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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EThe connection between the brain and the heart is supported by the description of arrhythmias associated with the central nervous system. This article discusses noninvasive methods to assess sympathetic tone through sensors on the skin to assist with better describing and possibly even preventing these types of arrhythmic events. Other topics include the use of left cardiac sympathetic denervation to treat ischemic arrhythmias, and experimental data that support human clinical trials of device-based neuromodulation in patients with heart failure.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EArrhythmias\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EEpisodic \u0026amp; Paroxysmal Disorders\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHeart Failure\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ECardiology \u0026amp; Cardiovascular Medicine\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EArrhythmias\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EEpisodic \u0026amp; Paroxysmal Disorders\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EHeart Failure\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003EInterventional Techniques \u0026amp; Devices\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EThe connection between the brain and the heart is supported by the description of arrhythmias associated with the central nervous system, stated Peng-Sheng Chen, MD, Indiana University, Indianapolis, Indiana, USA. These include arrhythmias that occur in relation to seizure disorders, sudden unexpected death in epilepsy (SUDEP), congenital long-QT syndrome (LQTS) in patients with genetic arrhythmias, and stress cardiomyopathy. Dr. Chen and colleagues are working to develop noninvasive methods to assess sympathetic tone through sensors on the skin to assist with better describing and possibly even preventing these types of arrhythmic events.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003ESeizure activity elevates sympathetic tone and thus can be proarrhythmic, said Dr. Chen. Although sinus tachycardia (ST) is the most common cardiac arrhythmia during seizure, bradycardia has also been described in case reports [Carvalho KS et al. \u003Cem\u003ESeizure\u003C\/em\u003E 2004]. An epidemiologic study published in 1985 found the prevalence of SUDEP in patients aged 14 to 21 years to be 5.7 per 100,000 person-years. Assuming a prevalence of epilepsy of 7 per 1000 persons, the relative risk of SUDEP was calculated to be 188.6 per 1000 persons with epilepsy and 4.6 per 1000 persons without epilepsy [Annegers JF, Coan SP. \u003Cem\u003ESeizure\u003C\/em\u003E 1999].\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003ECommunication between the brain and the heart via the spinal cord, said Dr. Chen, is associated with ST, atrioventricular nodal conduction diseases, and sudden cardiac death (SCD) in patients with massively increased sympathetic output plus organic disease. A recent study showed that 13% of patients with SUDEP had a genetic variant that predisposed them to ventricular arrhythmias [Tu E et al. \u003Cem\u003EBrain Path\u003C\/em\u003E 2011].\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EAbnormal findings on electroencephalography are more common in patients with LQTS (12 of 17 patients vs 2 of 16 controls) [Haugaa KH et al. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2013]. Although the relationship between LQTS and seizure disorders has been recognized, it is unclear which precipitates the other, and it may be that the disorders share some genetic mutations [Chen LS, Spoonamore K. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2013].\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003EThe most accepted theory for the cause of stress-induced cardiomyopathy is the differential innervation of sympathetic nerves (SN) in the base of the heart [Lyon AR et al. \u003Cem\u003ENat Clin Pract Cardiovasc Med\u003C\/em\u003E 2008]. Excessive and prolonged sympathetic stimulation during stress leads to a negative inotropic effect because of activation of b\u003Csub\u003E2\u003C\/sub\u003E receptors, which are increased in number in the apical area secondary to reduced SN innervation.\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ELEFT CARDIAC SYMPATHETIC DENERVATION\u003C\/h2\u003E\n         \u003Cp id=\u0022p-7\u0022\u003ELeft cardiac sympathetic denervation (LCSD) has been shown to effectively treat ischemic arrhythmias, LQTS, and catecholaminergic polymorphic ventricular tachycardia (CPVT) and to prevent SCD after myocardial infarction (MI). Peter J. Schwartz, MD, Center for Cardiac Arrhythmias of Genetic Origin, IRCCS Istituto Auxologico Italiano, Milan, Italy, reviewed experimental and clinical data.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EHistorically, the description of a reflex excitation of the SN by acute myocardial ischemia, which resulted in ventricular fibrillation (VF) led to experimental work showing that LCSD through the blocking the left stellate ganglion reduced VF and SCD and could raise the threshold for VF by 70% without the use of drugs. LCSD also increased the ventricular refractory period, VF threshold, and myocardial reactive hyperemia.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EThe Italian Sudden Death Prevention Group study, conducted before beta-blockers were standard treatment for MI, showed that LCSD and oxprenolol had a similar lower rate of SCD (\u223c3%) compared with placebo (\u223c20%) for patients who had an MI with VF or ventricular tachycardia (VT). A recent retrospective analysis reported that LCSD or bilateral CSD in patients with cardiomyopathy and refractory VT or VT storms significantly reduced implantable cardioverter-defibrillator (ICD) shocks (p\u0026lt;0.001); 30% of patients in the LCSD group and 48% in the bilateral CSD group had continued freedom from ICD shocks, and 90% of the patients had significant reductions in ICD shock burden [Vaseghi M et al. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2014].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EIn high-risk patients with LQTS, LCSD reduced any cardiac event by 91% and life-threatening events by 64% [Schwartz PJ et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2004]. Prior to treatment, 99% of the patients were symptomatic, 48% had experienced cardiac arrest, 75% had recurrences despite \u03b2-blocker use, and the mean corrected QT interval was 543\u00b165 ms. The impact on ICD shocks is shown in \u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E.\u003C\/p\u003E\n         \u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/15922\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/15922\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15922\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-11\u0022 class=\u0022first-child\u0022\u003EICD Multiple Shocks and LCSD\u003C\/p\u003E\n            \u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-14\u0022\u003ECPVT is associated with a very poor quality of life because of the frequency of ICD shocks. The long-term efficacy of LCSD was first shown in 3 patients who had experienced life-threatening cardiac events and after a mean follow-up period of 8 years had a 90% reduction in major arrhythmic events [Wilde AAM et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2008]. The multinational CPVT registry has shown that LCSD prevented, suppressed, or significantly reduced major cardiac events in 91% of 55 high-risk patients receiving optimal medical therapy. Prof. Schwartz recommended LCSD therapy in addition to \u03b2-blockers as a rationale approach for high-risk patients with CPVT, either alone or complementing ICDs used as a safety net.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ENEUROMODULATION TO TREAT HEART FAILURE\u003C\/h2\u003E\n         \u003Cp id=\u0022p-15\u0022\u003EPaul J. Wang, MD, Stanford University School of Medicine, Palo Alto, California, USA, reviewed experimental data that support human clinical trials of device-based neuromodulation in patients with heart failure (HF) to determine its safety and efficacy. The imbalance of parasympathetic and sympathetic systems in HF led to the hypothesis that modulating the autonomic nervous system would improve HF [Lopshire JC, Zipes DP. \u003Cem\u003ECurr Cardiol Rep\u003C\/em\u003E 2012].\u003C\/p\u003E\n         \u003Cp id=\u0022p-16\u0022\u003ESympathetic activation is compensatory in early HF but is deleterious in late HF, leading to decreased responsiveness of the myocardium to adrenergic stimuli [Lopshire JC et al. \u003Cem\u003ECurr Cardiol Rep\u003C\/em\u003E 2012]. Changes in cellular processes such as abnormal calcium handling and apoptosis occur, and abnormal cardiac reflexes can develop, which suppress the inhibitory arterial baroreceptor reflex and enhance excitatory sympathetic afferent and arterial chemoreceptor reflexes. Decreased parasympathetic tone increased heart rate and decreased heart rate variability, correlated with increased mortality, and increased vagal afferent activation (eg, cardiac cytokine and neurohumoral activity) and was associated with changes in parasympathetic ganglionic signaling and a decrease in postganglionic muscarinic receptor density and function.\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EExperimental data for the benefit of spinal cord stimulation (SCS) and vagal nerve stimulation (VNS) were also reviewed. SCS at the T1 level delivered before and during coronary artery occlusion reduced infarct size, significantly increased the sinus cycle length and AH interval, and ischemia-mediated ventricular arrhythmias were reduced in a canine model [Lopshire JC, Zipes DP et al. \u003Cem\u003ECurr Cardiol Rep\u003C\/em\u003E 2012]. Another animal study demonstrated a significant decrease in spontaneous and ischemic ventricular arrhythmias with SCS, medical therapy, or SCS plus medical therapy, compared with control. The SCS and the SCS plus medical therapy treatment groups also had significant improvements in resting heart rate, systolic blood pressure, and oxygen saturation, along with recovery of left ventricular ejection fraction (LVEF) and significant reversal of left ventricular (LV) dilatation. Two studies of SCS neuromodulation are under way in humans: the randomized, single-blind Determining the Feasibility of Spinal Cord Neuromodulation for the Treatment of Chronic Heart Failure trial [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01112579\u0026amp;atom=%2Fspmdc%2F14%2F9%2F32.atom\u0022\u003ENCT01112579\u003C\/a\u003E] for safety and efficacy in advanced HF and the nonrandomized Spinal Cord Stimulation For Heart Failure study [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01362725\u0026amp;atom=%2Fspmdc%2F14%2F9%2F32.atom\u0022\u003ENCT01362725\u003C\/a\u003E] in systolic HF.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EVNS in experimental models reduced ventricular arrhythmias and mortality, slowed HF progression in a canine model, reduced heart rate, significantly improved LVEF, and reduced LV volumes. In combination with \u03b2-blocker therapy, VNS produced the greatest reduction in LVEF, decreased circulating cytokines and myocyte hypertrophy, and restored baroreflex control to normal [Lopshire JC et al. \u003Cem\u003ECurr Cardiol Rep\u003C\/em\u003E 2012]. The Phase 2 Cardio-Fit trial [De Ferrari GM et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2011] demonstrated that VNS significantly improved LVEF from 22% to 29%, reduced LV systolic volumes at 6 months, and improved quality of life. The Increase of Vagal Tone in CHF [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01303718\u0026amp;atom=%2Fspmdc%2F14%2F9%2F32.atom\u0022\u003ENCT01303718\u003C\/a\u003E], vagal Nerve Stimulation: Safeguarding Heart Failure Patients [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT02113033\u0026amp;atom=%2Fspmdc%2F14%2F9%2F32.atom\u0022\u003ENCT02113033\u003C\/a\u003E], and Barostim Hope for Heart Failure [\u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT01720160\u0026amp;atom=%2Fspmdc%2F14%2F9%2F32.atom\u0022\u003ENCT01720160\u003C\/a\u003E] studies of VNS are currently under way.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2014 MD Conference Express\u00ae\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/14\/9\/32.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzp73h\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzp73h\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}