Transient cardiac electrophysiological changes in a rat model of subarachnoid haemorrhage: a brain-heart interaction.

AIMS: Subarachnoid haemorrhage (SAH) is one of the causes of sudden cardiac death (SCD). However, the time course of ventricular arrhythmias and potential mechanisms responsible for this effect after SAH remain unknown. OBJECTIVE: This study aims to investigate the effect of SAH on ventricular electrophysiological changes and its potential mechanisms in long-term phase. METHODS AND RESULTS: We examined the ventricular electrophysiological remodelling and potential mechanisms in a Sprague Dawley rat model of SAH at six time points (baseline, and Days 1, 3, 7, 14 and 28) and explored the potential mechanisms. We measured the ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT) and left stellate ganglion (LSG) activity at different time points before and after SAH. We also detected neuropeptide Y (NPY) levels in plasma and myocardial tissues by enzyme-linked immunosorbent assay, and quantified NPY 1 receptor (NPY1R) protein and mRNA expression levels by western blotting and quantitative real-time reverse transcription-polymerase chain reaction, respectively. Subarachnoid haemorrhage gradually prolonged QTc intervals, shortened ventricular ERP and reduced VFT during the acute phase, peaking at Day 3. However, no significant changes were observed from Days 14 to 28 compared to Day 0. Subarachnoid haemorrhage gradually increased LSG activity, increased NPY concentrations and up-regulated NPY1R expression in the acute phase of SAH, peaking at Day 3. However, no significant variations were found from Days 14 to 28 compared to Day 0. CONCLUSION: Subarachnoid haemorrhage increases the transient susceptibility of VAs in the acute phase, and the underlying mechanisms for this response included increased sympathetic activity and up-regulated NPY1R expression.

QNZ exposure induces development toxicity and mechanisms of hatching inhibition in large-scale loach (Paramisgurnus dabryanus) embryos.

QNZ is a quinazoline-type NF-κB inhibitor and is one of the hot anti-inflammatory drug candidates in recent years. With its development and application, QNZ will inevitably enter the aquatic environment posing a threat to aquatic organisms. To investigate the potential toxicity of QNZ in the early life stages of the organism, this study exposed embryos of large-scale loach (Paramisgurnus dabryanus) to 0, 20, 40, 60, and 80 nM of QNZ. The hatching of embryos was significantly inhibited and hatching time was delayed. We explored the mechanism of hatching delay and failure. The results suggested that QNZ exposure reduced the number of hatching gland cells (HGCs) and hatching enzyme activity. Also, the frequency of spontaneous movements was inhibited by interfering with the expression of genes related to the cholinergic system and skeletal muscle development. Further, QNZ exposure induces a series of morphological changes (spine deformation, pericardial edema, tail deformation, and yolk sac edema) in embryos and newly-hatched larvae, and finally increased the deformity rate and mortality rate of newly-hatched larvae. The information presented in this study will provide a scientific basis for further studies into the potential toxicity of QNZ on aquatic organisms.

Association between adiponectin-to-leptin ratio and heart rate variability in new-onset paroxysmal atrial fibrillation: A retrospective cohort study.

BACKGROUND: The adiponectin-to-leptin (A/L) ratio has been identified as a potential surrogate biomarker for metabolic disorders. However, it remains unknown whether the serum A/L ratio is associated with heart rate variability in paroxysmal atrial fibrillation (AF). METHODS: For this retrospective study, we included consecutive patients who underwent 24-h long-range electrocardiogram examination in our center for paroxysmal AF. The results of echocardiography, heart rate variability tests, and blood tests were also retrieved. Multivariate line regression analysis was performed to evaluate identify factors independently associated with heart rate variability. RESULTS: Among the 85 included patients with paroxysmal AF, the median A/L ratio was 1.71. Univariate analysis indicated that patients with a low A/L ratio (<1.71, n = 42) had a lower high-frequency (HF) power and a higher hs-CRP level, low-frequency (LF) power, and LF/HF ratio than those with a high A/L ratio (≥1.71, n = 43). Multivariate linear regression analysis showed that the serum leptin concentration was independently and positively associated with LF (ß = 0.175, p = .028), while the serum adiponectin concentration was independently and positively associated with HF (ß = 0.321, p = .001). Moreover, the A/L ratio was independently and negatively associated with the LF/HF ratio (ß = -0.276, p = .007). CONCLUSIONS: The A/L ratio was independently and negatively associated with the LF/HF ratio in patients with new-onset paroxysmal AF.

Bedside temporary transvenous cardiac pacing lead placement in patients with tricuspid valve surgery without guidance of X-ray: A single-center experience.

BACKGROUND: It is difficult to insert cardiac pacing leads in patient with tricuspid valve surgery (TVS). The aim of this study was to evaluate safety and effectiveness of a novel technique applied for bedside temporary pacemaker placement (TPP) in patients with TVS. METHODS: We investigated patients with TVS who required bedside TPP without X-ray guidance in cardiac intensive care unit between January 2019 and March 2022. They were divided into Novel pre-shaped group (N = 21) and Control group (routine pre-shaped group, N = 26). The ordinary bipolar electrodes were applied in both groups. In Novel pre-shaped group, electrodes were reshaped by a novel technique with three-curve with anterior tip method, while electrodes were shaped by traditional strategy in Control group. We evaluated the operation duration, first-attempt success rate of the lead placement, pacing threshold, success rate of lead placement, the rate of leads displacement, and complications. RESULTS: Compared with that in Control group, the procedure time was significantly shortened and the first-attempt success rate of lead placement was obviously increased in Novel pre-shaped group (both p < 0.05). Although there was a slight reduction in complications in Novel pre-shaped group when compared with that in Control group. However, there were no statistical significance in pacing threshold, the success rate of lead placement, the rate of leads displacement, and complications when compared between two groups. CONCLUSIONS: We propose a novel technique, three-curve with anterior tip method, is a feasible and effective bedside method to insert emergency temporary pacing leads in patients with TVS.

Real-time intracardiac echocardiography validation of saline-enhanced radiofrequency needle-tip ablation: lesion characteristics and gross pathology correlation.

AIMS: With the implementation of saline-enhanced radiofrequency (SERF) needle-tip ablation, real-time validation of lesion formation is needed for the controllable creation of transmural lesions. The aim of the study was to analyse the ability of two-dimensional intracardiac echocardiography (2D-ICE) to guide and validate SERF ablation in real-time. METHODS AND RESULTS: Fifty-six SERF energy deliveries at left ventricular sites of 11 dogs guided by 2D-ICE were analysed (power: 15-50 W; time: 25-120 s; irrigation saline: 60°C with 10 mL/min flow rate). Catheter tip/tissue orientation and lesion formation could be well detected by 2D-ICE in 49 (87.5%) energy deliveries. Gross pathology analysis confirmed excellent 2D-ICE lesion localization, the ability to detect transmural lesions (70% sensitivity, 47% specificity) and positive correlation between 2D-ICE and the corresponding gross pathology measurements of 'maximal lesion depth'; (repeated measures correlation: rrm = 0.43, P = 0.012) and 'depth at maximal lesion width' (D@MW; rrm = 0.51, P = 0.003). The median angle between SERF catheter tip and endocardium was 76° [interquartile range (IQR) 58-83°]. The more perpendicular the catheter tip/tissue orientation was the deeper D@MW (rrm = 0.32, P = 0.045). Grade 3 microbubbles on 2D-ICE during ablation, indicating inadequate catheter tip/tissue contact, was associated with smaller lesion volumes than with Grade 1 microbubbles (284.8 mm3 [IQR 151.3-343.1] vs. 2114.1 mm3 [IQR 1437.0-3026.3], P < 0.001). CONCLUSION: With excellent lesion localization and a 70% detection rate of transmural lesions, 2D-ICE is well suited to validate SERF ablation lesion formation in real-time. The catheter tip/tissue angle impacts the lesion formation and through perpendicular catheter positioning, deeper intramural areas of the myocardium can be reached.

Acute left atrial ridge lesion after cryoballoon ablation: How does this affect left atrial appendage closure combined procedure?

BACKGROUND: Acute left atrial ridge (LAR) lesions have been observed following atrial fibrillation (AF) ablation. However, LAR lesions had not yet been quantitatively evaluated and their influence on procedure combining cryoballoon (CB) ablation with left atrial appendage closure (LAAC) remained to be explored. METHODS: The profile of LAR lesions was measured by transesophageal echocardiography (TEE) in 117 consecutive nonvalvular AF patients, who underwent the combined procedure of CB ablation and LAAC. We thoroughly investigated how LAR lesions correlated with baseline variables and clinical outcomes. RESULTS: A total of 95 out of 96 available TEE images presented prominent acute LAR lesions. In terms of dimensions, there was a greater change in width (Δwidth = 3.6 ± 2.3 mm) than the thickness (Δthickness = 2.6 ± 3.5 mm), and the outer ostium was narrowed (Δouter ostium diameter = -3.4 ± 4.0 mm), while the inner ostium remained unchanged. A higher nadir temperature when freezing the left superior pulmonary vein (LSPV) led to an LAR lesion with a two times greater width (adjusted odds ratio = 1.16; 95% confidence interval, 1.02-1.31). In the evaluation of LAAC outcomes, four patients implanted with Watchman devices had minimal residual flow at the inferior border, while two implanted with LAmbre devices developed residual flow at the LAR side. Clinical outcomes were similar between groups divided by lesion size. CONCLUSION: Acute LAR lesions frequently occurred following the CB ablation combined procedure, and lesion width positively correlates with LSPV nadir temperature. The presence of these lesions affects the measurement of pacifier devices but has little impact on that of occluder devices.

Low-Intensity Ultrasound Modulation May Prevent Myocardial Infarction-induced Sympathetic Neural Activation and Ventricular Arrhythmia.

BACKGROUND: Low-intensity focused ultrasound (LIFU) has been shown to be a beneficial tool for autonomic nervous system modulation, but its effect on the left stellate ganglion (LSG) remains unknown. OBJECTIVE: To seek the effect of LIFU on myocardial infarction (MI)-induced LSG activation and ventricular arrhythmias (VAs). METHODS: In this study, 20 dogs were included and randomly divided into the LIFU (LIFU & MI, n = 8), Sham (sham LIFU & MI, n = 8), and Control group (sham LIFU & sham MI, n = 4). For each LIFU intervention (1.0-2.0 W, 10 minutes) of the LSG, the LSG function, ventricular effective refractory period (ERP), and temperature were tested pre-intervention and postintervention. Thereafter, MI was induced by left anterior artery ligation and VAs were recorded for 1 hour. At the end, both the LSG and the heart were extracted for biomedical and histological analysis. RESULTS: In the Sham group, no significant change was shown in ventricular ERP or LSG function for any intensity settings of sham LIFU intervention when compared with the group baseline. In the LIFU group, however, both 1.5 and 2.0 W LIFU modulation of LSG resulted in significant prolongation of ERP and attenuation of LSG function. Furthermore, the incidence of VAs was significantly attenuated in the LIFU group compared with the Sham group. Moreover, histological analysis showed that no damage or apoptosis was observed in LSG although a statistically significant increase was shown in temperature (maximal increase <1°C) with 1.5 and 2.0 W LIFU intervention. CONCLUSION: LIFU stimulation may be a safe and beneficial tool for LSG attenuation and VA prevention in the MI canine model.

Effects of dechlorane plus on intestinal barrier function and intestinal microbiota of Cyprinus carpio L.

Dechlorane Plus (DP) is a typical polychlorinated flame retardant that has been emerged in chemical products. Due to its accumulation and amplification effect, the toxicity of DP has become a widespread environmental safety issue. However, whether DP can affect the intestinal tract of teleost fish remains largely unclear. To understand its effects on the intestinal barrier, morphological characteristics and intestinal microbiome of common carp, different concentrations (30, 60 and 120 µg/L) of DP were exposed to common carps for 4 weeks. The results indicated that DP evidently shortened the intestinal folds and damaged the intestinal epithelium layer. In addition, the mRNA expression levels of occludin, claudin-2 and zonula occludens-1 (ZO-1) were significantly decreased with increasing DP concentrations. Furthermore, the relative abundance of some microbiota species were also changed significantly. Our study first demonstrated that DP could cause damage to the intestinal epithelium and destroy the intestinal barrier and increase the relative abundance of pathogenic bacteria, thereby increasing the probability of contact between intestinal epithelium and pathogenic bacteria, which in turn lead to an increased susceptibility to various diseases and poor health. In summary, our findings reveal that chronic DP exposure can have a harmful effect on the intestinal flora balance and is potentially linked to human disease.

Light-emitting diode therapy protects against ventricular arrhythmias by neuro-immune modulation in myocardial ischemia and reperfusion rat model.

BACKGROUND: Sympathetic overactivation and inflammation are two major mediators to post-myocardial ischemia-reperfusion (I/R)-induced ventricular arrhythmia (VA). The vicious cycle between microglia and sympathetic activation plays an important role in sympathetic hyperactivity related to cardiovascular diseases. Recently, studies have shown that microglial activation might be attenuated by light-emitting diode (LED) therapy. Therefore, we hypothesized that LED therapy might protect against myocardial I/R-induced VAs by attenuating microglial and sympathetic activation. METHODS: Thirty-six male anesthetized rats were randomized into four groups: control group (n = 6), LED group (n = 6), I/R group (n = 12), and LED+I/R group (n = 12). I/R was generated by left anterior descending artery occlusion for 30 min followed by 3 h reperfusion. ECG and left stellate ganglion (LSG) neural activity were recorded continuously. After 3 h reperfusion, a programmed stimulation protocol was conducted to test the inducibility of VA. Furthermore, we extracted the brain tissue to examine the microglial activation, and the peri-ischemic myocardium to examine the expression of NGF and inflammatory cytokines (IL-1ß, IL-18, IL-6, and TNF-α). RESULTS: As compared to the I/R group, LED illumination significantly inhibited the LSG neural activity (P < 0.01) and reduced the inducibility of VAs (arrhythmia score 4.417 ± 0.358 vs. 3 ± 0.3257, P < 0.01) in the LED+I/R group. Furthermore, LED significantly attenuated microglial activation and downregulated the expression of inflammatory cytokines and NGF in the peri-infarct myocardium. CONCLUSIONS: LED therapy may protect against myocardial I/R-induced VAs by central and peripheral neuro-immune regulation.

Noninvasive light emitting diode therapy: A novel approach for postinfarction ventricular arrhythmias and neuroimmune modulation.

BACKGROUND: Sympathetic neural activation plays a key role in the incidence and maintenance of acute myocardial infarction (AMI) induced ventricular arrhythmia (VA). Furthermore, previous studies showed that AMI might induce microglia and sympathetic activation and that microglial activation might contribute to sympathetic activation. Recently, studies showed that light emitting diode (LED) therapy might attenuate microglial activation. Therefore, we hypothesized that LED therapy might reduce AMI-induced VA by attenuating microglia and sympathetic activation. METHODS: Thirty anesthetized rats were randomly divided into three groups: the Control group (n = 6), AMI group (n = 12), and AMI + LED group (n = 12). Electrocardiogram (ECG) and left stellate ganglion (LSG) neural activity were continuously recorded. The incidence of VAs was recorded during the first hour after AMI. Furthermore, we sampled the brain and myocardium tissue of the different groups to examine the microglial activation and expression of nerve growth factor (NGF), interleukin-18 (IL-18), and IL-1ß, respectively. RESULTS: Compared to the AMI group, LED therapy significantly reduced the incidence of AMI-induced VAs (ventricular premature beats [VPB] number: 85.08 ± 13.91 vs 27.5 ± 9.168, P < .01; nonsustained ventricular tachycardia (nSVT) duration: 34.39 ± 8.562 vs 9.005 ± 3.442, P < .05; nSVT number: 18.92 ± 4.52 vs 7.583 ± 3.019, P < .05; incidence rate of SVT/VF: 58.33% vs. 8.33%, P < .05) and reduced the LSG neural activity (P < .01) in the AMI + LED group. Furthermore, LED significantly attenuated microglial activation and reduced IL-18, IL-1ß, and NGF expression in the peri-infarct myocardium. CONCLUSION: LED therapy may protect against AMI-induced VAs by suppressing sympathetic neural activity and the inflammatory response.

Efficacy and safety of cryoballoon ablation for Chinese patients over 75 years old: A comparison with a younger cohort.

INTRODUCTION: Cryoballoon ablation (CBA) results in satisfactory outcomes for drug-resistant atrial fibrillation (AF) patients. However, the efficacy and safety of CBA have not yet been tested in the Chinese elderly population. Therefore, this study compared the recurrence of AF and complications of CBA in patients ≥75 years and <75 years. METHODS: A total of 677 patients (<75 years, n = 550; ≥ 75 years, n = 127) with paroxysmal (n = 603) or persistent (n = 74) non-valvular drug-resistant AF were included. The efficacy was assessed by the recurrence of AF, and the safety was evaluated by peri- and post-procedural complications. RESULTS: The CHA2DS2-VASc (2.6 ± 1.7 vs 4.8 ± 1.6, P < .01) and HAS-BLED (1.8 ± 0.8 vs 2.0 ± 0.8, P = .01) scores were significantly higher in the elderly group. The instant pulmonary vein isolation success rate was comparable (99.11% younger vs 98.98% older, P = .99). After a mean follow-up time of 12.8 ± 9.6 months, the 1-year freedom from AF rate was 80.6% vs 85.8% in the older and younger groups, respectively, while the survival analysis showed a nonsignificant difference in the rate of freedom from AF (log-rank P = .46). Cox regression showed that age was not a predictive factor for AF recurrence and was not dichotomized (hazard ratio [HR] = 0.868, 95% confidence interval [CI] 0.509-1.481; P = .6046) or continuous (HR = 0.990, 95% CI, 0.968-1.012, P = .3642). Similar complications rates were observed, including stroke (1.0% younger vs 0.93% older, P = .95) and major hemorrhagic events (1.2% younger vs 0% elder, P = .25). CONCLUSIONS: The efficacy and safety profiles of CBA in patients older than 75 years are comparable with those in younger patients.

Low-Level Vagus Nerve Stimulation Attenuates Myocardial Ischemic Reperfusion Injury by Antioxidative Stress and Antiapoptosis Reactions in Canines.

BACKGROUND: Low-level vagus nerve stimulation (LL-VNS) has been demonstrated to protect myocardium against acute ischemia/reperfusion (I/R) injury. However, the underlying mechanism of this protective effect remains unknown. OBJECTIVE: This study aimed to test the hypothesis that LL-VNS exerts cardioprotective effect on acute I/R injury in canines via antioxidative stress and antiapoptosis reactions. METHOD: Thirty anesthetized mongrel dogs were randomly divided into three groups: I/R group (N = 12, the left anterior descending coronary artery was occluded for 1 hour following by 1 hour reperfusion), LL-VNS group (N = 9, I/R plus LL-VNS), and sham group (N = 9, sham surgery without LL-VNS). The voltage threshold was set at 80% of the voltage required to slow the sinus rate. Infarct size was assessed with Evans Blue and triphenyltetrazolium chloride. Activity assays, TUNEL staining, and western blotting were performed to determine markers of oxidative stress and apoptosis. RESULTS: LL-VNS significantly decreased the incidence of ventricular arrhythmias, increased vagal tone, as confirmed by heart rate viability, and reduced infarct size compared with the I/R group. This improvement was associated with a reduction in myocardial neutrophil infiltration, the inhibition of oxidative stress, and the suppression in cardiomyocyte apoptosis. In contrast, the lack of LL-VNS in the I/R group induced the opposite effect compared with the sham group. CONCLUSION: LL-VNS exerts protective effects on myocardial I/R injury. Its potential mechanisms involve the suppression of oxidative stress and cellular apoptosis.

The Use of Noninvasive Vagal Nerve Stimulation to Inhibit Sympathetically Induced Sinus Node Acceleration: A Potential Therapeutic Approach for Inappropriate Sinus Tachycardia.

BACKGROUND: Hyperactivity of the cardiac sympathetic nervous system may underlie the pathogenesis of inappropriate sinus tachycardia (IST). Studies have proven that cervical vagal stimulation could inhibit stellate ganglion neural activity. SUBJECTS: To investigate whether noninvasive vagal nerve stimulation (NVNS) could inhibit sympathetically induced sinus node acceleration by reducing right stellate ganglion (RSG) neural activity. METHODS: Sixteen anesthetized dogs were randomly divided into NVNS group (with NVNS, n = 8) and control group (with sham NVNS, n = 8). NVNS was delivered to the vagus nerve innervating at the right tragus with a voltage of 80% below the threshold, the minimal voltage to slow the sinus rate or atrioventricular conduction. The maximal sinus rate accelerations induced by high-frequency stimulation (HFS) of RSG and RSG neural activity were measured at baseline and 3 hours after NVNS. At the end, SK2, c-fos, and NGF protein expression in RSG were examined in both groups. RESULTS: Compared to baseline, the maximal sinus node acceleration induced by RSG stimulation and the RSG neural activity were both significantly attenuated after 3 hours of NVNS (P < 0.05 for both). However, these indices did not change significantly in the control group (P > 0.05). SK2 expression in RSG was significantly higher and c-fos and NGF expressions were significantly lower in the NVNS group than those in the control group (P < 0.05). CONCLUSION: Noninvasive vagal nerve stimulation may suppress RSG activity possibly by modulating SK2, c-fos, and NGF expressions in RSG, thus inhibiting sympathetically induced sinus node acceleration.

Left-sided Noninvasive Vagus Nerve Stimulation Suppresses Atrial Fibrillation by Upregulating Atrial Gap Junctions in Canines.

BACKGROUND: We have previously shown that right-sided low-level tragus nerve stimulation (LL-TS) is an effective approach for the treatment of atrial fibrillation (AF) induced by rapid atrial pacing (RAP) and acts by preventing the loss of atrial connexins (Cxs). Whether a left-sided approach would achieve the same effect remains unknown. OBJECTIVE: We hypothesized that left-sided LL-TS would inhibit AF by preserving atrial Cxs as effectively as right-sided LL-TS. METHODS: Bilateral thoracotomies allowed the attachment of multielectrode catheters to the pulmonary vein and non-pulmonary vein sites in 32 anaesthetized beagles. The dogs were randomly divided into 3 groups: RAP group (9 hours of RAP at the left appendage, n = 10), LL-TS group (9-hour RAP plus LL-TS, n = 12), and control group (sham RAP without LL-TS, n = 10). Alligator clips were clipped on the tragus of the left ear for electrical stimulation (20 Hz, 1 millisecond square waves). A voltage of stimulation setting at 80% below the threshold that slowed the sinus rate was defined as LL-TS. Electrophysiological parameters were measured at baseline and 9 hours after pacing. Connexin proteins from atrial tissues were measured at the end of the protocol. RESULTS: RAP induced a significant reduction in the effective refractory period and an increase in AF inducibility (P < 0.05). However, left-sided LL-TS reversed the effective refractory period reduction induced by RAP and the increase in AF inducibility. It also shortened the AF duration and prolonged the AF cycle length, which are associated with Cx40 and Cx43 upregulation (P < 0.05). CONCLUSIONS: We propose that left-sided LL-TS exerts its anti-AF effects through upregulation of Cxs as effectively as right-sided LL-TS, suggesting that LL-TS for AF suppression is not unique to the right tragus nerve.

Low-level transcutaneous electrical stimulation of the auricular branch of vagus nerve ameliorates left ventricular remodeling and dysfunction by downregulation of matrix metalloproteinase 9 and transforming growth factor ß1.

Vagus nerve stimulation improves left ventricular (LV) remodeling by downregulation of matrix metalloproteinase 9 (MMP-9) and transforming growth factor ß1 (TGF-ß1). Our previous study found that low-level transcutaneous electrical stimulation of the auricular branch of the vagus nerve (LL-TS) could be substituted for vagus nerve stimulation to reverse cardiac remodeling. So, we hypothesize that LL-TS could ameliorate LV remodeling by regulation of MMP-9 and TGF-ß1 after myocardial infarction (MI). Twenty-two beagle dogs were randomly divided into a control group (MI was induced by permanent ligation of the left coronary artery, n = 8), an LL-TS group (MI with long-term intermittent LL-TS, n = 8), and a normal group (sham ligation without stimulation, n = 6). At the end of 6 weeks follow-up, LL-TS significantly reduced LV end-systolic and end-diastolic dimensions, improved ejection fraction and ratio of early (E) to late (A) peak mitral inflow velocity. LL-TS attenuated interstitial fibrosis and collagen degradation in the noninfarcted myocardium compared with the control group. Elevated level of MMP-9 and TGF-ß1 in LV tissue and peripheral plasma were diminished in the LL-TS treated dogs. LL-TS improves cardiac function and prevents cardiac remodeling in the late stages after MI by downregulation of MMP-9 and TGF-ß1 expression.

Left renal nerves stimulation facilitates ischemia-induced ventricular arrhythmia by increasing nerve activity of left stellate ganglion.

INTRODUCTION: Renal sympathetic nerve (RSN) activity plays a key role in systemic sympathetic hyperactivity. Previous studies have shown that cardiac sympathetic hyperactivity, especially the left stellate ganglion (LSG), contributes to the pathogenesis of ventricular arrhythmias (VAs) after acute myocardial infarction (AMI). METHODS AND RESULTS: Twenty-eight dogs received 3 hours of continuous left-sided electrical stimulation of RSN (LRS; Group-1, n = 9), sham RSN stimulation (Group-2, n = 9), or LSG ablation plus 3 hours of LRS (Group-3, n = 10) were included. AMI was induced by ligating the proximal left anterior descending coronary artery. LRS was performed using electrical stimulation on the adventitia of left renal artery at the voltage increasing the systolic blood pressure (BP) by 10%. BP, heart rate variability (HRV), serum norepinephrine (NE) level, and LSG function were measured at baseline and the end of each hour of LRS. C-fos and nerve growth factor (NGF) protein expressed in the LSG were examined in Group-1 and Group-2. Compared with baseline, 3 hours of LRS induced a significant increase in BP, sympathetic indices of HRV, serum NE level, and LSG function. The incidence of VAs in Group-1 was significantly higher than other groups. The expression of c-fos and NGF protein in the LSG was significantly higher in Group-1 than Group-2. CONCLUSION: Three hours of LRS induces both systemic and cardiac sympathetic hyperactivity and increases the incidence of ischemia-induced VAs.

Renal sympathetic denervation modulates ventricular electrophysiology and has a protective effect on ischaemia-induced ventricular arrhythmia.

Recently, a beneficial effect of renal sympathetic denervation (RSD) has been seen in patients with ventricular electrical storm. However, the effect of RSD on ventricular electrophysiology remains unclear. Thirty-three mongrel dogs were included in the present study. Renal sympathetic denervation was performed by radiofrequency ablation of the adventitial surface of the renal artery. In group 1 (n = 8), programmed stimulation was performed before and after RSD to determine the ventricular effective refractory period (ERP) and action potential duration (APD) restitution properties. The same parameters were measured in five other animals that underwent sham RSD to serve as controls. In group 2 (n = 10), acute myocardial ischaemia (AMI) was induced by ligating the proximal left anterior descending coronary artery after the performance of RSD, and the incidence of ventricular arrhythmia (VA) was calculated during 1 h of recording. In another 10 dogs (group 3), AMI was induced and VA was measured with sham RSD. In group 1, RSD significantly prolonged ventricular ERP and APD, reduced the maximal slope (Smax) of the restitution curve and suppressed APD alternans at each site. Renal sympathetic denervation also significantly decreased the spatial dispersion of ERP, APD and Smax. In the five control animals, no significant electrophysiological change was detected after sham RSD. The occurrence of spontaneous VA during 1 h of AMI in group 2 was significantly lower than that in group 3. These data suggest that RSD stabilizes ventricular electrophysiological properties in normal hearts and reduces the occurrence of VA in hearts experiencing AMI.

Spinal cord stimulation suppresses focal rapid firing-induced atrial fibrillation by inhibiting atrial ganglionated plexus activity.

OBJECTIVE: This study was designed to demonstrate that spinal cord stimulation (SCS) could suppress high-frequency stimulation (HFS)-induced focal atrial fibrillation (AF) at atrial and pulmonary vein (PV) sites by inhibiting atrial ganglionated plexus (GP) activity. METHODS: Multielectrode catheters were attached to atria and all PV sites. SCS was performed at the T1-T5 spinal region for 1 hour. At the baseline state and the end of 1 hour of SCS, 40 milliseconds of HFS was delivered 2 milliseconds after atrial pacing to determine the AF threshold at each site. One electrode was attached to the superior left GP so that HFS to this site induced sinus rate slowing. Microelectrodes inserted into the anterior right GP recorded neural firing. RESULTS: SCS induced a significant increase in AF threshold at all sites (all P < 0.05). The sinus rate slowing response induced by superior left GP stimulation was blunted by SCS (17% ± 3.6% vs. 39% ± 3.8%, P < 0.05). The frequency (32 ± 4 vs. 87 ± 6 impulses per minute, P < 0.05) and amplitude (0.16 ± 0.02 vs. 0.42 ± 0.04 mv, P < 0.05) of the neural activity recorded from the anterior right GP were markedly inhibited by SCS. CONCLUSIONS: SCS may prevent episodic AF caused by rapid PV and non-PV firing through modulating GP activity.

Carotid baroreceptor stimulation prevents arrhythmias induced by acute myocardial infarction through autonomic modulation.

: Electrical carotid baroreceptor stimulation (CBS) has shown therapeutic potential for resistant hypertension and heart failure by resetting autonomic nervous system, but the impacts on arrhythmias remains unclear. This study evaluated the effects of CBS on ventricular electrophysiological properties in normal dog heart and arrhythmias after acute myocardial infarction (AMI). In the acute protocol, anesthetized open chest dogs were exposed to 1 hour left anterior descending coronary occlusion as AMI model. Dogs were received either sham treatment (Control group, n = 8) or CBS (CBS group, n = 8), started 1 hour before AMI. CBS resulted in pronounced prolongation of ventricular effective refractory period and reduction of the maximum action potential duration restitution slope (from 0.85 ± 0.15 in the baseline state to 0.67 ± 0.09 at the end of 1 hour, P < 0.05) before AMI. Number of premature ventricular contractions (277 ± 168 in the Control group vs. 103 ± 84 in the CBS group, P < 0.05) and episodes of ventricular tachycardia/ventricular fibrillation (7 ± 3 in the Control group vs. 3 ± 2 in the CBS group, P < 0.05) was decreased compared with the control group during AMI. CBS buffered low-frequency/high-frequency ratio raise during AMI. Ischemic size was not affected by CBS. CBS may have a beneficial impact on ventricular arrhythmias induced by AMI through modulation of autonomic tone.

Wearable ultrasound devices: An emerging era for biomedicine and clinical translation.

In recent years, personalized diagnosis and treatment have gained significant recognition and rapid development in the biomedicine and healthcare. Due to the flexibility, portability and excellent compatibility, wearable ultrasound (WUS) devices have become emerging personalized medical devices with great potential for development. Currently, with the development of the ongoing advancements in materials and structural design of the ultrasound transducers, WUS devices have improved performance and are increasingly applied in the medical field. In this review, we provide an overview of the design and structure of WUS devices, focusing on their application for diagnosis and treatment of various diseases from a clinical application perspective, and then explore the issues that need to be addressed before clinical translation. Finally, we summarize the progress made in the development of WUS devices, and discuss the current challenges and the future direction of their development. In conclusion, WUS devices usher an emerging era for biomedicine with great clinical promise.