provide some anatomical insight to explain the current study findings (12). The authors establish the isthmus to be an anatomically heterogeneous region, with the anterior aspect being consistently muscular, while the posterior membranous and the middle trabeculated aspects having variable ratios of muscle fibers to fibrofatty tissue, with myocardial bundles extending from terminal crest toward the Eustachian ridge to cover the mouth of the coronary sinus. In refractory atrial flutter following endocardial CT ablation, it maybe that ablation from the CS allows the elimination of residual conduction through these muscle fibers which is critical for maintenance of tachycardia.In conclusion, Chaumont et al should be congratulated for elegantly demonstrating the multi-layer physiological architecture of typical atrial flutter—a reflection of the anatomic complexity and heterogeneity of the cavotricuspid isthmus and its inputs, and of the atrial musculature in general. Appreciation of this complexity will undoubtedly empower us to characterize and treat this arrhythmia and others more effectively.

Atrial fibrillation (AF) is the most common sustained arrhythmia and is a significant public health burden.1,2 Many mutations in ion-channel and non ion-channel structural genes are linked to AF especially in patients with family history and no risk factors.3 The pulmonary vein muscle sleeves are the main trigger for AF. 4 Many studies showed that pulmonary vein isolation (PVI) via catheter ablation is superior to medical therapy in decreasing all-cause mortality, hospitalizations and recurrence 5-7. Though it is still controversial, vagal denervation and targeting the major atrial ganglionated plexi (GP) have been reported by Pappone et al. to improve the outcome after PVI.8 GP ablation has been associated with QT prolongation and ventricular arrhythmias9. PVI affects the atrial GP, modifies the intrinsic cardiac autonomic nervous system and could lead to QT prolongation and lethal ventricular arrhythmias such as torsade de pointe and ventricular tachycardia.10In their study published in this issue of the Journal of Cardiovascular Electrophysiology, Chikata et. al investigated the effect of PVI on the QT interval in patients with paroxysmal AF, and identified associated predisposing factors . 11 This was a retrospective observational study of 117 patients (out of 280 patients who were screened) with paroxysmal AF who underwent PVI via cryoballoon, hotballoon and radiofrequency at Toyama Prefectural Center in Japan between January 2016 and June 2019. The authors assessed 12 lead electrocardiograms (ECGs) at baseline and after four hours, one day, one month and three months. At each evalulaion point, they included only patients with sinus rhythm and excluded those taking antiarrhythmic drugs, drugs known to prolong QT intervals, patients undergoing renal transplant or having electrolyte imbalances in order to eliminate possible confounding factors. They measured the QRS, heart rate, QT interval and calculated QTc using the Bazett, Fridericia, Framingham and Hodges formulas at each evaluation point. All patients underwent PVI under conscious sedation with the same anesthesia regimen. They performed Cavotricuspid isthmus line ablation only if the Cavotricuspid isthmus dependent atrial flutter was noted, and they did not perform any intentional GP ablation. The study showed that QTc interval calculated by Bazett formula and the Fridericia formula was significantly prolonged at each time point ,whereas that of the Framingham formula and the Hodges formula was significantly prolonged only in the acute phase. The authors attributed this discrepancy to how each formula correlates with heart rate (HR). Since PVI could lead to autonomic denervation, a reflex increase in heart rate can be expected especially during the acute phase following the procedure. Furthermore, the study showed that in the acute phase post PVI, women had significantly prolonged QTc interval as compared to their baseline and to men (P < 0.05).The authors explained that QTc calculated by the Bazzet formula is more prone to error especially at elevated heart rates seen post PVI. In the setting of tachycardia, the QTc can be expected to prolong since the R-R interval shortens to a greater extent than the QT. Hence, the Bazzet’s QTc formula will overcorrect and overestimate the prevalence of the QT interval at heart rate greater than 100 bpm, and linear regression methods to correct the QT interval (such as Hodges) are better for clinical use. Women are known to have a longer baseline QT interval and are more prone to develop torsade de pointe than men12. That could be explained by the hormonal effect on the expression of ion channels and by the difference in autonomic regulation between genders.13,14 Chikata at al show a possible association between gender and QT prolongation post PVI that might be explained by a difference in inflammatory response or a distinguished genetic predisposition found more frequently in women. Further investigation is warranted via prospective studies with larger sample size in the future to corroborate the findings especially with the relatively small sample size and the fact that it was a single center study.References:1. Wolf PA, Abbott RD, Kannel WB. Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke . Aug 1991;22(8):983-8. doi:10.1161/01.str.22.8.9832. Chung MK, Refaat M, Shen WK, et al. Atrial Fibrillation: JACC Council Perspectives. J Am Coll Cardiol. Apr 2020; 75 (14): 1689-1713.3. Feghaly J, Zakka P, London B, MacRae CA, Refaat MM. Genetics of Atrial Fibrillation. Journal of the American Heart Association . Oct 16 2018;7(20):e009884. doi:10.1161/jaha.118.0098844. Haïssaguerre M, Jaïs P, Shah DC, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. The New England journal of medicine. Sep 3 1998;339(10):659-66. doi:10.1056/nejm1998090333910035. Asad ZUA, Yousif A, Khan MS, Al-Khatib SM, Stavrakis S. Catheter Ablation Versus Medical Therapy for Atrial Fibrillation: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Circulation Arrhythmia and electrophysiology . Sep 2019;12(9):e007414. doi:10.1161/circep.119.0074146. Refaat MM, Ballout J, Mansour M. Ablation of Atrial Fibrillation in Congenital Heart Disease. Arrhythm Electrophysiol Rev. Dec 2017; 6 (4): 191-4.7. Oral H, Knight BP, Tada H, et al. Pulmonary vein isolation for paroxysmal and persistent atrial fibrillation. Circulation . Mar 5 2002;105(9):1077-81. doi:10.1161/hc0902.1047128. Pappone C, Santinelli V, Manguso F, et al. Pulmonary vein denervation enhances long-term benefit after circumferential ablation for paroxysmal atrial fibrillation. Circulation . Jan 27 2004;109(3):327-34. doi:10.1161/01.cir.0000112641.16340.c79. He B, Lu Z, He W, et al. Effects of ganglionated plexi ablation on ventricular electrophysiological properties in normal hearts and after acute myocardial ischemia. International journal of cardiology . Sep 20 2013;168(1):86-93. doi:10.1016/j.ijcard.2012.09.06710. Münkler P, Wutzler A, Attanasio P, et al. Ventricular Tachycardia (VT) Storm After Cryoballoon-Based Pulmonary Vein Isolation. The American journal of case reports . Sep 11 2018;19:1078-1082. doi:10.12659/ajcr.90899911. Chikata A. Prolongation of QT interval after pulmonary vein isolation for paroxysmal atrial fibrillation Journal of Cardiovascular Electrophysiology . 2020;12. Drici MD, Burklow TR, Haridasse V, Glazer RI, Woosley RL. Sex hormones prolong the QT interval and downregulate potassium channel expression in the rabbit heart. Circulation . Sep 15 1996;94(6):1471-4. doi:10.1161/01.cir.94.6.147113. Chen YJ, Lee SH, Hsieh MH, et al. Effects of 17beta-estradiol on tachycardia-induced changes of atrial refractoriness and cisapride-induced ventricular arrhythmia. J Cardiovasc Electrophysiol . Apr 1999;10(4):587-98. doi:10.1111/j.1540-8167.1999.tb00716.x14. Huikuri HV, Pikkujämsä SM, Airaksinen KE, et al. Sex-related differences in autonomic modulation of heart rate in middle-aged subjects. Circulation . Jul 15 1996;94(2):122-5. doi:10.1161/01.cir.94.2.122

Introduction: Brugada syndrome is associated with ventricular arrhythmia leading to sudden cardiac death. Risk stratification is challenging, as major arrhythmic events (MAE) are rare. We assessed the utility of drug challenge testing in Brugada syndrome by a systematic review and meta-analysis. Methods and results: We comprehensively searched the databases of MEDLINE and EMBASE from inception to May 2019. Included studies compared the incidence of MAE between spontaneous and drug challenge induced Type-1. Data were combined using the random-effects, generic inverse variance method, to calculate pooled incidence and odds ratio (OR). Mixed-effects Poisson regression was used to calculated incidence rate ratio (IRR). Eighteen studies from 2006 to 2018 were included (4,099 patients, mean follow-up 4.5 years). Pooled annual incidences of MAE in spontaneous, drug challenge induced (regardless of symptoms), asymptomatic drug challenge induced, and symptomatic drug challenge induced Type-1 were 23.8 (95% confidence interval [CI]: 19.8-27.8), 6.5 (95% CI: 3.9-9.1), 2.1 (95% CI: -0.3-4.4), and 19.6 (95% CI: 9.9-29.3) per 1,000 person-years respectively. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was not statistically different (IRR=1.0, 95%CI: 0.6-1.7). The presence of ventricular tachyarrhythmia during drug challenge testing was a predictor of MAE (OR=3.73, 95% CI: 1.77-7.86, p=0.001). Conclusions: The incidence of MAE in drug challenge induced Type-1 in asymptomatic patients is low. The incidence of MAE between symptomatic drug challenge induced and asymptomatic spontaneous Type-1 was similar. Ventricular tachyarrhythmia during drug challenge testing could be a useful risk marker for MAE in Brugada syndrome.

Multipolar mapping has primarily been studied in complex arrhythmia substrates or re-entrant circuits. Chieng et al. use a Case-Control design to compare multipolar mapping and point-by-point mapping with an ablation catheter for focal atrial and ventricular tachycardias, showing reduced procedure times and earlier electrograms in the multipolar mapping group but no difference in clinical outcomes. It is plausible that faster mapping and better delineation of earliest signals may translate to improved clinical outcomes if studied in a randomized trial in a larger population. Future multipolar mapping systems will guide the operator toward the focus in real-time and may even triangulate the source in three dimensions, giving an estimate of depth within the myocardium or likely focus in the opposite chamber.

Introduction: The clinical efficacy and safety of hot balloon ablation (HBA) for treatment of persistent AF (PerAF) remain unclear. We aimed to evaluate the clinical efficacy and safety of HBA vs. cryoballoon ablation (CBA) as treatment for PerAF. Methods: Of 195 consecutive patients who underwent initial catheter ablation for PerAF (AF lasting >7 days but <12 months), 158 propensity score-matched (79 HBA and 79 CBA) patients were included in our study. All patients who underwent HBA received applications of energy to the upper posterior LA wall with a larger balloon in addition to single shots to each pulmonary vein (PV) ostium, whereas those who underwent CBA received simple single-shot applications. The electrically isolated surface area (ISA), including the PV antrum and part of the posterior LA wall, was assessed by high-resolution mapping. Results: Success of the PV isolation with balloon shots alone did not differ between HBA and CBA (81% vs. 85%; P = 0.52). The ISA was generally wide in both groups and significantly larger in the HBA group than in the CBA group (61 ± 16% vs. 51 ± 12%, P < 0.001). The incidence of procedure-related complications did not differ significantly (HBA 4% vs. CBA 1%; P = 0.62) nor did the arrhythmia recurrence rate (HBA 11% vs. CBA 18% at 18 months; P = 0.26). Conclusion: Despite the difference in protocols, HBA and CBA performed for PerAF appear comparable in terms of wide antral lesion creation, clinical efficacy, and safety.

Idiopathic ventricular arrhythmias (VA) is defined as premature ventricular complexes (PVCs) or ventricular tachycardias (VT) that occur in the absence of structural heart disease. Endocardial radiofrequency (RF) ablation is often curative for idiopathic VA. The success of the procedure depends on the ability to localize the abnormal foci accurately. These arrhythmias typical originate from the right ventricular outflow tract (RVOT), specifically from the superior septal aspect, but can also originate from the left ventricular outflow tract (LVOT) and the coronary cusps.1 The QRS electrocardiogram (ECG) characteristics have been helpful in patients with VAs, patient with accessory pathways and patients who have pacemakers.2 VAs originating from the RVOT have typical ECG findings with a left bundle branch block (LBBB) morphology and an inferior axis.3In the current issue of the Journal of Cardiovascular Electrophysiology, Hisazaki et al. describe five patients with idiopathic VA suggestive of RVOT origin and who required ablation in the left-sided outflow tract (OT) in addition to the initial ablation in the RVOT for cure to be achieved. Patients exhibited monomorphic, LBBB QRS pattern with an inferior axis on ECG, consistent with the morphology of VAs originating from the RVOT. Interestingly, all patients had a common distinct ECG pattern: qs or rs (r ≤ 5 mm) pattern in lead I, Q wave ratio[aVL/aVR]>1, and dominant S-waves in leads V1 and V2. Mapping of the right ventricle demonstrated early local activation time during the VA in the posterior portion of the RVOT, matching the QRS morphology obtained during pacemapping. Despite RF energy delivery to the RV, the VAs recurred shortly after ablation in four patients and had no effect at all in one patient. A change in the QRS morphology was noted on the ECG that had never been observed before the procedure. The new patterns were suggestive of left-sided OT origin: the second VAs exhibited an increase in the Q wave ratio [aVL/aVR] and R wave amplitude in lead V1, decrease in the S wave amplitude in lead V1, and a counterclockwise rotation of the precordial R-wave transition. Early activation of the second VA could not be found in the RVOT, and the earliest activation time after mapping the LV was found to be relatively late. Real-time intracardiac echocardiography and 3D mapping systems were used to determine the location immediately contralateral to the initial ablation site in the RVOT. Energy was then delivered to that site which successfully eliminated the second VA. The authors postulated that the second VAs shared the same origins as the first VAs, and the change in QRS morphology is likely attributed to a change in the exit point or in the pathway from the origin to the exit point. The authors further explained that the VAs originated from an intramural area of the superior basal LV surrounded by the RVOT, LVOT and the transitional zone from the great cardiac vein to the anterior interventricular vein (GCV-AIV).A limitation of this study is that GCV-AIV ablation was not attempted; however, the authors’ approach is safer and was successful in eliminating VA. Another limitation is that left-sided OT mapping was not initially performed. Nevertheless, given the ECG characteristics, local activation time, and mapping, it was appropriate to attempt a RVOT site ablation.Overall, the authors should be commended for their effort to describe in detail patients with idiopathic VAs that required ablation in the left-sided OT following ablation in the RVOT. Although change in QRS morphology after ablation has been previously described, the authors were the first to describe the ECG patterns of these patients.4–7 The results of this study have important clinical implications. First, the authors have demonstrated the importance of anatomical approach from the left-sided OT for cure to be achieved. Second, insight into the location of the origin of the VA may be helpful to physicians managing patients with VAs from the RVOT. Finally, continuous monitoring of the ECG during ablation for a change in QRS morphology should be considered to identify patients who will require further ablation. We have summarized in Table 1 important ECG characteristics indicative VA of specific origins, based on the findings of this study and previous studies in the literature.3,8–15

Pulmonary Vein Isolation (PVI) remains the cornerstone for catheter ablation for atrial fibrillation (AF). Achieving durable PVI safely with Radiofrequency Catheter Ablation (RFCA) has proven challenging until recently, even with the use of Contact Force (CF) sensing catheters and electroanatomical mapping1. Ablation success rates improve markedly, including in persistent AF, when permanent PVI can be achieved1,2, which only underscores the critical role of the Pulmonary Veins (PV) in AF arrhythmogenesis.Historically, the only way to assess PVI durability has been through invasive electrophysiology study, with all its associated risk, inconvenience, and costs. This price appears particularly galling to pay if the PVs are found to be isolated at repeat study, as is now becoming increasingly common3. Multiple randomised studies have failed to show additional benefit from ablating extra-PV structures4,5, and the best outcomes following repeat AF ablation procedures are restricted to those where PV reconnection is identified and treated6. As such, there remains a pressing need for a non-invasive tool that can accurately assess PVI durability, and ideally, the size and location of residual gaps. As Magnetic Resonance Imaging (MRI) has increasingly been shown capable of delineating atrial scar, there is much anticipation that it may serve this important purpose7.RFCA and Cryoballoon ablation (CBA) are by far the most common modalities used for PVI, and there is remarkable equivalence in their clinical results8. However, the handling of the two technologies in the catheter laboratory is very different, and ultrahigh density mapping has shown important differences in the number and location of chronic gaps between the two9. The use of MRI in characterizing these differences has not been well described so far.In this issue of the journal, Kurose and colleagues present a small but elegant study10, in which 30 consecutive patients who underwent PVI (18 with CBA, 12 with RFCA) were assessed by LGE-MRI two months later, where lesion width and visual gap(s) around each vein were assessed. The RF applications were delivered using a CF sensing catheter, with a target lesion size index (LSI) of 5, and an inter-lesion distance of <6mm. They found that the mean lesion width on MRI was significantly wider in the CBA group (8.1±2.2 mm) as compared to the RFCA group (6.3±2.2 mm), p=0.032. However, there were more visual gaps seen in the CBA group, especially in the bottom segments of the two inferior veins. In the RFCA group, gaps were seen most often seen in the left posterior segments where the target LSI value could not be achieved because of esopheageal temperature rise. Furthermore, the number of gaps visualised on MRI was linked to freedom from AF at 12 months; receiver operating characteristic curve analysis suggested a cut off value of less than 5 visual gaps per patient as being predictive of a good outcome.The authors deserve to be congratulated for their study, which builds on their previous work where LGE-MRI was used to compare chronic lesions between CBA and RFCA with non-CF sensing catheters11. It is notable that whilst the lesion width in their previous study was also significantly greater in the CBA group than the RFCA group, the mean number of gaps in the RFCA group was higher. This suggests that the modern technique of delivering LSI-guided contiguous RFCA lesions has resulted in a material improvement in PVI durability, something that is borne out in clinical studies too3.Some limitations of the work should be mentioned. Patients were not randomised to RFCA or CBA; rather, patients undergoing CBA were pre-selected with those with left common PV or large PVs excluded. The ablation technique used for CBA was unusual in that the use of RFCA was allowed if PVI could not be achieved after a single 3-minute freeze. This low bar for defining CBA failure led to as many as 3 patients out of 25 being excluded from the study. Many readers will feel that the mean procedural times of 129 minutes and fluoroscopy times of 39 minutes for CBA are much longer than what is the norm today. They may also find the RF powers used in this study unusual; only 30W was used on the anterior wall, and 20-25W on the posterior wall, which was reduced even further if esophageal temperature rise was observed. The field is moving towards using higher power short duration (HPSD) RF applications, and as HPSD lesions have been shown to be wider12, it is possible that the gaps on the posterior wall identified in this study may not have been present had HPSD applications been used. Finally, the definition of visual gap on MRI used in this study, a non-LGE site larger than 4 mm, almost certainly overestimated the number of true gaps. For instance, the authors observed at least one visual gap in each of the 16 segments around the PVs in more than 10% CB patients; this is at odds with data obtained with ultrahigh density mapping9, and also with the good clinical outcomes reported here. Future research should look at correlating these MRI-visualised gaps with actual gaps seen on repeat electrophysiological study, so that the clinical significance of these can be better defined.What can we take away from this study? Firstly, the use of MRI to assess post-ablation scar is now a reality in many labs, allowing assessment of PVI durability to help decide whether or not to offer a repeat procedure to a patient with AF recurrence. Secondly, the evolution of the RFCA technique to include target lesion indices and inter-lesion distance has made RFCA at least as effective as CBA in achieving durable PVI. Finally, this is an area ripe for further research, and we look forward to similarly valuable contributions from Kurose and colleagues in the future.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and often occurs with heart failure (HF) [1]. AF prevalence increases with increasing severity of HF: for instance its prevalence ranges from 5 percent in patients with New York Heart Association (NYHA) functional class I HF to 40 percent in patients with NYHA class IV HF [2]. Its presence with HF plays a significant prognostic role and increases morbidity and mortality. Heart Failure with reduced ejection fraction (HFrEF) is associated with cardiac arrhythmias [3]. HFrEF is also one of the indications for Cardiac resynchronization therapy (CRT) placement [4]. Therefore, many patients undergoing CRT implantation will concomitantly have HF and AF. As the benefit from CRT in HF patients has been established, the data on patients with both HF and AF is limited, because patients with atrial arrhythmias were excluded from most of the major CRT trials, such as CARE-HF and COMPANION [5]. However, a number of observational studies and small randomized clinical trials suggest a benefit from CRT in AF and HF patients such as a CRT-mediated ejection fraction (EF) increase [6, 7]. Other studies showed a high non-response rate in patients with AF as compared to those in sinus rhythm (SR) [8]. Thus, it is important to determine whether CRT has a beneficial role in these patients to decide on adding an atrial lead at the time of CRT implantation especially in patients with longstanding-persistent AF.In their published study, Ziegelhoeffer et al. investigated the outcomes of CRT placement with an atrial lead in patients with HF and AF. This was done by conducting a retrospective analysis of all patients with AF who received CRT for HF at the Kerckhoff Heart Center since June 2004 and were observed until July 2018- completing a 5-year follow-up. The authors identified 328 patients and divided them into 3 subgroups: paroxysmal (px) AF, persistent (ps) AF, and longstanding-persistent (lp) AF, with all patients receiving the same standard operative management. During the observation period, the authors analyzed the rhythm course of the patients, cardiac parameters (NYHA class, MR, LVEF, left atrial diameter) and performed a subgroup analysis for patients who received an atrial lead. The study showed that all groups had a high rate of sinus rate (SR) conversion and rhythm maintenance at 1 and 5 years. Specifically, the patients who received an atrial lead among the lp AF group were shown to have a stable EF, less pronounced  left ventricular end-systolic diameter (LVESD) and  left ventricular end diastolic diameter (LVEDD) and lower mitral regurgitation (MR) rates at one year follow-up as compared to the group without atrial lead placement. Moreover, the results of the lp group were similar to the ps-AF group, although the latter had a lower number of participants (n=4) without initial implantation of the atrial lead. The authors attributed the improvement in cardiac function and SR conversion to CRT and the implantation of an additional atrial lead.Although some studies showed that CRT therapy reduced secondary MR in HF [9, 10], this study additionally suggests that CRT with an atrial lead was associated with improved myocardial function and improvement of interventricular conduction delay triggering cardiac remodeling in patients with HF and AF. Although the results showed better cardiac function in the subgroup analysis of the patients with an additional atrial lead, these results were reported as percentages with no level of significance specified, hence statistical significance of the difference in the described parameters (such as LVESD, LVEDD) could not be determined. Further investigation via prospective studies is needed with larger sample size in the future to further support the results of the study especially that it was done in a single center and had a relatively small sample size.References:1. Chung MK, Refaat M, Shen WK, et al. Atrial Fibrillation: JACC Council Perspectives. J Am Coll Cardiol. Apr 2020; 75 (14): 1689-1713.2. Maisel, W.H. and L.W. Stevenson, Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy. Am J Cardiol, 2003. 91 (6a): p. 2d-8d.3. AlJaroudi WA, Refaat MM, Habib RH, et al. Effect of Angiotensin Converting Enzyme Inhibitors and Receptor Blockers on Appropriate Implantable Cardiac Defibrillator Shock: Insights from the GRADE Multicenter Registry. Am J Cardiol Apr 2015; 115 (7): 115(7):924-31.4. Yancy, C.W., et al., 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol, 2013. 62 (16): p. e147-239.5. Cleland, J.G., et al., The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J Med, 2005.352 (15): p. 1539-49.6. Leclercq, C., et al., Comparative effects of permanent biventricular and right-univentricular pacing in heart failure patients with chronic atrial fibrillation. Eur Heart J, 2002. 23 (22): p. 1780-7.7. Upadhyay, G.A., et al., Cardiac resynchronization in patients with atrial fibrillation: a meta-analysis of prospective cohort studies. J Am Coll Cardiol, 2008. 52 (15): p. 1239-46.8. Wilton, S.B., et al., Outcomes of cardiac resynchronization therapy in patients with versus those without atrial fibrillation: a systematic review and meta-analysis. Heart Rhythm, 2011. 8 (7): p. 1088-94.9. van Bommel, R.J., et al., Cardiac resynchronization therapy as a therapeutic option in patients with moderate-severe functional mitral regurgitation and high operative risk. Circulation, 2011.124 (8): p. 912-9.10. Breithardt, O.A., et al., Acute effects of cardiac resynchronization therapy on functional mitral regurgitation in advanced systolic heart failure. J Am Coll Cardiol, 2003. 41 (5): p. 765-70.

A document by Youssef Jalloul. Click on the document to view its contents.

Cardiac pacing is the only effective therapy for patients with symptomatic brady-arrhythmia. Traditional right ventricular apical pacing causes electrical and mechanical dyssynchrony resulting in left ventricular dysfunction, recurrent heart failure and atrial arrhythmias. Physiological pacing activates the normal cardiac conduction thereby providing synchronized contraction of ventricles. Though His bundle pacing (HBP) acts as an ideal physiological pacing modality, it is technically challenging and associated with troubleshooting issues during follow up. Left bundle branch pacing (LBBP) has been suggested as an effective alternative to overcome the limitations of HBP as it provides low and stable pacing threshold, lead stability and correction of distal conduction system disease. This paper will focus on the implantation technique, troubleshooting, clinical implications and a review of published literature of LBBP

A 53- year old woman presented with recurrent episodes of paroxysmal tachycardia with a structurally normal heart. She had undergone an electrophysiology study in an outside hospital which revealed orthodromic atrioventricular reentrant tachycardia (ORT) using a concealed left posterolateral accessory pathway (AP), for which radiofrequency ablation was performed. But tachycardia recurred three months later. In view of significant symptoms, she came to us for a repeat procedure. The AH and HV intervals were 77 ms and 45 ms respectively. Narrow complex tachycardia with a cycle length (CL) of 300 ms was easily and repeatedly induced and terminated (Figure 1, left panel) by a premature ventricular complex (PVC). Shortly another tachycardia with CL of 255 ms was induced and terminated (Figure 1, right panel) by a premature ventricular complex. Later, during another tachycardia, a spontaneous change was seen (Figure 2). Are we dealing with a single tachycardia mechanism?

The field of electrophysiology continues to move further towards low fluoroscopy procedures. The deleterious effects of radiation exposure and of the radiation protection clothing themselves are the primary drivers of this approach. Radiation exposure is known to increase the risk of cancer and cataracts for all operators, and namely those who are subjected to accumulating doses of radiation over time. (1). Proper radiation protective clothing can significantly decrease these risks however this strategy has serious weaknesses. For instance, the protective clothing does not cover the whole body, leaving the face and the skull exposed. Roguin et al (2) showed that the risk of radiation exposure to the unprotected areas of the body is real and has serious consequences. In a cohort of 31 interventional cardiologists who developed brain cancer, the investigators showed that 22 (85%) of them had left sided tumors, and 17 (55%) of them had glioblastoma multiforme. This remarkable finding suggests that the dose left side of the brain, the side that gets more radiation exposure, is much more likely to develop a cancer that carries a poor prognosis and a median expected survival of 12 months. Furthermore, the radiation protective clothing itself can cause orthopedics injuries common among interventional cardiologists such those of the spine and the knees. Given the deleterious effects of radiation, low fluoroscopy approaches are welcomed by the electrophysiology community if they can show a safety profile similar to that with the use of fluoroscopy.The transseptal puncture (TSP) is arguably the most critical step during which fluoroscopy is used. In this study Singh et al describe an approach for TSP under electoanatomic guidance. The authors then retrospectively compare the total procedure duration, fluoroscopy time, radiation exposures, and complications related to the TSP using this method with those of conventional fluoroscopy. This was a single center study that included 145 consecutive patients, with no previous history of cardiac surgery, who underwent de novo and redo AF ablations between June 2018 and April 2019. These patients were then compared to cases performed by the same operators before June 2018. The procedure was done under conscious sedation. A dense electroanatomic map of the right atrium was acquired using CARTO 3 Fast Anatomical Mapping and Confidence Software, with emphasis on the atrial septum, His Bundle, coronary sinus ostium, and superior vena cava. The authors observed that the fossa ovalis was an area of low voltage potential (0.37±0.19 mV vs 1.73±0.74 mV) and low impedance (125±11 Ω vs 138±15 Ω), and electrically distinct from the rest of the atrial septum. The authors were able to localize the fossa ovalis using a combination of anatomical landmarks and the use of a voltage threshold of 0.75mV. The transseptal needle was then advanced through this desired location. The authors reported no significant complications related to the TSP.The authors argue that the safety profile is like the TSP under fluoroscopy, however this is a single center study. In fact the most senior operator performed three- quarters of all the procedures. Given the high risk of such an approach, the main question for the wide adoption of such a technique will again be safety in the hands of less experienced operators. A major factor that can increase the safety profile as well as the preciseness of the TSP is the routine use of ICE. ICE can confirm the precise positioning of the needle even in cases with unusual atrial septal anatomies (floppy, bulging, hypertrophic septum or in the presence of devices such as CardioSEAL or other atrial septal defect occlusion devices). Furthermore, ICE can confirm the location of the needle in the LA with microbubble injections after the TSP; it can confirm the location of the wire thus making it safer to advance the sheath knowing that it will not end up in the LAA or causing a perforation. As such ICE is arguably more important in the low fluoroscopy approach than in a one with fluoroscopy.Low fluoroscopy approach to TSP is a welcomed change in the field of electrophysiology given the significant adverse outcomes of radiation and radiation protective clothing to providers. The main concern in such a change is the safety and precise localization of the TSP. New technologies are allowing the development of new approaches such as the one described by Troisi et al to achieve the goal of safe low fluoroscopy procedures.References:Klein LW, Miller DL, Balter S, et al. Occupational health hazards in the interventional laboratory: time for a safer environment. Radiology 2009; 250:538-544.Roguin A, Goldstein J, Bar O, Goldstein JA. Brain and neck tumors among physicians performing interventional procedures. Am J Cardiol 2013;111(9):1368-72.

Long QT syndrome (LQTS) is characterized by prolongation of the QT interval on the electrocardiogram (ECG). Clinically, LQTS is associated with the development of Torsades de Pointes (TdP), a well-defined polymorphic ventricular tachycardia and the development of sudden cardiac death (1). The most common type is the acquired form caused mainly by drugs, it is also known as the drug induced LQTS (diLQTS) (2-5). The diLQTS is caused by certain families of drugs which can markedly prolong the QT interval on the ECG most notably antiarrhythmic drugs (class IA, class III), anti-histamines, antipsychotics, antidepressants, antibiotics, antimalarial, and antifungals (2-5). Some of these agents including the antimalarial drug hydroxycholoquine and the antibiotic azithromycin which are being used in some countries as therapies for the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)(6,7). However, these drugs have been implicated in causing prolongation of the QT interval on the ECG (2-5).There is a solution for monitoring this large number of patients which consists of using mobile ECG devices instead of using the standard 12-lead ECG owing to the difficulty of using the 12-lead ECG due to its medical cost and increased risk of transmitting infection. These mobile ECG devices have been shown to be effective in interpreting the QT interval in patients who are using QT interval prolonging drugs (8, 9). However, the ECG mobile devices have been associated with decreased accuracy to interpret the QT interval at high heart rates (9). On the other hand, some of them have been linked with no accuracy to interpret the QT interval (10). This can put some patients at risk of TdP and sudden cardiac death.In this current issue of the Journal of Cardiovascular electrophysiology, Krisai P et al. reported that the limb leads underestimated the occurrence of diLQTS and subsequent TdP compared to the chest leads in the ECG device, this occurred in particular with the usage of mobile standard ECG devices which use limb leads only. To illuminate these findings, the authors have studied the ECGs of 84 patients who have met the requirements for this study, which are diLQTS and subsequent TdP. Furthermore, the patients in this study were also taking a QT interval prolonging drug. Krisai P et al. additionally reported the morphology of the T-wave in every ECG and classified them into flat, broad, notched, late peaked, biphasic and inverted. The authors showed that in 11.9% of these patients the ECG was non reliable in diagnosing diLQTS and subsequent Tdp using only limb leads due to T-wave flattening in these leads, in contrast to chest leads where the non- interpretability of the QT interval was never attributable to the T-wave morphology but to other causes. The authors further examined the QT interval duration in limb leads and chest leads and found that the QT interval in limb leads was shorter compared to that of the chest leads, but reported a high variability in these differences. Therefore, it should be taken into account when screening patients with diLQTS using only mobile ECG devices and these patients should be screened using both limb leads and chest leads. Moreover, the authors have highlighted the limitations of using ECG mobile devices as limb leads to interpret the QT interval especially in high heart rates (when Bazett’s equation overcorrects the QTc and overestimates the prevalence of the QT interval) and have advocated the usage of ECG mobile devices as chest leads instead of limb leads due to their superior ability to interpret the QT interval.The authors should be praised for their efforts in illustrating the difference in the QT interval interpretability between the chest leads and the limb leads in patients with diLQTS. The authors also pointed out the limitation of using mobile ECG devices as limb leads for the diagnosis of diLQTS and recommended their usage as chest leads by applying their leads onto the chest due to their better diagnostic accuracy for detecting the diLQTS. The study results are very relevant, it further expanded the contemporary knowledge about the limitation of the QT interval interpretability using ECG mobile device only (11). Future investigation is needed to elucidate the difference in chest and limb leads interpretability of the QT interval and to assess the ability of the mobile ECG devices to interpret the QT interval.ReferencesRefaat MM, Hotait M, Tseng ZH: Utility of the Exercise Electrocardiogram Testing in Sudden Cardiac Death Risk Stratification. Ann Noninvasive Electrocardiol 2014; 19(4): 311-318.Kannankeril P, Roden D, Darbar D. Drug-Induced Long QT Syndrome. Pharmacological Reviews. 2010;62(4):760-781.Nachimuthu S, Assar M, Schussler J. Drug-induced QT interval prolongation: mechanisms and clinical management. Therapeutic Advances in Drug Safety. 2012;3(5):241-253.Jankelson L, Karam G, Becker M, Chinitz L, Tsai M. QT prolongation, torsades de pointes, and sudden death with short courses of chloroquine or hydroxychloroquine as used in COVID-19: A systematic review. Heart Rhythm. 2020 ; S1547-5271(20)30431-8.Li M, Ramos LG. Drug-Induced QT Prolongation And Torsades de Pointes. P T . 2017;42(7):473-477.Singh A, Singh A, Shaikh A, Singh R, Misra A. Chloroquine and hydroxychloroquine in the treatment of COVID-19 with or without diabetes: A systematic search and a narrative review with a special reference to India and other developing countries. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2020;14(3):241-246.Hashem A, Alghamdi B, Algaissi A, Alshehri F, Bukhari A, Alfaleh M et al. Therapeutic use of chloroquine and hydroxychloroquine in COVID-19 and other viral infections: A narrative review. Travel Medicine and Infectious Disease. 2020; 35:101735.Chung E, Guise K. QTC intervals can be assessed with the AliveCor heart monitor in patients on dofetilide for atrial fibrillation. J Electrocardiol. 2015;48(1):8-9.Garabelli P, Stavrakis S, Albert M et al. Comparison of QT Interval Readings in Normal Sinus Rhythm Between a Smartphone Heart Monitor and a 12-Lead ECG for Healthy Volunteers and Inpatients Receiving Sotalol or Dofetilide. Journal Cardiovasc Electrophysiol. 2016;27(7):827-832.Bekker C, Noordergraaf F, Teerenstra S, Pop G, Bemt B. Diagnostic accuracy of a single‐lead portable ECG device for measuring QTc prolongation. Annals Noninvasive Electrocardiol. 2019;25(1): e12683.Malone D, Gallo T, Beck J, Clark D. Feasibility of measuring QT intervals with a portable device. American Journal of Health-System Pharmacy. 2017;74(22):1850-1851.

Incisional atrial tachycardia (AT) with multiple penetrating points on one surgical incision has not been reported. We present a case of incisional AT following mitral annuloplasty with a superior transseptal approach, in which two reconduction sites were part of the reentrant circuit. Radiofrequency ablation at the reconduction site successfully terminated the tachycardia. A total of four penetrating points were found on the incision line, and radiofrequency ablation at these sites was completed. Detailed mapping with consideration of possible reconduction sites along the incision line should be performed to avoid further instances of AT following open heart surgery.

Background Atrial tachyarrhythmias (ATAs) are common within the three-month blanking period following catheter ablation of atrial fibrillation (AF). However, little evidence is available regarding the current guidelines on the blanking period after surgical AF ablation. We investigate the incidence and significance of early recurrence of atrial tachyarrhythmia (ERAT) and evaluate the optimal blanking period after surgical AF ablation. Methods Data from 259 patients who underwent surgical AF ablation from 2009 to 2016 were collected. ERAT was defined as documented ATA episodes lasting for 30 seconds. A multivariate Cox proportional hazard model was constructed to evaluate the role of ERAT as a predictor of late recurrences (LR) for AF. Results In total, 127 patients (49.0%) experienced their last episodes of ERAT during the first (n=65), second (n=14), or third (n=48) month of the three-month blanking period (p<0.001). One-year freedom from ATAs was 97.8% in patients without ERAT compared with 95.4%, 64.3%, and 8.3% in patients with ERAT in the first, second, and third month after the index procedure, respectively (p<0.001). Hazard ratios of LR according to the timing of the last episode of ERAT first, second, and third month after the procedure were 2.84, 16.70, and 119.75, respectively. Conclusions The ERAT occurred in 49.0% of patients within the first three months after surgical ablation. The occurrence of ERAT within three months after surgical AF ablation was a significant independent predictor of LR. Hence, the currently accepted three-month blanking period needs to be redefined in patients with AF surgical ablation.

Introduction：LAmbre occluder (Lifetech Scientific, Shenzhen, China), a new device for left atrial appendage (LAA) occlusion, is increasingly used, but the procedure for retrieval after dislodgement has rarely reported in human. Methods and Results：An 80-year-old male patient with permanent atrial fibrillation underwent the implantation of LAA occlusion device. The occluder dislodged to left atrium (LA) at the end of procedure. We failed to retrieve device in LA with a LASSO catheter and forceps with the 8.5F sheath. After it suddenly flowing into aortic arch, we successfully retrieved with a 14F flexible sheath and forceps. We also discussed reasons for the device dislodgment and reported experiences for device retrieval. Conclusion: Combination of the 14F flexible sheath and forceps could be used to retrieve the dislocation of LAA occlusion device.

We present a case report of severed epicardial atrial lead salvage using an IS-1 lead extender. A 37-year-old male with single ventricle physiology, Fontan palliation, sinus node dysfunction, recurrent atrial tachycardias and atrial fibrillation resulting in failing Fontan physiology presented with failure of the atrial pacing lead. The patient was initially paced with an epicardial system that had to be removed due to pocket infection, and the epicardial leads were cut and abandoned. Given his significant sinus node dysfunction he required atrial pacing to allow for rhythm control. The failing Fontan physiology of the patient precluded him from undergoing surgery for epicardial lead placement or a complex intravascular lead placement procedure (although anatomically feasible). We considered the option of salvaging the existing epicardial atrial leads to provide atrial pacing, allowing for rhythm control and improvement of his failing Fontan physiology as a bridge to a more permanent pacing solution. This case report is important because it demonstrates how a lead extender can be used to salvage a severed pacemaker lead. This may be useful for patients in whom implantation of new leads is not promptly feasible due to patient anatomy and/or clinical status.