Ambient temperature and ambulatory blood pressure: An hourly-level, longitudinal panel study.

BACKGROUND: Variations of blood pressure (BP) related to air temperature have been reported previously; however, no evidence is available regarding the association of hourly ambient temperature with ambulatory blood pressure. METHODS: We conducted a longitudinal panel study among 1895 patients from an outpatient department who received repeated ambulatory blood pressure monitoring in Urumqi, China between July 2020 and December 2021. We obtained hourly ambient temperature from the nearest monitoring station to the residential address, and measured 4 ambulatory blood pressure indicators. Linear mixed-effect model combined with distributed lag models were applied to investigate the cumulative associations of hourly temperature with BP. RESULTS: A total of 97,466 valid blood pressure measurements were evaluated. We observed almost linear and monotonically decreasing relationships between temperature and blood pressure. The effects occurred in the same hour, attenuated thereafter and became insignificant approximately 36 h. A 10 °C decrease in temperature was significantly associated with increments of 0.84 mmHg in systolic blood pressure, 0.56 mmHg in diastolic blood pressure, 1.38 mmHg in mean arterial pressure, and 0.66 mmHg in pulse pressure over lag 0 to 36 h. Stronger associations were found among patients of female sex, age between 18 and 65 years, overweight or obesity, minority, less education or in the cold season, as well as those without hypertension or with coronary heart disease, or did not take anti-hypertension medication. CONCLUSION: Our study provides robust evidence that hourly ambient temperature is inversely associated with ambulatory blood pressure. It also highlights a linear relationship between decreased ambient temperature and elevated BP, which may have implications for the prevention and management of hypertension in susceptible populations.

lncRNA GAS5 regulates myocardial infarction by targeting the miR-525-5p/CALM2 axis.

Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of cardiovascular diseases, especially in myocardial infarction (MI). However, the underlying molecular mechanism of how lncRNA involves and affect MI still remains unclear. This study aimed to investigate the expression of lncRNA growth arrest-specific transcript 5 (GAS5) and its effects on myocardial cells' proliferation, cell cycle, and apoptosis. The possible mechanisms involved in GAS5, calmodulin 2 (CALM2), and microRNA (miR)-525-5p were also explored. The messenger RNA (mRNA) level of CALM2, GAS5, and miR-525-5p in postmyocardial infarction (MI) and normal cells were examined by quantitative real-time polymerase chain reaction (RT-qPCR). Western blot analysis assay was conducted to detect the protein levels of CALM2. The changes of cell cycle/apoptosis and cell viability of post-MI myocardial cells (PMMC) were determined by flow cytometry analysis and MTT (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide) assay after knockdown of GAS5 or CALM2, respectively. Dual luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR-525-5p and GAS5, CALM2 in myocardial. Hypoxic preconditioning was performed in normal cells, which constructed a simulated MI environment, and the effect of GAS5 on cardiomyocyte apoptosis was detected. Our data showed that the expression of GAS5 and CALM2 in PMMC was significantly upregulated, while the expression of miR-525-5p was downregulated. Overexpression of GAS5 and CALM2 profoundly promoted the apoptosis of myocardial cell. However, the proliferation of myocardial cell was inhibited by the upregulation of GAS5 and CALM2. Moreover, GAS5 was proved to be the target of miR-525-5p and GAS5 downregulated the expression of miR-525-5p and CALM2. In addition, lncRNA GAS5 promotes MI, while CALM2 induced MI can be reversed by miR-525-5p. These data suggested that lncRNA GAS5 promoted the development and progression of MI via targeting of the miR-525-5p/CALM2 axis and it has the potential to be explored as a therapeutic target for the treatment of MI in the future.

Fluctuation correlation spectroscopy and its applications in homogeneous analysis.

Fluctuation correlation spectroscopy (FCS) is a single-molecule/particle detection technique based on measuring signal fluctuations in a highly focused detection volume. Multiple-parameter information can be obtained from the FCS measurement including the amplitude, characteristic diffusion time of correlation curve, and brightness of the adopted probes. The multiple-parameter change is related with physical or chemical change occurring in the probes. Meanwhile, the detection method has advantages such as short sample time in seconds, sample volume with low limit in femtoliters, and mixing to detection without any separations. These advantages make the FCS technique suitable for homogeneous analysis. In this review, we summarized recent novel applications of FCS and its variants in homogeneous analysis including nucleic acid analysis, protein analysis, enzyme activity assay, direct characterization of nanoparticles in solution, and others. Graphical abstract.

Time-dependent cervical vagus nerve stimulation and frequency-dependent right atrial pacing mediates induction of atrial fibrillation.

OBJECTIVE: This study aimed to investigate the effects of right cervical vagus trunk simulation (RVTS) and/or right atrial pacing (RAP) on the induction of atrial fibrillation (AF). METHODS: Twenty-four healthy adult dogs were randomly divided into four groups: RAP groups comprising RAP500 (RAP with 500 beats/min) and RAP1000 (RAP with 1000 beats/min) and RVTS groups comprising RVTS and RAP500+RVTS. All dogs underwent 12-h intermittent RAP and/or RVTS once every 2 h. The AF induction rate, AF duration, atrial effective refractory period (ERP), and dispersion of ERP (dERP) were compared after every 2 h of RAP or/and RVTS. RESULTS: All groups had successful AF induction. The RAP1000 group had the highest AF induction rate and the longest AF duration. The RAP1000 group also had a shortened ERP in comparison to the other groups as well as the maximum dERP. Compared to the RAP500 group, RAP500+RVTS had an increased capacity to induce AF as measured by the AF induction rates, AF duration, ERP, and dERP. CONCLUSION: Increased tension in the vagus nerve and the intrinsic cardiac autonomic nervous system plays an important role in AF induction through different potential mechanisms. Interventions involving the vagus nerve and/or intrinsic cardiac autonomic nervous system can be a future potential therapy for AF.

Valproic acid regulates Ang II-induced pericyte-myofibroblast trans-differentiation via MAPK/ERK pathway.

Myocardial fibrosis (MF) plays an important part in cardiovascular diseases. The main cytological characteristics of MF is the increased number of myofibroblasts, which have multiple sources such as EMT, EndMT, myeloid progenitors, monocytes, and fibrocytes. Recent data showed that pericytes may represent a major source of myofibroblasts in kidney fibrosis. Valproic acid (VPA) is a kind of short-chain fatty acid. It was reported in recent studies that VPA regulates gene expression and influences various signal pathways. HDACs inhibitors can hinder the growth of tumor cells and differentiation of stem cells. And little is known about the effects of HDACs inhibitors on myofibroblasts transdiffererntiaton. This study focused on the role of HDACs in pericyte-myofibroblast trans-differentiation and how HDACs inhibitor VPA influenced proliferation, migration, viability and myofibroblast trans-differentiation of pericytes for the first time. Rat cardiac fibrosis model was induced by Ang II. Immunohistochemistry was employed to examine cardiac fibrosis and flow cytometry was used to analyze whether inflammatory cells involve VPA-induced trans-differentiation. Pericytes proliferation, migration and differentiation to myofibroblasts were performed to examine the role of VPA on pericyte trans-differentiation. Immunoblot and qPCR were applied to identify the signal transduction involving in VPA-induced trans-differentiation. In vivo study showed that HDAC inhibitor VPA blocks cardiac fibrosis, and inflammation inhibition was not involved in this process. VPA treatment inhibited Ang II pericyte proliferation, migration and transdifferentiation to myofibroblast. Furthermore, the inhibition of α-SMA expression by VPA was related to reduce phosphorylation of ERK, and a pharmacological inhibitor of MEK suppressed Ang II-induced α-SMA expression. HDAC4 knockdown resulted in inhibiting Ang II-mediated α-SMA expression as well as the phosphorylation of ERK. Moreover, the inhibitors of protein phosphatase 2A and 1 (PP2A and PP1) restored the Ang II-stimulated α-SMA expression from the inhibitory effect of VPA. Together, the current data indicate that the differentiation of pericytes to myofibroblasts is HDAC4 dependent and requires phosphorylation of ERK.

Relationship between abnormal vagus nerve tension and basal ganglia cerebral infarction induced paroxysmal atrial fibrillation.

OBJECTIVE: To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension. METHODS: A total of 1483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups. RESULTS: In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). The incidence trend of cerebral infarction in basal ganglia was age-related, in the >79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group. CONCLUSION: Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.

microRNA-208a in an early stage myocardial infarction rat model and the effect on cAMP-PKA signaling pathway.

The expression level of microRNA-208a (miR-208a) in a rat model with myocardial infarction and the effect of cAMP-PKA signaling pathway in early stage of myocardial infarction in rats were investigated. The early myocardial infarction model was established in 12 male Sprague-Dawley rats by ligation of the anterior descending coronary artery, and 12 rats were selected as the control group (sham operation group). Reverse-transcription quantitative PCR was conducted to detect the expression levels of miR-208a in the myocardium of and the expression levels of miR­208a in the serum of rats in the two groups. Western blot analysis was used to evaluate the expression levels of cAMP-PKA protein in the rat tissues in the two groups. After stimulating high levels of miR­208a expression in human myocardial cells (HCM), western blot analysis was used to detect the cAMP-PKA protein levels. The expression levels of miR­208a in myocardial tissues in rats with myocardial infarction were significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The expression levels of miR­208a in the early stage of myocardial infarction rats were also significantly higher than those in the control group, and the difference was statistically significant (P<0.05). The level of cAMP-PKA protein in myocardial tissue in rats with chronic myocardial infarction was also significantly higher. Transfection of human myocardial cells with miR­208a analogue significantly increased the cAMP-PKA protein levels in human myocardial cells. In conclusion, the over-expression of miR-208a in myocardial infarction tissue and the high levels of this miRNA in the serum, may be involved in the process of myocardial infarction by influencing the cAMP-PKA signaling pathway in myocardial cells.

Neuromodulation for cardiac arrhythmia.

The autonomic nervous system is known to play a significant role in the genesis and maintenance of arrhythmias. Neuromodulation, mostly designed to increase the parasympathetic tone and suppress the sympathetic tone, has become an emerging therapeutic strategy for the treatment of arrhythmias. Emerging therapeutic approaches include cervical vagal stimulation, transcutaneous auricular vagal stimulation, baroreceptor activation therapy spinal cord stimulation, ganglionated plexi ablation, renal sympathetic denervation, and left cardiac sympathetic denervation.

Autonomic Remodeling: How Atrial Fibrillation Begets Atrial Fibrillation in the First 24 Hours.

BACKGROUND: The mechanism(s) of how atrial fibrillation (AF) sustains itself in the first 24 hours is not well understood. OBJECTIVE: We sought to investigate the role of autonomic remodeling in the first 24 hours of AF simulated by rapid atrial pacing (RAP). METHODS: Forty-eight rabbits were divided into 6 groups. One group (n = 8) was euthanized after baseline recordings. Another group (n = 8) did not receive RAP during the 24-hour period to serve as controls. In the other 4 groups, rabbits were euthanized after RAP for 4, 8, 12, or 24 hours (n = 8 for each). Before and after designated hours of RAP, atrial effective refractory period, heart rate variability, and left vagal and sympathetic nerve activity (VNA and SNA, respectively) were determined. The right and left atrial tissues were obtained for immunocytochemical analysis for growth-associated protein 43 (GAP43), tyrosine hydroxylase (TH), and choline acetyltransferase (ChAT). RESULTS: RAP resulted in progressively shortened atrial effective refractory period and slower heart rate. In the first 12 hours of RAP, both SNA and VNA progressively increased. Then, VNA remained stably elevated but SNA began to attenuate. The high-frequency component and low-frequency/high-frequency ratio of heart rate variability followed the trend of VNA and SNA, respectively. The density of GAP43-positive, ChAT-positive, and TH-positive neural elements in the right and left atria was progressively higher with RAP. CONCLUSIONS: AF resulted in progressive autonomic remodeling, manifesting as nerve sprouting, sympathetic and vagal hyperinnervation. Autonomic remodeling may play an important role in sustaining AF in the first 24 hours.

The expression and functional evidence for voltage-dependent potassium channel Kv1.3 in lymphocytes during aging in spontaneously hypertensive rats.

AIMS: Our previous studies showed that expression and functional profile of voltage-dependent potassium channels Kv1.3 were increased in lymphocytes of spontaneously hypertensive rats (SHR) compared to normotensive rats, suggesting a crucial role for lymphocyte Kv1.3 in the development of hypertension. Here, we further investigated whether the expression and functional profile of Kv1.3 was related to increased blood pressure in SHR with age of 4, 8, 16 and 24 wk. METHODS: Systolic blood pressure was measured through pressure device around the tail. mRNA and protein expression were assessed by real-time PCR and western blot in lymphocytes of SHR. Current density of Kv channels in lymphocytes was measured by patch-clamp. RESULTS: Systolic blood pressure was elevated in an age-dependent manner (ANOVA P < 0.05). mRNA and protein level of Kv1.3 were significantly increased in an age-dependent manner in lymphocyte of SHR (ANOVA P < 0.05). Moreover, the current density of Kv was dramatically enhanced in an age-dependent manner (ANOVA P < 0.05). CONCLUSION: The systolic blood pressure positively correlated with expression as well as current density of potassium channels in lymphocytes of SHR at age of 8, 16 and 24 wk. In conclusion, Kv1.3 channels were upregulated in an age-dependent manner in SHR and correlates with systolic blood pressure during aging. The present study implies that Kv1.3 blockers may be applied as a therapeutic treatment for the development of hypertension during aging.

Structural changes in the progression of atrial fibrillation: potential role of glycogen and fibrosis as perpetuating factors.

BACKGROUND: Previous studies of the goat heart subjected to prolonged atrial pacing induced sustained atrial fibrillation (AF). Structural changes included marked accumulation of glycogen in atrial myocytes. AIMS: In the present study, we hypothesized that glycogen deposition in canine atrial myocytes promotes paroxysmal forms of AF and is involved in fibrosis development in the later stages of AF. MATERIAL & METHODS: In dogs under pentobarbital anesthesia, tissues were obtained from the right and left atrial appendages (LAA/RAA). Periodic acid Schiff (PAS) and Masson's trichrome staining of the LAA/RAA from normal dogs, and those subjected to atrial pacing induced AF for 48 h or 8 weeks determined glycogen and collagen concentrations, respectively, using morphometric analysis. RESULTS: At baseline, there was a significant greater concentration of glycogen in the LAA than the RAA (P ≤ 0.05). Compared to the RAA, the LAA glycogen, was dense and locked against the intercalated discs. After pacing induced AF for 48 hours and 8 weeks there was a marked increase in glycogen deposition, significantly greater than in the baseline state (P ≤ 0.05). There was a similar and progressive increase in collagen concentrations in each group (P ≤ 0.05). CONCLUSIONS: The differential in glycogen concentration, in conjunction with other factors, neural and electrophysiological, provide a basis for the greater propensity of the left atrium for paroxysmal AF, at baseline and 48 hours of pacing induced AF. The marked increase in collagen at 8 weeks of pacing provides a substrate for sustained AF. Evidence is presented linking glycogen accumulation and fibrosis as factors in the persistent forms of AF.

Glucagon-like peptide-1 protects against cardiac microvascular endothelial cells injured by high glucose.

OBJECTIVE: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. METHODS: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. RESULTS: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (P<0.05). CONCLUSIONS: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.

Obstructive Sleep Apnoea and Atrial Fibrillation.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and is associated with significant morbidity and mortality. Obstructive sleep apnoea (OSA) is common among patients with AF. Growing evidence suggests that OSA is associated with the initiation and maintenance of AF. This association is independent of obesity, body mass index and hypertension. OSA not only promotes initiation of AF but also has a significant negative impact on the treatment of AF. Patients with untreated OSA have a higher AF recurrence rate with drug therapy, electrical cardioversion and catheter ablation. Treatment with continuous positive airway pressure (CPAP) has been shown to improve AF control in patients with OSA. In this article, we will review and discuss the pathophysiological mechanisms of OSA that may predispose OSA patients to AF as well as the standard and emerging therapies for patients with both OSA and AF.

Low-level vagosympathetic trunk stimulation inhibits atrial fibrillation in a rabbit model of obstructive sleep apnea.

BACKGROUND: Atrial fibrillation (AF) is highly associated with obstructive sleep apnea (OSA) in which AF is triggered by hyperactivity of the cardiac autonomic nervous system. Previous studies showed that low-level vagosympathetic trunk stimulation (LLVS), at voltages not slowing sinus rate or AV conduction, inhibits AF by suppressing the cardiac autonomic nervous system. OBJECTIVE: The purpose of this study was to investigate whether LLVS delivered at the right vagosympathetic trunk suppresses AF in a rabbit model of OSA. METHODS: Eleven rabbits received a tracheostomy under general anesthesia. The endotracheal tube was clamped at end expiration for 1 minute to simulate OSA. Over a period of 4 hours, OSA was delivered every 6 minutes. Effective refractory period (ERP), blood pressure, intraesophageal pressure, and blood gases (O2, CO2, pH) were measured before and after each episode of OSA. AF duration and ERP were measured by programmed stimulation. Group 1 rabbits (n = 6) received LLVS (50% below that which slowed the sinus rate) in the first 3 hours. Group 2 rabbits (n = 5) only received OSA. RESULTS: Group 1 ERP began to lengthen progressively from the second hour compared to group 2. AF duration increased in the first hour for both groups but began to shorten progressively after the first hour in group 1 rabbits. Blood pH, O2 or CO2 level, intraesophageal pressure, and hypertensive response during OSA were not different between the 2 groups. CONCLUSION: LLVS is capable of suppressing ERP shortening and AF induced by OSA. LLVS may serve as a new therapeutic approach to treat OSA-induced AF.

A comparison of the efficacy of surgical renal denervation and pharmacologic therapies in post-myocardial infarction heart failure.

OBJECTIVE: Although renal denervation (RD) has been shown to be effective in treating post- myocardial Infarction (MI) heart failure (HF) in animal models and clinical trials, its utility as a standalone treatment without traditional drug treatment for post-MI HF still needs to be investigated. METHODS: Rats were randomly assigned into seven experimental groups: N group (control group with no MI and no RD, n = 10), MI group (MI, n = 20), RD group (renal denervation, n = 10), RD-3d+MI group (RD performed three days before MI, n = 15), ß-blocker-3d+MI group (Metoprolol treated three days before MI, n = 15), ACEI-3d+MI group (Perindopril treated three days before MI, n = 15), and ARB-3d+MI group (Losartan treated three days before MI, n = 15). Cardiac function, autonomic nervous system parameters, and neuroendocrine activities were evaluated 8 weeks post MI. RESULTS: Compared to ß-blockers, ACEIs, and ARBs, RD alone provided significantly better cardiac remodeling and function, enhanced water and sodium excretion, and improved autonomic modulation. CONCLUSIONS: In this post-MI HF animal model, surgical RD provides effective autonomic modulation, inhibition of the RAAS, improved cardiac remodeling, and preserved renal function, without affecting normal circulation and cardiopulmonary function in normal rats. Compared to ß-blocker, ACEI, and ARB single-drug therapies, RD alone is more efficacious. These results suggest that RD may be an effective treatment option for HF, especially in patients who have contraindications to drug therapy.

The effects of subclinical hypothyroidism on serum lipid level and TLR4 expression of monocyte in peripheral blood of rats.

OBJECTIVE: To observe effect of subclinical hypothyroidism (SCH) on serum lipid level and expression of toll-like receptor 4 (TLR4) in rats' peripheral blood mononuclear cells (PBMC). METHODS: Fifty Wistar female rats were divided into three groups: normal control (NC group; n=10), sham group (n=10), and L-T-4 (L-thyroxine) group (n=30, with thyroidectomy, fed with rich-calcium water after operation. 5 weeks later, abdominal subcutaneous injection of L-T-4: 0.95 µg/100g/d). 8 weeks later, the rats were killed then the peripheral blood was collected to determine the levels of serum thyroid-stimulating hormone (TSH), total thyroid hormone (TT4), total cholesterol (TC) and low density lipoprotein cholesterin (LDL-C). Rats in L-T-4 group were divided into normal lipid (NL) group) and high lipid (HL) group) according to lipid value of NC group. Monocytes were separated from blood to determine TLR4 expression by flow cytometry. RESULTS: In NL and HL groups TSH were higher than in NC and Sham groups (p<0.05). TT4 have no significant differences (p>0.05). TLR4, TLR4 mRNA, NF-κB (p65) were increased (p<0.05). TNF-α, IL-6 and IL-1ß were higher than in NC and sham groups (p<0.01). There were no significant differences of TLR4, TLR4 mRNA, NF-κB (p65), TNF-α, IL-6 and IL-1ß expression between NL and HL groups (p>0.05). CONCLUSION: TLR4, TLR4 mRNA, NF-κB (p65) of PBMC and TNF-α, IL-6, IL-1ß expression in serum were all increased in SCH rats, which was not related to serum dyslipidemia.

Effect of interconnection between cervical vagus trunk, epicardial fat pad on sinus node function, and atrial fibrillation.

BACKGROUND: The epicardial fat pad (FP) integrates the autonomic innervation between the extrinsic and intrinsic cardiac autonomic nervous system and affects atrial electrophysiology and pathophysiology. METHODS: Eighteen dogs were divided into two groups: sequential ablation of sinoatrial node FP (SAN-FP) and atrioventricular node FP (AVN-FP). Sinus rate (SR), atrial fibrillation (AF) inducibility, and effective refractory period (ERP) changes during electrical stimulation of the vagus trunk were detected before and after ablation. RESULTS: In the SAN-FP group, the SR slowing, increasing AF inducibility, and ERP shortening that induced by vagus trunk stimulation were significantly attenuated by isolated SAN-FP ablation, compared with the same group prior to ablation (all P < 0.05). Subsequent AVN-FP ablation following SAN-FP ablation almost cannot produce further attenuation during vagus trunk stimulation, compared with isolated SAN-FP ablation (P > 0.05). In the AVN-FP group, SR slowing, increasing AF inducibility, and ERP shortening that induced by vagus trunk stimulation were completely eliminated by isolated AVN-FP ablation, compared with the same group prior to ablation (all P < 0.05). Subsequent SAN-FP ablation following AVN-FP ablation produced no further attenuation, compared with isolated AVN-FP ablation (P > 0.05). CONCLUSIONS: A neural pathway from the cervical vagus trunk to the sinus node and atrium runs through the SAN-FP, but eventually converges at the AVN-FP and also suggested that the AVN-FP serves as an "integration center" for the SAN-FP to modulate sinus node function. The AVN-FP may play a more critical role in the initiation and maintenance of AF.

Effect of the stellate ganglion on atrial fibrillation and atrial electrophysiological properties and its left-right asymmetry in a canine model.

OBJECTIVE: To investigate the effect of the stellate ganglion (SG) and its left-right asymmetry on atrial fibrillation (AF) inducibility, AF duration and atrial electrophysiological properties. METHODS: Sixteen adult mongrel dogs were randomly assigned to three groups. The control group (n=4) underwent 6 h rapid atrial pacing (RAP) only; the right SG (RSG) group (n=6) underwent 6 h RSG stimulation plus RAP; and the left SG (LSG) group (n=6) underwent 6 h LSG stimulation plus RAP. AF induction rate, AF duration, effective refractory period (ERP) and dispersion of ERP (dERP) were measured. RESULTS: In the RSG group, the induction rate of AF was significantly increased in sites in the right atrium (RA) compared with baseline (P<0.05). In the LSG group, the induction rate of AF was significantly increased (P<0.05) compared with baseline in the left atrium (LA), left superior pulmonary vein and left inferior pulmonary vein, respectively. Compared with RSG stimulation, right stellate ganglionectomy markedly decreased the AF induction rate of the RA (P<0.05). Compared with LSG stimulation, left stellate ganglionectomy markedly decreased the AF induction rate of the LA, the left superior pulmonary vein and the left inferior pulmonary vein (P<0.05). In the RSG group, the ERP was significantly shortened (P<0.05) and the dERP was significantly increased (P<0.05) in RA sites (P<0.05). The ERP was significantly shortened in the LSG group (P<0.05). The dERP was significantly increased (P<0.05) in LA and pulmonary vein sites (P<0.05). CONCLUSIONS: Unilateral electrical stimulation of the SG in combination with RAP can successfully establish a canine model of acute AF mediated by excessive sympathetic activity. SG stimulation facilitates AF induction and aggravates electrical remodelling in sites in the atrium and pulmonary vein. Inhibiting sympathetic nerve activation through unilateral stellate ganglionectomy can reduce AF initiation.