Mohamad El Moheb

and 1 more

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

Mohammad Ramadan

and 1 more

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.

Bachir Lakkis

and 1 more

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.

Rand Ibrahim

and 1 more

Sudden Cardiac Death (SCD) remains a global threat.1The most common causes of SCD are ischemic heart diseases and structural cardiomyopathies in the elderly. Additional causes can be arrhythmogenic, respiratory, metabolic, or even toxigenic.2,3,4 Despite the novel diagnostic tools and our deeper understanding of pathologies and genetic associations, there remains a subset of patients for whom a trigger is not identifiable. When associated with a pattern of Ventricular Fibrillation, the diagnosis of exclusion is deemed Idiopathic Ventricular Fibrillation (IVF).2,5 IVF accounts for 5% of all SCDs6 – and up to 23% in the young male subgroup5 – and has a high range of recurrence rates (11-45%).7,8,9 There are still knowledge gaps in the initial assessment, follow-up approach, risk stratification and subsequent management for IVF.1,10,11 While subsets of IVF presentations have been better characterized into channelopathies, such as Brugada’s syndrome (BrS), Long QT Syndrome (LQTS), Early Repolarization Syndrome (ERS), Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), much remains to be discovered.12,13 Implantable Cardioverter Device (ICD) placement as secondary prevention for IVF is the standard of care. This is warranted in the setting of high recurrence rates of arrhythmias (11-43%). Multiple studies have shown potential complications from ICDs and a significant number of cases experiencing inappropriate shock after ICD placement.14In their article, Stampe et al. aim to further understand clinical presentation and assessment, and risk factors for recurrent ventricular arrhythmias in IVF patients. Using a single-centered retrospective study, they followed a total of 84 Danish patients who were initially diagnosed with IVF and received a secondary ICD placement between December 2007 and June 2019. Median follow-up time was 5.2 years (ICR=2-7.6). To ensure detection of many possible underlying etiologies ranging from structural, ischemic, arrhythmogenic, metabolic, or toxicologic, the researchers found that a wide array of diagnostic tools were necessary: standard electrocardiograms (ECGs), high-precordial leads ECGs, standing ECGs, Holter monitoring, sodium-channel blocker provocation tests, exercise stress tests, echocardiograms, cardiac magnetic resonance imaging, coronary angiograms, cardiac computed tomography, electrophysiological studies, histological assessment, blood tests, toxicology screens, and genetic analysis.The study by Stampe et al. highlights the importance of thorough and continuous follow-up with rigorous evaluation: Three (3.6%) patients initially diagnosed with IVF were later found to have underlying cardiac abnormalities (LQTS and Dilated Cardiomyopathy) that explained their SCA. Like other studies, the burden of arrhythmia was found to be high, but unlike reported data, the overall prognosis of IVF was good. Despite the initial pattern of ventricular fibrillation in those who experienced appropriate ICD placement (29.6%), ventricular tachycardia and ventricular fibrillation had a comparable predominance. As for patients with inappropriate ICD placements, atrial fibrillation was a commonly identified pathological rhythm (16.7%). Recurrent cardiac arrest at presentation (19.8%) was a risk factor for appropriate ICD therapy (HR=2.63, CI=1.08-6.40, p=0.033). However, in contrast to previous studies, early repolarization detected on baseline ECG (12.5%), was not found to be a risk factor (p=0.842).The study by Stampe et al. has few limitations. First, the study design, a retrospective cohort, precluded standardized follow-up frequencies and diagnostic testing. Second, while the study was included many of the cofounders tested in previous studies (baseline characteristics, baseline ECG patterns, comorbidities), medication use was not included. Third, the follow-up period may have been insufficient to detect effect from some of the confounding factors. Finally, the sample size was small and it was from a single center.There are several strengths of the Stampe et al. study. Firstly, the wide range of diagnostic tests used at index presentation and during the follow-up period ensured meticulous detection of most underlying etiologies. Secondly, appropriate and well-defined inclusion and exclusion criteria were used. Thirdly, funding by independent parties ensured no influence on study design, result evaluation, and interpretation. Finally, the study has succeeded in improving our understanding of IVF. Future studies should include though a larger population size and a more diverse population.References:1.AlJaroudi WA, Refaat MM, Habib RH, Al-Shaar L, Singh M, 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):924-31.2. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS guideline for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: executive summary. J Am Coll Cardiol 2018;72:e91–e220.3. Refaat MM, Hotait M, London B: Genetics of Sudden Cardiac Death. Curr Cardiol Rep Jul 2015; 17(7): 6064. Priori SG, Wilde AA, Horie M, Cho Y, Behr ER, Berul C, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA, and APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm 2013;10:1932–1963.5. Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Endorsed by: Association for European Paediatric and Congenital Cardiology (AEPC). Eur Heart J 2015;36(41):2793-2867.6. Zipes DP, Wellens HJ. Sudden cardiac death. Circulation. 1998;98:2334–2351.7. Ozaydin M, Moazzami K, Kalantarian S, Lee H, Mansour M, Ruskin JN. Long-term outcome of patients with idiopathic ventricular fibrillation: a meta-analysis. J Cardiovasc Electrophysiol 2015;26:1095–1104.8. Herman AR, Cheung C, Gerull B, Simpson CS, Birnie DH, Klein GJ, et al. Outcome of apparently unexplained cardiac arrest: results from investigation and follow-up of the prospective cardiac arrest survivors with preserved ejection fraction registry. Circ Arrhythm Electrophysiol 2016;9:e003619.9. Siebermair J, Sinner MF, Beckmann BM, Laubender RP, Martens E, Sattler S, et al.Early repolarization pattern is the strongest predictor of arrhythmia recurrence in patients with idiopathic ventricular fibrillation: results from a single centre long-term follow-up over 20 years. Europace 2016;18:718-25.10. Refaat MM, Hotait M, Tseng ZH: Utility of the Exercise Electrocardiogram Testing in Sudden Cardiac Death Risk Stratification. Ann Noninvasive Electrocardiol 2014; 19(4): 311-318.11. Gray B, Ackerman MJ, Semsarian C, Behr ER. Evaluation after sudden death in the young: a global approach. Circ Arrhythm Electrophysiol 2019;12: e007453.12. Herman AR, Cheung C, Gerull B, Simpson CS, Birnie DH, Klein GJ, et al. Response to Letter Regarding Article, Outcome of apparently unexplained cardiac arrest: results from investigation and follow-up of the prospective cardiac arrest survivors with preserved ejection fraction registry”. Circ Arrhythm Electrophysiol 2016;9:e004012.13. Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, Potenza D, et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998;392:293–296.14. Baranchuk A, Refaat M, Patton KK, Chung M, Krishnan K, et al. What Should You Know About Cybersecurity For Cardiac Implantable Electronic Devices? ACC EP Council Perspective. J Am Coll Cardiol Mar 2018; 71(11):1284-1288.

Ahmed Eltarras

and 7 more

Introduction: In-hospital cardiac arrest(IHCA) constitutes a significant cause of morbidity and mortality. we devised this study to shed some light on it to better inform both hospitals and policymakers. Methods: We analyzed retrospective data from 680 IHCAs at the American University of Beirut Medical Center between July 1st, 2016, and May 2nd, 2019. Sociodemographic variables included age, sex, and comorbidities in the Charlson Comorbidity Index(CCI). IHCA variables were the day of the week, time from activation to arrival, event location, initial cardiac rhythm, the total number of IHCA events, and the months and years of the IHCAs. We considered the return of spontaneous circulation(ROSC) and survival to discharge(StD) to be our outcomes of interest. Results: The incidence of IHCA was 6.58 per 1000 hospital admissions. Non-shockable rhythms were 90.7% of IHCAs. Most IHCAs occurred in the Closed care units(87.9%) and on weekdays(76.5%). ROSC followed 56% of the IHCAs. Only 5.4% achieved StD. Survival outcomes were not significantly different between the time of the day and were higher in cases with a shockable rhythm. ROSC wasn’t significantly different between weekdays and weekends. however, StD was higher on weekdays. A high CCI was associated with decreased StD. Conclusion: The incidence of IHCA was high, and its outcomes were lower compared to other developed countries. Survival outcomes were better for patients who had a shockable rhythm and were similar between the time of the day. These findings may help inform hospitals and policymakers about the magnitude and quality of IHCA care in Lebanon

Khaled Sabeh

and 1 more

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.

Farah Abdulhai

and 1 more

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

Khaled Sabeh

and 1 more

Are all Non-sustained Ventricular Tachycardia the Same in Hypertrophic Cardiomyopathy Risk Stratification for Sudden Cardiac Death?Mohamad Khaled Sabeh MD1, Marwan M. Refaat MD21Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, Massachusetts - USA2Division of Cardiology, Department of Internal Medicine, American University of Beirut Medical Center Beirut, LebanonRunning Title: NSVT in HCM SCD Risk StratificationWords (excluding references): 664Disclosures: NoneFunding: NoneKeywords: Hypertrophic Cardiomyopathy, Non-sustained Ventricular Tachycardia, Cardiac Arrhythmias, Cardiovascular DiseasesCorrespondence:Marwan M. Refaat, MD, FACC, FAHA, FHRS, FASE, FESC, FACP, FRCPAssociate Professor of MedicineDirector, Cardiovascular Fellowship ProgramDepartment of Internal Medicine, Cardiovascular Medicine/Cardiac ElectrophysiologyDepartment of Biochemistry and Molecular GeneticsAmerican University of Beirut Faculty of Medicine and Medical CenterPO Box 11-0236, Riad El-Solh 1107 2020- Beirut, LebanonFax: +961-1-370814Clinic: +961-1-350000/+961-1-374374 Extension 5800Office: +961-1-350000/+961-1-374374 Extension 5353 or Extension 5366 (Direct)Email: mr48@aub.edu.lbCardiomyopathies with reduced systolic function predispose to sudden cardiac death (SCD) and many studies helped in decreasing that risk by Implantable Cardioverter Defibrillator (ICD) implantation and pharmacologic management (1-4). Many types of cardiomyopathies with preserved systolic function, including hypertrophic cardiomyopathy (HCM), can predispose to malignant ventricular arrhythmias and SCD. HCM is the most common inherited cardiac disease that affects 1 in 200 live births (5,6). SCD remains one of the main causes of death in HCM and the SCD rate peaks in early adulthood (7-14). Data from ICDs suggest that SCD in HCM is most commonly caused by ventricular fibrillation (VF) (15). One major clinical challenge is identifying patients at risk for SCD. Multiple studies showed that non-sustained ventricular tachycardia (NSVT) is a risk actor for SCD (16,17). However the strength of the data was variable across these studies due to difference in populations and the low sensitivity of Holter ECG. Moreover, other studies looked at the rate and duration of the ventricular arrhythmias and their relationship to SCD in HCM (17-19) yet the effect of the morphology of NSVT on SCD has not been well investigated.In this single center study Adduci et al . explore the prognostic impact of different NSVT morphologies in a cohort of 109 consecutive HCM patients. The study included patients who had an ICD implanted in the authors’ institution from January 2001 to December 2018. The ICDs were mostly implanted for primary prevention in HCM patient with 1) one or more risk factor including maximal LV thickness ≥30 mm, family history of SD in at least 1 first-degree relative <50 years of age, non-sustained ventricular tachycardia (NSVT), recent (≤ 6 months) unexplained syncope, 2) hypotensive blood pressure during exercise with at least one additional major risk factor for SD 3) end-stage HCM regardless of other established risk markers of SCD. Devices were interrogated on evaluation every 3 to 6 months and the data was assessed for appropriate or inappropriate ICD therapies. Two independent electrophysiologists analyzed the ICD near field and far field EGMs from the ventricular tachycardia runs. They classified the VTs as either monomorphic (MMVT) or polymorphic (PMVT).During a mean follow up of 71+/- 48 months, 377 NSVT episodes of NSVT were retrieved from ICD memory in 46 patients; of these episodes, 7(2%) were polymorphic and 370 (98%) were monomorphic (MM). The mean HR of The MM NSVT had an average HR of 171+/- 32 BPM and lasted for 17 +/- 12 beats while the PMVT were faster at 241BPM +/- and longer at 28+/- 16 beats. The appropriate intervention rate was 5.1% per year and interestingly NSVT did not predict the occurrence of ICD therapy. However patients with polymorphic NSVT had a statistically higher risk for ICD intervention as compared to monomorphic NSVT. Further analysis noted a trend for increased risk of ICD therapy with patients with >1 NSVT morphology. Moreover 75% of the treated VTs had been previously observed as NSVT.Risk stratification is very important in this young patient population; decreasing the risk threshold for ICD implants leads to missed arrhythmias and bad outcomes while increasing it increases the risk for complications from unnecessarily implanted devices. There are several types of ICDs: Transvenous ICD, Subcutaneous ICD and Extravascular ICD. The results of this study suggest that the risk of SCD in patients with PMVT and/or NSVT with multiple morphologies is different from that of patients with a MMVT, and that the presence of short MMVT doe not predict the future ICD therapies. As such, one may consider a conservative approach in low-risk patients with short bursts of slow MM NSVT, and a more aggressive approach in patients with frequent, rapid rate burst of PMVT. Although this study suggests that different NSVT morphologies affect the prognosis in HCM patients, the low number of events lacked the statistical power to redefine ICD candidacy. Larger multicenter studies are needed to confirm these findings and to help delineate the “at risk patients” who would truly benefit from ICDs.

Mohamad El Moheb

and 1 more

A Cardiac Sodium Channel Mutation Associated with Epinephrine-Induced Marked QT-ProlongationMohamad N. El Moheb MD1, Marwan M. Refaat MD21Division of Trauma Emergency Surgery and Surgical Critical Care, Massachusetts General Hospital, Boston, Massachusetts - USA2Division of Cardiology, Department of Internal Medicine, American University of Beirut Medical Center Beirut, LebanonRunning Title: SCN5A mutation associated with epinephrine-induced LQTSWords (excluding references): 746Disclosures: NoneFunding: NoneKeywords: Long QT Syndrome, Genetics, Variants, Cardiac Arrhythmias, Cardiovascular DiseasesCorrespondence:Marwan M. Refaat, MD, FACC, FAHA, FHRS, FASE, FESC, FACP, FRCPAssociate Professor of MedicineDirector, Cardiovascular Fellowship ProgramDepartment of Internal Medicine, Cardiovascular Medicine/Cardiac ElectrophysiologyDepartment of Biochemistry and Molecular GeneticsAmerican University of Beirut Faculty of Medicine and Medical CenterPO Box 11-0236, Riad El-Solh 1107 2020- Beirut, LebanonFax: +961-1-370814Clinic: +961-1-350000/+961-1-374374 Extension 5800Office: +961-1-350000/+961-1-374374 Extension 5353 or Extension 5366 (Direct)Email: mr48@aub.edu.lbThe hereditary long QT syndrome (LQTS) is an important cause of polymorphous ventricular tachycardia (torsades de pointes) and sudden cardiac death in otherwise young and healthy individuals. Clinically, this condition is caused by delayed ventricular repolarization and manifests as an abnormally prolonged QT interval on the electrocardiogram (ECG). The most common subtypes of LQTS are LQT1, LQT2, and LQT3 (1-10). The life-threatening arrhythmias occur most frequently during exercise in LQT1, upon auditory stimulation or emotional stress in LQT2, and at rest or during sleep in LQT3 (11). Patients with LQT1 have a mutation in the KCNQ1 gene which codes for the subunit of the slow outward potassium current channel (IKs) while patients with LQT3 have a mutation in the SCN5A gene, which codes for the cardiac voltage-dependent sodium channel (INa) (12). LQT1-affected individuals are more vulnerable to β-adrenergic modulation than LQT3-affected individuals. Exercise and epinephrine-infusion ECG tests are therefore useful in differentiating between the LQTS subtypes and optimizing therapeutic strategies in order to prevent sudden cardiac death. While beta-blockers have been established as the standard of care for the treatment of the LQT1 and LQT2 subtypes, their use in LQT3 remains controversial (13, 14). A new missense mutation has been recently identified in the SCN5A-encoding INA channels and was found to be associated with sinus node dysfunction and epinephrine-induced QT prolongation (1). This atypical phenotype of LQT3 has so far been observed in only one patient. Whether other mutations exist that can cause a similar manifestation has yet to determined.In the current issue of the Journal of Cardiovascular Electrophysiology, Nakajima et al. describe a family with LQT3 that exhibited epinephrine-induced marked QT prolongation. The SCN5A V1667I mutation was found to be responsible for this atypical phenotype which resulted in prolongation of the QT interval in the proband as well as in family members carrying the mutation. The SCN5A V1667I mutation is a gain of function mutation located in domain IV-segment 5 (DIV-S5) of the sodium channel encoding SCN5A gene. To elucidate the pathophysiology of the disease, the authors transfected a human kidney cell line (tsA-201) to induce expression of wild-type and mutated sodium channels and measured the membrane sodium currents (INA). They showed that SCN5A V1667I mutation was associated with larger INA peak density, depolarizing shift in steady-state inactivation (SSI) leading to increased window current, and accelerated recovery from depolarization. Additionally, an increased hump in the INA of V1667I mutant cells (V1667I-INA) was observed during a ramp pulse protocol consistent with increased window current. There was no difference in fast inactivation rate and steady-state activation between the V1667I-INA and wild-type INA(WT-INA). The authors further examined the effects of protein kinase A (PKA) activation on V1667I-INA to mimic the effect of epinephrine. PKA activation resulted in a less significant hyperpolarizing shift in SSI in V1667I-INA compared to WT-INA leading to increased window current. Additionally, V1667I mutation was found to be associated with accelerated recovery from depolarization, and increased hump during ramp pulse protocol in the setting of PKA activation. Chen et al. have also reported the case of an individual with a mutation in SCN5A who exhibited marked QT-prolongation after epinephrine infusion (1). However, contrary to the SCN5A V1667I mutation described by Nakajima et al, the SCN5A V2016M defect was a loss of function mutation causing a decrease in INA peak density. The clinical manifestations of the SCN5A mutations described by Chen et al. and Nakajima et al. are more comparable to individuals with the LQT1 subtype than those with the LQT3 subtype. Therefore, it should be considered whether certain patients with SCN5A would benefit from beta-blocker therapy.Overall, the authors should be commended on their efforts to describe for the first time a family with the SCN5A V1667I mutation and show that this mutation is associated with epinephrine-induced marked QT prolongation. The authors have also provided important insight into the electrophysiological properties of the mutant channels and the structure-function relationship of SCN5A. Further studies are needed to elucidate the precise molecular mechanisms of PKA activation on WT-INa and V1667I-INa. The results of this study have important clinical implications. The efficacy of beta-blockers for the treatment of LQTS has so far only been proven for the LQT1 and LQT2 subtypes, with conflicting results for the LQT3 subtype (13, 14). Given the marked QT prolongation in response to epinephrine infusion in carriers of the SCN5A V1667I mutation, certain LQT3 patients may benefit from beta-blocker therapy. Future studies should clarify whether beta-blockers are effective in these patients.

Youssef Jalloul

and 1 more

In 1999, Paul Myles et al. published an important paper outlining the details of a novel assessment tool to measure patients’ quality of recovery (QoR) post-anesthesia and surgery.[1] The following year, Paul Myles et al. published another article outlining the QoR-40. This study, as well as multiple other studies, further studied QoR-40’s validity, reliability, internal consistency, test-retest reliability, inter-rater reliability, and split-half coefficient.[1–3] It can be completed in a relatively short period (around five minutes).[3,4] However, its administration by the investigators provides more complete and timely data as compared to self-administration.[4] It has been translated into multiple languages and validated by these languages as well.[5] However, even though the QoR-40’s score has a maximum score of 200 with a range of 160, the minimal clinically important difference is only 4.8 units to translate into clinically relevant change. The difference between the mean QoR-40 scores post-cardiac surgery (with and without complications) was only four units while maintaining a wide standard deviation within groups.[5,6] QoR’s utility lies in its correlation with patient satisfaction as well as with another measure of patient well-being, the quality of life (QoL) score.[3] Furthermore, the QoR-40’s score three days post-cardiac surgery correlated well with the SF-36’s measure of QoL 3 months after the operation. Hence QoR-40 is helpful in assess patient’s short-term prognosis.[7] These findings hold even three years after the operation; however, the correlation level does decrease. [8]In this issue of the journal of cardiovascular electrophysiology, Wasserlauf et al. utilized the QoR-40 to measure the impact of the anesthesia used during cryoballoon ablation of paroxysmal atrial fibrillation.[9] Catheter ablation has become a common procedure for the management of paroxysmal atrial fibrillation with minor procedural complication. [10,11] Patients undergoing cryoballoon ablation for atrial fibrillation experience less pain than radiofrequency ablation. [12]Multiple sedative modalities can be utilized for cardiac catheter ablation. One modality is the use of a light anesthetic: It alerts the physician of patient discomfort, it comforts the physician and nursing staff and carries a lower risk of drug overdose. However, it does increase the patients’ intraoperative motion.[13] Other modalities include general anesthesia and deep sedation. However, it should be noted that conscious sedation does carry a risk of hypoventilation and aspiration. [14] In a previous study, no significant difference in complication rate was present following ventricular tachycardia ablation during minimal as compared to deep sedation. [15] Also, in another study, patients undergoing percutaneous epicardial access (for ventricular tachycardia or premature ventricular complex) had similar complication rates regardless of whether they did the procedure under general anesthesia or moderate/deep sedation. [16] Furthermore, in a study by Tang et al., patients who underwent non-conscious sedation during catheter ablation for atrial fibrillation had more transient anesthetic complications as compared to conscious sedation. However, these two groups did not reveal a difference in the procedure-related complication/success rates. [17] Finally, Wasserlauf et al. found moderate sedation to carry a lower procedure time without jeopardizing the complication and recurrence rate up to a median follow-up duration of 0.9 years. This paper studied patients undergoing cryoballoon ablation for paroxysmal atrial fibrillation. [18]Given the previously reported evidence supporting the use of conscious anesthesia during atrial fibrillation catheter ablation, Wasserlauf et al. set on a task to expand our knowledge of patients’ tolerance of moderate sedation during cryoballoon ablation. [9] Consequently, they studied patients undergoing cryoballoon ablation for paroxysmal atrial fibrillation under general anesthesia or moderate sedation. Within 24 hours after the procedure, patients would provide the QoR-40 and their likelihood to recommend the procedure and sedation method. The mean QoR-40 was greater than 180 in the two groups with a difference of less than 5 unites. Furthermore, the difference in the QoR-40 scores was not statistically significant. [9] These scores were better than scores observed by Myles in minor surgeries (178 ± 17) and cardiac surgeries without complications (176 ± 16). [6] Moreover, patients reported a high satisfaction rate with a high likelihood to recommend the procedures (83% and 89%) and a high likelihood to recommend the sedation method (94% and 85%) depending on the sedation method (general anesthesia and moderate sedation respectively). However, the difference was not statistically significant.[9] This result is similar to a previous study that found that 96% of patients would recommend radiofrequency ablation for atrial fibrillation.[19] What these results mean is that they support the use of moderate sedation as compared to general anesthesia, given the similar patient experience, but different procedure time, expense, and possible complications from general anesthesia. [9]This study, however, does have limitations. It was a single-center non-randomized study. The QoR-40 has sections that are heavily dependent on the medical center and staff; hence this is an important issue to consider. Furthermore, the assignment to anesthesia groups was not standardized, and the decision was dependent on physician and patient preference. Though understandable, the physician preference can be made to be dictated by a predefined set of criteria to minimize nonrandom assignment. Finally, we note that the QoR-40 scores presented by Wasserlauf et al. were the means and standard deviations. [9] When calculating the 95% confidence intervals of the difference of the mean QoR-40 scores of the two groups, we find that there is no statistically significant difference between the two groups.In conclusion, Wasserlauf et al. have added to our knowledge of cryoballoon ablation under moderate sedation which might become the more frequently adopted anesthesia strategy during AFib cryoablation.References:1. Myles PS, Hunt JO, Nightingale CE, et al. Development and psychometric testing of a quality of recovery score after general anesthesia and surgery in adults. Anesth Analg. 1999;88(1):83-90. doi:10.1097/00000539-199901000-000162. Myles PS, Weitkamp B, Jones K, Melick J, Hensen S. Validity and reliability of a postoperative quality of recovery score: The QoR-40. Br J Anaesth. 2000;84(1):11-15. doi:10.1093/oxfordjournals.bja.a0133663. Gornall BF, Myles PS, Smith CL, et al. Measurement of quality of recovery using the QoR-40: A quantitative systematic review. Br J Anaesth. 2013;111(2):161-169. doi:10.1093/bja/aet0144. Gower ST, Quigg CA, Hunt JO, Wallace SK, Myles PS. A comparison of patient self-administered and investigator-administered measurement of quality of recovery using the QoR-40. Anaesth Intensive Care. 2006;34(5):634-638. doi:10.1177/0310057x06034005145. Myles PS. Measuring quality of recovery in perioperative clinical trials. Curr Opin Anaesthesiol. 2018;31(4):396-401. doi:10.1097/ACO.00000000000006126. Myles PS. Clinically Important Difference in Quality of Recovery Scores. Anesth Analg. 2016;122(1):13-14. doi:10.1213/ANE.00000000000010607. Myles PS, Hunt JO, Fletcher H, Solly R, Woodward D, Kelly S. Relation between quality of recovery in hospital and quality of life at 3 months after cardiac surgery. Anesthesiology. 2001;95(4):862-867. doi:10.1097/00000542-200110000-000138. Myles PS, Viira D, Hunt JO. Quality of life at three years after cardiac surgery: Relationship with preoperative status and quality of recovery. Anaesth Intensive Care. 2006;34(2):176-183. doi:10.1177/0310057x06034002209. Wasserlauf, Jeremiah; Kaplan, Rachel; Walega, David; Arora, Rishi; Chicos, Alexandr; Kim, Susan; Lin, Albert; Verma, Nishant; Patil, Kaustubha; Knight, Bradley; Passman R. Patient-Reported Outcomes After Cryoballoon Ablation Are Equivalent Between Moderate Sedation And General Anesthesia. J Cardiovasc Electrophysiol. 2020.10. Chung MK, Refaat M, Shen WK, Kutyifa V, Cha YM, Di Biase L, Baranchuk A, Lampert R, Natale A, Fisher J, Lakkireddy DR. Atrial Fibrillation: JACC Council Perspectives. J Am Coll Cardiol. Apr 2020; 75 (14): 1689-1713.11. D’Avila A, Ptaszek LM, Yu PB, Walker JD, Wright C, Noseworthy PA, Myers A, Refaat M, Ruskin JN: Left Atrial-Esophageal Fistula After Pulmonary Vein Isolation. Circulation May 2007; 115(17): e432-3.12. Attanasio P, Huemer M, Shokor Parwani A, et al. Pain Reactions during Pulmonary Vein Isolation under Deep Sedation: Cryothermal versus Radiofrequency Ablation. PACE - Pacing Clin Electrophysiol. 2016;39(5):452-457. doi:10.1111/pace.1284013. Defaye P, Kane A, Jacon P, Mondesert B. Cryoballoon for pulmonary vein isolation: Is it better tolerated than radiofrequency? Retrospective study comparing the use of analgesia and sedation in both ablation techniques. Arch Cardiovasc Dis. 2010;103(6-7):388-393. doi:10.1016/j.acvd.2010.06.00414. Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation: Recommendations for Patient Selection, Procedural Techniques, Patient Management and Follow-up, Definitions, Endpoints, and Research Trial Design. Heart Rhythm. 2012;9(4):632-696.e21. doi:10.1016/j.hrthm.2011.12.01615. Wutzler A, Mueller A, Loehr L, et al. Minimal and deep sedation during ablation of ventricular tachycardia. Int J Cardiol. 2014;172(1):161-164. doi:10.1016/j.ijcard.2013.12.17516. Killu AM, Sugrue A, Munger TM, et al. Impact of sedation vs. general anaesthesia on percutaneous epicardial access safety and procedural outcomes. Europace. 2018;20(2):329-336. doi:10.1093/europace/euw31317. Tang RB, Dong JZ, Zhao W Du, et al. Unconscious sedation/analgesia with propofol versus conscious sedation with fentanyl/midazolam for catheter ablation of atrial fibrillation: A prospective, randomized study. Chin Med J (Engl). 2007;120(22):2036-2038. doi:10.1097/00029330-200711020-0001818. Wasserlauf J, Knight BP, Li Z, et al. Moderate Sedation Reduces Lab Time Compared to General Anesthesia during Cryoballoon Ablation for AF Without Compromising Safety or Long-Term Efficacy. PACE - Pacing Clin Electrophysiol. 2016;39(12):1359-1365. doi:10.1111/pace.1296119. Ezzat VA, Chew A, McCready JW, et al. Catheter ablation of atrial fibrillation - Patient satisfaction from a single-center UK experience. J Interv Card Electrophysiol. 2013;37(3):291-303. doi:10.1007/s10840-012-9763-5

Mohamad El Moheb

and 1 more

Catheter ablation is the current standard of care for the management of symptomatic atrial fibrillation (AFib) refractory to pharmacological therapy. One of the complications of this procedure is thermal injury to the esophagus due to its anatomical proximity to the posterior wall of the left atrium (1). Rarely (<1%), an atrioesophageal fistula can form connecting the lumen of damaged esophagus to the atrial chamber (2). This complication is almost always fatal and can result in exsanguination, air embolism, and sepsis (3, 4). With a growing number of catheter ablations being performed each year, the rate of atrioesophageal fistulas is only expected to rise (5). Other more frequent complications include esophageal wall erosions and ulcers (47%), and thermal injury to the vagus nerve plexus leading to esophageal dysmotility and gastroparesis (17%) (6, 7). Therefore, protecting the esophagus from thermal injuries is paramount in ablative procedures and several strategies have been devised to help mitigate this risk. Many physicians monitor the luminal esophageal temperature (LET) [ as a surrogate for intramural esophageal tissue temperature] with a single sensor or multisensor temperature probe and interrupt energy delivery when LET reaches 38°C or 39°C during radiofrequency ablation. However, this technique significantly impacts the procedural workflow due to the waiting periods for LET to return to baseline. Alternative strategies involve cooling of the esophagus with ice water or reducing the ablation lesion power, contact force and/or duration but this strategy may increase the chances for pulmonary vein reconnection (8). To that end, there has been a growing interest in mechanical devices capable of deflecting the esophagus away from the atrium protecting it from thermal injury.In the current issue of the Journal of Cardiovascular Electrophysiology, Houmsse et al. introduce a novel device capable of mobilizing the esophagus laterally to protect it from injury when performing catheter ablation for AFib. Although other devices have been developed and/or used for this purpose (such as the transesophageal echocardiography probe, endotracheal stylet, Esosure stylet and DV8 shaped balloon retractor), this is the only one to operate using vacuum suction allowing it to latch onto the esophageal wall. The device consists of four main components: outer extrusion, inner stacking plates, deflecting arm and control handle. The outer extrusion is inserted via a trochanter or a bougie into the esophagus and is the only portion of the retractor that comes in contact with the surrounding tissues. Small perforations at the distal end allow for vacuum suction to adhere to the esophagus and for a radiocontrast agent to be delivered to delineate the esophageal contour. The inner stacking plates are then introduced through the outer extrusion and are designed to allow movement of the deflecting arm in the medio-lateral plane only. The deflecting arm is connected to the distal end of the stacking plates through a pivot point and can be steered using the control handle. The authors have evaluated the effectiveness and safety of the device on canine and swine animal models by measuring the distance and direction of displacement of the esophagus, examining the cellular architecture after prolonged suction, measuring the LET, and assessing compatibility of device with electroanatomical mapping systems. A total of 68 deviations were performed on four canine models. The average rightward deflection was equal to 26.6 ± 2.5mm compared to 18.7 ± 2.3mm for the direct leftward deflection (p<0.001), and 96% of deviations did not have an esophageal trailing edge. With the exception of one study, the average distance displaced using the suction retractor was superior to other devices (9-13). The substantial distance of deflection and the minimal esophageal trailing edge significantly decreased the rise in LET from baseline (mean increase of 0.2°C vs 2.5°C without deflection). Examination of the esophageal tissue integrity following one hour of continuous suctioning revealed no change in the esophageal cellular architecture, and only minimal circular areas of hyperemia in mucosa due to the suction ports without injury to the muscularis layer. Finally, the retractor did not interfere with the electroanatomical mapping systems used (CARTO and EnSite).Despite its interesting findings, this study has several limitations that should be acknowledged. First, the study was performed on swine and canine animal models, which are known to have an anatomy close to humans; however, the safety profile of the device and its effectiveness in displacing the esophagus may not translate in humans. Second, subjects may exhibit symptoms secondary to extreme deviation of the esophagus in the absence of distortion of the cellular architecture. Clinical studies are needed to assess the safety profile and side effects of this esophageal retractor. Third, it is unclear whether these results would be reproducible under monitored anesthesia care. Finally, the fluoroscopic equipment tools lacked electronic caliper capabilities, and the measurements were performed using radiopaque rulers.Overall, the authors should be commended on their efforts to introduce and evaluate an inexpensive and innovative tool for esophageal protection during AFib ablation. This retractor addresses the limitations of other products that serve a similar purpose. In fact, the suctioning power of the product minimizes the trailing edge of the esophagus that could not be managed with other devices which left esophageal tissue in the ablation field (10, 13). In addition, the control handle offers significant flexibility in device manipulation allowing physicians to choose the site of angulation and the angle of deflection depending on the patient’s anatomy. Future studies should focus on evaluating the safety and effectiveness of this device in humans. Given the growing number of esophageal retracting devices, studies should also aim to determine the device that produces the best esophageal protection and most desirable outcomes of ablation.REFERENCES1. Chung MK, Refaat M, Shen WK, Kutyifa V, Cha YM, Di Biase L, Baranchuk A, Lampert R, Natale A, Fisher J, Lakkireddy DR. Atrial Fibrillation: JACC Council Perspectives. J Am Coll Cardiol. Apr 2020; 75 (14): 1689-1713.2. 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Acute pyloric spasm and gastric hypomotility: an extracardiac adverse effect of percutaneous radiofrequency ablation for atrial fibrillation. Journal of the American College of Cardiology. 2005;46(2):327-30.7. Schmidt M, Nölker G, Marschang H, Gutleben K-J, Schibgilla V, Rittger H, et al. Incidence of oesophageal wall injury post-pulmonary vein antrum isolation for treatment of patients with atrial fibrillation. Europace. 2008;10(2):205-9.8. Tran VN, Kusa S, Smietana J, Tsai W-C, Bhasin K, Teh A, et al. The relationship between oesophageal heating during left atrial posterior wall ablation and the durability of pulmonary vein isolation. Ep Europace. 2017;19(10):1664-9.9. Mateos JCP, Mateos EIP, Peña TGS, Lobo TJ, Mateos JCP, Vargas RNA, et al. Simplified method for esophagus protection during radiofrequency catheter ablation of atrial fibrillation-prospective study of 704 cases. Brazilian Journal of Cardiovascular Surgery. 2015;30(2):139-47.10. Bhardwaj R, Naniwadekar A, Whang W, Mittnacht AJ, Palaniswamy C, Koruth JS, et al. Esophageal Deviation During Atrial Fibrillation Ablation: Clinical Experience With a Dedicated Esophageal Balloon Retractor. JACC Clin Electrophysiol. 2018;4(8):1020-30.11. Herweg B, Johnson N, Postler G, Curtis AB, Barold SS, Ilercil A. Mechanical esophageal deflection during ablation of atrial fibrillation. Pacing and clinical electrophysiology. 2006;29(9):957-61.12. Palaniswamy C, Koruth JS, Mittnacht AJ, Miller MA, Choudry S, Bhardwaj R, et al. The extent of mechanical esophageal deviation to avoid esophageal heating during catheter ablation of atrial fibrillation. JACC: Clinical Electrophysiology. 2017;3(10):1146-54.13. Parikh V, Swarup V, Hantla J, Vuddanda V, Dar T, Yarlagadda B, et al. 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