5207Bilateral cardiac sympathetic denervation in structural heart disease

Abstract Background Left cardiac sympathetic denervation (LCSD) is an established therapy for refractory ventricular arrhythmias (VAs) in channelopathies. A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart dis...

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Published in:European heart journal 2019-10, Vol.40 (Supplement_1)
Main Authors: Dusi, V, Pugliese, L, Passarelli, I, Camporotondo, R, Driussi, M, Antonutti, M, Miani, D, Maurelli, M, Facchin, D, Savastano, S, Raineri, C, Rordorf, R, Oltrona Visconti, L, Proclemer, A, De Ferrari, G M
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container_issue Supplement_1
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container_title European heart journal
container_volume 40
creator Dusi, V
Pugliese, L
Passarelli, I
Camporotondo, R
Driussi, M
Antonutti, M
Miani, D
Maurelli, M
Facchin, D
Savastano, S
Raineri, C
Rordorf, R
Oltrona Visconti, L
Proclemer, A
De Ferrari, G M
description Abstract Background Left cardiac sympathetic denervation (LCSD) is an established therapy for refractory ventricular arrhythmias (VAs) in channelopathies. A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart disease (SHD). Purpose To describe our single-center experience with BCSD in SHD. Methods Nine patients (78% male, mean 55±18 yrs, mean LVEF 31±14%) with SHD and refractory VAs underwent BCSD. All had a Video-Assisted Thoracoscopic Surgery (VATS), in 2 cases associated with the robotic technique. The underlying cardiomyopathy (CMP) was non-ischemic (NICMP) in most cases (n=5, 55%), ischemic in 2 cases, arrhythmogenic right ventricular (ARVC) in one and related to lamin A/C deficiency in one. All patients had an ICD, 44% (n=4) a CRT-D. NYHA functional class I was present in 4 patients, the rest were in NYHA class II (n=3) or III (n=2). Three patients were candidates to heart transplant/LV assistance device. The arrhythmic burden pre BCSD included in 7 pts (78%) a history of electrical storm (ES); the median number of shocks/patient in the 12 months before BCSD was 5 (IQ range 3–18). Except for 2 patients with previous thyrotoxicosis, the remaining were either on amiodarone (n=6) or on sotalol (n=1) before BCSD. Main BCSD indications were represented by drug refractory fast VT in 7 pts (cycle
doi_str_mv 10.1093/eurheartj/ehz746.0065
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A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart disease (SHD). Purpose To describe our single-center experience with BCSD in SHD. Methods Nine patients (78% male, mean 55±18 yrs, mean LVEF 31±14%) with SHD and refractory VAs underwent BCSD. All had a Video-Assisted Thoracoscopic Surgery (VATS), in 2 cases associated with the robotic technique. The underlying cardiomyopathy (CMP) was non-ischemic (NICMP) in most cases (n=5, 55%), ischemic in 2 cases, arrhythmogenic right ventricular (ARVC) in one and related to lamin A/C deficiency in one. All patients had an ICD, 44% (n=4) a CRT-D. NYHA functional class I was present in 4 patients, the rest were in NYHA class II (n=3) or III (n=2). Three patients were candidates to heart transplant/LV assistance device. The arrhythmic burden pre BCSD included in 7 pts (78%) a history of electrical storm (ES); the median number of shocks/patient in the 12 months before BCSD was 5 (IQ range 3–18). Except for 2 patients with previous thyrotoxicosis, the remaining were either on amiodarone (n=6) or on sotalol (n=1) before BCSD. Main BCSD indications were represented by drug refractory fast VT in 7 pts (cycle &lt;250 msec) and by recurrent monomorphic VT episodes (mean cycle 351 msec) after endocardial VT ablation in 2 patients. Results No major complication occurred. One patient (NICMP, NYHA II), has an uneventful follow up (FU) of less than 1 month and was excluded from the efficacy analysis. The median FU in the remaining 8 patients is 10 months (IQ range 6–19), during which the median number of shocks/patients was 0.5 (IQ range 0–3). Overall, 4 patients (50%) had ICD shock recurrences. Two cases (mean LVEF 17.5%, NYHA class III) had an ES during severe hemodynamic instability and subsequently died because of cardiogenic shock respectively 1 and 7 months after BCSD. One case had three, not consecutive ICD shocks 20 months after BCSD in the setting of severe amiodarone-induced thyrotoxicosis. Finally, one patient received a single intra-hospital ICD shock 5 days after BCSD before reintroduction of full-dose beta-blockers. The figure summarizes ICD shocks burden in the 6 months before and after BCSD. Among the 5 patients with NICMP/ARVC (4 in NYHA class I), only 1 had a single ICD shock recurrence. ICD shocks pre versus post BCSD, n=8 Conclusions Our case series, although numerically small, has a good follow-up and is the first reported in Europe. The results are in agreement with the suggested remarkable efficacy of BCSD in patients with good functional capacity and fast VAs. Therefore, cardiac sympathetic denervation should always be considered in patients with SHD and refractory ventricular tachyarrhythmias, especially in case VT ablation is either not indicated or fails.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehz746.0065</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>European heart journal, 2019-10, Vol.40 (Supplement_1)</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. For permissions, please email: journals.permissions@oup.com. 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1395-ddf6927de1575c3c539e1c54affdd8a1f57d0a6bcea6684616f852368ad4264f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Dusi, V</creatorcontrib><creatorcontrib>Pugliese, L</creatorcontrib><creatorcontrib>Passarelli, I</creatorcontrib><creatorcontrib>Camporotondo, R</creatorcontrib><creatorcontrib>Driussi, M</creatorcontrib><creatorcontrib>Antonutti, M</creatorcontrib><creatorcontrib>Miani, D</creatorcontrib><creatorcontrib>Maurelli, M</creatorcontrib><creatorcontrib>Facchin, D</creatorcontrib><creatorcontrib>Savastano, S</creatorcontrib><creatorcontrib>Raineri, C</creatorcontrib><creatorcontrib>Rordorf, R</creatorcontrib><creatorcontrib>Oltrona Visconti, L</creatorcontrib><creatorcontrib>Proclemer, A</creatorcontrib><creatorcontrib>De Ferrari, G M</creatorcontrib><title>5207Bilateral cardiac sympathetic denervation in structural heart disease</title><title>European heart journal</title><description>Abstract Background Left cardiac sympathetic denervation (LCSD) is an established therapy for refractory ventricular arrhythmias (VAs) in channelopathies. A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart disease (SHD). Purpose To describe our single-center experience with BCSD in SHD. Methods Nine patients (78% male, mean 55±18 yrs, mean LVEF 31±14%) with SHD and refractory VAs underwent BCSD. All had a Video-Assisted Thoracoscopic Surgery (VATS), in 2 cases associated with the robotic technique. The underlying cardiomyopathy (CMP) was non-ischemic (NICMP) in most cases (n=5, 55%), ischemic in 2 cases, arrhythmogenic right ventricular (ARVC) in one and related to lamin A/C deficiency in one. All patients had an ICD, 44% (n=4) a CRT-D. NYHA functional class I was present in 4 patients, the rest were in NYHA class II (n=3) or III (n=2). Three patients were candidates to heart transplant/LV assistance device. The arrhythmic burden pre BCSD included in 7 pts (78%) a history of electrical storm (ES); the median number of shocks/patient in the 12 months before BCSD was 5 (IQ range 3–18). Except for 2 patients with previous thyrotoxicosis, the remaining were either on amiodarone (n=6) or on sotalol (n=1) before BCSD. Main BCSD indications were represented by drug refractory fast VT in 7 pts (cycle &lt;250 msec) and by recurrent monomorphic VT episodes (mean cycle 351 msec) after endocardial VT ablation in 2 patients. Results No major complication occurred. One patient (NICMP, NYHA II), has an uneventful follow up (FU) of less than 1 month and was excluded from the efficacy analysis. The median FU in the remaining 8 patients is 10 months (IQ range 6–19), during which the median number of shocks/patients was 0.5 (IQ range 0–3). Overall, 4 patients (50%) had ICD shock recurrences. Two cases (mean LVEF 17.5%, NYHA class III) had an ES during severe hemodynamic instability and subsequently died because of cardiogenic shock respectively 1 and 7 months after BCSD. One case had three, not consecutive ICD shocks 20 months after BCSD in the setting of severe amiodarone-induced thyrotoxicosis. Finally, one patient received a single intra-hospital ICD shock 5 days after BCSD before reintroduction of full-dose beta-blockers. The figure summarizes ICD shocks burden in the 6 months before and after BCSD. Among the 5 patients with NICMP/ARVC (4 in NYHA class I), only 1 had a single ICD shock recurrence. ICD shocks pre versus post BCSD, n=8 Conclusions Our case series, although numerically small, has a good follow-up and is the first reported in Europe. The results are in agreement with the suggested remarkable efficacy of BCSD in patients with good functional capacity and fast VAs. Therefore, cardiac sympathetic denervation should always be considered in patients with SHD and refractory ventricular tachyarrhythmias, especially in case VT ablation is either not indicated or fails.</description><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNqNkE1LxDAQQIMoWFd_gtA_0N0kbdL2qIsfCwteFLyFMZnQLN22JKmw_npbK549zWXezOMRcsvomtE63-DoGwQfDxtsvspCrimV4owkTHCe1bIQ5yShrBaZlNX7JbkK4UAprSSTCdkJTst710JED22qwRsHOg2n4wCxweh0arBD_wnR9V3qujREP-o4zts_X1PjAkLAa3JhoQ148ztX5O3x4XX7nO1fnnbbu32mWT45GGNlzUuDTJRC51rkNTItCrDWmAqYFaWhID80wqRbTJK2EjyXFZiCy8LmKyKWu9r3IXi0avDuCP6kGFVzD_XXQy091Nxj4ujC9ePwT-QbnkRpbw</recordid><startdate>20191001</startdate><enddate>20191001</enddate><creator>Dusi, V</creator><creator>Pugliese, L</creator><creator>Passarelli, I</creator><creator>Camporotondo, R</creator><creator>Driussi, M</creator><creator>Antonutti, M</creator><creator>Miani, D</creator><creator>Maurelli, M</creator><creator>Facchin, D</creator><creator>Savastano, S</creator><creator>Raineri, C</creator><creator>Rordorf, R</creator><creator>Oltrona Visconti, L</creator><creator>Proclemer, A</creator><creator>De Ferrari, G M</creator><general>Oxford University Press</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20191001</creationdate><title>5207Bilateral cardiac sympathetic denervation in structural heart disease</title><author>Dusi, V ; Pugliese, L ; Passarelli, I ; Camporotondo, R ; Driussi, M ; Antonutti, M ; Miani, D ; Maurelli, M ; Facchin, D ; Savastano, S ; Raineri, C ; Rordorf, R ; Oltrona Visconti, L ; Proclemer, A ; De Ferrari, G M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1395-ddf6927de1575c3c539e1c54affdd8a1f57d0a6bcea6684616f852368ad4264f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dusi, V</creatorcontrib><creatorcontrib>Pugliese, L</creatorcontrib><creatorcontrib>Passarelli, I</creatorcontrib><creatorcontrib>Camporotondo, R</creatorcontrib><creatorcontrib>Driussi, M</creatorcontrib><creatorcontrib>Antonutti, M</creatorcontrib><creatorcontrib>Miani, D</creatorcontrib><creatorcontrib>Maurelli, M</creatorcontrib><creatorcontrib>Facchin, D</creatorcontrib><creatorcontrib>Savastano, S</creatorcontrib><creatorcontrib>Raineri, C</creatorcontrib><creatorcontrib>Rordorf, R</creatorcontrib><creatorcontrib>Oltrona Visconti, L</creatorcontrib><creatorcontrib>Proclemer, A</creatorcontrib><creatorcontrib>De Ferrari, G M</creatorcontrib><collection>CrossRef</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dusi, V</au><au>Pugliese, L</au><au>Passarelli, I</au><au>Camporotondo, R</au><au>Driussi, M</au><au>Antonutti, M</au><au>Miani, D</au><au>Maurelli, M</au><au>Facchin, D</au><au>Savastano, S</au><au>Raineri, C</au><au>Rordorf, R</au><au>Oltrona Visconti, L</au><au>Proclemer, A</au><au>De Ferrari, G M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>5207Bilateral cardiac sympathetic denervation in structural heart disease</atitle><jtitle>European heart journal</jtitle><date>2019-10-01</date><risdate>2019</risdate><volume>40</volume><issue>Supplement_1</issue><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>Abstract Background Left cardiac sympathetic denervation (LCSD) is an established therapy for refractory ventricular arrhythmias (VAs) in channelopathies. A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart disease (SHD). Purpose To describe our single-center experience with BCSD in SHD. Methods Nine patients (78% male, mean 55±18 yrs, mean LVEF 31±14%) with SHD and refractory VAs underwent BCSD. All had a Video-Assisted Thoracoscopic Surgery (VATS), in 2 cases associated with the robotic technique. The underlying cardiomyopathy (CMP) was non-ischemic (NICMP) in most cases (n=5, 55%), ischemic in 2 cases, arrhythmogenic right ventricular (ARVC) in one and related to lamin A/C deficiency in one. All patients had an ICD, 44% (n=4) a CRT-D. NYHA functional class I was present in 4 patients, the rest were in NYHA class II (n=3) or III (n=2). Three patients were candidates to heart transplant/LV assistance device. The arrhythmic burden pre BCSD included in 7 pts (78%) a history of electrical storm (ES); the median number of shocks/patient in the 12 months before BCSD was 5 (IQ range 3–18). Except for 2 patients with previous thyrotoxicosis, the remaining were either on amiodarone (n=6) or on sotalol (n=1) before BCSD. Main BCSD indications were represented by drug refractory fast VT in 7 pts (cycle &lt;250 msec) and by recurrent monomorphic VT episodes (mean cycle 351 msec) after endocardial VT ablation in 2 patients. Results No major complication occurred. One patient (NICMP, NYHA II), has an uneventful follow up (FU) of less than 1 month and was excluded from the efficacy analysis. The median FU in the remaining 8 patients is 10 months (IQ range 6–19), during which the median number of shocks/patients was 0.5 (IQ range 0–3). Overall, 4 patients (50%) had ICD shock recurrences. Two cases (mean LVEF 17.5%, NYHA class III) had an ES during severe hemodynamic instability and subsequently died because of cardiogenic shock respectively 1 and 7 months after BCSD. One case had three, not consecutive ICD shocks 20 months after BCSD in the setting of severe amiodarone-induced thyrotoxicosis. Finally, one patient received a single intra-hospital ICD shock 5 days after BCSD before reintroduction of full-dose beta-blockers. The figure summarizes ICD shocks burden in the 6 months before and after BCSD. Among the 5 patients with NICMP/ARVC (4 in NYHA class I), only 1 had a single ICD shock recurrence. ICD shocks pre versus post BCSD, n=8 Conclusions Our case series, although numerically small, has a good follow-up and is the first reported in Europe. The results are in agreement with the suggested remarkable efficacy of BCSD in patients with good functional capacity and fast VAs. Therefore, cardiac sympathetic denervation should always be considered in patients with SHD and refractory ventricular tachyarrhythmias, especially in case VT ablation is either not indicated or fails.</abstract><pub>Oxford University Press</pub><doi>10.1093/eurheartj/ehz746.0065</doi></addata></record>
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title 5207Bilateral cardiac sympathetic denervation in structural heart disease
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