Title: Successful chemical ablation for intraventricular septal ventricular tachycardia in a case with previous myocardial infarction and stents in the left anterior descending artery stent. Alternative approach to the septal branch.Word count: 1888 (Full manuscript)Authors:Shin Hasegawa M.D. [email protected] Tanaka M.D.　[email protected] Uehara M.D.　[email protected] Yabuta M.D.　 [email protected] Kato M.D. Ph.D.　[email protected]:Department of Cardiology, Nagoya Tokushukai General Hospital.Corresponding author:Kazuo Kato M.D. Ph.D.　[email protected]:2-52, Kozoji-cho Kita, Kasugai, Aichi, Japan. 487-0016Sources of Funding:This research did not receive any specific grants from funding agencies in the public, commercial, or not-for-profit sectors.Disclosures:None.Data Availability Statement:The data that support the findings of this study are available from the corresponding author upon reasonable request.Keywords:ventricular tachycardia; trans-coronary ethanol ablation; previous myocardial infarction; septal perforator; coronary computed tomography angiographyKey clinical MessageTrans-coronary ethanol ablation for ventricular tachycardia originating from the ventricular septum is effective, but there are cases with no septal perforator from left anterior descending artery.CT and angiography can reveal the optimal vessel.IntroductionArrhythmia-substrate-based radiofrequency (RF) catheter ablation (RFCA) is an effective treatment for scar-related ventricular tachycardia (VT) in patients with a previous myocardial infarction.1However, energy delivery to deep myocardial origins, such as the ventricular septum, is challenging.Trans-coronary ethanol ablation (TCEA) is one of an effective treatments option for VT of deep myocardial origin, and its advantage in the treatment of VT of septal origin has been widely reported; however, its safety and efficacy have not yet been established.2,3,4 This method requires the target vessel to be in an appropriate location.5 Therefore, TCEA becomes difficult if a stent has been implanted previously in the culprit vessel. The following case describes a patient who developed VT from the ventricular septum with previous myocardial infarction (MI), which was treated with a stent implantation in the left anterior descending branch (LAD). The VT of this patient seemed to be difficult to treat with not only RFCA but also TCEA through the LAD. However, we could identify the septal branch from the high lateral branch (HL), then we could perform TCEA successfully through the HL.We believe this would be the first case of the septal VT in which chemical ablation of the ventricular septum could be successfully performed even with stenting in the LAD after MI.Case PresentationA 64-year-old man with dyslipidemia experienced an acute myocardial infarction in 2009 and underwent percutaneous coronary intervention (PCI) at another hospital, where a drug-eluting stent (DES) was implanted in the mid LAD. Subsequently, one DES was placed in the mid right coronary artery, and two DESs were placed in the proximal left coronary artery circumflex. DES was implanted for proximal LAD in our hospital with an overlap with the previous stent because of unstable angina pectoris in 2018.In 2019, the patient visited our institution because he suddenly developed chest pain during cycling. A 12-lead ECG showed sinus rhythm (SR) and ventricular premature contraction (VPC) with a right-bundle-branch-block (RBBB) waveform on the inferior axis. No de novo lesions were observed on multidetector computed tomography and coronary angiography (CAG), however, VT occurred occasionally in the ward with symptoms similar to the chest pain as he felt before admission. During VT, his vital signs were stable at 132/91 mmHg, and a 12-lead ECG showed 187 bpm with RBBB in the inferior axis. RFCA was performed after informed consent was obtained for all procedures, including TCEA that was approved by the review board of this institute.The patient was heparinized at the start of the procedure, and activated coagulation time was maintained for over 300 s. The three-dimensional mapping system used was EnSite Precision (Abbott, St Paul, MN, USA). Left ventricular (LV) potentials during SR were examined with the Advisor HD grid mapping catheter (Abbott, St. Paul, MN, USA), and no local abnormal ventricular activity (LAVA) was observed, however, a low voltage area in the septum was observed. Programed stimulation elicited a VT almost identical to clinical VT with earlier excitation of the ventricular septal base. However, VT was not sustained and entrainment pacing was not possible. The local ventricular potentials during VT from both ventricles preceded 28 ms earlier than the body surface ECG. RF energy was applied from the LV side, which was ineffective. The vessels feeding the earliest VT site were examined using computed tomography (CT) and CAG to find out the possibility of an origin from the intramural ventricular septum. Although there was no septal perforator from the LAD to the target region of the VT, a branch was observed from the HL branch.An angiographic catheter (6F SPB 3.75, ASAHI Intec, Tokyo, Japan) was cannulated into the left coronary artery from the radial artery, and a guidewire (0.014-inch Sionblue for coronary angioplasty, ASAHI Intec) was used to inflate the balloon catheter (15-mm length Emerge over-the-wire with a 1.25-mm nominal diameter for angioplasty, Boston, MA, USA) at the target branch. Immediately after injection of the contrast medium through over-the-wire lumen, the VPC disappeared, and VT was no longer observed. We ensured that the injection of ice-cold saline would not affect AV conduction after confirming the absence of shunting and then injected 3 ml of dehydrated ethanol (98%) twice at 1 ml per minute. The procedure was completed after it was determined that neither VPCs nor VTs were induced. The patient was discharged after implanted defibrillator, which revealed that there was no VT recurrence for the next two years.DiscussionDespite showing the RBBB morphology in this case, the earliest activation sites were located at both of the RV base and the LV base, suggesting that the VT might be originated from the ventricular septal base. TCEA has been one of the alternative approaches for ventricular arrhythmias (VA) originated from deep septal origin that can be hardly treated by endocardial or epicardial RFCA6.7, most of which has been performed in the septal branch diverging from the LAD. However, in our case, two stents were placed in the LAD after PCI, and there might not be an appropriate septal perforator for TCEA, but it branched from the HL. But frequency of septal branching from other than the LAD. Millar et al . reported a VT case associated with nonischemic cardiomyopathy treated with ethanol injection into septal branches from vessels other than the LAD,9 and the frequency is reported as 10.0-14.7%.8 TCEA may be feasible even in cases of deep septal-originated VAs with stents in the LAD after PCI, if the culprit area would be fed by other artery from other vessels as we could experience in this case. We had better search for an optimal vessel using CT or CAG to achieve successful TCEA even in case implanted stent to the culprit site.10Further large clinical trials are needed to assess the success rate and safety of chemical ablation in post-stenting VT cases.However, this report has the following limitations. First, LV and RV potentials were evaluated only in SR, and all of LAVAs in the LV and RV were recorded in SR. Other arrhythmogenic insight may have obtained if the ventricular activation sequence map would be obtained under right or left ventricular pacing. Second, the contrast injection alone could abolish the VPC, suggesting that the perfusion area might be culprit. We chose the coated guidewire for its better lubricity and cross ability, which unfortunately spoiled detecting the local information. If we would use uncoated wire so as to record local potentials, we could obtain further evidence for the culprit site.ConclusionTCEA might be effective in patients with VT originated from deep septal lesions associated with previous MI with a stent implantation in the LAD, if there are other septal feeding arteries to the VT origin than the LAD. Detailed evaluation of the coronary arteries using CT and CAG would be crucial for such patients requiring VT therapy originating from deep septal origin.Acknowledgments:None.Author contributions:Shin Hasegawa performed the conception, design, and data collection.Yukihiro Uehara, Akimitsu Tanaka, and Kazuo Kato　collected the data.References:1. Segal OR, Chow AW, Markides V, et al. Long-term results after ablation of infarct-related ventricular tachycardia. Heart Rhythm 2005;2:474-482.2. Sacher F, Sobieszczyk P, Tedrow U, et al. Transcoronary ethanol ventricular tachycardia ablation in the modern electrophysiology era. Heart Rhythm 2008;5:62-68.3. Neira V, Santangeli P, Futyma P, et al. Ablation strategies for intramural ventricular arrhythmias. Heart Rhythm 2020;17:1176-1184.4. Kim SS, Knight BP. Alcohol ablation for ventricular tachycardia: a distillation of modern cases. Heart Rhythm 2008;5:69-70.5. Tavares L, Valderrábano M. Retrograde venous ethanol ablation for ventricular tachycardia. Heart Rhythm 2019;16:478-483.6: Sosa E, Scanavacca M, D’Avila A, et al. Endocardial and epicardial ablation guided by nonsurgical transthoracic epicardial mapping to treat recurrent ventricular tachycardia. J Cardiovasc Electrophysiol 1998;9:229–239.7: Sosa E, Scanavacca M, d’Avila A, et al. Nonsurgical transthoracic epicardial catheter ablation to treat recurrent ventricular tachycardia occurring late after myocardial infarction. J Am Coll Cardiol 2000;35:1442–1449.8: Alkhouli M, M, Sajjad W, Lee J, et al. Prevalence of non–left anterior descending septal perforator culprit in patients with hypertrophic cardiomyopathy undergoing alcohol septal ablation. Am J Cardiol, 2016;117:1655-16609: Miller MA, Kini AS, Reddy VY, Dukkipati SR. Transcoronary ethanol ablation of ventricular tachycardia via an anomalous first septal perforating artery. Heart Rhythm 2011;8:1606-1607.10: Mahida S, Berte B, Yamashita S, et al. New ablation technologies and techniques. Arrhythm Electrophysiol Rev. 2014;3:107-112.Figure legends:Figure 1:(A) Left: 12-lead ECG during sinus rhythm (SR). right: 12-lead ECG during ventricular tachycardia (VT). The patient had sustained monomorphic VT with a right bundle branch block and wide QRS on the inferior axis.(B) Observation of the left ventricular (LV) endocardium with HD grid during VT showed the earliest potentials at the base of the LV septum.(C) During SR, the HD grid showed a low voltage area at the mid of the LV septal endocardium.Figure 2:(A) Irrigation catheter placed in the left ventricle, and HD grid placed in the right ventricle during ventricular tachycardia (VT).(B) The earliest VT potentials were almost the same during the use of the irrigation catheter and HD grid.(C) Pacing stimulation was performed at the earliest VT site from the left and right ventricles, and the morphology was more similar to VT in the left ventricle.(D) The RF energy was delivered in the left ventricular septal endocardium during VT.Figure 3:Coronary computed tomography (CT; volume rendering) showing stents implanted in the left coronary artery, Two stents were implanted in the left anterior descending branch (LAD) in 2009 (a) and 2018 (b), and also two stents were implanted in the left coronary artery circumflex (c,d).(B) No vessels returns to the base of the ventricular septum from LAD (red asterisk).(C) Coronary CT shows the HL branch (yellow star) and LAD. The septal perforator (white arrow) is seen at the base of the ventricular septum.(D) Ethanol injection into the septal perforator. A guiding catheter was canulated into the left coronary artery, and selective contrast was performed on the septal perforator (white arrow) branching from the HL branch (yellow star) with a microcatheter.(E) The contrasts did not shunt (black arrow).(F) Ventricular premature contractions were observed before ethanol administration but were suppressed after ethanol administration.

Introduction Exit block, which is difficult to strictly confirm and cannot be adopted for adenosine triphosphate (ATP) injections to provoke dormancy, is an essential concept of atrial fibrillation (AF) ablation. We investigated exit conduction using high frequency stimulation (HFS) and evaluated whether dormant “exit” conduction of the pulmonary veins (PVs) and left atrial posterior wall (LAPW) would remain in patients in which an encircling isolation of all PVs and LAPW isolation (Box PVI) were performed. Methods We enrolled 345 consecutive patients with various severities of AF undergoing a Box PVI and defined the procedure endpoint as complete bidirectional block with no dormant “entrance and exit” conduction of all PVs and the LAPW using HFS and ATP. Results Dormant “exit” conduction of the PVs with HFS delivered at the PV carina following an ATP injection remained in 0.9% after additional applications, and that for the LAPW was provoked in 5.5%, which remained in 1.4%. Our definition of a complete bidirectional Box PVI was satisfied in 79.7% and showed the best clinical outcome. In the non-paroxysmal AF group, there were significant differences in the recurrence rates between the groups with and without a complete LAPW isolation, however, the clinical outcome was independent of a complete LAPW isolation in the paroxysmal AF group. Conclusion HFS delivered at the PV carina and LAPW following a Box PVI could clearly elucidate true exit block, and a concomitant ATP injection could define dormant “exit” conduction, suggesting incomplete lesions that had been missed.