Background:Subcutaneous nerve stimulation (ScNS) can reduce atrial arrhythmia in canine models. Objective:This study aimed to test the hypothesis that ScNS can reduce the burden of paroxysmal atrial fibrillation (AF) by a randomized, sham-controlled clinical trial. Methods:Patients with drug-resistant symptomatic paroxysmal AF were randomized to receive ScNS (10 Hz, 3.5 mA output, 20 s on, and 1 min off) for 2 weeks. The AF burden was determined by ePatch recordings. Results:Of the 46 patients who consented, 12 patients (8 men and 4 women, 60.9 ± 10.2 years) were randomized. The change in AF burden at week 1 from eligibility week was not significantly different between the groups (P = .8102). The proportion of AF-free patients was 16.7% for each group (P = 1.000). The difference-in-difference (DID) estimates for weeks 1, 2, 3, and 12 (estimate ± SE) were -2.04 ± 10.84 (P = .8516), -2.44 ± 10.84 (P = .8228), -0.20 ± 10.84 (P = .986), and -18.11 ± 11.16 (P = .1126), respectively. The Stimulation Group shows a slower increase in %AF burden over time than the Sham Group (P = .027 for group and time interaction) when time is modeled linearly as a continuous variable in the mixed model. In Week 3, the ventricular rate (VR) during AF in the Stimulation Group was faster than in the Sham Group (P = .026). Conclusion:2 weeks of ScNS did not reduce the AF burden or control the VR in patients with paroxysmal AF. However, there was a slower increase in %AF burden over time in the Stimulation Group than in the Sham Group.

BACKGROUND Autonomic nerve activity is important in the mechanisms of paroxysmal atrial fibrillation (PAF). OBJECTIVE The purpose of this study was to test the hypothesis that a single burst of skin sympathetic nerve activity (SKNA) can toggle on and off PAF or premature atrial contraction (PAC) clusters. METHODS Simultaneous recording of SKNA and electrocardiogram (neuECG) recording was performed over 7 days in patients with PAF. RESULTS In study 1, 8 patients (7 men and 1 woman; age 62 +/- 8 years) had 124 episodes of PAF. An SKNA burst toggled both on and off PAF in 8 episodes (6.5%) (type 1), toggled on but not off in 12 episodes (9.7%) (type 2), and toggled on a PAC cluster followed by PAF in 4 episodes (3.2%) (type 3). The duration of these PAF episodes was <10 minutes. The remaining 100 episodes (80.6%) were associated with active SKNA bursts throughout PAF (type 4) and lasted longer than type 1 (P 5 .0185) and type 2 (P 5 .0027) PAF. There were 47 PAC clusters. Among them, 24 (51.1%) were toggled on and off, and 23 (48.9%) were toggled on but not off by an SKNA burst. In study 2, 17 patients (9 men and 8 women; age 58 +/- 12 years) had <10 minutes of PAF (4, 8, 0, and 31 of types 1, 2, 3, and 4, respectively). There were significant circadian variations of all types of PAF. CONCLUSION A single SKNA burst can toggle short-duration PAF and PAC cluster episodes on and off. The absence of continued SKNA after the onset might have affected the maintenance of these arrhythmias.

The autonomic nervous system plays a vital role in cardiac arrhythmias, including atrial fibrillation (AF). Therefore, reducing the sympathetic tone via neuromodulation methods may be helpful in AF control. Myocardial ischemia is associated with increased sympathetic tone and incidence of AF. It is an excellent disease model to understand the neural mechanisms of AF and the effects of neuromodulation. This review summarizes the relationship between autonomic nervous system and AF and reviews methods and mechanisms of neuromodulation. This review proposes that noninvasive or minimally invasive neuromodulation methods will be most useful in the future management of AF.

OBJECTIVE:Postural orthostatic tachycardia syndrome (POTS) is associated with abnormal blood pressure (BP) regulation and increased prevalence of nocturnal nondipping. We hypothesized that nocturnal nondipping of BP is associated with elevated skin sympathetic nerve activity (SKNA) in POTS. METHOD:We used an ambulatory monitor to record SKNA and electrocardiogram from 79 participants with POTS (36 ± 11 years, 72 women), including 67 with simultaneous 24-h ambulatory BP monitoring. RESULTS:Nocturnal nondipping of BP was present in 19 of 67 (28%) participants. The nondipping group had a higher average SKNA (aSKNA) from midnight of day 1 to 0100 h on day 2 than the dipping group ( P  = 0.016, P  = 0.030, respectively). The differences (Δ) of aSKNA and mean BP between daytime and night-time were more significant in the dipping group compared with the nondipping group (ΔaSKNA 0.160 ± 0.103 vs. 0.095 ± 0.099 μV, P  = 0.021, and Δmean BP 15.0 ± 5.2 vs. 4.9 ± 4.2 mmHg, P  < 0.001, respectively). There were positive correlations between ΔaSKNA and standing norepinephrine (NE) (r = 0.421, P  = 0.013) and the differences between standing and supine NE levels ( r  = 0.411, P  = 0.016). There were 53 (79%) patients with SBP less than 90 mmHg and 61 patients (91%) with DBP less than 60 mmHg. These hypotensive episodes were associated with aSKNA of 0.936 ± 0.081 and 0.936 ± 0.080 μV, respectively, which were both significantly lower than the nonhypotensive aSKNA (1.034 ± 0.087 μV, P  < 0.001 for both) in the same patient. CONCLUSION:POTS patients with nocturnal nondipping have elevated nocturnal sympathetic tone and blunted reduction of SKNA between day and night. Hypotensive episodes were associated with reduced aSKNA.

BACKGROUND:Chronic orthostatic intolerance (OI) is characterized by the development of tachycardia and other symptoms when assuming an upright body position.OBJECTIVE:The purpose of this study was to test the hypothesis that skin sympathetic nerve activity (SKNA) bursts are specific symptomatic biomarkers in patients with chronic OI.METHODS:We used an electrocardiogram monitor with a built-in triaxial accelerometer to simultaneously record SKNA and posture in ambulatory participants. Study 1 compared chronic OI (14 women and 2 men; mean age 35 ± 10 years) with reference control participants (14 women; mean age 31 ± 6 years). Study 2 included 17 participants with chronic OI (15 women and 2 men; mean age 39 ± 12 years) not yet treated with ivabradine, pyridostigmine, or β-blockers.RESULTS:In study 1, there were 124 episodes (8 ± 4 per participant) of postural changes, with 11 episodes (8.9%) associated with symptoms. In comparison, 0 of 104 postural changes (7 ± 3 per participant) in controls were symptomatic (P = .0011). In participants with chronic OI, the SKNA bursts associated with symptoms had higher burst frequencies, longer burst durations, and larger mean burst areas than did bursts during asymptomatic periods. However, SKNA bursts and tachycardia were asymptomatic in controls. We analyzed 110 symptomatic episodes in study 2 (6 ± 5 per participant). Among them, 98 (89.1%) followed at least 1 SKNA burst. In comparison, only 41 (37.3%) had heart rate exceed 100 beats/min 1 minute before symptom onset (P < .0001).CONCLUSION:SKNA bursts are a highly specific, albeit insensitive, symptomatic biomarker for chronic OI.

BACKGROUND:The role of sympathetic nerve activity to maintain sinus rate acceleration remains unclear.OBJECTIVE:The purpose of this study was to test the hypothesis that sustained (>30 seconds) sinus rate acceleration can be associated with either a sympathetic driven or a sympathetic toggled mechanism.METHODS:We used a patch monitor to record skin sympathetic nerve activity (SKNA) and electrocardiogram over 24 hours. Study 1 included chronic orthostatic intolerance (OI) (n = 18), atrial fibrillation (n = 7), and asymptomatic normal control (n = 19) groups. Study 2 included 17 participants with chronic OI not treated with ivabradine, pyridostigmine, or β-blockers.RESULTS:While a majority of sinus rate acceleration was driven by persistent SKNA in study 1, some episodes were toggled on and off by SKNA bursts without persistent SKNA elevation. The sympathetic toggled sinus rate acceleration episodes were found in 7 of 18 participants with chronic OI (39%), 2 of 7 participants with atrial fibrillation (29%), and 6 of 19 normal control participants (32%) (P = .847) and were faster and longer in the chronic OI group than in other groups. In study 2, there were a total of 11 episodes of sinus rate acceleration that persisted for >200 seconds. Among these episodes, 6 (35%) were toggled on and off by SKNA bursts.CONCLUSION:Sustained sinus rate acceleration (may be toggled on or off) is associated with SKNA bursts in participants with chronic OI, participants with atrial fibrillation, and normal controls. Patients with OI had more frequent and longer episodes than did other groups.

BACKGROUND Prostatitis seriously endangers the health of men. While they have been widely used in recent years, there remains a lack of systematic evaluation of the clinical efficacy of α-receptor blockers (α-RBs)/α-adrenergic receptor blockers (α-ARBs) in its treatment. Based on this, this study was developed to systematically evaluate the clinical effect of α-ARB in the treatment of prostatitis. METHODS Randomized controlled trials (RCTs) studying α-RBs or α-ARBs, placebos, or other measures to treat prostatitis were searched in Cochrane Library, PubMed, Embase, and CBM databases from establishment to December 2020. The quality of included articles was evaluated using the Cochrane System Review Manual and Jadad tools, and a meta-analysis was performed using Review Manager 5.3 software. RESULTS A total of six articles meeting the requirements were found and included 450 patients. Meta-analysis showed that the National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) score [mean difference (MD) =-1.76, 95% confidence interval (CI): (-3.35 to -0.17), and P=0.03], pain score [MD =-2.24, 95% CI: (-3.65 to -0.83), and P=0.002], voiding symptom score [MD =-1.21, 95% CI: (-2.06 to -0.35), and P=0.006], and quality of life score [MD =-1.40, 95% CI: (-1.48 to -1.33), and P<0.00001] for patients in the experimental group were lower in contrast to those in the control group after the treatment. DISCUSSION The use of α-ARB could significantly improve the treatment effect of patients with prostatitis and improve their quality of life.

BACKGROUND:Sympathetic nerve activity, heart rate (HR), and blood pressure (BP) all have very low frequency (VLF), low frequency (LF), and high frequency (HF) oscillations.OBJECTIVE:The purpose of this study was to test the hypothesis that the frequency spectra of subcutaneous nerve activity (ScNA), stellate ganglion nerve activity (SGNA), HR, and BP are important to cardiac arrhythmogenesis.METHODS:We used radiotransmitters to record SGNA, ScNA, HR, and BP in 6 ambulatory dogs and determined the dominant frequency and paroxysmal atrial tachyarrhythmias (PATs) episodes in 3-minute windows over a 24-hour period.RESULTS:The frequency spectra determined in ScNA reflected that in SGNA. HF oscillations were present in both ScNA and SGNA at all time but could be overshadowed by the much larger LF and VLF burst activities. The dominant frequency could occur in any of the 3 frequency bands. There were circadian variations with more frequent occurrences of HF oscillations at night. HF oscillations in HR and BP matched HF oscillations in SGNA and ScNA. PATs occurred only when dominant frequencies of SGNA and ScNA were in the LF and VLF bands.CONCLUSION:HF oscillations in BP and HR correlate with HF oscillations in sympathetic nerve activity and are present at all time. HF oscillations can be overshadowed by the much larger LF and VLF burst activities. PATs occur only when LF or VLF, but not when HF, is the dominant frequency. The frequency spectra determined in ScNA reflect that in SGNA.

BACKGROUND:Subcutaneous nerve stimulation (ScNS) remodels the stellate ganglion and reduces stellate ganglion nerve activity (SGNA) in dogs. Acute myocardial infarction (MI) increases SGNA through nerve sprouting. OBJECTIVE:The purpose of this study was to test the hypothesis that ScNS remodels the stellate ganglion and reduces SGNA in ambulatory dogs with acute MI. METHODS:In the experimental group, a radio transmitter was implanted during the first sterile surgery to record nerve activity and an electrocardiogram, followed by a second sterile surgery to create MI. Dogs then underwent ScNS for 2 months. The average SGNA (aSGNA) was compared with that in a historical control group (n = 9), with acute MI monitored for 2 months without ScNS. RESULTS:In the experimental group, the baseline aSGNA and heart rate were 4.08±0.35 μV and 98±12 beats/min, respectively. They increased within 1 week after MI to 6.91±1.91 μV (P=.007) and 107±10 beats/min (P=.028), respectively. ScNS reduced aSGNA to 3.46±0.44 μV (P<.039) and 2.14±0.50 μV (P<.001) at 4 and 8 weeks, respectively, after MI. In comparison, aSGNA at 4 and 8 weeks in dogs with MI but no ScNS was 8.26±6.31 μV (P=.005) and 10.82±7.86 μV (P=0002), respectively. Immunostaining showed confluent areas of remodeling in bilateral stellate ganglia and a high percentage of tyrosine hydroxylase-negative ganglion cells. Terminal deoxynucleotidyl transferase dUTP nick end labeling was positive in 26.61%±11.54% of ganglion cells in the left stellate ganglion and 15.94%±3.62% of ganglion cells in the right stellate ganglion. CONCLUSION:ScNS remodels the stellate ganglion, reduces SGNA, and suppresses cardiac nerve sprouting after acute MI.

The convenience of obtaining perfect photos with mobile devices not only promotes the quality of modern life, but also facilitates privacy hacker for crimes like taking images secretly. Such dilemma causes widely concerns and calls for forensic community to reverse-engineer the evil images, which can be seen as a source identification problem. In recent years, convolutional neural network (CNN) has jumped to the crown jewel due to its high performance in image recognition. In this light, we devise a CNN-based system named FATE (Fingerprints Automatically Targeting and Extracting) which can identify the image source out of various models of mobile devices. To verify our FATE system, we first set up a dataset consisted of images from six different model mobile devices, then we train FATE on our dataset and test it with real data. Besides, we introduce another two stat-of-the-art CNN models for comparison. The results show that our FATE beats down the rivals and achieves an accuracy of 98.5% in recognition.

Class IIa histone deacetylases (HDACs) critically regulate cardiac function through the repression of the activity of myocyte enhancer factor 2 (MEF2)-dependent gene programs. Protein kinase D (PKD) and Ca2+/Calmodulin-dependent kinase II (CaMKII) activate MEF2 by phosphorylating distinct HDAC isoforms and thereby creating 14-3-3 binding sites for nucleo-cytoplasmic shuttling. Recently, it has been shown that this process is counteracted by cyclic AMP (cAMP)-dependent signaling. Here, we investigated the specific mechanisms of how cAMP-dependent signaling regulates distinct HDAC isoforms and determined their relative contributions to the protection from pathological MEF2 activation. We found that cAMP is sufficient to induce nuclear retention and to blunt phosphorylation of the 14-3-3 binding sites of HDAC5 (Ser259/498) and HDAC9 (Ser218/448) but not HDAC4 (Ser246/467/632). These regulatory events could be observed only in cardiomyocytes and myocyte-like cells but not in non-myocytes, pointing to an indirect myocyte-specific mode of action. Consistent with one previous report, we found that blunted phosphorylation of HDAC5 and HDAC9 was mediated by protein kinase A (PKA)-dependent inhibition of PKD. However, we show by the use of neonatal cardiomyocytes derived from genetic HDAC mouse models that endogenous HDAC5 but not HDAC9 contributes specifically to the repression of endogenous MEF2 activity. HDAC4 contributed significantly to the repression of MEF2 activity but based on the mechanistic findings of this study combined with previous results we attribute this to PKA-dependent proteolysis of HDAC4. Consistently, cAMP-induced repression of agonist-driven cellular hypertrophy was blunted in cardiomyocytes deficient for both HDAC5 and HDAC4. In conclusion, cAMP inhibits MEF2 through both nuclear accumulation of hypo-phosphorylated HDAC5 and through a distinct HDAC4-dependent mechanism.

neuECG, the simultaneous noninvasive recording of ECG and skin sympathetic nerve activity (SKNA), directly records sympathetic nerve activity over a long period of time. It can be used to measure sympathetic tone in healthy subjects and in subjects with non-cardiovascular diseases. The electrical activity that can be measured on the surface of the skin originates from the heart, the muscle or nerve structures. Because the frequency content of nerve activity falls in a higher frequency range than that of the ECG and myopotential, it is possible to use high-pass or band-pass filtering to specifically isolate the SKNA. neuECG is voltage calibrated and does not require invasive procedures to impale electrodes in nerves and thus has advantages over microneurography. Here, we present a protocol that takes <10 min to set up. The neuECG can be continuously recorded over a 24-h period or longer. We also describe methods to efficiently analyze neuECG from humans using commercially available hardware and software to facilitate adoption of this technology in clinical research.

Our research laboratory recently invented a new method (neuECG) to simultaneously and non‐invasively record electrocardiogram (ECG) and skin sympathetic nerve activity (SKNA) from humans using standard ECG patch electrodes. These methods are non‐invasive and stable over long periods of time. However, because the neuECG analyses required custom written software, these methods have not been widely used or tested by the scientific community. The purpose of the present study was to develop a method for neuECG recording and analyses using commercially available hardware and software. We used ADInstruments PowerLab to record bipolar electrical signals from the skin of thorax and arms. Wide bandwidth and high sampling rate (10,000/s) were used for recording. The data were then analyzed offline using LabChart Pro 8 software. The digitized neuECG signals are amplified and band‐pass filtered between 0.05 Hz and 150 Hz to display ECG and between 500 Hz and 1,000 Hz to show the SKNA (μV). We full‐wave rectify then integrate all digitized SKNA signals using leaky integrator with 100 ms time constant and display the results over time to simulate the display methods of microneurography (iSKNA, μV.s). For quantitative analyses, we divide the absolute sum of the voltage samples by the number of digitized samples in the chosen window to obtain the aSKNA (μV). We can also examine the distribution of the aSKNA and determine a threshold to separate baseline activity from the burst activity. As compared with the microneurography studies, the neuECG does not require invasive procedures to impale electrodes in nerves and is voltage calibrated. The latter characteristics allow investigators to compare aSKNA, iSKNA and burst duration between subjects or groups. Figure shows the actual neuECG recording. SKNA band‐pass filtered from the digitized signal was converted to iSKNA and aSKNA. Down arrows show premature ventricular contractions. The dotted line indicates the commencement of cold water pressor test that elevated the aSKNA (red double headed arrows) and heart rate. We conclude that neuECG can be recorded and analyzed using commercially‐available hardware and software. These new methods may facilitate the testing and use of this novel technology in experimental biology research.Support or Funding InformationThis study was supported in part by NIH Grants 1OT2OD028190, R01 HL139829, R56 HL71140, TR002208‐01 (Dr. Chen), R42DA043391 (Dr Everett), a Charles Fisch Cardiovascular Research Award endowed by Dr Suzanne B. Knoebel of the Krannert Institute of Cardiology (Drs. Kusayama and Everett), a Medtronic‐Zipes Endowment, and the Indiana University Health‐Indiana University School of Medicine Strategic Research Initiative (Dr. Chen).Example of actual neuECG recordingFigure 1

Background Subcutaneous nerve stimulation (ScNS) damages the stellate ganglion and improves rhythm control of atrial fibrillation (AF) in ambulatory dogs. Objective The purpose of this study was to test the hypothesis that thoracic ScNS can improve rate control in persistent AF. Methods We created persistent AF in 13 dogs and randomly assigned them to ScNS (n = 6) and sham control (n = 7) groups. 18F-2-Fluoro-2-deoxyglucose positron emission tomography/magnetic resonance imaging of the brain stem was performed at baseline and at the end of the study. Results The average stellate ganglion nerve activity reduced from 4.00 ± 1.68 μV after the induction of persistent AF to 1.72 ± 0.42 μV (P = .032) after ScNS. In contrast, the average stellate ganglion nerve activity increased from 3.01 ± 1.26 μV during AF to 5.52 ± 2.69 μV after sham stimulation (P = .023). The mean ventricular rate during persistent AF reduced from 149 ± 36 to 84 ± 16 beats/min (P = .011) in the ScNS group, but no changes were observed in the sham control group. The left ventricular ejection fraction remained unchanged in the ScNS group but reduced significantly in the sham control group. Immunostaining showed damaged ganglion cells in bilateral stellate ganglia and increased brain stem glial cell reaction in the ScNS group but not in the control group. The 18F-2-fluoro-2-deoxyglucose uptake in the pons and medulla was significantly (P = .011) higher in the ScNS group than the sham control group at the end of the study. Conclusion Thoracic ScNS causes neural remodeling in the brain stem and stellate ganglia, controls the ventricular rate, and preserves the left ventricular ejection fraction in ambulatory dogs with persistent AF.

Background: In 2018, diagnosis-related group-based prospective payment system (DRG-PPS) was implemented nationwide by China that did not fully consider the additional costs caused by healthcare associated infections (HAIs). HAIs can increase hospitalization costs, but only a few studies have been conducted in China. We aimed to assess the additional costs caused by HAIs. Methods: A retrospective matched case-control (1:1) study was performed in one of the largest tertiary hospitals in Sichuan Province, China. A multiple linear regression was used to identify confounding factors, and the propensity score matching (PSM) method was used to balance confounding factors between cases and controls. On this basis, we estimated the additional costs caused by HAIs. Results: Of the 109,294 inpatients observed, 1912 had HAI. After the PSM method was implemented, 1686 cases were successfully matched. Median hospitalization costs were (sic)5613.03 for patients with HAIs and (sic)3414.83 for patients without HAIs (P< 0.001), resulting in an absolute difference of (sic)2198.19. With the exception of pathological diagnosis costs, surgical treatment costs and disposable medical material costs for surgery, all other types of costs for the cases with HAIs were larger. Conclusions: Patients with HAIs incurred greater hospitalization costs than non-HAI patients, which warrants closer attention if we are to reform the payment method of medical insurance in China. (C) 2019 The Authors. Published by Elsevier Limited on behalf of King Saud Bin Abdulaziz University for Health Sciences.

OBJECTIVES This study was designed to test the hypothesis that low-level vagal nerve stimulation (VNS) reduces the ventricular rate (VR) during atrial fibrillation (AF) through the activation of the inferior vena cava (IVC)-inferior atrial ganglionated plexus nerve activity (IAGPNA). BACKGROUND Increased IVC-IAGPNA can suppress atrioventricular node conduction and slow VR in canine models of AF. METHODS Persistent AF was induced in 6 dogs and the IVC-IAGPNA, right vagal nerve activity, left vagal nerve activity, and an electrocardiogram were recorded. After persistent AF was documented, VNS was programed to 14 s "on" and 1.1 min "off." After 1 week, the VNS was reprogramed to 3 min off and stimulation continued for another week. Neural remodeling of the stellate ganglion (SG) was assessed with tyrosine hydroxylase staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling staining. RESULTS Average IVC-IAGPNA was increased during both VNS 1.1 min off (8.20 +/- 2.25 mu V [95% confidence interval (CI): 6.33 to 9.53 mu V]; p = 0.002) and 3 min off (7.96 +/- 2.03 mu V [95% CI: 6.30 to 9.27 mu V]; p = 0.001) versus baseline (7.14 +/- 2.20 mu V [95% CI: 5.35 to 8.52 mu V]). VR was reduced during both VNS 1.1 min off (123.29 +/- 6.29 beats/min [95% CI: 116.69 to 129.89 beats/min]; p = 0.001) and 3 min off (120.01 +/- 4.93 beats/min [95% CI: 114.84 to 125.18 beats/min]; p = 0.001) compared to baseline (142.04 +/- 7.93 bpm [95% CI: 133.72 to 150.37]). Abnormal regions were observed in the left SG, but not in the right SG. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling-positive neurons were found in 22.2 +/- 17.2% [95% CI: 0.9% to 43.5%] of left SG cells and 12.8 +/- 8.4% [95% CI: 2.4% to 23.2%] of right SG cells. CONCLUSIONS Chronic low-level VNS increases IVC-IAGPNA and damages bilateral stellate ganglia. Both mechanisms could contribute to the underlying mechanism of VR control during AF. (C) 2018 by the American College of Cardiology Foundation.

In the present work, we studied the microstructure, thermal and magnetic properties of a Gd48Co50Nb2 amorphous ribbon for the purpose of revealing the mechanism of the table-like magnetic entropy change (−ΔSm) profile of the ribbon. It was found that the amorphous ribbon was fully amorphous with only short-range orders. The two-step magnetic phase transitions indicate that there are two amorphous phases in the Gd48Co50Nb2 amorphous ribbon. The table-like −ΔSm profile of the Gd48Co50Nb2 amorphous ribbon is supposed to be due to the superposition of two −ΔSm peaks corresponding to two separated amorphous phases with different magnetic properties. The amorphous ribbon is expected to be a good candidate for magnetic refrigerant because of its high maximum −ΔSm and high effective refrigeration capacity of the specific table-like −ΔSm profile.

BACKGROUND We recently reported that skin sympathetic nerve activity (SKNA) can be used to estimate sympathetic tone in humans. In animal models, vagal nerve stimulation (VNS) can damage the stellate ganglion, reduce stellate ganglion nerve activity, and suppress cardiac arrhythmia. Whether VNS can suppress sympathetic tone in humans remains unclear. OBJECTIVE The purpose of this study was to test the hypothesis that VNS suppresses SKNA in patients with drug-resistant epilepsy. METHODS ECG patch electrodes were used to continuously record SKNA in 26 patients with drug-resistant epilepsy who were admitted for video electroencephalographic monitoring. Among them, 6 (2 men, age 40 +/- 11 years) were previously treated with VNS and 20 (7 men, age 37 +/- 8 years) were not. The signals from ECG leads I and II were filtered to detect SKNA. RESULTS VNS had an on-time of 30 seconds and off-time of 158672 seconds, with output of 1.9260.42 mA at 24.17 +/- 2.01 Hz. Average SKNA during VNS off-time was 1.06 mV (95% confidence interval [CI] 0.93-1.18) in lead I and 1.13 mV (95% CI 0.99-1.27) in lead II, which was significantly lower than 1.38 mV (95% CI 1.01-1.75; P = .036) and 1.38 mV (95% CI 0.98-1.78; P = .035) in the control group, respectively. Heart rate was 65 bpm (95% CI 59-71) in the VNS group, which was significantly lower than 77 bpm (95% CI 71-83) in the control group. CONCLUSION Patients with VNS had significantly lower SKNA than those without VNS.