Percutaneous coronary intervention vs . medical therapy in patients on dialysis with coronary artery disease in China.

BACKGROUND: The available evidence regarding the benefits of percutaneous coronary intervention (PCI) on patients receiving dialysis with coronary artery disease (CAD) is limited and inconsistent. This study aimed to evaluate the association between PCI and clinical outcomes as compared with medical therapy alone in patients undergoing dialysis with CAD in China. METHODS: This multicenter, retrospective study was conducted in 30 tertiary medical centers across 12 provinces in China from January 2015 to June 2021 to include patients on dialysis with CAD. The primary outcome was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Secondary outcomes included all-cause death, the individual components of MACE, and Bleeding Academic Research Consortium criteria types 2, 3, or 5 bleeding. Multivariable Cox proportional hazard models were used to assess the association between PCI and outcomes. Inverse probability of treatment weighting (IPTW) and propensity score matching (PSM) were performed to account for potential between-group differences. RESULTS: Of the 1146 patients on dialysis with significant CAD, 821 (71.6%) underwent PCI. After a median follow-up of 23.0 months, PCI was associated with a 43.0% significantly lower risk for MACE (33.9% [ n  = 278] vs . 43.7% [ n  = 142]; adjusted hazards ratio 0.57, 95% confidence interval 0.45-0.71), along with a slightly increased risk for bleeding outcomes that did not reach statistical significance (11.1% vs . 8.3%; adjusted hazards ratio 1.31, 95% confidence interval, 0.82-2.11). Furthermore, PCI was associated with a significant reduction in all-cause and cardiovascular mortalities. Subgroup analysis did not modify the association of PCI with patient outcomes. These primary findings were consistent across IPTW, PSM, and competing risk analyses. CONCLUSION: This study indicated that PCI in patients on dialysis with CAD was significantly associated with lower MACE and mortality when comparing with those with medical therapy alone, albeit with a slightly increased risk for bleeding events that did not reach statistical significance.

Comprehensive Investigation into the Impact of Degradation of Recycled Polyethylene and Recycled Polypropylene on the Thermo-Mechanical Characteristics and Thermal Stability of Blends.

The impact of degradation on plastics is a critical factor influencing their properties and behavior, particularly evident in polyethylene (PE) and polypropylene (PP) and their blends. However, the effect of photoaging and thermal degradation, specifically within recycled polyethylene (rPE) and recycled polypropylene (rPP), on the thermo-mechanical and thermostability aspects of these blends remains unexplored. To address this gap, a range of materials, including virgin polyethylene (vPE), recycled polyethylene (rPE), virgin polypropylene (vPP), recycled polypropylene (rPP), and their blends with different ratios, were comprehensively investigated. Through a systematic assessment encompassing variables such as melting flow index (MFI), functional groups, mechanical traits, crystallization behavior, microscopic morphology, and thermostability, it was found that thermo-oxidative degradation generated hydroxyl and carboxyl functional groups in rPE and rPP. Optimal mechanical properties were achieved with a 6:4 mass ratio of rPE to rPP, as validated by FTIR spectroscopy and microscopic morphology. By establishing the chemical model, the changes in the system with an rPE-rPP ratio of 6:4 and 8:2 were monitored by the molecular simulation method. When the rPE-rPP ratio was 6:4, the system's energy was lower, and the number of hydrogen bonds was higher, which also confirmed the above experimental results. Differential scanning calorimetry revealed an increased crystallization temperature in rPE, a reduced crystallization peak area in rPP, and a diminished crystallization capacity in rPE/rPP blends, with rPP exerting a pronounced influence. This study plays a pivotal role in enhancing recycling efficiency and reducing production costs for waste plastics, especially rPE and rPP-the primary components of plastic waste. By uncovering insights into the degradation effects and material behaviors, our research offers practical pathways for more sustainable waste management. This approach facilitates the optimal utilization of the respective performance characteristics of rPE and rPP, enabling the development of highly cost-effective rPE/rPP blend materials and promoting the efficient reuse of waste materials.

Cypher/ZASP drives cardiomyocyte maturation via actin-mediated MRTFA-SRF signalling.

Rationale: Cardiomyocytes (CMs) undergo dramatic structural and functional changes in postnatal maturation; however, the regulatory mechanisms remain greatly unclear. Cypher/Z-band alternatively spliced PDZ-motif protein (ZASP) is an essential sarcomere component maintaining Z-disc stability. Deletion of mouse Cypher and mutation in human ZASP result in dilated cardiomyopathy (DCM). Whether Cypher/ZASP participates in CM maturation and thereby affects cardiac function has not been answered. Methods: Immunofluorescence, transmission electron microscopy, real-time quantitative PCR, and Western blot were utilized to identify the role of Cypher in CM maturation. Subsequently, RNA sequencing and bioinformatics analysis predicted serum response factor (SRF) as the key regulator. Rescue experiments were conducted using adenovirus or adeno-associated viruses encoding SRF, both in vitro and in vivo. The molecular mechanisms were elucidated through G-actin/F-actin fractionation, nuclear-cytoplasmic extraction, actin disassembly assays, and co-sedimentation assays. Results: Cypher deletion led to impaired sarcomere isoform switch and morphological abnormalities in mitochondria, transverse-tubules, and intercalated discs. RNA-sequencing analysis revealed significant dysregulation of crucial genes related to sarcomere assembly, mitochondrial metabolism, and electrophysiology in the absence of Cypher. Furthermore, SRF was predicted as key transcription factor mediating the transcriptional differences. Subsequent rescue experiments showed that SRF re-expression during the critical postnatal period effectively rectified CM maturation defects and notably improved cardiac function in Cypher-depleted mice. Mechanistically, Cypher deficiency resulted in the destabilization of F-actin and a notable increase in G-actin levels, thereby impeding the nuclear localisation of myocardin-related transcription factor A (MRTFA) and subsequently initiating SRF transcription. Conclusion: Cypher/ZASP plays a crucial role in CM maturation through actin-mediated MRTFA-SRF signalling. The linkage between CM maturation abnormalities and the late-onset of DCM is suggested, providing further insights into the pathogenesis of DCM and potential treatment strategies.

The combined effect of triglyceride-glucose index and high-sensitivity C-reactive protein on cardiovascular outcomes in patients with chronic coronary syndrome: A multicenter cohort study.

BACKGROUND: The triglyceride-glucose (TyG) index and high-sensitivity C-reactive protein (hsCRP) are the commonly used biomarkers for insulin resistance and systemic inflammation, respectively. We aimed to investigate the combined association of TyG and hsCRP with the major adverse cardiovascular events (MACE) in patients with chronic coronary syndrome (CCS). METHODS: A total of 9421 patients with CCS were included in this study. The primary endpoint was defined as a composite of MACE covering all-cause death, nonfatal myocardial infarction, and revascularization. RESULTS: During the 2-year follow-up period, 660 (7.0%) cases of MACE were recorded. Participants were divided equally into three groups according to TyG levels. Compared with the TyG T1 group, the risk of MACE was significantly higher in the TyG T3 group. It is noteworthy that among patients in the highest tertile of TyG, hsCRP >3 mg/L was significantly associated with an increased risk of MACE, whereas the results were not significant in the medium to low TyG groups. When patients were divided into six groups according to hsCRP and TyG, the Cox regression analysis showed that patients in the TyG T3 and hsCRP >3 mg/L group had a significantly higher risk of MACE than those in the TyG T1 and hsCRP ≤3 mg/L group. However, no significant interaction was found between TyG and hsCRP on the risk of MACE. CONCLUSION: Our study suggests that the concurrent assessment of TyG and hsCRP may be valuable in identifying high-risk populations and guiding management strategies among CCS patients.

Modifiable risk factors mediating the impact of educational inequality on heart failure: A Mendelian randomization study.

BACKGROUND: Heart failure (HF) is a rapidly growing global disease burden with high mortality rates. We aimed to utilize mendelian randomization (MR) analyses to investigate the association between educational attainment (EA) and HF, and to evaluate the contribution of modifiable risk factors as mediators. METHODS: We applied a two-sample MR approach based on the largest genome-wide association studies (GWAS) to investigate the causal relationship between EA and HF. Data collection was conducted in July 2023. We then conducted mediation analyses to explore whether body mass index (BMI), blood pressure, and type 2 diabetes mellitus (T2DM) mediate the effect of EA on HF, and utilized multivariable MR to estimate the proportion of mediation attributed to these factors. RESULTS: Genetically predicted 3.4 years of additional education was associated with a decrease in the risk of HF (OR 0.76 for each 3.4 years of schooling; 95% CI 0.72, 0.81). BMI, T2DM, systolic blood pressure, and diastolic blood pressure mediated 40.82% (95% CI: 28.86%, 52.77%), 18.00% (95% CI: 12.10%, 23.90%), 11.60% (95% CI: 7.63%, 15.56%), and 7.80% (95% CI: 4.63%, 10.96%) of the EA-HF association, respectively. All risk factors combined were estimated to mediate 63.81% (95% CI: 45.91%, 81.71%) of the effect of EA on HF. CONCLUSION: Higher EA has a protective effect against the risk of HF, and potential mechanisms may include regulation of BMI, blood pressure, and blood glucose. Further research is needed to understand whether interventions targeting these factors could influence the association between EA and HF risk.

Altered lipid metabolism promoting cardiac fibrosis is mediated by CD34+ cell-derived FABP4+ fibroblasts.

Hyperlipidemia and hypertension might play a role in cardiac fibrosis, in which a heterogeneous population of fibroblasts seems important. However, it is unknown whether CD34+ progenitor cells are involved in the pathogenesis of heart fibrosis. This study aimed to explore the mechanism of CD34+ cell differentiation in cardiac fibrosis during hyperlipidemia. Through the analysis of transcriptomes from 50,870 single cells extracted from mouse hearts and 76,851 single cells from human hearts, we have effectively demonstrated the evolving cellular landscape throughout cardiac fibrosis. Disturbances in lipid metabolism can accelerate the development of fibrosis. Through the integration of bone marrow transplantation models and lineage tracing, our study showed that hyperlipidemia can expedite the differentiation of non-bone marrow-derived CD34+ cells into fibroblasts, particularly FABP4+ fibroblasts, in response to angiotensin II. Interestingly, the partial depletion of CD34+ cells led to a notable reduction in triglycerides in the heart, mitigated fibrosis, and improved cardiac function. Furthermore, immunostaining of human heart tissue revealed colocalization of CD34+ cells and fibroblasts. Mechanistically, our investigation of single-cell RNA sequencing data through pseudotime analysis combined with in vitro cellular studies revealed the crucial role of the PPARγ/Akt/Gsk3ß pathway in orchestrating the differentiation of CD34+ cells into FABP4+ fibroblasts. Through our study, we generated valuable insights into the cellular landscape of CD34+ cell-derived cells in the hypertrophic heart with hyperlipidemia, indicating that the differentiation of non-bone marrow-derived CD34+ cells into FABP4+ fibroblasts during this process accelerates lipid accumulation and promotes heart failure via the PPARγ/Akt/Gsk3ß pathway.

Midterm Outcomes of Percutaneous Intramyocardial Septal Radiofrequency Ablation for Hypertrophic Cardiomyopathy: A Single-Center, Observational Study.

BACKGROUND: Percutaneous intramyocardial septal radiofrequency ablation (PIMSRA) has been reported to be safe and effective at midterm follow-up to treat drug-refractory hypertrophic obstructive cardiomyopathy in a single center. However, data from other centers are lacking. This retrospective cohort study aimed to investigate the efficacy and safety of PIMSRA from another independent center. METHODS AND RESULTS: PIMSRA was performed in 76 patients with hypertrophic obstructive cardiomyopathy in our center from April 2020 to June 2023. The primary outcome was the reduction of left ventricular outflow tract gradient after 6 months or more post-PIMSRA. Secondary outcomes were periprocedural major adverse clinical events. Sixty-one patients returned to the hospital for follow-up 6 to 30 (median, 14) months after the procedure. At the last follow-up of the 61 patients, the maximum septal thickness decreased from a median of 23.6 (interquartile range, 20.5-26.4) to 19.1 (interquartile range, 16.0-22.1) mm (P<0.001) and the left ventricular outflow tract peak gradient at rest decreased from a median of 70.0 (interquartile range, 29.1-107.5) to 20.0 (interquartile range, 10.8-48.8) mm Hg (P<0.001). The percentage of patients with symptoms of New York Heart Association functional class III/IV decreased from 51% to 0%. Of all 76 patients, there was no in-hospital or 30-day death, no right or left branch block, and no permanent pacemaker implantation. Six (8%) patients had pericardial effusion, with 1 experiencing cardiac tamponade and ventricular fibrillation, and 1 (1%) patient developed septal branch aneurysm that was treated with coil occlusion. CONCLUSIONS: PIMSRA allows for the reduction in the left ventricular outflow tract gradient and enhances symptomatic improvement, with a limited incidence of adverse events and complications among patients with hypertrophic obstructive cardiomyopathy.

Percutaneous endocardial septal radiofrequency ablation on syncope in patients with hypertrophic obstructive cardiomyopathy: a short-term safety and efficacy study.

Background: Syncope is a serious consequence in patients with hypertrophic obstructive cardiomyopathy (HOCM). Percutaneous endocardial septal radiofrequency ablation (PESA) has emerged as a promising intervention to alleviate symptoms and enhance the quality of life for HOCM patients. However, little is known about the effects of PESA on syncope in HOCM. The authors aimed to study the effects of PESA on syncope in patients with HOCM. Materials and methods: Nineteen patients with HOCM and syncope were enrolled. The left ventricular outflow tract gradient (LVOTG) of the patients was more than 50 mmHg despite medication. The participants underwent PESA under the guidance of intracardiac echocardiography (ICE) combined with a three-dimensional electrophysiological mapping system. The patients were followed for 3 (3-5.5) months. Results: The mean age of the patients was 54.8±13.7 years. Out of the 19 participants, 7 (37%) were females. During the follow-up, the syncope was completely alleviated in 14 patients (73.7%) or the syncope episodes were reduced greater than or equal to 80% in 16 patients (84.2%). The mean NYHA functional class significantly improved from 2.2±0.7 at baseline to 1.7±0.6 during follow-up (P=0.002). The LVOTG and septal thickness showed a decreasing trend from baseline to follow-up (LVOTG: P=0.083, septal thickness: P=0.086). Conclusion: The authors' investigation provides evidence supporting the effectiveness of PESA in reducing syncope episodes in patients with HOCM.

CircARCN1 aggravates atherosclerosis by regulating HuR-mediated USP31 mRNA in macrophages.

AIMS: Circular RNAs (circRNAs) are considered important regulators of biological processes, but their impact on atherosclerosis development, a key factor in coronary artery disease (CAD), has not been fully elucidated. We aimed to investigate their potential use in patients with CAD and the pathogenesis of atherosclerosis. METHODS AND RESULTS: Patients with stable angina (SA) or acute coronary syndrome (ACS) and controls were selected for transcriptomic screening and quantification of circRNAs in blood cells. We stained carotid plaque samples for circRNAs and performed gain- and loss-of-function studies in vitro. Western blots, protein interaction analysis, and molecular approaches were used to perform the mechanistic study. ApoE-/- mouse models were employed in functional studies with adeno-associated virus-mediated genetic intervention. We demonstrated elevated circARCN1 expression in peripheral blood mononuclear cells from patients with SA or ACS, especially in those with ACS. Furthermore, higher circARCN1 levels were associated with a higher risk of developing SA and ACS. We also observed elevated expression of circARCN1 in carotid artery plaques. Further analysis indicated that circARCN1 was mainly expressed in monocytes and macrophages, which was also confirmed in atherosclerotic plaques. Our in vitro studies provided evidence that circARCN1 affected the interaction between HuR and ubiquitin-specific peptidase 31 (USP31) mRNA, resulting in attenuated USP31-mediated NF-κB activation. Interestingly, macrophage accumulation and inflammation in atherosclerotic plaques were markedly decreased when circARCN1 was knocked down with adeno-associated virus in macrophages of ApoE-/- mice, while circARCN1 overexpression in the model exacerbated atherosclerotic lesions. CONCLUSIONS: Our findings provide solid evidence macrophagic-expressed circARCN1 plays a role in atherosclerosis development by regulating HuR-mediated USP31 mRNA stability and NF-κB activation, suggesting that circARCN1 may serve as a factor for atherosclerotic lesion formation.

A novel approach to terminate roof-dependent atrial flutter with epicardial conduction through septopulmonary bundle.

Atrial flutter, a prevalent cardiac arrhythmia, is primarily characterized by reentrant circuits in the right atrium. However, atypical forms of atrial flutter present distinct challenges in terms of diagnosis and treatment. In this study, we examine three noteworthy clinical cases of atypical atrial flutter, which offer compelling evidence indicating the implication of the lesser-known Septopulmonary Bundle (SPB). This inference is based on the identification of distinct electrocardiographic patterns observed in these patients and their favorable response to catheter ablation, which is a standard treatment for atrial flutter. Remarkably, in each case, targeted ablation at the anterior portion of the left atrial roof effectively terminated the arrhythmia, thus providing further support for the hypothesis of SPB involvement. These insightful observations shed light on the potential significance of the SPB in the etiology of atypical atrial flutter and introduce a promising therapeutic target. We anticipate that this paper will stimulate further exploration into the role of the SPB in atrial flutter and pave the way for the development of targeted ablation strategies.

Effect of SARA Fractions on Fatigue Properties of Hard Asphalt.

The fatigue performance of hard asphalt is an important factor that affects the service life of asphalt pavement. In order to comprehensively explore the influence of chemical components on the fatigue performance of hard asphalt, and to eliminate the chemical instability between the microstructure of asphalt from different oil sources, seven kinds of hard asphalt were designed and prepared with saturates, aromatics, resins, and asphaltenes (SARA) extracted from the same hard asphalt. Rheological, time sweep and linear amplitude sweep (LAS) tests were carried out to evaluate the fatigue properties. The results show that the complex modulus of asphalt binds increased rapidly with an increase of asphaltene and resins and that the colloidal structure was strengthened, which would increase the fatigue factor. In the time sweep test, the strength of the colloidal structure significantly affected the fatigue life, and the fatigue life was different under different test stresses. In the viscoelastic continuum damage (VECD) model, the cumulative damage was related to the modulus, while with the increase of asphaltene and resins, the fatigue life showed a trend of first increasing and then decreasing. The linear regression analysis showed that the fatigue life of hard asphalt had a good correlation with strain sensitivity. This study investigated the applicability of different fatigue evaluation methods and revealed the influence of four components on the fatigue properties of hard asphalt. The results provide significant insights in the improvement of the fatigue performance of both hard asphalt and corresponding mixtures.

Sodium catalytic phenylpentazole cracking: a theoretical study.

This work presents an in-depth investigation into the cracking reaction mechanism of phenylpentazole (C6H5N5) under the catalytic influence of sodium metal, utilizing density functional theory. The geometries of the reactants, transition states, intermediates, and products are meticulously optimized employing the GGA/PW91/DNP level of theory. Also, a rigorous analysis is undertaken, encompassing various key factors including configuration parameters, Mulliken charges, densities of states, and reaction energies. Three distinct reaction pathways are comprehensively examined, shedding light on the intricate details and intricacies of each pathway. The results show that a remarkable outcome in which the activation energy of the C6H5N5 cracking reaction releases N2, facilitated by catalytic metal Na, reveals a strikingly reduced value of a mere 5.2 kcal mol-1 compared to the previously reported activation energies ranging from 20 to 30 kcal mol-1. Evidently, this significantly lowered barrier can be readily surpassed at typical room temperatures, exhibiting practical applicability. Notably, the alkali metal Na effectively serves as a catalyst, successfully diminishing the activation energy required for N2 production through the pyrolysis of pentazole compounds. This breakthrough discovery provides a theoretical basis for experimental research on the low-temperature cracking of pentazole compounds. It also offers valuable insights for the development and application of new high energy density materials, contributing to the creation of a green and low-carbon circular economic system.

TUDCA alleviates atherosclerosis by inhibiting AIM2 inflammasome and enhancing cholesterol efflux capacity in macrophage.

Cholesterol efflux capacity (CEC) dysfunction in macrophages is important in atherosclerosis. However, the mechanism underlying CEC dysfunction remains unclear. We described the characteristics of ATF4 and inflammasome activation in macrophages during atherosclerosis through scRNA sequencing analysis. Then model of hyperlipemia was established in ApoE-/- mice; some were treated with tauroursodeoxycholic acid (TUDCA). TUDCA decreased the ATF4, Hspa, and inflammasome activation, reduced plaque area of the artery, and promoted CEC in macrophages. Furthermore, TUDCA abolished oxLDL-induced foam cell formation by inhibiting activation of the PERK/eIF2α/ATF4 and AIM2 inflammasome in macrophages. Further assays revealed ATF4 binding to AIM2 promoter, promoting its transcriptional activity significantly. Then we discovered that ATF4 affected AIM2-mediated foam cell formation by targeting ABCA1, which could be blocked by TUDCA. Our study demonstrated that TUDCA alleviates atherosclerosis by inhibiting AIM2 inflammasome and enhancing CEC of macrophage, which provided possibilities for the development of therapies.

Clinical outcomes of radiofrequency catheter ablation guided by intracardiac echocardiography for Chinese atrial fibrillation patients: a single-center, retrospective study.

Background: Intracardiac echocardiography (ICE) is a novel technology with certain advantages in treatment of atrial fibrillation (AF), yet there is limited research on the use of ICE in radiofrequency ablation for AF treatment in China. The aim of this study was to investigate the total fluoroscopy time and dose, safety, and effectiveness of ICE guided vs. traditional fluoroscopy (non-ICE) guided radiofrequency ablation for AF in China. Methods: We conducted a single-center retrospective analysis of patients who underwent ICE or traditional fluoroscopy-guided radiofrequency ablation for AF. The primary endpoint of this study was total fluoroscopy time, and the secondary endpoints included total fluoroscopy dose, acute surgery failure, transseptal puncture time, ablation time, total procedure time, and 6-month surgery success (no AF recurrence or atrial flutter). As an exploratory analysis, outcomes of interest by different types of AF were examined. Results: A total of 97 patients were included in the analysis. Forty-eight were in the ICE group and 49 were in the non-ICE group with comparable demographic and clinical characteristics at the baseline. None of patients experienced acute surgery failure with no major procedure-related complications occurred. The fluoroscopic time and dose were significantly lower in the ICE group compared to the non-ICE group (0.00 vs. 9.67±4.88 min, P<0.001; 0.00 vs. 77.10±44.28 mGy/cm2, P<0.001, respectively). There were no statistically significant differences in transseptal puncture time, ablation time and total procedure time between the two groups. There were two AF recurrences observed during the 6-month follow-up in each group (P>0.99). Conclusions: ICE significantly reduced the fluoroscopic time and dose for radiofrequency catheter ablation in AF patients. There were no significant differences in safety or effectiveness outcomes between the ICE and non-ICE groups.

Genetically predicted systemic inflammation and the risk of atrial fibrillation: A bidirectional two-sample Mendelian randomization study.

Background: Systemic inflammation has been proposed to be associated with the incidence of atrial fibrillation (AF), but whether it is a cause or a consequence of AF remains uncertain. We sought to explore the causal associations between systemic inflammation and AF using bidirectional Mendelian randomization (MR) analysis. Methods: Independent genetic variants strongly associated with AF were selected as instrumental variables from the largest genome-wide association study (GWAS) with up to 1,030,836 individuals. Regarding inflammation traits, genetic associations with 41 inflammatory cytokines and 5 inflammatory biomarkers were obtained from their corresponding GWASs databases. Effect estimates were primarily evaluated using the inverse-variance weighted (IVW) method, supplemented by sensitivity analyses using MR-Egger, weighted median, and MR-PRESSO methods. Results: In our initial MR analyses, we observed suggestive associations of genetically predicted interleukin-17 (IL-17), interleukin-2 receptor subunit alpha (IL-2rα), and procalcitonin (PCT) with AF. One standard deviation (SD) increase in IL-17, IL-2rα, and PCT caused an increase in AF risk by 6.3 % (OR 1.063, 95 %CI 1.011---1.118, p = 0.018), 4.9 % (OR 1.049, 95 %CI 1.007---1.094, p = 0.023) and 3.4 % (OR 1.034, 95 %CI 1.005---1.064, p = 0.022), respectively. Furthermore, our reverse MR analyses indicated that genetically predicted AF contributed to a suggestive increase in the levels of macrophage inflammatory protein-1ß (MIP1ß) (ß 0.055, 95 %CI 0.006 to 0.103, p = 0.028), while a decrease in the levels of fibrinogen (Fbg) (ß -0.091, 95 %CI -0.140 to -0.041, p < 0.001), which remained significant after multiple test correction. Conclusions: Our MR study identified several inflammatory biomarkers with suggestive causal associations regarding the upstream and downstream regulation of AF occurrence, offering new insights for therapeutic exploitation of AF. Further research is required to validate the underlying link between systemic inflammation and AF in larger cohorts.

Focal atrial tachycardias originating from the aorta-mitral continuity: Anatomical and electrophysiological characteristics.

BACKGROUND: The aorta-mitral annulus conjunction (AMC) is an uncommon site of origin of focal atrial tachycardias (ATs). Hence, the electrophysiological and ablation target characteristics are poorly described. OBJECTIVE: The purpose of this study was to describe the characteristics of AMC ATs in detail. METHODS: The study enrolled 650 patients with ATs, 21 (3.2%) of whom had ATs originating from the AMC. A comprehensive evaluation, including electrocardiography, electrophysiology study, computed tomography scan, and intracardiac echocardiography, was performed. RESULTS: The majority (19, 90.5%) of ATs occurred spontaneously. The mean age of this group was 48.9 ± 21.6 years, with 12 being female (57.1%). Seventeen patients had a typical biphasic P wave with a prominent positive component. The earliest activation site in the right atrium was near the His bundle, with average activation -10.3 ± 6.0 ms preceding the P wave. The successful ablation targets were distributed as follows: 1 case at 9 o'clock, 6 cases at 10 o'clock, 7 cases at 11 o'clock, 6 cases at 12 o'clock, and 1 case in the left coronary cusp. The local AMC potential differed from the commonly perceived annular potential and was characterized by a prominent A wave and a smaller V wave (atrial-to-ventricular ratio > 1). The angle of encroachment on the left atrial anterior wall, compressed by the left coronary cusp, was significantly smaller in the AMC ATs group than in the control group consisted of 40 patients who underwent coronary artery CT scans because of the chest pain but without atrial arrhythmias were randomly selected, which may have contributed to the arrhythmia substrate (141.7° ± 11.5° vs 155.2° ± 13.9°; P = .026). CONCLUSION: A new strategy for mapping AMC ATs has been introduced. The ablation target should have an atrial-to-ventricular ratio of >1.

Prognostic implications of premature ventricular contractions and non-sustained ventricular tachycardia in light-chain cardiac amyloidosis.

AIMS: Premature ventricular contractions (PVC) and non-sustained ventricular tachycardia (NSVT) are commonly observed in light chain cardiac amyloidosis (AL-CA), but their association with prognosis is still unclear. We aimed to evaluate the prognostic value of PVCs and NSVT in patients with moderate-to-advanced AL-CA. METHODS AND RESULTS: We retrospectively included patients with AL-CA at modified 2004 Mayo stages II-IIIb between February 2014 and December 2020. Twenty-four-hour Holter recordings were assessed on admission. The outcomes included (i) new onset of adverse ventricular arrhythmia (VA) or sudden cardiac death (SCD) and (ii) cardiac death during follow-up. Of the 143 patients studied (60.41 ± 11.06 years, male 64.34%), 132 (92.31%) had presence of PVC, and 50 (34.97%) had NSVT on Holter. Twelve (8.4%) patients died in hospital and 131 patients were followed up (median 24.4 months), among whom 71 patients had cardiac death, and 15 underwent adverse VA/SCD. NSVT [hazard ratio (HR): 13.57, 95% confidence interval (CI): 3.06-60.18, P < 0.001], log-transformed PVC counts (HR: 1.46, 95%CI: 1.15-1.86, P = 0.002) and PVC burden (HR: 1.43 95%CI:1.14-1.80, P = 0.002) were predictive of new onset of adverse VA/SCD. The highest tertile of PVC counts (HR: 2.33, 95%CI: 1.27-4.28, P = 0.006) and PVC burden (HR: 2.58, 95%CI: 1.42-4.69, P = 0.002), rather than NSVT (HR: 1.16, 95%CI: 0.67-1.98, P = 0.603), was associated with cardiac death. Higher PVC counts/burden provided incremental value on modified 2004 Mayo stage in predicting cardiac death, with C index increasing from 0.681 to 0.712 and 0.717, respectively (P values <0.05). CONCLUSION: PVC count, burden, and NSVT significantly correlated with adverse VA/SCD during follow-up in patients with AL-CA. Higher PVC counts/burdens added incremental value for predicting cardiac death.

Development and validation of a novel score for predicting perioperative major adverse cardiovascular events in patients with stable coronary artery disease undergoing noncardiac surgery.

BACKGROUND: A model developed specifically for stable coronary artery disease (SCAD) patients to predict perioperative major adverse cardiovascular events (MACE) has not been previously reported. METHODS: The derivation cohort consisted of 5780 patients with SCAD undergoing noncardiac surgery at the First Affiliated Hospital of Zhejiang University School of Medicine, from January 1, 2013 until May 31, 2021. The validation cohort consisted of 2677 similar patients from June 1, 2021 to May 31, 2023. The primary outcome was a composite of MACEs (death, resuscitated cardiac arrest, myocardial infarction, heart failure, and stroke) intraoperatively or during hospitalization postoperatively. RESULTS: Six predictors, including Creatinine >90 µmol/L, Hemoglobin <110 g/L, Albumin <40 g/L, Leukocyte >10 ×109/L, high-risk Surgery (general abdominal or vascular), and American Society of Anesthesiologists (ASA) class (III or IV), were selected in the final model (CHALSA score). Each patient was assigned a CHALSA score of 0, 1, 2, 3, or > 3 according to the number of predictors present. The incidence of perioperative MACEs increased steadily across the CHALSA score groups in both the derivation (0.5%, 1.4%, 2.9%, 6.8%, and 23.4%, respectively; p < 0.001) and validation (0.3%, 1.5%, 4.1%, 9.2%, and 29.2%, respectively; p < 0.001) cohorts. The CHALSA score had a higher discriminatory ability than the revised cardiac risk index (C statistic: 0.827 vs. 0.695 in the validation dataset; p < 0.001). CONCLUSIONS: The CHALSA score showed good validity in an external dataset and will be a valuable bedside tool to guide the perioperative management of patients with SCAD undergoing noncardiac surgery.

The China Hypertrophic Cardiomyopathy Project (CHCMP): The Rationale and Design of a Multicenter, Prospective, Registry Cohort Study.

Hypertrophic cardiomyopathy (HCM) is associated with adverse outcomes, such as heart failure, arrhythmia, and mortality. Sudden cardiac death (SCD) is a common cause of death in HCM patients, and identification of patients at a high risk of SCD is crucial in clinical practice. The China Hypertrophic Cardiomyopathy Project is a hospital-based, multicenter, prospective, registry cohort study of HCM patients, covering a total of 3000 participants and with a 5-year follow-up plan. A large number of demographic characteristics and clinical data will be fully collected to identify prognostic factors in Chinese HCM patients. Furthermore, the main purpose of this study is to integrate demographic and clinical characteristics to establish new 5-year SCD risk predictive equations for Chinese HCM patients by the use of machine learning technologies. The project has crucial clinical significance for risk stratification and determination of HCM patients with high risk of adverse outcomes. CLINICAL TRIALS REGISTRATION: ChiCTR2300070909.