The comparison between the novel technique and conventional method in the catheter ablation of premature ventricular contractions originating from the free wall of tricuspid annulus.

BACKGROUND: This study aimed to assess the safety and effectiveness of a novel technique for catheter ablation in patients with premature ventricular contraction (PVC) from the free wall of tricuspid annulus (TV). HYPOTHESIS: We hypothesized that the novel technique is more efficacious than the traditional approach. METHODS: We retrospectively investigated 59 consecutive patients with PVC originating from the free wall of TV between January 2013 and November 2021. The patients were divided into two groups: the reversed S-curve technique group (RST, n = 26) and the reversed C-curve technique group (RCT, n = 33). The RST under the support of a steerable sheath was used in RST group, while the RCT under the support of a nonsteerable sheath was used in the RCT group. Systematic mapping and radiofrequency ablation were preferentially performed under the valve in all patients. RESULTS: Compared to the RCT group, total procedural time and fluoroscopic exposure time were significantly shorter in RST group. Two patients experienced cardiac tamponade in the RCT group, while no complications were observed in RST group (p = .498). The success rate was significantly higher in RST group compared to RCT group (81.9% vs. 100%, p = .029). Three patients in RCT group failed to ablate during the operation but were successfully ablated using the novel method. During regular follow-up, no patients in the RST group had a recurrence, while three patients in the RCT group did (p = .274). CONCLUSIONS: It suggests that the reserved S-curve technique, supported by a steerable sheath, is a feasible and effective method for ablating PVC originating from the free wall of TV.

Multimodal data-driven prognostic model for predicting new-onset ST-elevation myocardial infarction following emergency percutaneous coronary intervention.

OBJECTIVES: We developed a nomogram model derived from inflammatory indices, clinical data, and imaging data to predict in-hospital major adverse cardiac and cerebrovascular events (MACCEs) following emergency percutaneous coronary intervention (PCI) in patients with new-onset ST-elevation myocardial infarction (STEMI). METHODS: Patients with new-onset STEMI admitted between June 2020 and November 2022 were retrospectively reviewed. Data pertaining to coronary angiograms, clinical data, biochemical indices, and in-hospital clinical outcomes were derived from electronic medical records. Lasso regression model was employed to screen risk factors and construct a prediction model. RESULTS: Overall, 547 patients with new-onset STEMI who underwent PCI were included and assigned to the training cohort (n = 384) and independent verification cohort (n = 163). Six clinical features (age, diabetes mellitus, current smoking, hyperuricemia, neutrophil-to-lymphocyte ratio, and Gensini score) were selected by LASSO regression to construct a nomogram to predict the risk of in-hospital MACCEs. The area-under-the-curve (AUC) values for in-hospital MACCEs risk in the training and independent verification cohorts were 0.921 (95% CI 0.881-0.961) and 0.898 (95% CI 0.821-0.976), respectively. It was adequately calibrated in both training cohort and independent verification cohorts, and predictions were correlated with actual outcomes. Decision curve analysis demonstrated that the nomogram was capable of predicting in-hospital MACCEs with good clinical benefit. CONCLUSIONS: Our prediction nomogram based on multi-modal data (inflammatory indices, clinical and imaging data) reliably predicted in-hospital MACCEs in new-onset STEMI patients with emergency PCI. This prediction nomogram can enable individualized treatment strategies.

Predicting long-term prognosis after percutaneous coronary intervention in patients with new onset ST-elevation myocardial infarction: development and external validation of a nomogram model.

BACKGROUND: The triglyceride glucose (TyG) index is a well-established biomarker for insulin resistance (IR) that shows correlation with poor outcomes in patients with coronary artery disease. We aimed to integrate the TyG index with clinical data in a prediction nomogram for the long-term prognosis of new onset ST-elevation myocardial infarction (STEMI) following primary percutaneous coronary intervention (PCI) . METHODS: This retrospective study included new-onset STEMI patients admitted at two heart centers for emergency PCI from December 2015 to March 2018 in development and independent validation cohorts. Potential risk factors were screened applying least absolute shrinkage and selection operator (LASSO) regression. Multiple Cox regression was employed to identify independent risk factors for prediction nomogram construction. Nomogram performance was assessed based on receiver operating characteristic curve analysis, calibration curves, Harrell's C-index and decision curve analysis (DCA). RESULTS: In total, 404 patients were assigned to the development cohort and 169 to the independent validation cohort. The constructed nomogram included four clinical variables: age, diabetes mellitus, current smoking, and TyG index. The Harrell's C-index values for the nomogram were 0.772 (95% confidence interval [CI]: 0.721-0.823) in the development cohort and 0.736 (95%CI: 0.656-0.816) in the independent validation cohort. Significant correlation was found between the predicted and actual outcomes in both cohorts, indicating that the nomogram is well calibrated. DCA confirmed the clinical value of the development prediction nomogram. CONCLUSIONS: Our validated prediction nomogram based on the TyG index and electronic health records data was shown to provide accurate and reliable discrimination of new-onset STEMI patients at high- and low-risk for major adverse cardiac events at 2, 3 and 5 years following emergency PCI.

CTRP1 Aggravates Cardiac Fibrosis by Regulating The NOX2/P38 Pathway in Macrophages.

OBJECTIVE: C1q/TNF-related proteins 1 (CTRP1) is a recently identified adiponectin associated with obesity-linked disorders and adverse cardiovascular events. The effect of CTRP1 on cardiac fibrosis has not yet been fully elucidated; thus, we aimed to explore this association. MATERIALS AND METHODS: In this experimental study, a mouse model of cardiac fibrosis was established by administering isoproterenol (ISO) (subcutaneously injecting 10 mg/kg/day for 3 days and then 5 mg/kg/day for 11 days). Mice were also injected with recombinant CTRP1 protein (200 µg/kg) 14 days after the final ISO administration. Adult mouse fibroblasts were isolated and stimulated with transforming growth factor (TGF) ß1, followed by treatment with recombinant CTRP1. Primary bone marrow-derived macrophages were isolated from C57BL/6J mice and treated with recombinant CTRP1 as well. RESULTS: CTRP1 level was increased in mouse plasma and heart tissue 2 weeks after ISO injection. Our findings indicated that recombinant CTRP1 injection aggravated ISO-induced cardiac fibrosis and dysfunction. However, recombinant CTRP1 did not alter TGFß1-induced fibroblast proliferation and activation or collagen transcription. Recombinant CTRP1 exacerbated ISO-induced macrophage infiltration and inflammatory response. We determined that macrophages treated with recombinant CTRP1 showed increased pro-inflammatory cytokine release. Fibroblasts co-cultured with macrophages treated with recombinant CTRP1 showed increased proliferation and collagen transcription. We also found that CTRP1 upregulated the NADPH oxidase 2 (NOX2)/p38 pathway in macrophages. When we inhibited p38 signaling, the pro-inflammatory effect of CTRP1 on macrophages was counteracted. Fibroblasts co-cultured with macrophages treated with a p38 inhibitor also showed limited proliferation and collagen transcription. CONCLUSION: Cardiac fibrosis was aggravated with the activation of the NOX2/p38 pathway in macrophages after CTRP1 treatment.

Prediction of major adverse cardiovascular events in patients with acute coronary syndrome: Development and validation of a non-invasive nomogram model based on autonomic nervous system assessment.

Background: Disruption of the autonomic nervous system (ANS) can lead to acute coronary syndrome (ACS). We developed a nomogram model using heart rate variability (HRV) and other data to predict major adverse cardiovascular events (MACEs) following emergency coronary angiography in patients with ACS. Methods: ACS patients admitted from January 2018 to June 2020 were examined. Holter monitors were used to collect HRV data for 24 h. Coronary angiograms, clinical data, and MACEs were recorded. A nomogram was developed using the results of Cox regression analysis. Results: There were 439 patients in a development cohort and 241 in a validation cohort, and the mean follow-up time was 22.80 months. The nomogram considered low-frequency/high-frequency ratio, age, diabetes, previous myocardial infarction, and current smoking. The area-under-the-curve (AUC) values for 1-year MACE-free survival were 0.790 (95% CI: 0.702-0.877) in the development cohort and 0.894 (95% CI: 0.820-0.967) in the external validation cohort. The AUCs for 2-year MACE-free survival were 0.802 (95% CI: 0.739-0.866) in the development cohort and 0.798 (95% CI: 0.693-0.902) in the external validation cohort. Development and validation were adequately calibrated and their predictions correlated with the observed outcome. Decision curve analysis (DCA) showed the model had good discriminative ability in predicting MACEs. Conclusion: Our validated nomogram was based on non-invasive ANS assessment and traditional risk factors, and indicated reliable prediction of MACEs in patients with ACS. This approach has potential for use as a method for non-invasive monitoring of health that enables provision of individualized treatment strategies.

Serum Lipopolysaccharide Is Associated with the Recurrence of Atrial Fibrillation after Radiofrequency Ablation by Increasing Systemic Inflammation and Atrial Fibrosis.

Objectives: The gut microbiota and its metabolites are linked to inflammation and contribute to the progression of atrial fibrillation (AF), but the predictive value of the gut microbiota-derived metabolite lipopolysaccharide (LPS) for AF recurrence (RAF) is unknown. This study is aimed at investigating (1) the correlation between LPS and RAF and (2) its relationship with inflammation and atrial fibrosis. Method: We performed a single-centre retrospective analysis in 159 AF patients. Fasting plasma samples were collected, and an enzyme-linked immunosorbent assay was used to determine the levels of serum LPS, interleukin-6 (IL-6), collagen type-1 C-terminal telopeptide (CITP), and transforming growth factor-ß1 (TGFß1). The cumulative risk for RAF was evaluated with Kaplan-Meier analysis. Cox proportional hazard analysis was carried out to predict the hazard of RAF. The correlations among LPS and IL-6, CITP, TGFß1, and left atrial diameter (LAD) were analysed by Pearson's correlation coefficient. Subsequent univariate and multivariable linear regression analyses were carried out to evaluate the connection between clinical variables and Log-LPS. Results: All 159 AF patients were included in this study. The proportion of persistent atrial fibrillation was 40.3%, the mean age was 61.9 ± 10.1 years, the proportion of males was 61.6%, and the mean LPS was 56.5 ± 29.5 pg/mL. After all patients were divided into tertiles according to the circulating LPS level, a total of 44 RAF occurred: 10 in the first tertile, 15 in the second tertile, and 19 in the third tertile (log-rank test P = 0.037). Heart failure (hazard ratio 2.029, P = 0.041), LAD (hazard ratio 1.064, P = 0.022), Log-LPS (hazard ratio 5.686, P = 0.043), and CITP (hazard ratio 6.841, P = 0.033) independently predicted the risk of RAF. In all patients, univariate analysis showed that heart failure, LAD, hs-CRP, IL-6, CITP, and TGF-ß1 were connected with Log-LPS. Multivariate linear regression analysis indicated that IL-6 and hs-CRP were independently and positively connected with Log-LPS. Conclusions: Our results indicated that circulating LPS was a predictor of RAF and may contribute to RAF incidence after ablation by increasing systemic inflammation and atrial fibrosis.

New permanent bundle-branch block and long-term prognosis of patients with new onset ST-elevation myocardial infarction who underwent percutaneous coronary intervention.

Aim: The aim of the study was to evaluate the potential predictive value of permanent RBBB and LBBB for longer-term prognosis in patients with new-onset STEMI who underwent percutaneous coronary intervention (PCI). Methods: Patients with new-onset STEMI that underwent emergency PCI at our department from June 2012 to September 2020 were included in the study. Gensini score (GS) was employed to evaluate the severity of coronary lesions. The primary endpoint of the study was the occurrence of major adverse cardiac and cerebrovascular events (MACCEs), the composite of cardiac mortality, recurrence of myocardial infarction, cardiac shock, stroke, stent thrombosis, or revascularization. We also set all-cause mortality as a secondary endpoint. Results: Out of the 547 patients, 29 patients had new-onset permanent LBBB, 51 patients had new-onset permanent RBBB, and 467 patients had no bundle-branch block (BBB). The occurrence of no BBB, new permanent LBBB, or RBBB was not associated with the severity of coronary artery lesions as evaluated by the GS. After follow-up at an average of 43.93 months, MACCEs occurred in 52 patients. Kaplan-Meier analysis showed that patients with new-onset RBBB were at greater risk for MACCEs compared to those with new onset LBBB (χ2 = 5.107, p = 0.021). Also, an independent correlation was found between new permanent RBBB and LBBB and MACCEs risk. The adjusted hazard ratios (HRs) were 6.862 [95% confidence interval (CI) of 3.764-12.510] for the new-onset permanent RBBB and 3.395 (95% CI of 1.280-9.005) for LBBB, compared to those with no BBB, respectively (both p < 0.05). Conclusion: New onset permanent RBBB in patients with new onset STEMI who underwent PCI may be correlated independently with increased risk of poor long-term prognosis.

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.

Serum total bilirubin and long-term prognosis of patients with new-onset non-ST elevation myocardial infarction: a cohort study.

BACKGROUND: The potential prognostic role of total bilirubin (TBIL) in patients with new-onset non-ST elevation myocardial infarction (NSTEMI) is not fully understood. This study aims to evaluate the potential predictive value of TBIL for long-term prognosis in patients with new-onset NSTEMI. METHODS: Patients with new-onset NSTEMI that underwent emergency coronary angiography in our department from June 2015 to March 2020 were included. Baseline TBIL was measured at admission. SYNTAX scores were used to indicate the severity of coronary lesions. The association between TBIL and SYNTAX scores was analyzed using multivariate logistic regression. The patients were followed for the incidence of major adverse cardiac and cerebrovascular events (MACCEs). The association between TBIL and MACCEs was analyzed using Kaplan-Meier survival methods. RESULTS: In total 327 patients were included in this study. Patients were divided according to tertiles of TBIL (first tertile < 10.23 µmol/L, n = 109; second tertile 10.23-14.30 µmol/L, n = 109; and third tertile ≥ 14.30 µmol/L, n = 109). TBIL was independently associated with the severity of coronary lesions in patients with NSTEMI, with an adjusted odds ratio (OR) and 95% confidence interval (CI) for the third tertile and the second tertile compared with the first tertile of TBIL of 2.259 (1.197-4.263) and 2.167 (1.157-4.059), respectively (both p < 0.05). After a mean follow-up of 30.33 months, MACCE had occurred in 57 patients. TBIL was independently associated with the increased risk of MACCEs, with an adjusted hazard ratio (HR) and 95% CI for the third tertile and the second tertile compared with the first tertile of TBIL of 2.737 (1.161-6.450) and 3.272 (1.408-7.607), respectively (both p < 0.05). CONCLUSIONS: Higher myocardial infarction admission TBIL might independently predict poor prognosis in patients with NSTEMI.

Clinical characteristics and the severity of coronary atherosclerosis of different subtypes of bundle-branch block.

BACKGROUND: Right bundle-branch block (RBBB) and left bundle-branch block (LBBB) play a role in the pathogenesis and progression of coronary artery disease (CAD). However, the clinical features and the severity of coronary artery disease associated with different subtypes of bundle-branch block, according to time of new appearance, is not well characterized in patients with no known CAD. METHODS: We retrospectively analyzed data pertaining to consecutive patients with RBBB or LBBB who underwent coronary angiography. The severity of coronary lesions was evaluated using the SYNTAX score. The differential effect of new-onset RBBB, old RBBB, new-onset LBBB, and old LBBB on the severity of CAD and its association with clinical characteristics was quantified. Multivariate logistic regression analysis was performed to evaluate the effect of RBBB and LBBB on the degree of coronary atherosclerosis in patients without known CAD. RESULTS: Out of the 243 patients, 72 patients had old LBBB, 37 had new-onset LBBB, 93 patients had old RBBB, and 41 patients had new-onset RBBB. On univariate analysis, age, systolic blood pressure, diastolic blood pressure, creatinine, serum glucose, and glycosylated hemoglobin level were associated with high SYNTAX score (p < .05 for all). Patients in the new-onset RBBB, old RBBB, new-onset LBBB, and old LBBB groups showed significant differences in baseline characteristics and coronary atherosclerosis (p < .05 for all). However, there were no significant between-group differences with respect to the degree of coronary atherosclerosis as assessed by SYNTAX score. CONCLUSIONS: New-onset RBBB, old RBBB, new-onset LBBB, and old LBBB were not associated with the severity of coronary lesions as assessed by SYNTAX score in patients without known CAD.

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.

LL-VNS attenuates SK2 expression and incidence of arrhythmias following acute myocardial infarction in rats.

Objectives: Our previous study has demonstrated that low-level vagus nerve stimulation (LL-VNS) protects the heart against ventricular arrhythmias (VAs) induced by acute myocardial infarction (AMI). However, the potential mechanisms by which it influences ventricular electrophysiology remain unknown. Materials and methods: Forty-five rats were divided into three groups: a Control group (sham AMI followed by sham LL-VNS, n = 15), an AMI group (AMI followed by sham LL-VSN for 60 mins, n = 15), and an AMI + LL-VNS group (AMI followed by LL-VSN for 60 mins, n = 15). Heart rate variability (HRV), ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and left stellate ganglion (LSG) activity were measured at baseline and during AMI. Finally, myocardial tissues were collected for tissue analysis. Results: AMI directly induced hyperactivity in the LSG and reduced vagal tone as indexed by HRV. AMI also decreased VFT, and shortened ERP but increased ERP dispersion. AMI resulted in an increase in expression of ventricular small-conductance Ca2+-activated K+ (SK2). However, LL-VNS significantly mitigated or eliminated the effects of AMI. Conclusion: LL-VNS altered the electrophysiological properties of the ventricles through inhibition of cardiac sympathetic nervous activity and reduction in SK2 expression.

Pulsed Field Ablation of Superior Vena Cava: Feasibility and Safety of Pulsed Field Ablation.

Background: Studies have shown that pulsed field ablation (PFA) has excellent effectiveness and safety in pulmonary vein isolation (PVI). However, there are few reports about the application of PFA, especially the alternating current (AC) biphase PFA, in superior vena cava (SVC) isolation, and its effectiveness and safety are still unclear. Objective: To investigate the efficacy and safety of the AC biphase PFA for SVC isolation, and to provide evidence for the clinical use of PFA for SVC. Methods: Eight pigs and two dogs were included in the study. PFA was delivered to these pigs and dogs. Pacing threshold and electrogram data were recorded before and after PFA. Voltage mapping of SCV was obtained before, after, and 3 weeks after PFA. At the end, all animals were euthanatized for gross pathology analysis. Results: For eight pigs, the median pacing threshold was 1.5 (1.4, 2.75) mA before PFA, while > 6.0 mA after PFA for all animals. The average electrogram amplitude reduction was 61.33 ± 24.90% for ablations with the initial amplitude≥0.5 mv. For two dogs, pacing threshold change and electrogram amplitude reduction were also observed. No phrenic palsy or sinus node injury was observed during PFA in any animal. Furthermore, voltage mapping showed that the voltage amplitude was significantly decreased in all animals and this could be kept for more than 3 weeks. Moreover, transmural tissue damage with reserved vessel and nerve were shown, no SVC stenosis was found at 3 weeks after PFA. Conclusion: PFA can effectively isolate SVC. Transmural tissue damage of SVC can be achieved without phrenic palsy, sinus node injury nor SVC stenosis.

Association between Serum Adiponectin and Atrial Fibrillation: A Case-Control Study Stratified by Age and Gender.

BACKGROUND: Circulating adiponectin has been suggested to be associated with atrial fibrillation (AF). However, whether the association differs by age and gender remains unknown. We performed a case-control study to evaluate the above association. METHODS: AF patients who underwent 24-hour long-range 12-channel electrocardiogram examination at our center were included in this study, and people with normal sinus rhythm (NSR) were included as controls. All participants underwent echocardiography and heart rate variability tests. Biochemical parameters and adiponectin levels were also evaluated. Receiver operating characteristic (ROC) analyses were used to determine the predictive efficacy of adiponectin for AF, and multivariate logistic regression analysis was performed to evaluate the potential independent predictors of AF. RESULTS: Overall, 84 patients with AF and 84 people with NSR were included. Serum adiponectin was significantly higher in AF patients compared to that in controls (P < 0.001). ROC analysis showed that higher serum adiponectin (>6.098 µg/mL) had predictive efficacy for AF, with an area under the curve of 0.660 (95% confidence interval [CI]: 577-0.742). The results of multivariate logistic regression analysis showed that higher adiponectin was an independent predictor of AF in the overall participants (odds ratio [OR] 1.224, 95% CI 1.018-1.471, P=0.032). Subgroup analysis showed that higher adiponectin was independently associated with AF in women (OR 1.893, 95% CI 1.160-3.089, P=0.011) and in patients aged < 65 years (OR 1.453, 95% CI 1.023-2.064, P=0.037), but not in men or those aged ≥ 65 years. CONCLUSIONS: Higher serum adiponectin level was independently associated with higher odds for AF in women and in participants <65 years old, but not in men or those aged ≥65 years.

Ultrasonic Neuromodulation and Sonogenetics: A New Era for Neural Modulation.

Non-invasive ultrasonic neural modulation (UNM), a non-invasive technique with enhanced spatial focus compared to conventional electrical neural modulation, has attracted much attention in recent decades and might become the mainstream regimen for neurological disorders. However, as ultrasonic bioeffects and its adjustments are still unclear, it remains difficult to be extensively applied for therapeutic purpose, much less in the setting of human skull. Hence to comprehensively understand the way ultrasound exerts bioeffects, we explored UNM from a basic perspective by illustrating the parameter settings and the underlying mechanisms. In addition, although the spatial resolution and precision of UNM are considerable, UNM is relatively non-specific to tissue or cell type and shows very low specificity at the molecular level. Surprisingly, Ibsen et al. (2015) first proposed the concept of sonogenetics, which combined UNM and mechanosensitive (MS) channel protein. This emerging approach is a valuable improvement, as it may markedly increase the precision and spatial resolution of UNM. It seemed to be an inspiring tool with high accuracy and specificity, however, little information about sonogenetics is currently available. Thus, in order to provide an overview of sonogenetics and prompt the researches on UNM, we summarized the potential mechanisms from a molecular level.

Effects of Kindlin-2 on proliferation and migration of VSMC and integrinß1 andß3 activity via FAK-PI3K signaling pathway.

Vascular hyperplasia after vascular trauma is one of the difficult problems in clinical treatment. Nowadays, there is no effective treatment for vascular hyperplasia. Previous studies have shown that integrinß1 andß3 activity play an important role in vascular hyperplasia. Kindlin-2 has been shown to modulate integrinß1 andß3 activity in cancer. Therefore, in this study, we hope to explore the relationship between Kindlin-2 and vascular hyperplasia. We overexpressed or knocked down Kindlin-2 by adenovirus. The results showed that Kindlin-2 overexpression could regulate integrinß1 andß3 activity through FAK-PIK3 signaling pathways ex vivo and in vivo, thereby affecting the proliferation and migration of VSMC, and then it causes the consequences of vascular hyperplasia. Therefore, Our results show that Kindlin-2 may be a potential target for the treatment of vascular hyperplasia.

Serum N-Acetylneuraminic Acid Is Associated with Atrial Fibrillation and Left Atrial Enlargement.

PURPOSE: Recent studies have indicated that N-acetylneuraminic acid (Neu5Ac) plays a key role in severe coronary artery diseases, involving RhoA signaling pathway activation, which is critically involved in cardiac fibrosis. There is convincing evidence from many studies that left atrium fibrosis is involved in the pathophysiology of AF. Therefore, we speculated that Neu5Ac may be associated with atrial fibrillation (AF) and involved in the development of AF. This study aims to investigate the clinical relationship between Neu5Ac and AF and left atrial enlargement. METHODS: Forty-five patients with AF (AF group) and forty-five patients with non-AF (control group) matched for age, sex, and hospitalization date were recruited for our study. Plasma concentrations of Neu5Ac from peripheral venous blood were analyzed using enzyme-linked immunosorbent assay (ELISA). The baseline characteristics, plasma level of Neu5Ac, and echocardiographic characteristics were evaluated. RESULTS: The plasma level of Neu5Ac was significantly higher in the AF group than in the control group (107.66 ± 47.50 vs 77.87 ± 39.09 ng/ml; P < 0.05); the left atrial diameters were positively correlated with the plasma Neu5Ac level (R = 0.255; P < 0.05). The plasma Neu5Ac level (R = 0.368; P < 0.05) and the left atrial diameters (R = 0.402; P < 0.05) were positively correlated with AF history times. Neu5Ac (odds ratio 1.018, 95% CI 1.003-1.032; P < 0.05) and the left atrial diameter (odds ratio 1.142, 95% CI 1.020-1.280; P < 0.05) were independent risk factors for AF in multivariate regression analysis. CONCLUSIONS: Serum Neu5Ac is associated with atrial fibrillation, and the mechanism may involve left atrial enlargement.

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.

Low testosterone level in middle-aged male patients with coronary artery disease.

BACKGROUND: Endogenous testosterone has been shown to provide a protective role in the development of cardiovascular diseases in men. This study investigated the changes of testosterone level and its relationship to the severity of coronary artery stenosis in middle-aged men with coronary artery disease (CAD). METHODS: Serum testosterone concentration was measured in 87 middle-aged men patients with CAD including stable angina pectoris (SAP), unstable angina pectoris (USAP) and acute myocardial infarction (AMI). All patients underwent coronary angiography and the severity of coronary stenosis was estimated by the Gensini coronary score. The patients with the severity of coronary artery stenosis of less than 50% served as control group. RESULTS: The levels of testosterone in SAP group (488.2 ± 96.8ng/dl), USAP group (411.6 ± 128.6ng/dl) and AMI group (365.3 ± 116.6ng/dl) were significantly lower than that in control group (562.8 ± 110.2ng/dl) (all p<0.05). When compared with another group among SAP, USAP and AMI groups, the level of testosterone in the AMI group was the lowest, the USAP group was the median while the SAP group was the highest (all p<0.05). There was a significant correlation between angiographic Gensini score and testosterone level (n=87, r=-0.513, p<0.05). Multiple regression analysis found that testosterone and BMI were independent predictors for CAD (testosterone: odds ratio 0.311, 95% confidence interval 0.174-0.512; BMI: odds ratio 1.905, 95% confidence interval 1.116-2.973). CONCLUSION: The present study showed that middle-aged male patients with CAD present a lower level of serum testosterone and the testosterone level was negatively correlated with the severity of coronary artery stenosis.