Hybrid meat batter system: effects of plant proteins (pea, brown rice, faba bean) and concentrations (3-12%) on texture, microstructure, rheology, water binding, and color.

A lean meat batter system was mixed with four plant proteins at 3, 6, 9, and 12% (w/w): pea protein A (PA), pea protein B (PB), brown rice protein (BR) and faba bean protein (FB). Texture profile analysis (TPA) revealed that increasing plant protein levels hardened the hybrid meat batters, with PA and PB leading to the hardest gels. TPA results were supported by micrographs, demonstrating that the two pea proteins formed large aggregates, contributing to a firmer hybrid meat gel. Dynamic rheology showed that the incorporation of plant proteins lowered the storage modulus (G') during the heating stage (20 to 72°C), yet the 6% PA treatment produced a final G' (after cooling) closest to the control (CL). Nuclear Magnetic Resonance (NMR) T2 relaxometry also demonstrated that plant proteins reduced the water mobility in hybrid meat batters. Results were in line with the cooking loss, except for a higher cooking loss in the BR formulation compared to the CL. Color measurement showed that increasing plant protein levels led to darker and yellower meat batters; however, the effect on redness varied among treatments. Overall, the findings suggest that pea proteins have superior functionality and compatibility within a lean poultry meat protein system, compared to BR and FB tested here.

Effects of low-density lipoprotein cholesterol on sleep apnea: Insights from a rat model of cardiovascular autonomic dysregulation.

INTRODUCTION: The levels of low-density lipoprotein (LDL) cholesterol in plasma are important risk factors for coronary heart disease. Several reports suggest that elevated plasma cholesterol is associated with cardiac arrhythmias. In a subsequent study investigating LDL cholesterol levels and the frequency of LDL cholesterol measurements, a positive correlation was observed between the severity of sleep apnea and visit-to-visit LDL cholesterol variability. Our objective was to assess the effects of hypercholesterolemia on cardiac autonomic activity, disordered sleep patterns, and increased incidence of arrhythmias in freely moving rats. METHODS: Wireless transmission of polysomnographic recordings was performed in control and high cholesterol male rats during normal daytime sleep. Spectral analyses were conducted on the electroencephalogram and electromyogram (EMG) recordings to distinguish active waking, quiet sleep, and paradoxical sleep. Heart rate variability power spectrum analysis was used to measure cardiac autonomic activity. RESULTS: The high cholesterol group exhibited a higher low-frequency (LF)/high-frequency (HF) power ratio during all sleep stages compared to the control group. Additionally, the frequency of sleep interruptions was increased in the high cholesterol group compared to the control group. CONCLUSIONS: Our results show significant sleep fragmentation with sympathetic hyperactivity after exposure to high cholesterol. This indicates that high cholesterol may increase the risk of sleep apnea and poor sleep quality by disrupting autonomic homeostasis.

Renal sympathetic denervation ameliorates the activated inflammatory response through JAK-STAT pathway in a chronic obstructive sleep apnea animal model.

OBJECTIVES: Obstructive sleep apnea (OSA) is known to increase the risk of cardiovascular disease and inflammation plays a significant role in this process. Renal denervation (RDN) is a novel approach aimed at reducing sympathetic nervous system activity. The role of RDN in the inflammatory response to chronic OSA (COSA) is currently unclear. The main objective was to study inflammatory mechanisms in the rabbit heart with COSA and the effects of RDN. METHODS: Eighteen rabbits were randomized into three groups: sham control, COSA, and COSA-RDN. COSA and COSA-RDN groups received liquid silicone injections, while the sham control group received normal saline. We performed combined surgical and chemical RDN through bilateral retroperitoneal flank incisions in the COSA-RDN group after silicone injections. The inflammatory mechanisms were assessed through immunoblotting, real-time PCR, and ELISA after the experiment. RESULTS: H&E staining showed immune cell infiltration in COSA, which decreased after RDN treatment. The level of α7nAChR was significantly reduced in COSA compared to the sham control but was restored to a similar level in the COSA-RDN group. Furthermore, the expressions of p-JAK2 and p-STAT3 were significantly reduced in COSA but showed an up-regulation following RDN treatment. Similarly, levels of the inflammatory markers IL-6, IL-1ß and TNF-α were markedly increased in COSA but decreased after RDN therapy. We observed NF-κB activation in the COSA rabbit model, which decreased after RDN treatment, as evidenced by decreased NF-κB expression. CONCLUSIONS: Our study suggests that RDN treatment may prevent COSA-associated heart inflammation via the JAK2-STAT3 signaling pathway.

Neural mechanism facilitating PM2.5-related cardiac arrhythmias through cardiovascular autonomic and calcium dysregulation in a rat model.

Particulate matter < 2.5 µm (PM2.5) exposure is associated with increased arrhythmia events and cardiovascular mortality, but the detailed mechanism remained elusive. In the current study, we aimed to investigate the autonomic alterations in a rodent model after acute exposure to PM2.5. Twelve male WKY rats were randomized to control and PM2.5 groups. All were treated with 2 exposures of oropharyngeal aerosol inhalations (1 µg PM2.5 per gram of body weight in 100 µL normal saline for the PM2.5 group) separately by 7 days. Polysomnography and electrocardiography were surgically installed 7 days before oropharyngeal inhalation and monitored for 7 days after each inhalation. Physiologic monitors were used to define active waking (AW), quiet sleep (QS), and paradoxical sleep (PS). Autonomic regulations were measured by heart rate variability (HRV). The protein expression of ventricular tissue of the 2 groups was compared at the end of the experiment. In sleep pattern analysis, QS interruption of the PM2.5 group was significantly higher than the control group (0.52 ± 0.13 events/min, 0.35 ± 0.10 events/min, p = 0.002). In HRV analysis, the LF/HF was significantly higher for the PM2.5 group than the control group (1.15 ± 0.16, 0.64± 0.30, p = 0.003), largely driven by LF/HF increase during the QS phase. Ionic channel protein expression from Western blots showed that the PM2.5 group had significantly lower L-type calcium channel and higher SERCA2 and rectifier potassium channel expressions than the control group, respectively. Our results showed that acute PM2.5 exposure leads to interruption of QS, sympathetic activation, and recruitment of compensatory calcium handling proteins. The autonomic and calcium dysregulations developed after PM 2.5 exposure may explain the risk of sleep disturbance and sleep-related arrhythmia.

Renal denervation reverses ventricular structural and functional remodeling in failing rabbit hearts.

Renal denervation (RDN) suppresses the activity of the renin-angiotensin-aldosterone system and inflammatory cytokines, leading to the prevention of cardiac remodeling. Limited studies have reported the effects of renal denervation on ventricular electrophysiology. We aimed to use optical mapping to evaluate the effect of RDN on ventricular structural and electrical remodeling in a tachycardia-induced cardiomyopathy rabbit model. Eighteen rabbits were randomized into 4 groups: sham control group (n = 5), renal denervation group receiving RDN (n = 5), heart failure group receiving rapid ventricular pacing for 1 month (n = 4), and RDN-heart failure group (n = 4). Rabbit hearts were harvested for optical mapping. Different cycle lengths were paced (400, 300, 250, 200, and 150 ms), and the results were analyzed. In optical mapping, the heart failure group had a significantly slower epicardial ventricular conduction velocity than the other three groups. The RDN-heart failure, sham control, and RDN groups had similar velocities. We then analyzed the 80% action potential duration at different pacing cycle lengths, which showed a shorter action potential duration as cycle length decreased (P for trend < 0.01), which was consistent across all groups. The heart failure group had a significantly longer action potential duration than the sham control and RDN groups. Action potential duration was shorter in the RDN-heart failure group than the heart failure group (P < 0.05). Reduction of conduction velocity and prolongation of action potential duration are significant hallmarks of heart failure, and RDN reverses these remodeling processes.

Post-ablation augmentation of skin sympathetic nerve activity predicts a poor outcome of idiopathic ventricular arrhythmias.

BACKGROUND: The neuromodulation effect after ventricular arrhythmia (VA) ablation is unclear. The study aimed to investigate skin sympathetic nerve activity (SKNA) changes in patients receiving catheter ablations for idiopathic VA. METHODS: Of 43 patients with drug-refractory symptomatic VA receiving ablation, SKNA was continuously recorded for 10 min during resting from electrocardiogram lead I configuration and bipolar electrodes on the right arm 1 day before and 1 day after ablation. RESULTS: Twenty-two patients with acute procedure success and no recurrence during follow-ups were classified as sustained success group (group 1). Other 21 patients were classified as failed ablation group (group 2). Baseline SKNA showed no significant difference between the two groups. Post-ablation SKNA in group 2 was significantly higher than in group 1. In patients with ablation involved right ventricular outflow tract (RVOT), the post-ablation SKNA was also significantly higher in group 2. In contrast, there was no difference in post-ablation SKNA between groups in patients receiving non-RVOT ablation. CONCLUSION: The neuromodulation response after RVOT ablation may correspond to the sympathetic nerve distribution at RVOT. Augmentation of sympathetic activity after VA ablation indicates an unsuccessful VA suppression, especially in patients receiving ablation of RVOT VA.

Effects of renal denervation on sleep apnea and arrhythmia in rats with myocardial infarction.

BACKGROUND: Sympathetic hyperactivity and poor sleep quality have been reported in patients with myocardial infarction (MI). Sleep is an important modulator of cardiovascular function. We aimed to evaluate the effects of renal denervation (RDN) on cardiac autonomic activity and disordered sleep patterns in rats with MI. METHODS: Wireless transmission of polysomnographic recordings was performed in sham and left coronary artery (LCA) ligation male rats during normal daytime sleep before and after RDN. Spectral analyses of electroencephalogram and electromyogram (EMG) recordings were performed to define active waking, quiet sleep, and paradoxical sleep. Cardiac autonomic activity was measured by analyzing the power spectrum of heart rate variability. Central sleep apnea events were measured by analyzing the EMG recordings of the diaphragm. RESULTS: In the LCA ligation group, there was a higher low-frequency (LF)/high-frequency (HF) power ratio during sleep; the LF/HF ratio decreased significantly in the rats that underwent RDN in all sleep stages when compared with that in the rats that did not. The frequency of sleep interruptions increased without RDN in the LCA ligation group when compared with that in the sham group. This change was ameliorated and prevented with RDN in the LCA ligation group. CONCLUSIONS: Our results demonstrate significant sleep fragmentation with sympathetic hyperactivity after MI and that RDN prevents autonomic dysfunction and disordered sleep. RDN may then reduce sleep apnea and sleep-related sudden cardiac death after MI by restoring autonomic homeostasis.

Renal artery denervation prevents ventricular arrhythmias in long QT rabbit models.

Long QT syndrome (LQTS) is commonly presented with life-threatening ventricular arrhythmias (VA). Renal artery denervation (RDN) is an alternative antiadrenergic treatment that attenuates sympathetic activity. We aimed to evaluate the efficacy of RDN on preventing VAs in LQTS rabbits induced by drugs. The subtypes of LQTS were induced by infusion of HMR-1556 for LQTS type 1 (LQT1), erythromycin for LQTS type 2 (LQT2), and veratridine for LQTS type 3 (LQT3). Forty-four rabbits were randomized into the LQT1, LQT2, LQT3, LQT1-RDN, LQT2-RDN, and LQT3-RDN groups. All rabbits underwent cardiac electrophysiology studies. The QTc interval of the LQT2-RDN group was significantly shorter than those in the LQT2 group (650.08 ± 472.67 vs. 401.78 ± 42.91 ms, p = 0.011). The QTc interval of the LQT3-RDN group was significantly shorter than those in the LQT3 group (372.00 ± 22.41 vs. 335.70 ± 28.21 ms, p = 0.035). The VA inducibility in all subtypes of the LQT-RDN groups was significantly lower than those in the LQT-RDN groups, respectively (LQT1: 9.00 ± 3.30 vs. 47.44 ± 4.21%, p < 0.001; LQT2: 11.43 ± 6.37 vs. 45.38 ± 5.29%, p = 0.026; LQT3: 10.00 ± 6.32 vs. 32.40 ± 7.19%, p = 0.006). This study demonstrated the neuromodulation of RDN leading to electrical remodeling and reduced VA inducibility of the ventricular substrate in LQT models.

Evidence of Ventricular Arrhythmogenicity and Cardiac Sympathetic Hyperinnervation in Early Cirrhotic Cardiomyopathy.

Cirrhotic cardiomyopathy (CMP) is associated with altered cardiac electrophysiological (EP) properties, which leads to the risk of ventricular arrhythmias (VAs). We aimed to evaluate the EP properties, autonomic, and structural remodeling in a rabbit model with early liver cirrhosis (LC). Twelve rabbits were assigned to the sham and LC groups. The early-stage LC was induced by the ligation of the common bile duct. All rabbits received an EP study, VA inducibility test, myocardial, and liver histology staining. Western blot analyses of protein expression and tyrosine hydroxylase stain for sympathetic nerves were performed. The effective refractory period the LC group was significantly longer than the sham group [i.e., left ventricle (LV) 205.56 ± 40.30 vs. 131.36 ± 7.94 ms; right ventricle (RV) 206.78 ± 33.07 vs. 136.79 ± 15.15 ms; left atrium (LA) 140.56 ± 28.75 vs. 67.71 ± 14.29 ms; and right atrium (RA) 133.78 ± 40.58 vs. 65.43 ± 19.49 ms, all p < 0.01], respectively. The VA inducibility was elevated in the LC group when compared with the sham group (i.e., 21.53 ± 7.71 vs. 7.76 ± 2.44%, p = 0.013). Sympathetic innervation (102/µm2/mm2) was increased in all cardiac chambers of the LC group compared with the sham group (i.e., LV 9.11 ± 4.86 vs. 0.17 ± 0.15, p < 0.01; RV 4.36 ± 4.95 vs. 0.18 ± 0.12, p = 0.026; LA 6.79 ± 1.02 vs. 0.44 ± 0.20, p = 0.018; and RA 15.18 ± 5.12 vs. 0.10 ± 0.07, p = 0.014), respectively. Early LC is presented with an increased ventricular vulnerability, structural heterogeneity, and sympathetic innervation. Close monitoring for fatal arrhythmias is warranted in patients with early stages of LC.

Renal denervation prevents myocardial structural remodeling and arrhythmogenicity in a chronic kidney disease rabbit model.

BACKGROUND: The electrophysiological (EP) effects and safety of renal artery denervation (RDN) in chronic kidney disease (CKD) are unclear. OBJECTIVE: The purpose of this study was to investigate the arrhythmogenicity of RDN in a rabbit model of CKD. METHODS: Eighteen New Zealand white rabbits were randomized to control (n = 6), CKD (n = 6), and CKD-RDN (n = 6) groups. A 5/6 nephrectomy was selected for the CKD model. RDN was applied in the CKD-RDN group. All rabbits underwent cardiac EP studies for evaluation. Immunohistochemistry, myocardial fibrosis, and renal catecholamine levels were evaluated. RESULTS: The CKD group (34.8% ± 9.2%) had a significantly higher ventricular arrhythmia (VA) inducibility than the control (8.6% ± 3.8%; P <.01) and CKD-RDN (19.5% ± 6.3%; P = .01) groups. In the CKD-RDN group, ventricular fibrosis was significantly decreased compared to the CKD group (7.4% ± 2.0 % vs 10.4% ± 3.7%; P = .02). Sympathetic innervation in the CKD group was significantly increased compared to the control and CKD-RDN groups [left ventricle: 4.1 ± 1.8 vs 0.8 ± 0.5 (102 µm2/mm2), P <.01; 4.1 ± 1.8 vs 0.9± 0.6 (102 µm2/mm2), P <.01; right ventricle: 3.6 ± 1.0 vs 1.0 ± 0.4 (102 µm2/mm2), P <.01; 3.6 ± 1.0 vs 1.0 ± 0.5 (102 µm2/mm2), P <.01]. CONCLUSION: Neuromodulation by RDN demonstrated protective effects with less structural and electrical remodeling, leading to attenuated VAs. In a rabbit model of CKD, RDN plays a therapeutic role by lowering the risk of VA caused by autonomic dysfunction.

Delayed association of acute particulate matter 2.5 air pollution exposure with loss of complexity in cardiac rhythm dynamics: insight from detrended fluctuation analysis.

There is a delayed (lag 1 to 2 days) correlation between acute PM 2.5 (particulate matter < 2.5 µm in aerodynamic diameter) exposure and cardiovascular events, but the underlying mechanism remained unclear. We aimed to investigate the delayed impact of acute PM 2.5 exposures on cardiac autonomics through linear and nonlinear heart rate variability (HRV) analyses. Among 6912 patients who had received 24-h Holter ECG between October 1, 2015, to October 31, 2016, 56 patients (31 males, 70.3 ± 12.7 years old) were enrolled. We classified the patients as high (> 35.4 µg/m3) or low (< 35.4 µg/m3) PM 2.5 groups according to their PM 2.5 exposures on the day of Holter recordings (day 0) lag 1 and lag 2 days. Linear and nonlinear HRV parameters〔Detrended fluctuation analysis (DFA) slopes 1 and 2〕were compared. Baseline characteristics were similar between groups. Linear and nonlinear HRV parameters were similar between high- and low-exposure groups on day 0 and lag 1 day, respectively. However, DFA slope 1 was significantly lower in the high-exposure group on lag 2 days (0.784 ± 0.201 vs. 0.964 ± 0.274, p = 0.021). DFA slope 1 of the high-exposure group was significantly lower on daytime periods (9 am to 9 pm, 8 am to 4 pm and 4 pm to 12 pm) but not on nighttime periods. High lag 2 days PM 2.5 exposure is associated with low DFA slope 1 and the relationship is diurnal. This suggests that air pollution might have a delayed impact on the cardiovascular autonomic system.

A Neurofeedback Protocol for Executive Function to Reduce Depression and Rumination: A Controlled Study.

OBJECTIVE: Rumination is a maladaptive emotional-regulation strategy that is strongly associated with depression. Impaired executive function can lead to difficulties in disengaging from rumination, thus exacerbating depression. In this study, we inspect an electroencephalograph neurofeedback protocol that enhance the target peak alpha frequency (PAF) activation in the prefrontal region. We examine the protocol's effects on depression and rumination. METHODS: We randomly assigned 30 dysphoric participants into either the neurofeedback training group or the control group. We then evaluated their depression, rumination, and executive function at pre- and posttraining so as to examine the effects of the neurofeedback. RESULTS: The results show that this neurofeedback protocol can specifically enhance participants' target PAF. The participants' executive function performances significantly improved after undergoing 20 neurofeedback sessions. Compared with those in the control group, those in the neurofeedback group had significantly fewer depressive symptoms and significantly reduced rumination. Moreover, as target PAF and executive function improved, depression and rumination both declined. CONCLUSION: Our data are in line with those of previous studies that indicated a relationship between upper-band alpha activity and executive function. This PAF neurofeedback can effectively enhance participants' executive function, which can reduce rumination and ameliorate depression. This neurofeedback training is based on basic cognitive neuroscience, so it sheds light on depression's pathological factors and etiology.

The Impact of Estrogen Supplementation to Autonomic and Sleep Modulations in Free-Moving Spontaneously Hypertensive Rats.

Sleep and estrogen levels have an impact on neural regulation and are associated with cardiovascular (CV) events. We investigated the effects of estrogen on heart rate variability (HRV) and circadian cycle in spontaneously hypertensive rats (SHRs). Polysomnographic recording was performed in seven male and seven female SHRs during sleep. The electroencephalogram (EEG) and electromyogram (EMG) were evaluated to define active waking (AW), quiet sleep (QS), and paradoxical sleep (PS) stages. Cardiac activities were measured by RR interval of the electrocardiogram (ECG), mean arterial pressure (MAP), and power spectrum of HRV.In ECG, estrogen prolonged the RR interval in total sleep when compared with that at baseline in male SHRs (203.74 ± 6.61 versus 181.30 ± 8.06 ms, P < 0.001) and in female SHRs (169.21 ± 6.43 versus 160.76 ± 10.66 ms, P < 0.05). In HRV, the estrogen increased the high frequency (HF) in total sleep when compared with that at baseline in male SHRs (1.03 ± 0.28 versus 0.60 ± 0.43 ln (ms2), P < 0.001) and in female SHRs (0.71 ± 0.26 versus 0.42 ± 0.19 ln (ms2), P < 0.05).In male SHRs, estrogen increased the frequency of QS (26.50 ± 4.85 versus 20.79 ± 5.07, P < 0.01) and PS (25.64 ± 5.18 versus 20.14 ± 4.75, P < 0.05) stages when compared with baseline. In female SHRs, estrogen increased the percentage of delta waves in total sleep (79.87% ± 3.10% versus 76.71% ± 2.74%, P < 0.05) when compared with that at baseline.In HRV, estrogen leads to neuromodulation by increased parasympathetic tone in all SHRs, suggesting a lower risk to CV events. In sleep analyses, estrogen in male SHRs caused poor sleep quality. In contrast, estrogen in female SHRs demonstrated improved quality of sleep and decreased risk of hypertension.

Renal denervation ameliorates the risk of ventricular fibrillation in overweight and heart failure.

AIMS: Both obesity and heart failure (HF) are associated with sudden cardiac death. The current study aimed to investigate the effects of overweight and HF on the substrate for ventricular fibrillation (VF), and whether renal denervation (RDN) can protect the heart from sympathetic activation and cardiac remodelling in HF rabbits fed with high-fat diet (HFD). METHODS AND RESULTS: Twenty-four rabbits randomized into control group fed with regular diet (Control), HFD, HFD-HF, and HFD-HF-RDN groups. Rapid ventricular pacing of 400 b.p.m. for 4 weeks was applied in HFD-HF and HFD-HF-RDN. Surgical and chemical RDNs were approached through bilateral retroperitoneal flank incisions in HFD-HF-RDN. All rabbits received electrophysiological study and a VF inducibility test. The ventricular myocardium was harvested for trichrome stain. After 3 months, mean body weight was heavier in HFD, compared with control (3.5 ± 0.1 kg vs. 2.6 ± 0.1 kg, P < 0.01). No differences in body weight among the three groups fed with HFD were observed. The ventricular refractory periods were longer in HFD-HF and HFD-HF-RDN than in control. An extension of ventricular fibrosis was observed in HFD and HFD-HF compared with control, and the degree of ventricular fibrosis was suppressed in HFD-HF-RDN compared with HFD-HF. The level of tyrosine hydroxylase staining was reduced in HFD-HF-RDN compared with HFD and HFD-HF. Importantly, VF inducibility was lower in HFD-RDN-HF (10 ± 4%), when compared with those in HFD-HF (58 ± 10%, P < 0.01) and HFD (42 ± 5%, P < 0.05), respectively. CONCLUSION: Our results suggest that overweight and HF increase sympathetic activity, structural remodelling, and VF inducibility, but RDN prevents them.

Gastroesophageal reflux disease and atrial fibrillation: Insight from autonomic cardiogastric neural interaction.

BACKGROUND: The relationship between gastroesophageal reflux disease (GERD) and atrial fibrillation (AF) has been previously reported. However, the detailed mechanism remains unknown. In this study, we investigated the effects of acid reflux on the intrinsic cardiac autonomic nervous system, atrial/ventricular electrophysiology, and AF inducibility. METHODS: Eighteen rabbits were randomized into three groups: acid reflux (group 1, n = 6), control (group 2, n = 6), and acid reflux with periesophageal vagal blockade (group 3, n = 6). Atrial and ventricular effective refractory periods (ERPs) and AF inducibility were checked at baseline and then hourly until 5 hours after the experiment. RESULTS: Three hours after the experiment, atrial ERP prolongation was noted in groups 2 and 3 (P < .05), whereas shortening of the atrial ERPs was observed in group 1, compared with the baseline. However, no changes were observed in ventricular ERPs in the three groups. The AF inducibility was higher in group 1 than in groups 2 and 3. Pathological examination showed clear esophageal mucosal breaks in groups 1 and 3. CONCLUSIONS: In this study, we found that the antimuscarinic blockade prevents GERD induced changes to atrial electrophysiology and susceptibility to AF-making it highly likely that autonomic activity is important in mediating this effect.

Ultra-rapid high-density mapping system with the phase singularity technique is feasible in identifying rotors and focal sources and predicting AF termination.

INTRODUCTION: Phase singularity (PS) mapping provides additional insight into the AF mechanism and is accurate in identifying rotors. The study aimed to evaluate the feasibility of PS mapping in identifying AF rotors using data obtained from an automatic ultra-rapid high-resolution mapping system with a high-density mini-basket catheter. METHODS: Twenty-three pigs underwent rapid right atrial (RA) pacing (RAP 480 bpm) for 5 weeks before the experiment. During AF, RA endocardial automatic continuous mappings with a mini-basket catheter were generated using an automatic ultra-rapid mapping system. Both fractionation mapping and waveform similarity measurements using a PS mapping algorithm were applied on the same recording signals to localize substrates maintaining AF. RESULTS: Seventeen (74%) pigs developed sustained AF after RAP. Three were excluded because of periprocedural ventricular arrhythmia and corrupted digital data. RA fractionation maps were acquired with 6.17 ± 4.29 minutes mean acquisition time, 13768 ± 12698 acquisition points mapped during AF from 581 ± 387 beats. Fractionation mapping identified extensively distributed (66.7%) RA complex fractionated atrial electrogram (CFAE), whereas the nonlinear analysis identified high similarity index (SI > 0.7) parts in limited areas (23.7%). There was an average of 1.67 ± 0.87 SI sites with 0.43 ± 0.76 rotor/focal source/chamber. AF termination occurred in 11/16 (68.75%) AF events in 14 pigs during ablation targeting max CFAE. There was a higher incidence of rotor/focal source at AF termination sites compared with non-AF termination sites (54.5% vs 0%, P = 0.011). CONCLUSIONS: The data obtained from ultra-rapid high-density automatic mapping is feasible and effective in identifying AF rotors/focal sources using PS technique, and those critical substrates were closely related to AF procedural termination.

Ambient fine particulate matter (PM2.5) exposure is associated with idiopathic ventricular premature complexes burden: A cohort study with consecutive Holter recordings.

BACKGROUND: Epidemiological evidence has shown an association between ambient fine particulate matter (PM2.5) exposure and cardiovascular mortality. Increased ventricular premature complex (VPC) burden can cause left ventricular dilatation and dysfunction. We aimed to investigate the relationship between acute PM2.5 exposure and VPC burden in patients without structural heart disease. METHODS: We reviewed 26 820 patients who underwent 24-hour Holter electrocardiogram (ECG) recordings between 1 Jan 2013 and 1 Dec 2016. We enrolled patients with significant idiopathic (structurally normal heart) VPC burden defined as ≥30 VPCs/h (Lown grade 2) who had at least two Holter ECG recordings. The VPC burden between the studies on high and low PM2.5 exposure dates was compared in 24 and 12 hours time periods. RESULT: Sixty-seven patients (31 men, 56.49 ± 18.35 years) were enrolled. Patients were exposed to 25.63 ± 11.47 and 14.66 ± 7.51 µg/m 3 of PM2.5 during the high and low study dates, respectively. The overall VPC counts (10,490.69 ± 10,681.63/day) and burden (10.22% ± 10.17%) were significantly higher on the days with higher PM2.5 exposure compared with low PM2.5 exposure dates (8293.31 ± 9009.09; P = 0.014% and 9.14% ± 12.73%, P = 0.012, respectively). Compared with low PM2.5 exposure dates, the VPC burden on high exposure dates was significantly higher from 9 am to 9 pm (5.85% ± 6.41% vs 4.84% ± 6.97%; P = 0.025) but not at nocturnal periods. CONCLUSION: Our study demonstrated a significantly higher VPC burden on high PM2.5 exposure date. The burden was increased in the daytime but not at nighttime. This result suggests that daytime PM2.5 exposure may be associated with ventricular arrhythmia burden in the healthy population.

Diurnal cardiac sympathetic hyperactivity after exposure to acute particulate matter 2.5 air pollution.

BACKGROUND: Ambient fine particulate matter (PM2.5) exposure is associated with increased cardiovascular and cardiac arrhythmias events, but the detailed mechanism remains unclear. OBJECTIVE: We aimed to investigate the effect of PM2.5 (particulate matter < 2.5 µm in aerodynamic diameter) on the cardiac autonomics through a heart rate variability (HRV) analysis. METHOD: Among 6912 patients who had underwent 24-hour Holter ECG recordings between Oct 1st 2015 and Oct 31st 2016, 46 (25 males, 69.3 ±â€¯12.1 years old) were enrolled with confirmation of living in an environment with a reported PM2.5 level and were classified as elevated (Group 1, >36 µg/m3, 50.73 ±â€¯8.50) or low (Group 2, <11 µg/m3, 6.06 ±â€¯1.00) PM2.5 group. The Holter recordings and HRV parameters were evaluated. RESULT: The baseline characteristics including the comorbidities and medications were similar between the 2 groups. The Holter ECG parameters were also similar. There were no significant HRV differences between the two groups for the 24-hour interval analysis. However, the LF/HF ratio was significantly higher in Group 1 than Group 2 in the 9 am to 9 pm (p = 0.028), 8 am to 4 pm (p = 0.024), and 4 pm to 12 pm (p = 0.025) periods, respectively, but not for the nocturnal HRV parameters. CONCLUSION: Our study demonstrated that an elevated PM2.5 exposure had a significant association with an increased daytime LF/HF ratio suggesting a diurnal difference in the response to PM2.5 exposure.