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Damiani D, Agosta VT, D'Andria Ursoleo J, Bottussi A, Licheri M, Muriana P, Monaco F. Perioperative and long-term outcomes of bilateral cardiac sympathetic denervation via video-assisted thoracoscopic surgery in patients with refractory ventricular arrhythmias. Int J Cardiol 2025; 421:132890. [PMID: 39672471 DOI: 10.1016/j.ijcard.2024.132890] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/01/2024] [Revised: 12/01/2024] [Accepted: 12/04/2024] [Indexed: 12/15/2024]
Abstract
BACKGROUND Bilateral cardiac sympathetic denervation (CSD) performed via video-assisted thoracoscopic (VAT) surgery shows potential in managing ventricular tachycardia (VT), thereby reducing arrhythmic burden. In this setting, the scarcity of studies addressing both perioperative and long-term outcomes creates a substantial gap in the optimal management of patients with multiple comorbidities and limited treatment options. This observational study aimed to assess the medical comorbidities, as well as the short- and long-term outcomes of patients who underwent CSD for VT refractory to catheter ablation and medical therapy at a referral tertiary teaching hospital. MATERIALS We retrospectively analyzed data of all patients with VT who underwent bilateral CSD-VAT surgery at a single center. Unadjusted Kaplan-Meier survival curves were generated to analyze the survival rates at 1-year and 2-years following the procedure. RESULTS Ten consecutive patients were unrolled between August 2014 and March 2024. Bilateral CSD-VAT surgery was successfully performed in all patients. Pre-operative ejection fraction was 33 % (26-41). Two patients (22 %) suffered cardiogenic shock and 1 vasoplegia. Half (50 %) of the patients necessitated inotrope/vasopressor support and 1 an intra-aortic balloon pump. Median hospital stay was 12 (9-19) days. Three (33 %) patients required postoperative ICU admission. All patients were alive upon hospital discharge. Neither major surgical complications nor complications typically associated with VAT-CSD (e.g., Horner's syndrome) were observed. The 1-year survival was 80 % while the survival at 24 months was 60 %. CONCLUSIONS CSD-VAT is a feasible rescue treatment in patients with refractory VT and is associated with limited intra- and postoperative complications alongside an acceptable long-term survival rate.
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Affiliation(s)
- Diana Damiani
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Viviana Teresa Agosta
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Jacopo D'Andria Ursoleo
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Alice Bottussi
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Margherita Licheri
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Piergiorgio Muriana
- Department of Thoracic Surgery, IRCCS San Raffaele Scientific Institute, Milan, Italy
| | - Fabrizio Monaco
- Department of Anesthesia and Intensive Care, IRCCS San Raffaele Scientific Institute, Milan, Italy.
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Hanna DB, Karimianpour A, Mamprejew N, Fiechter C, Verghese D, Navas V, Sharma D. The role of cardiac sympathetic denervation for ventricular arrhythmias: an updated systematic review and meta-analysis. J Interv Card Electrophysiol 2025:10.1007/s10840-025-01997-x. [PMID: 39875720 DOI: 10.1007/s10840-025-01997-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/19/2024] [Accepted: 01/09/2025] [Indexed: 01/30/2025]
Abstract
INTRODUCTION The role of the sympathetic nervous system in the initiation and continuation of ventricular tachyarrhythmias (VTA) is well established. However, whether CSD reduces implantable cardioverter-defibrillator (ICD) shocks and recurrent VTA is still uncertain. METHODS A comprehensive literature search was performed at Medline and Embase until March 2023. The primary outcome was the rate of ICD shocks and VTA per patient-year in our pooled analysis of all included articles. Analyses were conducted using Comprehensive Meta-Analysis software. RESULTS Initial search yielded 1324 scientific studies with a total of 15 studies fitting our inclusion criteria. ICD shocks at 1 year post-CSD revealed an event rate of 69.8% (95% CI, 56.4-80.4% with 50% heterogeneity) (I2 statistic). ICD shocks at 6 months had an event rate of 59.1% (95% CI, 46.9-70.4%; 47 I2). Analysis of our pooled studies showed that 64.3% of individuals achieved freedom from VTA at 1 year post-CSD (95% CI, 42.3-81.5%; 26% I2), while 62.3% were free from recurrent VTA 6 months post-CSD (95% CI, 51.2-72.2%; 40% I2). Time to mortality directly caused by recurrent VTA post-CSD was subdivided into short-term (0-30 days), intermediate-term (31-364 days), and long-term (≥ 365). Mortality for the short-term tertile was 8.9% (95% CI, 5.0-15.4%; 0% I2), medium-term was 5.3% (95% CI, 2.4-11.3%; 0% I2), and long-term 5.2% (95% CI, 2.4-10.9%; 0% I2). CONCLUSION CSD seems to be promising as an acceptable treatment strategy for recurrent VTA refractory to traditional pharmacological or ablation therapy.
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Affiliation(s)
- Daniel B Hanna
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA.
| | | | - Nicole Mamprejew
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA
| | - Chris Fiechter
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA
| | - Dhiran Verghese
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA
| | - Viviana Navas
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA
| | - Dinesh Sharma
- Rooney Heart Institute, 311 9th St N #201, Naples, FL, 34102, USA
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Ebert M, Thomsen Y, Richter S. [Role of ventricular tachycardia ablation in patients with systolic heart failure]. Herzschrittmacherther Elektrophysiol 2025:10.1007/s00399-024-01064-4. [PMID: 39843809 DOI: 10.1007/s00399-024-01064-4] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/01/2024] [Accepted: 12/12/2024] [Indexed: 01/24/2025]
Abstract
Patients with systolic heart failure (HF) and structural heart disease often suffer from ventricular tachycardias (VTs), which lead to increased morbidity and mortality. Despite advancements in pharmacological therapy and the use of implantable cardioverter-defibrillators, treatment options are limited due to side effects and decreased effectiveness. Catheter ablation (CA) has emerged as a promising therapy for drug-refractory VTs, especially in patients with structural heart disease. This article reviews current knowledge on the indications, efficacy, and long-term prognosis of CA in patients with HF. Additionally, it discusses the importance of preprocedural planning, risk stratification, and emerging therapeutic strategies such as mechanical circulatory support and stereotactic arrhythmia radioablation. The complex relationship between VT and HF, as well as potential risks like acute hemodynamic decompensation, are also addressed.
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Affiliation(s)
- M Ebert
- Sektion Rhythmologie, Klinik für Innere Medizin und Kardiologie, Herzzentrum Dresden, Medizinische Fakultät und Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 76, 01307, Dresden, Deutschland.
| | - Y Thomsen
- Sektion Rhythmologie, Klinik für Innere Medizin und Kardiologie, Herzzentrum Dresden, Medizinische Fakultät und Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 76, 01307, Dresden, Deutschland
| | - S Richter
- Sektion Rhythmologie, Klinik für Innere Medizin und Kardiologie, Herzzentrum Dresden, Medizinische Fakultät und Universitätsklinikum Carl Gustav Carus, Technische Universität Dresden, Fetscherstr. 76, 01307, Dresden, Deutschland
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Kanthasamy V, Ang R, Sridhar A, Vyas S, Whittaker-Axon S, Schilling R, Honarbakhsh S, Papageorgiou N, Creta A, Ahluwalia N, Hunter R, Finlay M. Subclavian Ansae Stimulation on Cardiac Hemodynamics and Electrophysiology in Atrial Fibrillation: A Target for Sympathetic Neuromodulation. JACC Clin Electrophysiol 2024:S2405-500X(24)00931-9. [PMID: 39797853 DOI: 10.1016/j.jacep.2024.10.023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/28/2024] [Revised: 09/23/2024] [Accepted: 10/21/2024] [Indexed: 01/13/2025]
Abstract
BACKGROUND The sympathetic autonomic nervous system plays a major role in arrhythmia development and maintenance. Historical preclinical studies describe preferential increases in cardiac sympathetic tone upon selective stimulation of the subclavian ansae (SA), a nerve cord encircling the subclavian artery. OBJECTIVES This study sought to define, for the first time, the functional anatomy and physiology of the SA in humans using a percutaneous approach. METHODS The authors prospectively recruited patients undergoing catheter ablation for paroxysmal atrial fibrillation (AF) under general anesthesia. SA stimulation (SAS) was performed on the left and/or the right (L/SAS and/or R/SAS, respectively) within the subclavian artery using an ablation catheter introduced via a femoral arterial sheath. Stimulation involved up to 70 V, 10 Hz, and a 2- to 4-millisecond pulse width for 15 to 30 seconds. Invasive blood pressure (BP), heart rate, and electrophysiological parameters were recorded. A positive response was a ≥10% increase in BP or heart rate from baseline. RESULTS Seventeen patients (median age 60 years [quartile 1-quartile 3: 58-67 years];11 male subjects; paroxysmal AF duration 24 months [quartile 1-quartile 3: 10-60 months) underwent the stimulation protocol before their clinical AF ablation procedure. A positive hemodynamic response was observed in 11 patients; of these, arrhythmia was inducible in 5 patients. The median sinus cycle length decreased after stimulation, and there was a larger decrease with R/SAS (L/SAS 1,008 milliseconds to 926 milliseconds [P = 0.037] vs R/SAS 1,029.5 milliseconds to 917 milliseconds [P = 0.005]). Both L/SAS and R/SAS led to a notable increase in median systolic BP (L/SAS 81 mm Hg to 128 mm Hg [P = 0.005] vs R/SAS 85 mm Hg to 104 mm Hg [P = 0.007]) and a similar trend in diastolic BP. In addition, there was a demonstrable decrease in interatrial conduction time and increase in P-wave dispersion. CONCLUSIONS This study represents the first successful application of selective SAS in humans. The SA is a potentially important site for targeted autonomic neuromodulation therapy.
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Affiliation(s)
- Vijayabharathy Kanthasamy
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom
| | - Richard Ang
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom
| | | | - Sandip Vyas
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom
| | | | - Richard Schilling
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom
| | - Shohreh Honarbakhsh
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom
| | | | - Antonio Creta
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom
| | - Nikhil Ahluwalia
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom
| | - Ross Hunter
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom
| | - Malcolm Finlay
- St Bartholomew's Hospital, Barts Health NHS Trust, London, United Kingdom; William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.
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Leung HT, Kwok SY, Lau M, Lee LKF, Tsao S. Case Report: The unrelenting journey-successful resolution of catecholaminergic polymorphic ventricular tachycardia (CPVT) through right cardiac sympathetic denervation in a teenager after left cardiac sympathetic denervation. Front Cardiovasc Med 2024; 11:1477359. [PMID: 39735866 PMCID: PMC11671521 DOI: 10.3389/fcvm.2024.1477359] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2024] [Accepted: 11/25/2024] [Indexed: 12/31/2024] Open
Abstract
Background Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited arrhythmia disorder characterized by ventricular arrhythmia triggered by adrenergic stimulation. Case presentation A 9-year-old boy presented with convulsions following physical exertion. Bidirectional ventricular tachycardia (VT) during a treadmill test led to the diagnosis of catecholaminergic polymorphic ventricular tachycardia (CPVT). Genetic testing revealed a pathogenic variant of RYR2:c.720G>A (p.ArG2401His). Nadolol was initially started. However, he experienced aborted VT arrest three years later. Flecainide was thus added as dual therapy and he underwent left cardiac sympathetic denervation (LCSD). Subsequently, a transvenous implantable cardioverter-defibrillator (ICD) was implanted because he still had several episodes of bidirectional VT. Despite a good compliance to medication, the patient still had exercise induced VT episodes with new onset of atrial fibrillation. High dose nadolol was required and amiodarone was added. Despite maximizing the dosage of these three antiarrhythmics, the patient continued to experience multiple episodes of ventricular fibrillation with appropriate ICD shocks and persistent atrial arrhythmias. Right cardiac sympathetic denervation (RCSD) was performed as the last modality of treatment. Patient had a total elimination of VT post bilateral sympathectomy. He remained asymptomatic on follow up. A follow-up treadmill test showed no recurrence of exercise-induced PVCs and VT. Conclusion We illustrated the challenges and the complex decision-making process encountered in managing refractory CPVT. In patients unresponsive to conventional therapies, RCSD in additional to LCSD is a safe and effective alternative treatment. A history of LCSD should not preclude physicians from considering RCSD in children with refractory CPVT.
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Affiliation(s)
- Hei-To Leung
- Department of Paediatrics and Adolescent Medicine, Hong Kong Children's Hospital, Kowloon, Hong Kong SAR, China
| | - Sit-Yee Kwok
- Department of Paediatrics and Adolescent Medicine, Hong Kong Children's Hospital, Kowloon, Hong Kong SAR, China
| | - Ming Lau
- Department of Cardiothoracic Surgery, Queen Mary Hospital, Pok Fu Lam, Hong Kong SAR, China
| | - Lucius Kwok-Fai Lee
- Department of Cardiothoracic Surgery, Queen Mary Hospital, Pok Fu Lam, Hong Kong SAR, China
| | - Sabrina Tsao
- Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, Pok Fu Lam, Hong Kong SAR, China
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Vrabec T, Bender S, Chan SA, Cha S, Haridas S, Hanna P, Ajijola OA, Shivkumar K, Smith C, Ardell JL. Bioelectronic block of stellate ganglia mitigates pacing-induced heterogeneous release of catecholamine and neuropeptide Y in the infarcted pig heart. J Physiol 2024. [PMID: 39557601 DOI: 10.1113/jp286924] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2024] [Accepted: 10/23/2024] [Indexed: 11/20/2024] Open
Abstract
The sympathetic nervous system modulates cardiac contractile and electrophysiological function and contributes to adverse remodelling following myocardial infarction (MI). Axonal modulation therapy (AMT), directed at the sympathetic chain, blocks efferent sympathetic outflow to the heart and is a strategy to transiently and controllably mitigate chronic MI-associated sympatho-excitation. In porcine models, we evaluated scalable AMT, directed at the paravertebral chain, in blocking reflex-mediated pacing-induced sympatho-excitation post-MI. The level of sympatho-excitation was assessed by dynamic interstitial measurement of noradrenaline (NA) and neuropeptide Y (NPY). In anaesthetized normal (n = 5) and age-matched pigs 6 weeks post-MI induction (n = 10), we electrically stimulated the right sympathetic chain and determined levels of direct current block applied at the T1-T2 level sufficient to reduce the evoked changes in heart rate and/or contractility by 25-75%. Reflex-mediated neural release of NA and NPY into the interstitial space during programmed pacing (PP) was assessed using fast-scanning cyclic voltammetry and capacitive immunoprobes. Normal animals demonstrated homogeneous NA and NPY release profiles during PP. In contrast, for MI animals PP evoked differential NA and NPY release in remote and MI border zones of the left ventricle. Right-sided AMT mitigated NA and NPY pacing-induced release in the remote left ventricle with a positive correlation to increasing AMT levels. Pacing-induced NA and NPY release in the MI border zone was not mitigated by AMT. Differential effects of AMT on NA and NPY may underlie the anti-arrhythmic effects of partial stellate ganglion block in the setting of chronic MI. KEY POINTS: Programmed cardiac pacing evokes homogeneous noradrenaline (NA) and neuropeptide Y (NPY) release in equivalent areas (e.g. medial and lateral aspects) of the normal left ventricle. Programmed cardiac pacing evokes differential NA and NPY release in remote and border zones of the infarcted left ventricle. Axonal modulation therapy (AMT), using a graded direct current block applied to the stellate ganglia, can proportionally modulate cardiac sympathetic reflexes. Unilateral AMT mitigates NA and NPY release in remote left ventricular tissue, with release negatively correlated to increasing AMT levels. Heterogeneities in NA and NPY between the border and remote tissues are reduced by progressive AMT.
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Affiliation(s)
- Tina Vrabec
- Department of Physical Medicine & Rehabilitation, MetroHealth Medical Center, Cleveland, OH, USA
- Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH, USA
| | - Shane Bender
- Department of Physical Medicine & Rehabilitation, MetroHealth Medical Center, Cleveland, OH, USA
- Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH, USA
| | - Shyue-An Chan
- Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
| | - Steven Cha
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
| | - Sahil Haridas
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
| | - Peter Hanna
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
| | - Olujimi A Ajijola
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
| | - Kalyanam Shivkumar
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
| | - Corey Smith
- Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
| | - Jeffrey L Ardell
- David Geffen School of Medicine, University of California - Los Angeles (UCLA) Cardiac Arrhythmia Center, Los Angeles, CA, USA
- UCLA Neurocardiology Research Program of Excellence, Los Angeles, CA, USA
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Khan S, Abdo DBFK, Mushtaq V, Ahmed N, Bai K, Neelam F, Malik M, Malik J. Cardiac Implantable Electronic Devices in Cardiac Transplant Patients: A Comprehensive Review. Cardiol Rev 2024:00045415-990000000-00368. [PMID: 39707617 DOI: 10.1097/crd.0000000000000817] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/23/2024]
Abstract
A fraction of patients (approximately 10%) undergoing heart transplantation require permanent pacemaker (PPM) implantation due to sinus node dysfunction or atrioventricular block, occurring either shortly after surgery or later. The incidence of PPM implantation has declined to less than 5% with the introduction of bicaval anastomosis transplantation surgery. Pacing dependency during follow-up varies among recipients. A smaller subset (1.5-3.4%) receives implantable cardioverter-defibrillators (ICDs), but data on their use in transplant recipients are limited, primarily from cohort studies and case series. Sudden cardiac death affects around 10% of transplant recipients, attributed to various nonarrhythmic factors such as acute rejection, late graft failure, and cardiac allograft vasculopathy-induced ischemia. This review offers a comprehensive analysis of the existing data concerning the role of PPMs and ICDs in this population, encompassing leadless PPMs, subcutaneous ICDs, unique considerations, and future directions.
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Affiliation(s)
- Shayan Khan
- From the Department of Cardiology, Pakistan Institute of Medical Sciences, Islamabad, Pakistan
| | | | - Varda Mushtaq
- Department of Medicine, Liaquat University of Medical and Health Sciences, Jamshoro, Pakistan
| | - Najeeb Ahmed
- Department of Medicine, Liaquat University of Medical and Health Sciences, Jamshoro, Pakistan
| | - Kajal Bai
- Department of Medicine, Chandka Medical College, Larkana, Pakistan
| | - Fnu Neelam
- Department of Medicine, Jinnah Sindh Medical University, Karachi, Pakistan
| | - Maria Malik
- Department of Cardiovascular Medicine, Cardiovascular Analytics Group, Islamabad, Pakistan
| | - Jahanzeb Malik
- Department of Cardiovascular Medicine, Cardiovascular Analytics Group, Islamabad, Pakistan
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Hu H, Wu H, Zhu T, Cheng Y, Guo W, Tan T, Hu C, Jiang H, Wang S. Long-term transcranial ultrasound stimulation regulates neuroinflammation to ameliorate post-myocardial infarction cardiac arrhythmia and remodeling. Heart Rhythm 2024:S1547-5271(24)03442-8. [PMID: 39413944 DOI: 10.1016/j.hrthm.2024.10.017] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/25/2024] [Revised: 10/01/2024] [Accepted: 10/08/2024] [Indexed: 10/18/2024]
Abstract
BACKGROUND Sympathetic overactivation and neuroinflammation in the paraventricular nucleus (PVN) are crucial factors in post-myocardial infarction (MI) cardiac remodeling and ventricular arrhythmias (VAs). Prior study has indicated that low-intensity focused ultrasound stimulation could attenuate sympathetic neuroinflammation within the PVN to prevent the occurrence of VAs in an acute MI model. Meanwhile, the cGAS-STING pathway has shown potential to ameliorate the neuroinflammatory response. However, the effect and mechanisms of long-term transcranial ultrasound stimulation (LTUS) for modulating neuroinflammation in the chronic stage of MI remain unclear. OBJECTIVE This study aimed to ascertain whether LTUS could mitigate post-MI neuroinflammation and improve cardiac arrhythmia and remodeling through the cGAS-STING pathway. METHODS Thirty-six SD rats were equally randomized to the sham group (pseudo-MI modeling), chronic MI group (MI modeling), and LTUS group (MI modeling and long-term ultrasound stimulation). Transcranial ultrasound stimulation (15 min/d) was conducted on the PVN for 4 consecutive weeks. After 4-week intervention, echocardiography, electrophysiologic experiments, and histopathologic staining were performed to assess the role of LTUS on post-MI neuroinflammation and cardiac remodeling. RESULTS The results indicated that LTUS significantly facilitated microglial M1 to M2 polarization through the cGAS-STING signaling pathway within the PVN. Furthermore, LTUS inhibited MI-induced sympathetic neuroinflammation, thereby improving cardiac dysfunction, ameliorating cardiac remodeling, and reducing VA inducibility. CONCLUSION Long-term ultrasound stimulation of the PVN was found to alleviate post-MI neuroinflammation and to improve cardiac remodeling, which might inspire novel insights and clinical strategies for noninvasive neuromodulation and the treatment of post-MI VAs.
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Affiliation(s)
- Haoyuan Hu
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Huijun Wu
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Tongjian Zhu
- Department of Cardiology, Xiangyang Central Hospital, Xiangyang, China
| | - Ye Cheng
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Wei Guo
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Tuantuan Tan
- Department of Ultrasonography, Renmin Hospital of Wuhan University, Wuhan, China
| | - Changhao Hu
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Hong Jiang
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China.
| | - Songyun Wang
- Department of Cardiology, Renmin Hospital of Wuhan University; Cardiac Autonomic Nervous System Research Center of Wuhan University; Cardiovascular Research Institute, Wuhan University; Hubei Key Laboratory of Cardiology, Wuhan, China.
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Salavatian S, Wong B, Kuwabara Y, Fritz JR, Varghese CG, Howard-Quijano K, Armour JA, Foreman RD, Ardell JL, Mahajan A. Comparing the Memory Effects of 50-Hz Low-Frequency and 10-kHz High-Frequency Thoracic Spinal Cord Stimulation on Spinal Neural Network in a Myocardial Infarction Porcine Model. Neuromodulation 2024; 27:1177-1186. [PMID: 39078348 DOI: 10.1016/j.neurom.2024.06.002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/09/2024] [Revised: 05/29/2024] [Accepted: 06/06/2024] [Indexed: 07/31/2024]
Abstract
OBJECTIVE This study evaluated the effects of cessation of both conventional low-frequency (50 Hz) and high-frequency (10 kHz) spinal cord stimulation (SCS) on the cardiospinal neural network activity in pigs with myocardial infarction (MI). The objective is to provide an insight into the memory effect of SCS. MATERIALS AND METHODS In nine Yorkshire pigs, chronic MI was created by delivering microspheres to the left circumflex coronary artery. Five weeks after MI, anesthetized pigs underwent sternotomy to expose the heart for performing acute ischemia intervention, and laminectomy to expose the T1-T4 spinal regions for extracellular in vivo neural recording and SCS. Cardiac ischemic-sensitive neurons were identified by selective responsiveness to left anterior descending (LAD) coronary artery occlusion. SCS episodes were delivered in a random order between low- (50 Hz) and high- (10 kHz) frequency, for 1 minute, at 90% of the motor threshold current. Neural firing and synchrony of ischemic-sensitive spinal neurons were evaluated before vs after SCS. RESULTS Using a 64-channel microelectrode array, 2711 spinal neurons were recorded extracellularly. LAD ischemia excited 228 neurons that were labeled as ischemic-responsive neurons. The cessation of 50-Hz SCS caused a higher activation than did inhibition of ischemic-responsive neurons (41 activated vs 19 inhibited), whereas the cessation of 10-kHz SCS caused an opposite response with higher inhibition (11 activated vs 28 inhibited, p < 0.01 vs 50 Hz). Termination of low-frequency SCS caused an increase in ischemic-responsive neuronal firing rate compared with high-frequency SCS (50 Hz: 0.39 Hz ± 0.16 Hz, 10 kHz: -0.11 Hz ± 0.057 Hz, p < 0.01). In addition, SCS delivered at 50 Hz increased the number of synchronized pairs of neurons by 205 pairs, whereas high-frequency SCS decreased the number of synchronized pairs by 345 pairs (p < 0.01). CONCLUSIONS High-frequency (10 kHz) stimulation provides persistent suppression of the ischemia-sensitive neurons after termination of SCS. In contrast, the spinal neural network reverted to excitatory state after termination of low-frequency (50 Hz) stimulation.
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Affiliation(s)
- Siamak Salavatian
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Medicine, Division of Cardiology, University of Pittsburgh, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA
| | - Benjamin Wong
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA
| | - Yuki Kuwabara
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - Jonathan R Fritz
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - Christopher G Varghese
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - Kimberly Howard-Quijano
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - J Andrew Armour
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA
| | - Robert D Foreman
- Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - Jeffrey L Ardell
- Cardiac Arrhythmia Center and Neurocardiology Research Program of Excellence, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
| | - Aman Mahajan
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, USA; Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA.
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10
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Herring N, Ajijola OA, Foreman RD, Gourine AV, Green AL, Osborn J, Paterson DJ, Paton JFR, Ripplinger CM, Smith C, Vrabec TL, Wang HJ, Zucker IH, Ardell JL. Neurocardiology: translational advancements and potential. J Physiol 2024. [PMID: 39340173 DOI: 10.1113/jp284740] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2024] [Accepted: 09/03/2024] [Indexed: 09/30/2024] Open
Abstract
In our original white paper published in the The Journal of Physiology in 2016, we set out our knowledge of the structural and functional organization of cardiac autonomic control, how it remodels during disease, and approaches to exploit such knowledge for autonomic regulation therapy. The aim of this update is to build on this original blueprint, highlighting the significant progress which has been made in the field since and major challenges and opportunities that exist with regard to translation. Imbalances in autonomic responses, while beneficial in the short term, ultimately contribute to the evolution of cardiac pathology. As our understanding emerges of where and how to target in terms of actuators (including the heart and intracardiac nervous system (ICNS), stellate ganglia, dorsal root ganglia (DRG), vagus nerve, brainstem, and even higher centres), there is also a need to develop sensor technology to respond to appropriate biomarkers (electrophysiological, mechanical, and molecular) such that closed-loop autonomic regulation therapies can evolve. The goal is to work with endogenous control systems, rather than in opposition to them, to improve outcomes.
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Affiliation(s)
- N Herring
- Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK
| | - O A Ajijola
- UCLA Neurocardiology Research Center of Excellence, David Geffen School of Medicine, Los Angeles, CA, USA
| | - R D Foreman
- Department of Biochemistry and Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA
| | - A V Gourine
- Centre for Cardiovascular and Metabolic Neuroscience, University College London, London, UK
| | - A L Green
- Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK
| | - J Osborn
- Department of Surgery, University of Minnesota, Minneapolis, MN, USA
| | - D J Paterson
- Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK
| | - J F R Paton
- Manaaki Manawa - The Centre for Heart Research, Department of Physiology, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand
| | - C M Ripplinger
- Department of Pharmacology, University of California Davis, Davis, CA, USA
| | - C Smith
- Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH, USA
| | - T L Vrabec
- Department of Physical Medicine and Rehabilitation, School of Medicine, Case Western Reserve University, Cleveland, OH, USA
| | - H J Wang
- Department of Anesthesiology, University of Nebraska Medical Center, Omaha, NE, USA
| | - I H Zucker
- Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA
| | - J L Ardell
- UCLA Neurocardiology Research Center of Excellence, David Geffen School of Medicine, Los Angeles, CA, USA
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11
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Sarkar A, Ajijola OA. Pathophysiologic Mechanisms in Cardiac Autonomic Nervous System and Arrhythmias. Card Electrophysiol Clin 2024; 16:261-269. [PMID: 39084719 DOI: 10.1016/j.ccep.2023.11.001] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 08/02/2024]
Abstract
The autonomic nervous system, including the central nervous system and the cardiac plexus, maintains cardiac physiology. In diseased states, autonomic changes through neuronal remodeling generate electrical mechanisms of arrhythmia such as triggered activity or increased automaticity. This article will focus on the pathophysiological mechanisms of arrhythmia to highlight the role of the autonomic nervous system in disease and the related therapeutic interventions.
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Affiliation(s)
- Abdullah Sarkar
- UCLA Cardiac Arrhythmia Center and Neurocardiology Research program of Excellence, Los Angeles, CA, USA
| | - Olujimi A Ajijola
- UCLA Cardiac Arrhythmia Center and Neurocardiology Research program of Excellence, Los Angeles, CA, USA.
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12
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Brady S, Matthia E, Antoine S, Aranda J, Miles W, Vilaro J, Al-Ani M, Oduntan O, Guo Y, Li Y, Ahmed M, Parker A. Outcome of Patients With Systolic Heart Failure Who Underwent Sympathectomy for Ventricular Arrhythmia. Am J Cardiol 2024; 225:37-40. [PMID: 38866354 DOI: 10.1016/j.amjcard.2024.05.035] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/27/2024] [Revised: 05/19/2024] [Accepted: 05/24/2024] [Indexed: 06/14/2024]
Abstract
Cardiac sympathetic denervation (CSD) is a surgical procedure increasingly used for managing ventricular arrhythmia refractory to conventional medical therapy. Long-term outcomes of CSD in patients with systolic heart failure has not been well studied. This observational study aimed to evaluate the medical co-morbidities and outcomes of patients with systolic heart failure who underwent CSD performed as treatment for ventricular arrhythmia refractory to conventional therapy. A retrospective analysis in adult patients with ventricular arrhythmia and systolic heart failure who underwent unilateral or bilateral CSD at a single center was performed. Unadjusted Kaplan-Meier survival curves were constructed to evaluate survival after CSD. Between June 1, 2011 and March 31, 2021, 32 adult patients (age 62 ± 11.6 years, 88% male, left ventricular ejection fraction 22% ± 8.2%) with systolic heart failure underwent unilateral left (n = 4), unilateral right (n = 1), or bilateral CSD (n = 27). Mean survival after CSD was 613 ± 745 days, and the mean time from CSD to death was 291 ± 447 days. The cumulative probability of survival 1 year after CSD was 61.4%. In this single-center observational study, CSD performed for refractory ventricular arrhythmia showed favorable survival in patients with systolic heart failure. In conclusion, this study lays the groundwork for a more in-depth analysis of the potential survival benefits of CSD in this patient group.
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Affiliation(s)
- Steven Brady
- Department of Medicine, University of Florida, Gainesville, Florida.
| | - Eldon Matthia
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - Steve Antoine
- Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, Texas
| | - Juan Aranda
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - William Miles
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - Juan Vilaro
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - Mohammad Al-Ani
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - Olusola Oduntan
- Division of Thoracic Surgery, Department of Surgery, University of Florida, Gainesville, Florida
| | - Yi Guo
- Department of Health Outcomes and Biomedical Informatics, College of Medicine, University of Florida, Gainesville, Florida
| | - Yujia Li
- Department of Pharmaceutical Outcomes and Policy, College of Pharmacy, University of Florida, Gainesville, Florida
| | - Mustafa Ahmed
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
| | - Alex Parker
- Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida
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13
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Markman TM, Marchlinski FE, Callans DJ, Frankel DS. Programmed Ventricular Stimulation: Risk Stratification and Guiding Antiarrhythmic Therapies. JACC Clin Electrophysiol 2024; 10:1489-1507. [PMID: 38661601 DOI: 10.1016/j.jacep.2024.02.034] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2024] [Accepted: 02/13/2024] [Indexed: 04/26/2024]
Abstract
Electrophysiologic testing with programmed ventricular stimulation (PVS) has been utilized to induce ventricular tachycardia (VT), thereby improving risk stratification for patients with ischemic and nonischemic cardiomyopathies and determining the effectiveness of antiarrhythmic therapies, especially catheter ablation. A variety of procedural aspects can be modified during PVS in order to alter the sensitivity and specificity of the test including the addition of multiple baseline pacing cycle lengths, extrastimuli, and pacing locations. The definition of a positive result is also critically important, which has varied from exclusively sustained monomorphic VT (>30 seconds) to any ventricular arrhythmia regardless of morphology. In this review, we discuss the history of PVS and evaluate its role in sudden cardiac death risk stratification in a variety of patient populations. We propose an approach to future investigations that will capitalize on the unique ability to vary the sensitivity and specificity of this test. We then discuss the application of PVS during and following catheter ablation. The strategies that have been utilized to improve the efficacy of intraprocedural PVS are highlighted during a discussion of the limitations of this probabilistic strategy. The role of noninvasive programmed stimulation is also reviewed in predicting recurrent VT and informing management decisions including repeat ablations, modifications in antiarrhythmic drugs, and implantable cardioverter-defibrillator programming. Based on the available evidence and guidelines, we propose an approach to future investigations that will allow clinicians to optimize the use of PVS for risk stratification and assessment of therapeutic efficacy.
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Affiliation(s)
- Timothy M Markman
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Francis E Marchlinski
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - David J Callans
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - David S Frankel
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
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14
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Li M, Sorensen M, Johnson MA, Ingram SL, Andresen MC, Habecker BA. Hypertension increases sympathetic neuron activity by enhancing intraganglionic cholinergic collateral connections. J Physiol 2024:10.1113/JP286601. [PMID: 39031543 PMCID: PMC11662085 DOI: 10.1113/jp286601] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/20/2024] [Accepted: 06/06/2024] [Indexed: 07/22/2024] Open
Abstract
Autonomic dysregulation, including sympathetic hyperactivity, is a common feature of hypertension (HT) and other cardiovascular diseases. The CNS plays a role in driving chronic sympathetic activation in disease, but several lines of evidence suggest that neuroplasticity in the periphery may also contribute. The potential contribution of postganglionic sympathetic neurons to sustained sympathetic hyperactivity is not well understood. We recently discovered that noradrenergic sympathetic neurons in the stellate ganglion (SG) have excitatory cholinergic collateral connections to other neurons within the ganglion. We hypothesize that remodelling of these neurons and increased cholinergic collateral transmission contributes to sustained sympathetic hyperactivity in cardiovascular diseases, including HT. To test that hypothesis, we examined the activity of sympathetic neurons in isolated SG under control conditions and after 1 week of HT induced by peripheral angiotensin II infusion, using whole-cell patch clamp recordings. Despite the absence of central inputs, we observed elevated spontaneous activity and synaptic transmission in sympathetic SG neurons from hypertensive mice that required generation of action potentials. Genetically disrupting cholinergic transmission in noradrenergic neurons decreased basal neuronal activity and prevented angiotensin II-mediated enhancement of activity. Similar changes in activity, driven by increased collateral transmission, were identified in cardiac projecting neurons and neurons projecting to brown adipose tissue. These changes were not driven by altered A-type K+ currents. This suggests that HT stimulates increased activity throughout the intraganglionic network of collateral connections, contributing to the sustained sympathetic hyperactivity characteristic in cardiovascular disease. KEY POINTS: Sympathetic neurons in ganglia isolated from angiotensin II-treated hypertensive mice are more active than neurons from control mice despite the absence of central activation. The enhanced activity is the result of a ganglionic network of cholinergic collaterals, rather than altered intrinsic excitability. Increased neuronal activity was observed in both cardiac neurons and brown adipose tissue-projecting neurons, which are not involved in cardiovascular homeostasis.
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Affiliation(s)
- Minghua Li
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, United States of America, 97239
| | - Michelle Sorensen
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, United States of America, 97239
| | - Morgan A. Johnson
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, United States of America, 97239
| | - Susan L. Ingram
- Department of Anesthesiology, University of Colorado Anschutz Medical Campus, Aurora, CO 80045
| | - Michael C. Andresen
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, United States of America, 97239
| | - Beth A. Habecker
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, OR, United States of America, 97239
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15
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Álvarez-Ortega C, Gómez-Martínez JD, Cardona-Gallardo MA, Torres-España NF, Pava-Molano LF, Sánchez-Ortiz ÁI, Velásquez-Galvis M. Cardiac Sympathetic Denervation as a Treatment for Ventricular Arrhythmias Refractory to Conventional Treatment: A Case Series. Interv Cardiol 2024; 19:e06. [PMID: 38808282 PMCID: PMC11131149 DOI: 10.15420/icr.2023.09] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/21/2023] [Accepted: 06/01/2023] [Indexed: 05/30/2024] Open
Abstract
Background Ventricular arrhythmias are a leading cause of sudden death. The objective of this study was to characterise the results of patients with ventricular arrhythmias refractory to standard medical management, undergoing Video-assisted thoracoscopic cardiac sympathetic denervation (VAT-CSD) during 2012-2022 in Cali, Colombia. Methods This was an observational retrospective study, using the Institutional General Thoracic Surgery Database for patient identification and retrospectively reviewing the clinical charts for data description and analysis. Results Clinical records of 19 patients who underwent VAT-CSD for ventricular arrhythmia were analysed. The patients were predominantly male (73.7%) with an mean age of 62 years. Ischaemic heart disease was the main underlying condition (52.6%); all individuals had a diagnosis of heart failure, with comorbidities such as hypertension (63.1%), acute MI (57.8%) and diabetes (26.3%) also present. The procedure was performed bilaterally in 89.4% of cases and was successful with minimal perioperative complications. Postoperative follow-up showed improvement in symptoms, including a significant reduction in the number of ICD shocks and emergency department visits. Conclusion VAT-CSD is a viable, safe and palliative therapeutic option for patients with ventricular arrhythmias who have not responded to conventional treatments, achieving a significant decrease in symptoms with low mortality and perioperative complications.
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16
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Bauer J, Vlcek J, Pauly V, Hesse N, Xia R, Mo L, Chivukula AS, Villgrater H, Dressler M, Hildebrand B, Wolf E, Rizas KD, Bauer A, Kääb S, Tomsits P, Schüttler D, Clauss S. Biomarker Periodic Repolarization Dynamics Indicates Enhanced Risk for Arrhythmias and Sudden Cardiac Death in Myocardial Infarction in Pigs. J Am Heart Assoc 2024; 13:e032405. [PMID: 38639363 PMCID: PMC11179938 DOI: 10.1161/jaha.123.032405] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/29/2023] [Accepted: 03/08/2024] [Indexed: 04/20/2024]
Abstract
BACKGROUND Periodic repolarization dynamics (PRD) is an electrocardiographic biomarker that captures repolarization instability in the low frequency spectrum and is believed to estimate the sympathetic effect on the ventricular myocardium. High PRD indicates an increased risk for postischemic sudden cardiac death (SCD). However, a direct link between PRD and proarrhythmogenic autonomic remodeling has not yet been shown. METHODS AND RESULTS We investigated autonomic remodeling in pigs with myocardial infarction (MI)-related ischemic heart failure induced by balloon occlusion of the left anterior descending artery (n=17) compared with pigs without MI (n=11). Thirty days after MI, pigs demonstrated enhanced sympathetic innervation in the infarct area, border zone, and remote left ventricle paralleled by altered expression of autonomic marker genes/proteins. PRD was enhanced 30 days after MI compared with baseline (pre-MI versus post-MI: 1.75±0.30 deg2 versus 3.29±0.79 deg2, P<0.05) reflecting pronounced autonomic alterations on the level of the ventricular myocardium. Pigs with MI-related ventricular fibrillation and SCD had significantly higher pre-MI PRD than pigs without tachyarrhythmias, suggesting a potential role for PRD as a predictive biomarker for ischemia-related arrhythmias (no ventricular fibrillation versus ventricular fibrillation: 1.50±0.39 deg2 versus 3.18±0.53 deg2 [P<0.05]; no SCD versus SCD: 1.67±0.32 deg2 versus 3.91±0.63 deg2 [P<0.01]). CONCLUSIONS We demonstrate that ischemic heart failure leads to significant proarrhythmogenic autonomic remodeling. The concomitant elevation of PRD levels in pigs with ischemic heart failure and pigs with MI-related ventricular fibrillation/SCD suggests PRD as a biomarker for autonomic remodeling and as a potential predictive biomarker for ventricular arrhythmias/survival in the context of MI.
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Affiliation(s)
- Julia Bauer
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Julia Vlcek
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Valerie Pauly
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Nora Hesse
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Ruibing Xia
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Li Mo
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Aparna Sharma Chivukula
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Hannes Villgrater
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Marie Dressler
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Bianca Hildebrand
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
| | - Eckhard Wolf
- Chair for Molecular Animal Breeding and Biotechnology, Gene Center and Department of Veterinary Sciences, LMU MunichMunichGermany
- Interfaculty Center for Endocrine and Cardiovascular Disease Network Modelling and Clinical Transfer (ICONLMU), LMU MunichMunichGermany
| | - Konstantinos D. Rizas
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
| | - Axel Bauer
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- University Hospital for Internal Medicine IIIMedical University of InnsbruckInnsbruckAustria
| | - Stefan Kääb
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Interfaculty Center for Endocrine and Cardiovascular Disease Network Modelling and Clinical Transfer (ICONLMU), LMU MunichMunichGermany
| | - Philipp Tomsits
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Dominik Schüttler
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
| | - Sebastian Clauss
- Department of Medicine IUniversity Hospital, LMU MunichMunichGermany
- German Center for Cardiovascular Research (DZHK), Partner Site Munich, Munich Heart AllianceMunichGermany
- Institute of Surgical Research at the Walter‐Brendel‐Centre of Experimental MedicineUniversity Hospital, LMU MunichMunichGermany
- Interfaculty Center for Endocrine and Cardiovascular Disease Network Modelling and Clinical Transfer (ICONLMU), LMU MunichMunichGermany
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17
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Lenarczyk R, Zeppenfeld K, Tfelt-Hansen J, Heinzel FR, Deneke T, Ene E, Meyer C, Wilde A, Arbelo E, Jędrzejczyk-Patej E, Sabbag A, Stühlinger M, di Biase L, Vaseghi M, Ziv O, Bautista-Vargas WF, Kumar S, Namboodiri N, Henz BD, Montero-Cabezas J, Dagres N. Management of patients with an electrical storm or clustered ventricular arrhythmias: a clinical consensus statement of the European Heart Rhythm Association of the ESC-endorsed by the Asia-Pacific Heart Rhythm Society, Heart Rhythm Society, and Latin-American Heart Rhythm Society. Europace 2024; 26:euae049. [PMID: 38584423 PMCID: PMC10999775 DOI: 10.1093/europace/euae049] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2024] [Accepted: 02/07/2024] [Indexed: 04/09/2024] Open
Abstract
Electrical storm (ES) is a state of electrical instability, manifesting as recurrent ventricular arrhythmias (VAs) over a short period of time (three or more episodes of sustained VA within 24 h, separated by at least 5 min, requiring termination by an intervention). The clinical presentation can vary, but ES is usually a cardiac emergency. Electrical storm mainly affects patients with structural or primary electrical heart disease, often with an implantable cardioverter-defibrillator (ICD). Management of ES requires a multi-faceted approach and the involvement of multi-disciplinary teams, but despite advanced treatment and often invasive procedures, it is associated with high morbidity and mortality. With an ageing population, longer survival of heart failure patients, and an increasing number of patients with ICD, the incidence of ES is expected to increase. This European Heart Rhythm Association clinical consensus statement focuses on pathophysiology, clinical presentation, diagnostic evaluation, and acute and long-term management of patients presenting with ES or clustered VA.
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Affiliation(s)
- Radosław Lenarczyk
- Medical University of Silesia, Division of Medical Sciences, Department of Cardiology and Electrotherapy, Silesian Center for Heart Diseases, Skłodowskiej-Curie 9, 41-800 Zabrze, Poland
| | - Katja Zeppenfeld
- Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
| | - Jacob Tfelt-Hansen
- The Department of Cardiology, The Heart Centre, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
- The Department of Forensic Medicine, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
| | - Frank R Heinzel
- Cardiology, Angiology, Intensive Care, Städtisches Klinikum Dresden Campus Friedrichstadt, Dresden, Germany
| | - Thomas Deneke
- Clinic for Interventional Electrophysiology, Heart Center RHÖN-KLINIKUM Campus Bad Neustadt, Bad Neustadt an der Saale, Germany
- Clinic for Electrophysiology, Klinikum Nuernberg, University Hospital of the Paracelsus Medical University, Nuernberg, Germany
| | - Elena Ene
- Clinic for Interventional Electrophysiology, Heart Center RHÖN-KLINIKUM Campus Bad Neustadt, Bad Neustadt an der Saale, Germany
| | - Christian Meyer
- Division of Cardiology/Angiology/Intensive Care, EVK Düsseldorf, Teaching Hospital University of Düsseldorf, Düsseldorf, Germany
| | - Arthur Wilde
- Department of Cardiology, Amsterdam UMC University of Amsterdam, Amsterdam, the Netherlands
- Amsterdam Cardiovascular Sciences, Heart Failure and arrhythmias, Amsterdam, the Netherlands
| | - Elena Arbelo
- Arrhythmia Section, Cardiology Department, Hospital Clínic, Universitat de Barcelona, Barcelona, Spain; IDIBAPS, Institut d'Investigació August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain
| | - Ewa Jędrzejczyk-Patej
- Department of Cardiology, Congenital Heart Diseases and Electrotherapy, Silesian Centre for Heart Diseases, Zabrze, Poland
| | - Avi Sabbag
- The Davidai Center for Rhythm Disturbances and Pacing, Chaim Sheba Medical Center, Tel Hashomer, Israel
- School of Medicine, Faculty of Medical and Health Sciences, Tel Aviv University, Tel Aviv, Israel
| | - Markus Stühlinger
- Department of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria
| | - Luigi di Biase
- Albert Einstein College of Medicine at Montefiore Hospital, New York, NY, USA
| | - Marmar Vaseghi
- UCLA Cardiac Arrythmia Center, Division of Cardiology, Department of Medicine, University of California, Los Angeles, CA, USA
| | - Ohad Ziv
- Case Western Reserve University, Cleveland, OH, USA
- The MetroHealth System Campus, Cleveland, OH, USA
| | | | - Saurabh Kumar
- Department of Cardiology, Westmead Hospital, Westmead Applied Research Centre, University of Sydney, Sydney, Australia
| | | | - Benhur Davi Henz
- Instituto Brasilia de Arritmias-Hospital do Coração do Brasil-Rede Dor São Luiz, Brasilia, Brazil
| | - Jose Montero-Cabezas
- Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands
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18
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Dusi V, Angelini F, Baldi E, Toscano A, Gravinese C, Frea S, Compagnoni S, Morena A, Saglietto A, Balzani E, Giunta M, Costamagna A, Rinaldi M, Trompeo AC, Rordorf R, Anselmino M, Savastano S, De Ferrari GM. Continuous stellate ganglion block for ventricular arrhythmias: case series, systematic review, and differences from thoracic epidural anaesthesia. Europace 2024; 26:euae074. [PMID: 38531027 PMCID: PMC11020261 DOI: 10.1093/europace/euae074] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/25/2023] [Accepted: 03/18/2024] [Indexed: 03/28/2024] Open
Abstract
AIMS Percutaneous stellate ganglion block (PSGB) through single-bolus injection and thoracic epidural anaesthesia (TEA) have been proposed for the acute management of refractory ventricular arrhythmias (VAs). However, data on continuous PSGB (C-PSGB) are scant. The aim of this study is to report our dual-centre experience with C-PSGB and to perform a systematic review on C-PSGB and TEA. METHODS AND RESULTS Consecutive patients receiving C-PSGB at two centres were enrolled. The systematic literature review follows the latest Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. Our case series (26 patients, 88% male, 60 ± 16 years, all with advanced structural heart disease, left ventricular ejection fraction 23 ± 11%, 32 C-PSGBs performed, with a median duration of 3 days) shows that C-PSGB is feasible and safe and leads to complete VAs suppression in 59% and to overall clinical benefit in 94% of cases. Overall, 61 patients received 68 C-PSGBs and 22 TEA, with complete VA suppression in 63% of C-PSGBs (61% of patients). Most TEA procedures (55%) were performed on intubated patients, as opposed to 28% of C-PSGBs (P = 0.02); 63% of cases were on full anticoagulation at C-PSGB, none at TEA (P < 0.001). Ropivacaine and lidocaine were the most used drugs for C-PSGB, and the available data support a starting dose of 12 and 100 mg/h, respectively. No major complications occurred, yet TEA discontinuation rate due to side effects was higher than C-PSGB (18 vs. 1%, P = 0.01). CONCLUSION Continuous PSGB seems feasible, safe, and effective for the acute management of refractory VAs. The antiarrhythmic effect may be accomplished with less concerns for concomitant anticoagulation compared with TEA and with a lower side-effect related discontinuation rate.
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Affiliation(s)
- Veronica Dusi
- Cardiology, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Torino, Italy
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Filippo Angelini
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Enrico Baldi
- Arrhythmia and Electrophysiology Unit, Division of Cardiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
| | - Antonio Toscano
- Department of Anaesthesia, Critical Care and Emergency, ‘Città della Salute e della Scienza’ Hospital, Torino, Italy
| | - Carol Gravinese
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Simone Frea
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Sara Compagnoni
- Department of Molecular Medicine, Section of Cardiology, University of Pavia, Viale Golgi 19, 27100 Pavia, Italy
| | - Arianna Morena
- Cardiology, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Torino, Italy
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Andrea Saglietto
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Eleonora Balzani
- Department of Surgical Sciences, University of Turin, Torino, Italy
| | - Matteo Giunta
- Department of Anaesthesia, Critical Care and Emergency, ‘Città della Salute e della Scienza’ Hospital, Torino, Italy
| | - Andrea Costamagna
- Department of Anaesthesia, Critical Care and Emergency, ‘Città della Salute e della Scienza’ Hospital, Torino, Italy
| | - Mauro Rinaldi
- Department of Surgical Sciences, University of Turin, Torino, Italy
- Department of Cardiovascular and Thoracic Surgery, ‘Città della Salute e della Scienza’ Hospital, Torino, Italy
| | - Anna Chiara Trompeo
- Department of Anaesthesia, Critical Care and Emergency, ‘Città della Salute e della Scienza’ Hospital, Torino, Italy
| | - Roberto Rordorf
- Arrhythmia and Electrophysiology Unit, Division of Cardiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
| | - Matteo Anselmino
- Cardiology, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Torino, Italy
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
| | - Simone Savastano
- Arrhythmia and Electrophysiology Unit, Division of Cardiology, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
| | - Gaetano Maria De Ferrari
- Cardiology, Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Torino, Italy
- Division of Cardiology, Cardiovascular and Thoracic Department, ‘Città della Salute e della Scienza’ Hospital, Corso Bramante 88/90, 10126 Torino, Italy
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Gurau A, Bosmans F, Barth A, Brock MV, Ha JS. Exploring Cardiac Sympathetic Denervation as a Treatment Approach for Recurrent Ventricular Arrhythmias: A Concise Review. JOURNAL OF CLINICAL & EXPERIMENTAL CARDIOLOGY 2024; 15:874. [PMID: 39649113 PMCID: PMC11623387] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Subscribe] [Scholar Register] [Indexed: 12/10/2024]
Abstract
Surgical Cardiac Sympathetic Denervation (CSD) has gained traction as a promising neuromodulatory therapy for Refractory Ventricular Tachyarrhythmias (RVT), particularly in patients with channelopathies and Ischemic (ICM) and Non-Ischemic Cardiomyopathies (NICM) who are refractory to conventional treatment. This mini review examines the pathophysiological role of the sympathetic nervous system in RVT and assesses the efficacy of Bilateral CSD (BCSD) through a literature review. Historical perspectives have traced the evolution of CSD from its initial use in intractable angina to its current application in ventricular arrhythmias. BCSD is associated with improved outcomes for refractory ventricular arrhythmias, with studies demonstrating approximately 60% reductions in implantable cardioverter defibrillator shocks and over 50% shock-and transplant-free survival at 1 year after BCSD. Notably, the 2017 AHA/ACC/HRS guidelines recommend Left CSD (LCSD) for certain etiologies of RVT, including congenital long QT syndrome, Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT), and VT/VF storm. Both Video-Assisted Thoracoscopic Surgery (VATS) and Robot-Assisted Thoracoscopic Surgery (RATS) BCSD are performed, with shorter operative times for RATS. Yet, most RVT CSD studies have a small sample size; therefore, complications may be underreported because the studies are underpowered. Although BCSD has superior reported outcomes with respect to left CSD, there may be confounding factors due to the selection of healthier patients for BCSD. Additional comparative effectiveness and cost-effectiveness data are needed to guide clinical practice. In conclusion, BCSD can restore the quality of life of severely impacted RVT patients; however, the benefits must be weighed against procedure-related risks, and further research should clarify the impact on long-term morbidity and mortality.
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Affiliation(s)
- Andrei Gurau
- Division of Thoracic Surgery, Johns Hopkins University School of Medicine, Baltimore, USA
| | - Frank Bosmans
- Department of Basic and Applied Medical Sciences, University of Ghent, Ghent, Belgium
| | - Andreas Barth
- Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore
| | - Malcolm V. Brock
- Division of Thoracic Surgery, Johns Hopkins University School of Medicine, Baltimore, USA
| | - Jinny S. Ha
- Division of Thoracic Surgery, Johns Hopkins University School of Medicine, Baltimore, USA
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20
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SUN Q, CHENG K, DAI X, YANG Z, WU X, XU C, QIU X, GAO X, LIU D, YANG Q. Effect of electroacupuncture at Neiguan (PC6) at different time points on myocardial ischemia reperfusion arrhythmia in rats. J TRADIT CHIN MED 2024; 44:113-121. [PMID: 38213246 PMCID: PMC10774726 DOI: 10.19852/j.cnki.jtcm.20231110.004] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/22/2023] [Accepted: 05/17/2023] [Indexed: 01/13/2024]
Abstract
OBJECTIVE To observe the effects of electroacupuncture at Neiguan (PC6) at different time points on reperfusion arrhythmia (RA) after myocardial ischemia and reperfusion in rats, and to investigate the correlation of this protective effect with nerve growth factor (NGF), tyrosine kinase A (TrkA), tyrosine hydroxylase (TH), and norepinephrine (NE). METHODS:A total of 72 Sprague-Dawley male rats were randomly divided into six groups (n = 12 rats/group): normal group (Norm), sham operation group (Sham), ischemia reperfusion group (I/R), pre-ischemic electroacupuncture group (EAI), pre-reperfusion electroacupuncture group (EAII), post-reperfusion electroacupuncture group (EAIII). The myocardial ischemia-reperfusion injury (MIRI) model was induced by occlusion of left anterior descending coronary artery for 20 min followed by reperfusion for 40 min in rats. With no intervention in the Norm group and only threading without ligation in the Sham group. Electroacupuncture pre-treatment at 20 min/d for 7 d before ligation in the EAⅠ group, 20 min of electroacupuncture before reperfusion in the EAII group and 20 min of electroacupuncture after reperfusion in the EAIII group. The electrocardiogram (ECG) of each group was recorded throughout the whole process, and the success of the MIRI model was determined based on the changs of J-point and T-wave in the ECG. The arrhythmia score was used to record premature ventricular contractions, ventricular tachycardia and ventricular fibrillation during the reperfusion period to assess the reperfusion induced arrhythmias. The expression levels of NGF, TrkA, TH protein were measured by Western blot. Moreover, the expression levels of plasma and myocardial NE levels were detected by enzyme linked immunosorbent assay. RESULTS The differences between Norm group and Sham group were not statistically significant in all indexes. Arrhythmia score, myocardial NGF, TrkA, TH, and NE expression were significantly higher in the I/R group compared with the Sham group. Arrhythmia score, myocardial NGF, TrkA, TH, and NE expression were significantly lower in each EA group compared with the I/R group. CONCLUSION Electroacupuncture at Neiguan (PC6) at different time points can reduce the incidence and severity of reperfusion arrhythmias in rats. This protective effect is related to electroacupuncture regulating NGF, TrkA, TH, NE expression and reducing sympathetic hyperactivation.
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Affiliation(s)
- Qianhui SUN
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Kai CHENG
- 2 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Xingye DAI
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Zhiwen YANG
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Xiaoling WU
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Chang XU
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Xinghua QIU
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Xiaofeng GAO
- 3 Beijing MedEx Technology Co., Ltd., Beijing 100029, China
| | - Daonan LIU
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
| | - Qirui YANG
- 1 School of Acupuncture and Tuina, Beijing University of Chinese Medicine, Beijing 100029, China
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21
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Trohman RG. Etiologies, Mechanisms, Management, and Outcomes of Electrical Storm. J Intensive Care Med 2024; 39:99-117. [PMID: 37731333 DOI: 10.1177/08850666231192050] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 09/22/2023]
Abstract
Electrical storm (ES) is characterized by three or more discrete sustained ventricular tachyarrhythmia episodes occurring within a limited time frame (generally ≤ 24 h) or an incessant ventricular tachyarrhythmia lasting > 12 h. In patients with an implantable cardioverterdefibrillator (ICD), ES is defined as three or more appropriate device therapies, separated from each other by at least 5 min, which occur within a 24-h period. ES may constitute a medical emergency, depending on the number arrhythmic episodes, their duration, the type, and the cycle length of the ventricular arrhythmias, as well as the underlying ventricular function. This narrative review was facilitated by a search of MEDLINE to identify peer-reviewed clinical trials, randomized controlled trials, meta-analyses, and other clinically relevant studies. The search was limited to English-language reports published between 1999 and 2023. ES was searched using the terms mechanisms, genetics, channelopathies, management, pharmacological therapy, sedation, neuraxial modulation, cardiac sympathetic denervation, ICDs, and structural heart disease. Google and Google scholar as well as bibliographies of identified articles were reviewed for additional references. This manuscript examines the current strategies available to treat ES and compares pharmacological and invasive treatment strategies to diminish ES recurrence, morbidity, and mortality.
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Affiliation(s)
- Richard G Trohman
- Section of Electrophysiology, Division of Cardiology, Department of Internal Medicine, Rush University Medical Center, Chicago, IL, USA
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22
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Wang Y, Liu Z, Zhou W, Wang J, Li R, Peng C, Jiao L, Zhang S, Liu Z, Yu Z, Sun J, Deng Q, Duan S, Tan W, Wang Y, Song L, Guo F, Zhou Z, Wang Y, Zhou L, Jiang H, Yu L. Mast cell stabilizer, an anti-allergic drug, reduces ventricular arrhythmia risk via modulation of neuroimmune interaction. Basic Res Cardiol 2024; 119:75-91. [PMID: 38172251 DOI: 10.1007/s00395-023-01024-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/14/2023] [Revised: 11/26/2023] [Accepted: 11/27/2023] [Indexed: 01/05/2024]
Abstract
Mast cells (MCs) are important intermediates between the nervous and immune systems. The cardiac autonomic nervous system (CANS) crucially modulates cardiac electrophysiology and arrhythmogenesis, but whether and how MC-CANS neuroimmune interaction influences arrhythmia remain unclear. Our clinical data showed a close relationship between serum levels of MC markers and CANS activity, and then we use mast cell stabilizers (MCSs) to alter this MC-CANS communication. MCSs, which are well-known anti-allergic agents, could reduce the risk of ventricular arrhythmia (VA) after myocardial infarction (MI). RNA-sequencing (RNA-seq) analysis to investigate the underlying mechanism by which MCSs could affect the left stellate ganglion (LSG), a key therapeutic target for modulating CANS, showed that the IL-6 and γ-aminobutyric acid (GABA)-ergic system may be involved in this process. Our findings demonstrated that MCSs reduce VA risk along with revealing the potential underlying antiarrhythmic mechanisms.
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Affiliation(s)
- Yuhong Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Zhihao Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Wenjie Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Jun Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Rui Li
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Chen Peng
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Liying Jiao
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Song Zhang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Zhihao Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Zhongyang Yu
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Ji Sun
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Qiang Deng
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Shoupeng Duan
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Wuping Tan
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Yijun Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Lingpeng Song
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Fuding Guo
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Zhen Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Yueyi Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Liping Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China
| | - Hong Jiang
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China.
| | - Lilei Yu
- Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China.
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23
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Yang H, Hu Y, Kong B, Zhou Y, Shuai W. Low-intensity pulsed ultrasound treatment mitigates ventricular arrhythmias via inhibiting microglia-mediated neuroinflammation in heart failure rat model. Int Immunopharmacol 2024; 126:111317. [PMID: 38048669 DOI: 10.1016/j.intimp.2023.111317] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/17/2023] [Revised: 11/11/2023] [Accepted: 11/27/2023] [Indexed: 12/06/2023]
Abstract
BACKGROUND Sympathetic overactivation plays an important role in heart failure (HF)-induced ventricular arrhythmias (VAs). Microglia-mediated neuroinflammation could contribute to sympathetic overactivation. A previous study demonstrated that low-intensity pulsed ultrasound (LIPUS) could inhibit neuroinflammation. However, whether LIPUS could attenuate HF-induced VAs via inhibiting microglia-mediated neuroinflammation remains largely unknown. METHODS Forth Sprague-Dawley male rats were averagely randomized into four groups: CTL (control) group, CTL + LIPUS group, HF group and HF + LIPUS. Surgical ligation of the coronary artery was used for induction of HF. In vivo electrophysiological study was performed to check VAs susceptibility. Left stellate ganglion (LSG) neural activity and heart rate variability (HRV) were used to test sympathetic nerve activity. RESULTS Compared to the HF group, LIPUS treatment significantly ameliorated HF-induced cardiac hypertrophy, fibrosis, and dysfunction. In addition, LIPUS treatment markedly inhibited HF-induced VAs susceptibility and reversed gap junction remodeling. LIPUS treatment obviously inhibited microglial activation and neuroinflammation in PVN, sympathetic hyperactivity in the LSG and proinflammatory cytokines releases in the ventricle. P2X7/NLRP3 signaling pathway may be involved in the anti-arrhythmic effect of LIPUS treatment following HF. CONCLUSIONS Our data demonstrated that LIPUS treatment protected against HF-induced VAs via alleviating microglia-mediated neuroinflammation, sympathetic overactivation and proinflammatory cytokines releases through inhibiting P2X7/NLRP3 signaling. This study provides novel insight into the therapeutic potential of LIPUS.
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Affiliation(s)
- Hongjie Yang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China
| | - Yugang Hu
- Department of Ultrasound Imaging, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China
| | - Bin Kong
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China
| | - Yanxiang Zhou
- Department of Ultrasound Imaging, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China.
| | - Wei Shuai
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China.
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24
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Ahmed A, Charate R, Bawa D, Ghazal R, Garg J, Pothineni NVK, Kabra R, Della Rocca DG, Atkins D, Lakkireddy P, Bommana S, Al-Ahmad A, Shenthar J, Padmanabhan D, Narasimhan C, DiBiase L, Romeya A, Gopinathannair R, Natale A, Lakkireddy D. Bilateral Cardiac Sympathetic Denervation for Refractory Multifocal Premature Ventricular Contractions in Patients With Nonischemic Cardiomyopathy. JACC Clin Electrophysiol 2024; 10:31-39. [PMID: 37943190 DOI: 10.1016/j.jacep.2023.09.014] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/04/2022] [Revised: 09/05/2023] [Accepted: 09/10/2023] [Indexed: 11/10/2023]
Abstract
BACKGROUND Bilateral cardiac sympathetic denervation (BCSD) for refractory life-threatening ventricular arrhythmias is a neuromodulatory intervention targeting sympathetically driven focal or re-entrant ventricular arrhythmias. OBJECTIVES This study sought to provide a more complete and successful option for intervention in patients in whom premature ventricular contraction (PVC) ablation is not feasible or has been unsuccessful. METHODS A total of 43 patients with >5% PVC burden and concomitant nonischemic cardiomyopathy (NICM) who previously failed medical and ablation therapies were referred for BCSD. All patients underwent bilateral video-assisted thoracoscopic surgical approach with T1-T4 sympathectomy. Primary effectiveness endpoints were postprocedural PVC burden resolution, improvement in left ventricular ejection fraction (LVEF), and cessation of antiarrhythmic drugs (AADs). Safety endpoints included peri- and postprocedural complications. Outcomes were assessed over a 1-year follow-up period. RESULTS Among the 43 patients who underwent BCSD, the mean age was 52.3 ± 14.7 years, 69.8% of whom were male patients. Presenting mean LVEF was 38.7% ± 7.8%, and PVC burden was 23.7% ± 9.9%. There were significant reductions in PVC burden postprocedurally (1.3% ± 1.1% post-BCSD, compared with 23.7% ± 9.9% pre-BCSD, P < 0.001) and improvements in LVEF (46.3% ± 9.5% post-BCSD, compared with 38.7% ± 7.8% pre-BCSD, P < 0.001). The rate of ICD therapies decreased from 81.4% (n = 35) to 11.6% (n = 5) (P < 0.001), leading to a significant reduction in use of AADs (100.0% to 11.6%, P < 0.001) and improvement in mean NYHA functional class (2.5 ± 0.5 to 1.4 ± 0.2, P < 0.001). Major intraoperative complications were seen in 4.7% of patients (hemothorax and chylothorax). Of the patients, 81.4% (n = 35) experienced no mortality or major complications over a 1-year follow-up period, with the remaining still within their first year postprocedure. CONCLUSIONS BCSD is effective for the management of refractory PVCs and ventricular tachycardia who have failed previous ablation therapy.
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Affiliation(s)
- Adnan Ahmed
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | - Rishi Charate
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | - Danish Bawa
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | - Rachad Ghazal
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | - Jalaj Garg
- Loma Linda University Health, Loma Linda, California, USA
| | | | - Rajesh Kabra
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | | | - Donita Atkins
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | | | - Sudha Bommana
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | - Amin Al-Ahmad
- Texas Cardiac Arrhythmia Institute, St David's Medical Center, Austin, Texas, USA
| | - Jayaprakash Shenthar
- Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India
| | - Deepak Padmanabhan
- Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, Karnataka, India
| | | | - Luigi DiBiase
- Montefiore Medical Center, Montefiore Medical Center, Bronx, New York, USA
| | - Ahmed Romeya
- Kansas City Heart Rhythm Institute, Overland Park, Kansas, USA
| | | | - Andrea Natale
- Texas Cardiac Arrhythmia Institute, St David's Medical Center, Austin, Texas, USA
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Al-Khatib SM. Cardiac Sympathetic Denervation for Ventricular Arrhythmias and Nonischemic Cardiomyopathy: The End of the Beginning. JACC Clin Electrophysiol 2024; 10:40-42. [PMID: 38069972 DOI: 10.1016/j.jacep.2023.10.025] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2023] [Accepted: 10/17/2023] [Indexed: 01/26/2024]
Affiliation(s)
- Sana M Al-Khatib
- Division of Cardiology and Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina, USA.
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26
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Barrett MS, Bauer TC, Li MH, Hegarty DM, Mota CMD, Amaefuna CJ, Ingram SL, Habecker BA, Aicher SA. Ischemia-reperfusion myocardial infarction induces remodeling of left cardiac-projecting stellate ganglia neurons. Am J Physiol Heart Circ Physiol 2024; 326:H166-H179. [PMID: 37947434 PMCID: PMC11213476 DOI: 10.1152/ajpheart.00582.2023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/19/2023] [Revised: 10/23/2023] [Accepted: 11/08/2023] [Indexed: 11/12/2023]
Abstract
Neurons in the stellate ganglion (SG) provide sympathetic innervation to the heart, brown adipose tissue (BAT), and other organs. Sympathetic innervation to the heart becomes hyperactive following myocardial infarction (MI). The impact of MI on the morphology of cardiac sympathetic neurons is not known, but we hypothesized that MI would stimulate increased cell and dendritic tree size in cardiac neurons. In this study, we examined the effects of ischemia-reperfusion MI on sympathetic neurons using dual retrograde tracing methods to allow detailed characterization of cardiac- and BAT-projecting neurons. Different fluorescently conjugated cholera toxin subunit B (CTb) tracers were injected into the pericardium and the interscapular BAT pads, respectively. Experimental animals received a 45-min occlusion of the left anterior descending coronary artery and controls received sham surgery. One week later, hearts were collected for assessment of MI infarct and SGs were collected for morphological or electrophysiological analysis. Cardiac-projecting SG neurons from MI mice had smaller cell bodies and shorter dendritic trees compared with sham animals, specifically on the left side ipsilateral to the MI. BAT-projecting neurons were not altered by MI, demonstrating the subpopulation specificity of the response. The normal size and distribution differences between BAT- and cardiac-projecting stellate ganglion neurons were not altered by MI. Patch-clamp recordings from cardiac-projecting left SG neurons revealed increased spontaneous excitatory postsynaptic currents despite the decrease in cell and dendritic tree size. Thus, increased dendritic tree size does not contribute to the enhanced sympathetic neural activity seen after MI.NEW & NOTEWORTHY Myocardial infarction (MI) causes structural and functional changes specifically in stellate ganglion neurons that project to the heart, but not in cells that project to brown adipose fat tissue.
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Affiliation(s)
- Madeleine S Barrett
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Temerity C Bauer
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Ming-Hua Li
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Deborah M Hegarty
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Clarissa M D Mota
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Chimezie J Amaefuna
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Susan L Ingram
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Beth A Habecker
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
| | - Sue A Aicher
- Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, United States
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27
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Paterson DJ, Shivkumar K. Bioelectronics for neurocardiology: diagnosis and therapeutics. Eur Heart J 2023; 44:4822-4825. [PMID: 37949823 DOI: 10.1093/eurheartj/ehad624] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/12/2023] Open
Affiliation(s)
- David J Paterson
- Burdon Sanderson Cardiac Science Centre, Sherrington Building, Department of Physiology, Anatomy & Genetics, University of Oxford, Parks Road, Oxford OX1 3PT, UK
| | - Kalyanam Shivkumar
- Department of Medicine, UCLA Cardiac Arrhythmia Center University of California, Los Angeles, 100 UCLA Medical Plaza, Suite 660, Los Angeles, CA 90095, USA
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Salavatian S, Robbins EM, Kuwabara Y, Castagnola E, Cui XT, Mahajan A. Real-time in vivo thoracic spinal glutamate sensing during myocardial ischemia. Am J Physiol Heart Circ Physiol 2023; 325:H1304-H1317. [PMID: 37737733 PMCID: PMC10908408 DOI: 10.1152/ajpheart.00299.2023] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/22/2023] [Revised: 09/18/2023] [Accepted: 09/18/2023] [Indexed: 09/23/2023]
Abstract
In the spinal cord, glutamate serves as the primary excitatory neurotransmitter. Monitoring spinal glutamate concentrations offers valuable insights into spinal neural processing. Consequently, spinal glutamate concentration has the potential to emerge as a useful biomarker for conditions characterized by increased spinal neural network activity, especially when uptake systems become dysfunctional. In this study, we developed a multichannel custom-made flexible glutamate-sensing probe for the large-animal model that is capable of measuring extracellular glutamate concentrations in real time and in vivo. We assessed the probe's sensitivity and specificity through in vitro and ex vivo experiments. Remarkably, this developed probe demonstrates nearly instantaneous glutamate detection and allows continuous monitoring of glutamate concentrations. Furthermore, we evaluated the mechanical and sensing performance of the probe in vivo, within the pig spinal cord. Moreover, we applied the glutamate-sensing method using the flexible probe in the context of myocardial ischemia-reperfusion (I/R) injury. During I/R injury, cardiac sensory neurons in the dorsal root ganglion transmit excitatory signals to the spinal cord, resulting in sympathetic activation that potentially leads to fatal arrhythmias. We have successfully shown that our developed glutamate-sensing method can detect this spinal network excitation during myocardial ischemia. This study illustrates a novel technique for measuring spinal glutamate at different spinal cord levels as a surrogate for the spinal neural network activity during cardiac interventions that engage the cardio-spinal neural pathway.NEW & NOTEWORTHY In this study, we have developed a new flexible sensing probe to perform an in vivo measurement of spinal glutamate signaling in a large animal model. Our initial investigations involved precise testing of this probe in both in vitro and ex vivo environments. We accurately assessed the sensitivity and specificity of our glutamate-sensing probe and demonstrated its performance. We also evaluated the performance of our developed flexible probe during the insertion and compared it with the stiff probe during animal movement. Subsequently, we used this innovative technique to monitor the spinal glutamate signaling during myocardial ischemia and reperfusion that can cause fatal ventricular arrhythmias. We showed that glutamate concentration increases during the myocardial ischemia, persists during the reperfusion, and is associated with sympathoexcitation and increases in myocardial substrate excitability.
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Affiliation(s)
- Siamak Salavatian
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
- Division of Cardiology, Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
- Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
| | - Elaine Marie Robbins
- Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
| | - Yuki Kuwabara
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
| | - Elisa Castagnola
- Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
| | - Xinyan Tracy Cui
- Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
- Center for Neural Basis of Cognition, Pittsburgh, Pennsylvania, United States
- McGowan Institute for Regenerative Medicine, Pittsburgh, Pennsylvania, United States
| | - Aman Mahajan
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
- Department of Bioengineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
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Melinosky K, Leng A, Johnson CR, Giuliano Verdi K, Etchill EW, Tandri H, Brock MV, Ha JS. Outcomes Comparison of Robot-Assisted and Video-Assisted Thoracoscopic Cardiac Sympathetic Denervation. INNOVATIONS-TECHNOLOGY AND TECHNIQUES IN CARDIOTHORACIC AND VASCULAR SURGERY 2023; 18:512-518. [PMID: 37997649 DOI: 10.1177/15569845231210282] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/25/2023]
Abstract
OBJECTIVE Cardiac sympathetic denervation (CSD) is a surgical antiadrenergic procedure that can reduce sustained ventricular tachyarrhythmia (VT). Video-assisted thoracoscopic surgery (VATS) is currently the standard approach used in CSD, and the practicality for robot-assisted thoracoscopic surgery (RATS) has yet to be investigated. METHODS We conducted a single-center retrospective study of all adult patients (N = 67) who underwent CSD from 2015 to 2021. We compared short-term outcomes of those treated with RATS versus VATS thoracic sympathectomy. For patients with VT, we examined the effectiveness of a RATS approach in reducing implantable cardioverter defibrillator (ICD) shock burden. RESULTS A total of 34 patients underwent RATS cardiac denervation, and 33 underwent VATS cardiac denervation. Those undergoing RATS denervation had a significantly shorter procedure duration with a median of 129 min (P = 0.008). Patients receiving the VATS approach were significantly more complicated by pneumothorax (P = 0.004) and overall complications (P = 0.01) when compared with the RATS approach. At 1 year after surgery, both groups had significant reductions in ICD shocks compared with before surgery, both decreasing from a median of 4 to 0 shocks (P < 0.001). In addition, at 1 year after surgery, the percentage of patients with persistent ICD shocks and the median of ICD shocks were similar between the groups. CONCLUSIONS The RATS approach to cardiac denervation has similar 1-year follow-up outcomes in reducing recurrent VT as the VATS approach. However, patients undergoing RATS denervation experienced better perioperative outcomes. This shows promise for robotic CSD to be an effective and safe therapeutic option for patients with malignant arrhythmias.
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Affiliation(s)
- Kelsey Melinosky
- Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
| | - Albert Leng
- Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
| | - Christopher R Johnson
- Division of Thoracic Surgery, Department of Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA
| | | | - Eric W Etchill
- Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
| | - Harikrishna Tandri
- Department of Cardiology, Vanderbilt University School of Medicine, Nashville, TN, USA
| | - Malcolm V Brock
- Division of Thoracic Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
| | - Jinny S Ha
- Division of Thoracic Surgery, Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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30
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Salamon RJ, Halbe P, Kasberg W, Bae J, Audhya A, Mahmoud AI. Parasympathetic and sympathetic axons are bundled in the cardiac ventricles and undergo physiological reinnervation during heart regeneration. iScience 2023; 26:107709. [PMID: 37674983 PMCID: PMC10477065 DOI: 10.1016/j.isci.2023.107709] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/15/2023] [Revised: 07/25/2023] [Accepted: 08/23/2023] [Indexed: 09/08/2023] Open
Abstract
Sympathetic innervation influences homeostasis, repair, and pathology in the cardiac ventricles; in contrast, parasympathetic innervation is considered to have minimal contribution and influence in the ventricles. Here, we use genetic models, whole-mount imaging, and three-dimensional modeling to define cardiac nerve architecture during development, disease, and regeneration. Our approach reveals that parasympathetic nerves extensively innervate the cardiac ventricles. Furthermore, we identify that parasympathetic and sympathetic axons develop synchronously and are bundled throughout the ventricles. We further investigate cardiac nerve remodeling in the regenerative neonatal and the non-regenerative postnatal mouse heart. Our results show that the regenerating myocardium undergoes a unique process of physiological reinnervation, where proper nerve distribution and architecture is reestablished, in stark contrast to the non-regenerating heart. Mechanistically, we demonstrate that physiological reinnervation during regeneration is dependent on collateral artery formation. Our results reveal clinically significant insights into cardiac nerve plasticity which can identify new therapies for cardiac disease.
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Affiliation(s)
- Rebecca J. Salamon
- Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
| | - Poorva Halbe
- Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
| | - William Kasberg
- Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
| | - Jiyoung Bae
- Department of Nutritional Sciences, Oklahoma State University, Stillwater, OK 74078, USA
| | - Anjon Audhya
- Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
| | - Ahmed I. Mahmoud
- Department of Cell and Regenerative Biology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA
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31
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van Weperen VYH, Ripplinger CM, Vaseghi M. Autonomic control of ventricular function in health and disease: current state of the art. Clin Auton Res 2023; 33:491-517. [PMID: 37166736 PMCID: PMC10173946 DOI: 10.1007/s10286-023-00948-8] [Citation(s) in RCA: 12] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/02/2023] [Accepted: 04/20/2023] [Indexed: 05/12/2023]
Abstract
PURPOSE Cardiac autonomic dysfunction is one of the main pillars of cardiovascular pathophysiology. The purpose of this review is to provide an overview of the current state of the art on the pathological remodeling that occurs within the autonomic nervous system with cardiac injury and available neuromodulatory therapies for autonomic dysfunction in heart failure. METHODS Data from peer-reviewed publications on autonomic function in health and after cardiac injury are reviewed. The role of and evidence behind various neuromodulatory therapies both in preclinical investigation and in-use in clinical practice are summarized. RESULTS A harmonic interplay between the heart and the autonomic nervous system exists at multiple levels of the neuraxis. This interplay becomes disrupted in the setting of cardiovascular disease, resulting in pathological changes at multiple levels, from subcellular cardiac signaling of neurotransmitters to extra-cardiac, extra-thoracic remodeling. The subsequent detrimental cycle of sympathovagal imbalance, characterized by sympathoexcitation and parasympathetic withdrawal, predisposes to ventricular arrhythmias, progression of heart failure, and cardiac mortality. Knowledge on the etiology and pathophysiology of this condition has increased exponentially over the past few decades, resulting in a number of different neuromodulatory approaches. However, significant knowledge gaps in both sympathetic and parasympathetic interactions and causal factors that mediate progressive sympathoexcitation and parasympathetic dysfunction remain. CONCLUSIONS Although our understanding of autonomic imbalance in cardiovascular diseases has significantly increased, specific, pivotal mediators of this imbalance and the recognition and implementation of available autonomic parameters and neuromodulatory therapies are still lagging.
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Affiliation(s)
- Valerie Y H van Weperen
- Division of Cardiology, Department of Medicine, UCLA Cardiac Arrythmia Center, University of California, 100 Medical Plaza, Suite 660, Los Angeles, CA, 90095, USA
| | | | - Marmar Vaseghi
- Division of Cardiology, Department of Medicine, UCLA Cardiac Arrythmia Center, University of California, 100 Medical Plaza, Suite 660, Los Angeles, CA, 90095, USA.
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32
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Salavatian S, Kuwabara Y, Wong B, Fritz JR, Howard-Quijano K, Foreman RD, Armour JA, Ardell JL, Mahajan A. Spinal neuromodulation mitigates myocardial ischemia-induced sympathoexcitation by suppressing the intermediolateral nucleus hyperactivity and spinal neural synchrony. Front Neurosci 2023; 17:1180294. [PMID: 37332861 PMCID: PMC10272539 DOI: 10.3389/fnins.2023.1180294] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2023] [Accepted: 05/16/2023] [Indexed: 06/20/2023] Open
Abstract
Introduction Myocardial ischemia disrupts the cardio-spinal neural network that controls the cardiac sympathetic preganglionic neurons, leading to sympathoexcitation and ventricular tachyarrhythmias (VTs). Spinal cord stimulation (SCS) is capable of suppressing the sympathoexcitation caused by myocardial ischemia. However, how SCS modulates the spinal neural network is not fully known. Methods In this pre-clinical study, we investigated the impact of SCS on the spinal neural network in mitigating myocardial ischemia-induced sympathoexcitation and arrhythmogenicity. Ten Yorkshire pigs with left circumflex coronary artery (LCX) occlusion-induced chronic myocardial infarction (MI) were anesthetized and underwent laminectomy and a sternotomy at 4-5 weeks post-MI. The activation recovery interval (ARI) and dispersion of repolarization (DOR) were analyzed to evaluate the extent of sympathoexcitation and arrhythmogenicity during the left anterior descending coronary artery (LAD) ischemia. Extracellular in vivo and in situ spinal dorsal horn (DH) and intermediolateral column (IML) neural recordings were performed using a multichannel microelectrode array inserted at the T2-T3 segment of the spinal cord. SCS was performed for 30 min at 1 kHz, 0.03 ms, 90% motor threshold. LAD ischemia was induced pre- and 1 min post-SCS to investigate how SCS modulates spinal neural network processing of myocardial ischemia. DH and IML neural interactions, including neuronal synchrony as well as cardiac sympathoexcitation and arrhythmogenicity markers were evaluated during myocardial ischemia pre- vs. post-SCS. Results ARI shortening in the ischemic region and global DOR augmentation due to LAD ischemia was mitigated by SCS. Neural firing response of ischemia-sensitive neurons during LAD ischemia and reperfusion was blunted by SCS. Further, SCS showed a similar effect in suppressing the firing response of IML and DH neurons during LAD ischemia. SCS exhibited a similar suppressive impact on the mechanical, nociceptive and multimodal ischemia sensitive neurons. The LAD ischemia and reperfusion-induced augmentation in neuronal synchrony between DH-DH and DH-IML pairs of neurons were mitigated by the SCS. Discussion These results suggest that SCS is decreasing the sympathoexcitation and arrhythmogenicity by suppressing the interactions between the spinal DH and IML neurons and activity of IML preganglionic sympathetic neurons.
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Affiliation(s)
- Siamak Salavatian
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
- Division of Cardiology, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, United States
| | - Yuki Kuwabara
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
| | - Benjamin Wong
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
| | - Jonathan R. Fritz
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
| | - Kimberly Howard-Quijano
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, United States
| | - Robert D. Foreman
- Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States
| | - J. Andrew Armour
- Cardiac Arrhythmia Center and Neurocardiology Research Program of Excellence, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States
| | - Jeffrey L. Ardell
- Cardiac Arrhythmia Center and Neurocardiology Research Program of Excellence, David Geffen School of Medicine at UCLA, Los Angeles, CA, United States
| | - Aman Mahajan
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA, United States
- Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, United States
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McCabe MD, Cervantes R, Kewcharoen J, Sran J, Garg J. Quelling the Storm: A Review of the Management of Electrical Storm. J Cardiothorac Vasc Anesth 2023:S1053-0770(23)00338-5. [PMID: 37296026 DOI: 10.1053/j.jvca.2023.05.029] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/12/2023] [Accepted: 05/17/2023] [Indexed: 06/12/2023]
Abstract
Heightened sympathetic input to the myocardium potentiates cardiac electrical instability and may herald an electrical storm. An electrical storm is characterized by 3 or more episodes of ventricular tachycardia, ventricular fibrillation, or appropriate internal cardiac defibrillator shocks within 24 hours. Management of electrical storms is resource-intensive and inevitably requires careful coordination between multiple subspecialties. Anesthesiologists have an important role in acute, subacute, and long-term management. Identifying the phase of an electrical storm and understanding the characteristics of each morphology may help the anesthesiologist anticipate the management approach. In the acute phase, management of an electrical storm is aimed at providing advanced cardiac life support and identifying reversible causes. After initial stabilization, subacute management focuses on dampening the sympathetic surge with sedation, thoracic epidural, or stellate ganglion blockade. Definitive long-term management with surgical sympathectomy or catheter ablation also may be warranted. Our objective is to provide an overview of electrical storms and the anesthesiologist's role in management.
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Affiliation(s)
- Melissa D McCabe
- Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, California.
| | - Richard Cervantes
- Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, California
| | - Jakrin Kewcharoen
- Cardiac Arrhythmia Service, Loma Linda University School of Medicine, Loma Linda, California
| | - Jasmine Sran
- Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, California
| | - Jalaj Garg
- Cardiac Arrhythmia Service, Loma Linda University School of Medicine, Loma Linda, California
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Chung WH, Lin YN, Wu MY, Chang KC. Sympathetic Modulation in Cardiac Arrhythmias: Where We Stand and Where We Go. J Pers Med 2023; 13:786. [PMID: 37240956 PMCID: PMC10221179 DOI: 10.3390/jpm13050786] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/02/2023] [Revised: 04/27/2023] [Accepted: 04/29/2023] [Indexed: 05/28/2023] Open
Abstract
The nuance of autonomic cardiac control has been studied for more than 400 years, yet little is understood. This review aimed to provide a comprehensive overview of the current understanding, clinical implications, and ongoing studies of cardiac sympathetic modulation and its anti-ventricular arrhythmias' therapeutic potential. Molecular-level studies and clinical studies were reviewed to elucidate the gaps in knowledge and the possible future directions for these strategies to be translated into the clinical setting. Imbalanced sympathoexcitation and parasympathetic withdrawal destabilize cardiac electrophysiology and confer the development of ventricular arrhythmias. Therefore, the current strategy for rebalancing the autonomic system includes attenuating sympathoexcitation and increasing vagal tone. Multilevel targets of the cardiac neuraxis exist, and some have emerged as promising antiarrhythmic strategies. These interventions include pharmacological blockade, permanent cardiac sympathetic denervation, temporal cardiac sympathetic denervation, etc. The gold standard approach, however, has not been known. Although neuromodulatory strategies have been shown to be highly effective in several acute animal studies with very promising results, the individual and interspecies variation between human autonomic systems limits the progress in this young field. There is, however, still much room to refine the current neuromodulation therapy to meet the unmet need for life-threatening ventricular arrhythmias.
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Affiliation(s)
- Wei-Hsin Chung
- Division of Cardiovascular Medicine, Department of Medicine, China Medical University Hospital, Taichung 40447, Taiwan
- UCLA Cardiac Arrhythmia Center, Ronald Reagan UCLA Medical Center, Los Angeles, CA 90024, USA
| | - Yen-Nien Lin
- Division of Cardiovascular Medicine, Department of Medicine, China Medical University Hospital, Taichung 40447, Taiwan
- School of Medicine, China Medical University, Taichung 404333, Taiwan
| | - Mei-Yao Wu
- School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 404333, Taiwan
- Department of Chinese Medicine, China Medical University Hospital, Taichung 40447, Taiwan
| | - Kuan-Cheng Chang
- Division of Cardiovascular Medicine, Department of Medicine, China Medical University Hospital, Taichung 40447, Taiwan
- School of Medicine, China Medical University, Taichung 404333, Taiwan
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Sridharan A, Tang A, Sorg JM, Hoftman NN, Lee JM, Yanagawa J, Vaseghi M. Effect of Bilateral Cardiac Sympathetic Denervation on Burden of Premature Ventricular Contractions. Circ Arrhythm Electrophysiol 2023; 16:e011546. [PMID: 36916281 PMCID: PMC10132769 DOI: 10.1161/circep.122.011546] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 03/16/2023]
Affiliation(s)
- Aadhavi Sridharan
- Department of Medicine, Division of Cardiology, UCLA Cardiac Arrhythmia Center, University of California, Los Angeles, CA
| | - Amber Tang
- Department of Medicine, Division of Cardiology, UCLA Cardiac Arrhythmia Center, University of California, Los Angeles, CA
| | - Julie M. Sorg
- Department of Medicine, Division of Cardiology, UCLA Cardiac Arrhythmia Center, University of California, Los Angeles, CA
| | - Nir N. Hoftman
- Department of Anesthesiology, University of California, Los Angeles
| | - Jay M. Lee
- Division of Thoracic Surgery, University of California, Los Angeles
| | - Jane Yanagawa
- Division of Thoracic Surgery, University of California, Los Angeles
| | - Marmar Vaseghi
- Department of Medicine, Division of Cardiology, UCLA Cardiac Arrhythmia Center, University of California, Los Angeles, CA
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Salavatian S, Robbins EM, Kuwabara Y, Castagnola E, Cui XT, Mahajan A. Real-time in vivo thoracic spinal glutamate sensing reveals spinal hyperactivity during myocardial ischemia. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2023:2023.03.11.531911. [PMID: 36993301 PMCID: PMC10054946 DOI: 10.1101/2023.03.11.531911] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 06/19/2023]
Abstract
Myocardial ischemia-reperfusion (IR) can cause ventricular arrhythmias and sudden cardiac death via sympathoexcitation. The spinal cord neural network is crucial in triggering these arrhythmias and evaluating its neurotransmitter activity during IR is critical for understanding ventricular excitability control. To assess the real-time in vivo spinal neural activity in a large animal model, we developed a flexible glutamate-sensing multielectrode array. To record the glutamate signaling during IR injury, we inserted the probe into the dorsal horn of the thoracic spinal cord at the T2-T3 where neural signals generated by the cardiac sensory neurons are processed and provide sympathoexcitatory feedback to the heart. Using the glutamate sensing probe, we found that the spinal neural network was excited during IR, especially after 15 mins, and remained elevated during reperfusion. Higher glutamate signaling was correlated with the reduction in the cardiac myocyte activation recovery interval, showing higher sympathoexcitation, as well as dispersion of the repolarization which is a marker for increased risk of arrhythmias. This study illustrates a new technique for measuring the spinal glutamate at different spinal cord levels as a surrogate for the spinal neural network activity during cardiac interventions that engage the cardio-spinal neural pathway. Graphical abstract
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Markman TM, Gugger D, Arkles J, Riley MP, Dixit S, Guandalini GS, Frankel DS, Epstein AE, Callans DJ, Singhal S, Marchlinski FE, Nazarian S. Neuromodulation for the Treatment of Refractory Ventricular Arrhythmias. JACC Clin Electrophysiol 2023; 9:161-169. [PMID: 36858681 DOI: 10.1016/j.jacep.2022.08.031] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/08/2022] [Revised: 08/25/2022] [Accepted: 08/29/2022] [Indexed: 11/07/2022]
Abstract
BACKGROUND Neuromodulation is increasingly recognized as a therapeutic strategy for patients with refractory ventricular arrhythmias (VAs). Percutaneous stellate ganglion blockade (SGB), transcutaneous magnetic stimulation (TcMS), and surgical cardiac sympathetic denervation (CSD) have all been utilized in this setting. OBJECTIVES This study sought to characterize contemporary use and outcomes of these neuromodulation techniques for patients with refractory VA. METHODS This retrospective cohort study included all patients at the Hospital of the University of Pennsylvania with antiarrhythmic drug (AAD)-refractory VA from 2019 to 2021 who were treated with SGB, TcMS, or CSD. RESULTS A total of 34 patients (age 61 ± 14 years, 15 polymorphic VAs [44%], refractory to 1.8 ± 0.8 AADs) met inclusion criteria. SGB was performed on 11 patients (32%), TcMS on 19 (56%), and CSD on 7 (21%). Neuromodulation was associated with a reduction in the number of episodes of sustained VAs from 7 [IQR: 4-12] episodes in the 24 hours before the initial neuromodulation strategy to 0 [IQR: 0-1] episodes in the subsequent 24 hours (P < 0.001). During 1.2 ± 1.1 years of follow-up, 21 (62%) experienced recurrent VAs, and among those patients, the median time to recurrence was 3 [IQR: 1-25] days. Outcomes were similar among patients with monomorphic and polymorphic VAs. Among patients who had an acute myocardial infarction within 30 days before neuromodulation, the burden of VAs decreased from 11 [IQR: 7-12] episodes to 0 episodes in the 24 hours after treatment. CONCLUSIONS Autonomic neuromodulation with SGB, TcMS, or CSD in patients with AAD-refractory VAs is safe and results in substantial acute reduction of VA although recurrent arrhythmias are common, and not all patients experience a reduction in arrhythmia burden.
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Affiliation(s)
- Timothy M Markman
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA.
| | - Douglas Gugger
- Department of Anesthesia, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Jeffrey Arkles
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Michael P Riley
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Sanjay Dixit
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Gustavo S Guandalini
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - David S Frankel
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Andrew E Epstein
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - David J Callans
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Sunil Singhal
- Thoracic Surgery Division, Department of Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Francis E Marchlinski
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Saman Nazarian
- Cardiovascular Division, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA
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Salamon RJ, Halbe P, Kasberg W, Bae J, Audhya A, Mahmoud AI. Defining Cardiac Nerve Architecture During Development, Disease, and Regeneration. BIORXIV : THE PREPRINT SERVER FOR BIOLOGY 2023:2022.12.31.522405. [PMID: 36711742 PMCID: PMC9881855 DOI: 10.1101/2022.12.31.522405] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 01/05/2023]
Abstract
Cardiac nerves regulate neonatal mouse heart regeneration and are susceptible to pathological remodeling following adult injury. Understanding cardiac nerve remodeling can lead to new strategies to promote cardiac repair. Our current understanding of cardiac nerve architecture has been limited to two-dimensional analysis. Here, we use genetic models, whole-mount imaging, and three-dimensional modeling tools to define cardiac nerve architecture and neurovascular association during development, disease, and regeneration. Our results demonstrate that cardiac nerves sequentially associate with coronary veins and arteries during development. Remarkably, our results reveal that parasympathetic nerves densely innervate the ventricles. Furthermore, parasympathetic and sympathetic nerves develop synchronously and are intertwined throughout the ventricles. Importantly, the regenerating myocardium reestablishes physiological innervation, in stark contrast to the non-regenerating heart. Mechanistically, reinnervation during regeneration is dependent on collateral artery formation. Our results reveal how defining cardiac nerve remodeling during homeostasis, disease, and regeneration can identify new therapies for cardiac disease.
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Sridharan A, Bradfield JS, Shivkumar K, Ajijola OA. Autonomic nervous system and arrhythmias in structural heart disease. Auton Neurosci 2022; 243:103037. [DOI: 10.1016/j.autneu.2022.103037] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/22/2021] [Revised: 09/21/2022] [Accepted: 09/21/2022] [Indexed: 11/28/2022]
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Cardiac Sympathetic Denervation for the Management of Ventricular Arrhythmias. J Interv Card Electrophysiol 2022; 65:813-826. [PMID: 35397706 DOI: 10.1007/s10840-022-01211-2] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/31/2022] [Accepted: 03/29/2022] [Indexed: 01/01/2023]
Abstract
BACKGROUND The autonomic nervous system contributes to the pathogenesis of ventricular arrhythmias (VA). Though anti-arrhythmic drug therapy and catheter ablation are the mainstay of management of VAs, success may be limited in patients with more refractory arrhythmias. Sympathetic modulation is increasingly recognized as a valuable adjunct tool for managing VAs in patients with structural heart disease and inherited arrhythmias. RESULTS In this review, we explore the role of the sympathetic nervous system and rationale for cardiac sympathetic denervation (CSD) in VAs and provide a disease-focused review of the utility of CSD for patients both with and without structural heart disease. CONCLUSIONS We conclude that CSD is a reasonable therapeutic option for patients with VA, both with and without structural heart disease. Though not curative, many studies have demonstrated a significant reduction in the burden of VAs for the majority of patients undergoing the procedure. However, in patients with unilateral CSD and subsequent VA recurrence, complete bilateral CSD may provide long-lasting reprieve from VA.
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Zhang S, Wang M, Jiao L, Liu C, Chen H, Zhou L, Wang Y, Wang Y, Liu Z, Liu Z, Zhou Y, Zhou H, Xu X, Li Z, Liu Z, Yu Z, Nie L, Yu L, Jiang H. Ultrasound-guided injection of botulinum toxin type A blocks cardiac sympathetic ganglion to improve cardiac remodeling in a large animal model of chronic myocardial infarction. Heart Rhythm 2022; 19:2095-2104. [PMID: 35948203 DOI: 10.1016/j.hrthm.2022.08.002] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/06/2022] [Revised: 07/20/2022] [Accepted: 08/01/2022] [Indexed: 12/14/2022]
Abstract
BACKGROUND Strategies to improve various cardiovascular diseases by blocking cardiac sympathetic ganglion have been increasingly available currently. Botulinum toxin type A (BTA), a typical neurotoxin, has been shown to block neural transmission in a safe and long-lasting manner. OBJECTIVE The aim of the present preclinical study was to assess the efficacy of BTA microinjection to alleviate cardiac remodeling after chronic myocardial infarction (MI) by blocking cardiac sympathetic ganglion in a canine model. METHODS Beagles were randomly divided into a control group (saline microinjection with sham surgery), an MI group (saline microinjection with MI), and an MI + BTA group (BTA microinjection with MI). Ultrasound-guided percutaneous BTA or saline injection into the left stellate ganglion (LSG) was performed followed by MI induction via left anterior descending artery occlusion (LADO) or sham surgery. After 30 days, electrocardiography, Doppler echocardiography, LSG function, neural activity, and ventricular electrophysiological detection were performed in all experimental dogs. At the end, LSG and ventricular tissues were collected for further detection. RESULTS BTA treatment significantly inhibited LSG function and neural activity and improved heart rate variability. Additionally, BTA application alleviated ventricular remodeling, ameliorated cardiac function, and prevented ventricular arrhythmias after 30-day chronic LADO-induced MI. CONCLUSION Ultrasound-guided percutaneous microinjection of BTA can block cardiac sympathetic ganglion to improve cardiac remodeling in a large animal model of chronic LADO-induced MI. Ultrasound-guided BTA microinjection has potential for clinical application as a novel cardiac sympathetic ganglion blockade strategy for MI.
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Affiliation(s)
- Song Zhang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Meng Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Liying Jiao
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Chengzhe Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Huaqiang Chen
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Liping Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Yueyi Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Yuhong Wang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Zhihao Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Zihan Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Yuyang Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Huixin Zhou
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Xiao Xu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Zeyan Li
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Zhihao Liu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Zhongyang Yu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Liqing Nie
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
| | - Lilei Yu
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China.
| | - Hong Jiang
- Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiac Autonomic Nervous System Research Center of Wuhan University, Wuhan, China; Hubei Key Laboratory of Autonomic Nervous System Modulation, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China
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Cauti FM, Capone S, Rossi P, Polselli M, Venuta F, Vannucci J, Bruno K, Pugliese F, Tozzi P, Bianchi S, Anile M. Cardiac sympathetic denervation for untreatable ventricular tachycardia in structural heart disease. Strengths and pitfalls of evolving surgical techniques. J Interv Card Electrophysiol 2022:10.1007/s10840-022-01404-9. [PMID: 36282370 DOI: 10.1007/s10840-022-01404-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/14/2022] [Accepted: 10/19/2022] [Indexed: 10/31/2022]
Abstract
Cardiac sympathetic denervation (CSD) is a valuable option in the setting of refractory ventricular arrhythmias in patient with structural heart disease. Since the procedure was introduced for non structural heart disease patients the techniques evolved and were modified to be adopted in several settings. In this state-of-the-art article we revised different techniques, their rationale, strengths, and pitfalls.
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Affiliation(s)
- Filippo Maria Cauti
- Arrhythmology Unit, Ospedale San Giovanni Calibita, Fatebenefratelli Isola Tiberina, Via Ponte Quattro Capi 39, 00186, Rome, Italy.
| | - Silvia Capone
- Arrhythmology Unit, Ospedale San Giovanni Calibita, Fatebenefratelli Isola Tiberina, Via Ponte Quattro Capi 39, 00186, Rome, Italy
- Cardiology Unit, Dipartimento Cuore E Grossi Vasi, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Pietro Rossi
- Arrhythmology Unit, Ospedale San Giovanni Calibita, Fatebenefratelli Isola Tiberina, Via Ponte Quattro Capi 39, 00186, Rome, Italy
| | - Marco Polselli
- Arrhythmology Unit, Ospedale San Giovanni Calibita, Fatebenefratelli Isola Tiberina, Via Ponte Quattro Capi 39, 00186, Rome, Italy
| | - Federico Venuta
- Thoracic Unit, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Jacopo Vannucci
- Thoracic Unit, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Katia Bruno
- Department of Anesthesiology, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Francesco Pugliese
- Department of Anesthesiology, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Pierfrancesco Tozzi
- Department of Anesthesiology, Policlinico Umberto I, Sapienza University, Rome, Italy
| | - Stefano Bianchi
- Arrhythmology Unit, Ospedale San Giovanni Calibita, Fatebenefratelli Isola Tiberina, Via Ponte Quattro Capi 39, 00186, Rome, Italy
| | - Marco Anile
- Thoracic Unit, Policlinico Umberto I, Sapienza University, Rome, Italy
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Zeppenfeld K, Tfelt-Hansen J, de Riva M, Winkel BG, Behr ER, Blom NA, Charron P, Corrado D, Dagres N, de Chillou C, Eckardt L, Friede T, Haugaa KH, Hocini M, Lambiase PD, Marijon E, Merino JL, Peichl P, Priori SG, Reichlin T, Schulz-Menger J, Sticherling C, Tzeis S, Verstrael A, Volterrani M. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J 2022; 43:3997-4126. [PMID: 36017572 DOI: 10.1093/eurheartj/ehac262] [Citation(s) in RCA: 1092] [Impact Index Per Article: 364.0] [Reference Citation Analysis] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/11/2022] Open
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Mittal S, Deepti S, Abraham J, Kashyap L, Suhani S, Parshad R. VATS cardiac sympathetic denervation for ventricular arrhythmias: initial experience in a tertiary care centre. Indian J Thorac Cardiovasc Surg 2022; 38:515-520. [PMID: 36050987 PMCID: PMC9424384 DOI: 10.1007/s12055-022-01361-y] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/28/2022] [Revised: 04/08/2022] [Accepted: 04/12/2022] [Indexed: 10/18/2022] Open
Abstract
Cardiac sympathetic denervation (CSD) is a useful therapeutic option for patients with ventricular arrhythmias (VAs) refractory to anti-arrhythmic agents and/or catheter ablation. However, the experience is mostly limited to non-structural heart disease in paediatric patients. The advent of video-assisted thoracoscopic surgery (VATS) with its reduced morbidity has encouraged the use of VATS CSD in patients with structural heart disease. In this series, we report the surgical and cardiac outcomes of VATS-guided CSD in four patients who presented with electrical storm in the setting of different structural cardiomyopathies. Four patients underwent VATS-guided CSD at our centre during the period 2019-2021 after failure of conventional medical and/or ablative treatment for the management of refractory VAs. All four patients presented with electrical storm with different cardiomyopathies including ischaemic (post-acute myocardial infarction) and non-ischaemic aetiologies (sarcoidosis, non-specific right ventricular cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy). A combined total of 349 implantable cardioverter defibrillator (ICD) shocks were registered in the 4 weeks preceding the procedure with mean shocks of 87 per patient. All four patients successfully underwent CSD through the VATS approach with no operative mortality or any major surgical morbidity. All patients had resolution of electrical storms with 75% of patients remaining free of ICD shocks at a mean follow-up of 14.87 months. One patient who remained free of ICD shocks and recurrent VAs died at 23 months after the procedure due to progressive heart failure and complications. VATS CSD is a safe and effective complementary therapeutic modality in patients with life-threatening refractory VAs and electrical storms irrespective of the underlying substrate. Supplementary Information The online version contains supplementary material available at 10.1007/s12055-022-01361-y.
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Affiliation(s)
- Sonali Mittal
- Department of Surgical Disciplines, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110 029 India
| | - Siddharthan Deepti
- Department of Cardiology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029 India
| | - Joyner Abraham
- Department of Surgical Disciplines, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110 029 India
| | - Lokesh Kashyap
- Department of Anaesthesiology and Critical Care Medicine, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029 India
| | - Suhani Suhani
- Department of Surgical Disciplines, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110 029 India
| | - Rajinder Parshad
- Department of Surgical Disciplines, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110 029 India
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Miki Y, Yoshimura S, Sasaki T, Takizawa R, Kimura K, Haraguchi Y, Sasaki W, Kishi S, Nakatani Y, Kaseno K, Goto K, Take Y, Nakamura K, Niwamae N, Kamiyoshihara M, Naito S. Bilateral Cardiac Sympathetic Denervation for Treatment-Resistant Ventricular Arrhythmias in Heart Failure Patients with a Reduced Ejection Fraction. Int Heart J 2022; 63:692-699. [PMID: 35908853 DOI: 10.1536/ihj.21-601] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
The sympathetic nervous system plays an important role in life-threatening ventricular arrhythmias (VAs). Bilateral cardiac sympathetic denervation (BCSD) is performed for refractory VAs. We sought to assess our institutional experience with BCSD in managing treatment-resistant monomorphic ventricular tachycardia (MMVT) in heart failure patients with a reduced ejection fraction (HFrEF).Four patients with HFrEF (EF 30.0 ± 8.2%, New York Heart Association [NYHA] class IV 1) underwent BCSD for MMVT (VT storm 3, repetitive VT requiring implantable cardioverter defibrillator [ICD] therapy 1) refractory to antiarrhythmic drugs, catheter ablation and ICD therapy. BCSD was effective for suppressing VT in 3 patients for whom deep sedation was effective for suppressing VT. One patient remained alive after 14 months of follow-up without episodes of VT. One patient died of acute myocardial infarction before discharge and 1 patient died from unknown cause at 3 days post-discharge. In contrast, BCSD was completely ineffective for suppressing VT in a patient with NYHA class IV for whom deep sedation and stellate ganglion block were ineffective. This patient died on the 10th post-CSD day, despite left ventricular assist device implantation. In all cases, BCSD was successfully performed without procedure-related complications.Despite the limited number of cases, our results showed that BCSD in patients with HFrEF suppressed refractory MMVT in acute-phase except for a patient with NYHA class IV; however, the prognoses were not good. BCSD may be a treatment option at an earlier stage of NYHA and a bridge to orthotopic heart transplantation, even if BCSD is effective for suppressing VAs.
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Affiliation(s)
- Yuko Miki
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | | | - Takehito Sasaki
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Ryoya Takizawa
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Kohki Kimura
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | | | - Wataru Sasaki
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Shohei Kishi
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Yosuke Nakatani
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Kenichi Kaseno
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Koji Goto
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Yutaka Take
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Kohki Nakamura
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
| | - Nogiku Niwamae
- Department of Cardiovascular Medicine, Japanese Red Cross Maebashi Hospital
| | | | - Shigeto Naito
- Division of Cardiology, Gunma Prefectural Cardiovascular Center
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46
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König S, Schröter T, Borger MA, Bertagnolli L, Nedios S, Darma A, Hindricks G, Arya A, Dinov B. Outcomes following cardiac sympathetic denervation in patients with structural heart disease and refractory ventricular arrhythmia. Europace 2022; 24:1800-1808. [DOI: 10.1093/europace/euac078] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2021] [Accepted: 05/02/2022] [Indexed: 11/13/2022] Open
Abstract
Abstract
Aim
Cardiac sympathetic denervation (CSD) has been introduced as a bailout therapy in patients with structural heart disease and refractory ventricular arrhythmias (VAs), but available data are scarce. Purpose of this study was to estimate immediate results, complications, and mid-term outcomes of CSD following recurrent VA after catheter ablation.
Methods and results
Adult patients who underwent CSD in the Heart Center Leipzig from March 2017 to February 2021 were retrospectively analysed. Follow-up (FU) was executed via implantable cardioverter defibrillator (ICD) interrogation, telephone interviews, and reviewing medical records. Twenty-one patients (age 63.7 ± 14.4 years, all men, 71.4% non-ischaemic cardiomyopathy, left ventricular ejection fraction 31.6 ± 12.6%) received CSD via video-assisted thoracoscopic surgery (90.5% bilateral, 9.5% left-sided only). Indication for CSD was monomorphic ventricular tachycardia in 76.2% and ventricular fibrillation in 23.8 with 71.4% of patients presenting with electrical storm before index hospitalization. Procedure-related major complications occurred in 9.5% of patients. In-hospital adverse events not related to surgery were common (28.6%) and two patients died during the index hospital stay. During FU (mean duration 9.1 ± 6.5 months), five more patients died. Of the remaining patients, 38.5 and 76.9% were free from any VA or ICD shocks, respectively.
Conclusions
The CSD showed additional moderate efficacy to suppress VAs, when performed as a bailout therapy after previously unsuccessful catheter ablation. At 9 months, it was associated with freedom of ICD shocks in two-thirds of patients. In a population with many comorbidities, the rate of CSD-related complications was acceptable, although there was an overall high risk of procedure unrelated adverse events and death.
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Affiliation(s)
- Sebastian König
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
- Leipzig Heart Institute , Leipzig , Germany
| | - Thomas Schröter
- Heart Center Leipzig at University of Leipzig, Department of Cardiac Surgery , Leipzig , Germany
| | - Michael A Borger
- Heart Center Leipzig at University of Leipzig, Department of Cardiac Surgery , Leipzig , Germany
| | - Livio Bertagnolli
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
| | - Sotirios Nedios
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
| | - Angeliki Darma
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
| | - Gerhard Hindricks
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
- Leipzig Heart Institute , Leipzig , Germany
| | - Arash Arya
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
| | - Borislav Dinov
- Department of Electrophysiology, Heart Center Leipzig at University of Leipzig , Strümpellstraße 39, Leipzig 04289 , Germany
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47
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Lee ACH, Tung R, Ferguson MK. Thoracoscopic sympathectomy decreases disease burden in patients with medically refractory ventricular arrhythmias. Interact Cardiovasc Thorac Surg 2022; 34:783-790. [PMID: 35015855 PMCID: PMC9070511 DOI: 10.1093/icvts/ivab372] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2021] [Revised: 11/22/2021] [Accepted: 12/08/2021] [Indexed: 11/13/2022] Open
Abstract
Abstract
OBJECTIVES
Thoracic sympathectomy has been shown to be effective in reducing implantable cardioverter-defibrillator (ICD) shocks and ventricular tachycardia recurrence in patients with channelopathies, but the evidence supporting its use for refractory ventricular arrhythmias in patients without channelopathies is limited. This is a single-centre cohort study of bilateral R1–R4 thoracoscopic sympathectomy for medically refractory ventricular arrhythmias.
METHODS
Clinical information was examined for all bilateral thoracoscopic R1–R4 sympathectomies for ventricular arrhythmias at our institution from 2016 through 2020.
RESULTS
Thirteen patients underwent bilateral thoracoscopic R1–R4 sympathectomy. All patients had prior ICD implant. Patients had a recent history of multiple ICD discharges (12/13), catheter ablation (10/13) and cardiac arrest (3/13). Ten patients were urgently operated on following transfer to our centre for sustained ventricular tachycardia. Seven patients had ventricular tachycardia ablations preoperatively during the same admission. Five patients were in intensive care immediately preoperatively, with 3 requiring mechanical ventilation. Three patients suffered in-hospital mortality. Kaplan–Meier analysis estimated 73% overall survival at 24-month follow-up. Among the 10 patients who survived to discharge, all were alive at a median follow-up of 8.7 months (interquartile range 0.6–26.7 months). Six of 10 patients had no further ICD discharges. Kaplan–Meier analysis estimated 27% ICD shock-free survival at 24 months follow-up for all patients. Three of 10 patients had additional ablations, while 2 patients underwent cardiac transplantation.
CONCLUSIONS
Bilateral thoracoscopic sympathectomy is an effective option for patients with life-threatening ventricular arrhythmia refractory to pharmacotherapy and catheter ablation.
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Affiliation(s)
- Andy Chao Hsuan Lee
- Section of Thoracic Surgery, Department of Surgery, The University of Chicago, Chicago, IL, USA
| | - Roderick Tung
- Division of Cardiology, Department of Internal Medicine, University of Arizona, Phoenix, AZ, USA
| | - Mark K Ferguson
- Section of Thoracic Surgery, Department of Surgery, The University of Chicago, Chicago, IL, USA
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Li L, Gao J, Gao L, Li L, Zhang H, Zhao W, Xu S. Bilateral Superior Cervical Sympathectomy Activates Signal Transducer and Activator of Transcription 3 Signal to Alleviate Myocardial Ischemia-Reperfusion Injury. Front Cardiovasc Med 2022; 9:807298. [PMID: 35433880 PMCID: PMC9010611 DOI: 10.3389/fcvm.2022.807298] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/02/2021] [Accepted: 03/10/2022] [Indexed: 11/23/2022] Open
Abstract
Background There is growing evidence about the effect of bilateral superior cervical sympathectomy on myocardial ischemia-reperfusion (I/R) injury. Studies have increasingly found that the signal transducer and activator of transcription 3 (STAT3) plays a protective role in myocardial I/R injury. However, the precise mechanism is unknown. The present study explored the bilateral superior cervical sympathectomy’s effect and potential mechanism in mice myocardial I/R injury. Methods The left heart I/R injury model was created by ligating the anterior descending branch of the coronary artery for 30 min followed by reperfusion. Bilateral superior cervical sympathectomy was performed before myocardial I/R injury. To evaluate the effect of bilateral superior cervical sympathectomy on the myocardium, we examined the myocardial infarct size and cardiac function. Then, myocardial apoptosis, inflammation, and oxidative stress were detected on the myocardium. Furthermore, the expression of STAT3 signal in myocardial tissue was measured by western blotting. To further examine the cardioprotective effect of STAT3 after bilateral superior cervical sympathectomy, the STAT3 inhibitor (static) was utilized to inhibit the phosphorylation of STAT3. Results The results showed that the myocardial I/R injury decreased and the cardiac function recovered in the myocardial I/R injury after cervical sympathectomy. Meanwhile, cervical sympathectomy reduced the myocardial distribution of the sympathetic marker tyrosine hydroxylase (TH) and systemic sympathetic tone. And levels of oxidative stress, inflammatory markers, and apoptosis were reduced in myocardial tissue. We also found that the STAT3 signal was activated in myocardial tissue after cervical sympathectomy. STAT3 inhibitor can partially reverse the myocardial protective effect of cervical sympathectomy. Conclusion Bilateral superior cervical sympathectomy significantly alleviated myocardial I/R injury in mice. And activation of the STAT3 signal may play an essential role in this.
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Markman TM, Pothineni NVK, Zghaib T, Smietana J, McBride D, Amankwah NA, Linn KA, Kumareswaran R, Hyman M, Arkles J, Santangeli P, Schaller RD, Supple GE, Frankel DS, Deo R, Lin D, Riley MP, Epstein AE, Callans DJ, Marchlinski FE, Hamilton R, Nazarian S. Effect of Transcutaneous Magnetic Stimulation in Patients With Ventricular Tachycardia Storm: A Randomized Clinical Trial. JAMA Cardiol 2022; 7:445-449. [PMID: 35171197 PMCID: PMC8851364 DOI: 10.1001/jamacardio.2021.6000] [Citation(s) in RCA: 25] [Impact Index Per Article: 8.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/20/2022]
Abstract
IMPORTANCE Autonomic neuromodulation provides therapeutic benefit in ventricular tachycardia (VT) storm. Transcutaneous magnetic stimulation (TcMS) can noninvasively and nondestructively modulate a patient's nervous system activity and may reduce VT burden in patients with VT storm. OBJECTIVE To evaluate the safety and efficacy of TcMS of the left stellate ganglion for patients with VT storm. DESIGN, SETTING, AND PARTICIPANTS This double-blind, sham-controlled randomized clinical trial took place at a single tertiary referral center between August 2019 and July 2021. The study included 26 adult patients with 3 or more episodes of VT in 24 hours. INTERVENTIONS Patients were randomly assigned to receive a single session of either TcMS that targeted the left stellate ganglion (n = 14) or sham stimulation (n = 12). MAIN OUTCOMES AND MEASURES The primary outcome was freedom from VT in the 24-hour period following randomization. Key secondary outcomes included safety of TcMS on cardiac implantable electronic devices, as well as burden of VT in the 72-hour period following randomization. RESULTS Among 26 patients (mean [SD] age, 64 [13] years; 20 [77%] male), a mean (SD) of 12.7 (10.3) episodes of VT occurred within the 24 hours preceding randomization. Patients had recurrent VT despite taking a mean (SD) of 2.0 (0.6) antiarrhythmic drugs (AADs), and 11 patients (42%) required mechanical hemodynamic support at the time of randomization. In the 24-hour period after randomization, VT recurred in 4 of 14 patients (29% [SD 47%]) in the TcMS group vs 7 of 12 patients (58% [SD 51%]) in the sham group (P = .20). In the 72-hour period after randomization, patients in the TcMS group had a mean (SD) of 4.5 (7.2) episodes of VT vs 10.7 (13.8) in the sham group (incidence rate ratio, 0.42; P < .001). Patients in the TcMS group were taking fewer AADs 24 hours after randomization compared with baseline (mean [SD], 0.9 [0.8] vs 1.8 [0.4]; P = .001), whereas there was no difference in the number of AADs taken for the sham group (mean [SD], 2.3 [0.8] vs 1.9 [0.5]; P = .20). None of the 7 patients in the TcMS group with a cardiac implantable electronic device had clinically significant effects on device function. CONCLUSIONS AND RELEVANCE In this randomized clinical trial, findings support the potential for TcMS to safely reduce the burden of VT in the setting of VT storm in patients with and without cardiac implantable electronic devices and inform the design of future trials to further investigate this novel treatment approach. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT04043312.
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Affiliation(s)
- Timothy M. Markman
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia,Penn Brain Science, Translation, Innovation, and Modulation Center, University of Pennsylvania, Philadelphia
| | - Naga Venkata K. Pothineni
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Tarek Zghaib
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Jeffrey Smietana
- Division of Cardiology, Temple University, Temple University Hospital, Philadelphia, Pennsylvania
| | - Daniel McBride
- Division of Cardiology, University of Michigan, Ann Arbor
| | - Nigel A. Amankwah
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Kristin A. Linn
- Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania, Philadelphia
| | - Ramanan Kumareswaran
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Matthew Hyman
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Jeffrey Arkles
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Pasquale Santangeli
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Robert D. Schaller
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Gregory E. Supple
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - David S. Frankel
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Rajat Deo
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - David Lin
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Michael P. Riley
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Andrew E. Epstein
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia,Cardiology Division, Corporal Michael J. Crescenz VA Medical Center, Philadelphia, Pennsylvania
| | - David J. Callans
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Francis E. Marchlinski
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Roy Hamilton
- Penn Brain Science, Translation, Innovation, and Modulation Center, University of Pennsylvania, Philadelphia,Department of Neurology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
| | - Saman Nazarian
- Division of Cardiology, University of Pennsylvania, Hospital of the University of Pennsylvania, Philadelphia
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50
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[Catheter ablation of ventricular tachycardia in patients with structural heart disease]. Herz 2022; 47:129-134. [PMID: 35262743 DOI: 10.1007/s00059-022-05103-z] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 02/02/2022] [Indexed: 11/04/2022]
Abstract
Ventricular cardiac rhythm disorders are potentially life-threatening arrhythmias. Ventricular tachycardia (VT) in patients with structural heart disease carries an increased risk of sudden cardiac death. Interventional radiofrequency catheter ablation is increasingly becoming the focus of treatment for ventricular arrhythmias. So far, no randomized study has been able to demonstrate a reduction in mortality; however, depending on the existing cardiomyopathy, interventional VT ablation has proven to be more effective for rhythm stabilization than antiarrhythmic therapy and is subsequently associated with improve quality of life through reduced implantable cardioverter defibrillator (ICD) treatment. The aim of this work is to discuss the pathophysiology, mechanism and treatment of VT with structural heart disease in order to define the role of catheter ablation.
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