BACKGROUND:The 'out of hours effect' applies to patients undergoing surgery during night shifts, weekends or holidays, who face higher risks of complications and mortality. The 7-day service policy was implemented to ensure consistent healthcare delivery. OBJECTIVE:To assess the association between surgical time and incidence of major peri-operative adverse cardiac and cerebral events (MACCE) and also the length of hospital stay, and whether this has changed following the implementation of the 7-day service. DESIGN:Nested case-control study. SETTING:Single-centre university hospital. Retrospective enrolment from January 2018 to December 2021. PATIENTS:The study included 2543 cases and 10 683 controls. MAIN OUTCOME MEASURES:The primary outcome was peri-operative MACCE. Patients who developed MACCE after noncardiac surgery were compared with controls randomly selected from those without MACCE (1 : 4 ratio). RESULTS:Night-shift procedures were associated with higher incidence of peri-operative MACCE (28.7 vs. 18.2%, P < 0.001), longer hospital stays (172 vs. 155 h, P < 0.01), and higher costs (48 529 vs. 37 962 yuan, P < 0.001). In multivariable logistic regression, night-shift surgery remained independently associated with MACCE [fully adjusted odds ratio (OR) 1.54, 95% confidence interval (CI), 1.3 to 1.8; P < 0.001]. Weekend surgery was not significantly associated with MACCE after full adjustment (OR 1.15, 95% CI, 0.96 to 1.38; P = 0.13), and results were consistent in a sensitivity model including both night-shift and weekend surgery (night shift OR 1.54, 95% CI, 1.3 to 1.82, P < 0.001; weekend OR 1.17, 95% CI, 0.97 to 1.4, P = 0.09). Following implementation of the 7-day service policy, night-shift procedures decreased [16.1% prepolicy vs. 3.7% postpolicy; standardised mean difference (SMD) 0.42] and weekend procedures increased (5.5 vs. 13.3%; SMD 0.27). In the postpolicy period, weekend surgery was associated with a shorter hospital stay (139 vs. 160 h, P < 0.001) without an increase in MACCE (18.7 vs. 19.4%, P = 0.53). CONCLUSION:Night-shift surgery was an independent risk factor for peri-operative MACCE in noncardiac surgery patients. The 7-day service policy reduced night-shift procedures and increased those at weekends, without increasing the risk of MACCE. It was also associated with shorter hospital stays. TRIAL REGISTRATION:Chinese Clinical Trial Registry identifier: ChiCTR1900024645.

Particulate matter (PM) is known to accelerate atherosclerosis through systemic inflammation, yet its specific impact on local coronary inflammation remains poorly understood. This large-scale retrospective cohort study investigated the long-term effects of PM exposure on coronary inflammation as assessed by the pericoronary fat attenuation index (FAI). We analyzed 5528 participants undergoing coronary computed tomography angiography (CCTA), including a longitudinal subcohort of 656 individuals with serial scans. FAI values for the left anterior descending, left circumflex, and right coronary arteries were extracted using a deep-learning-based pipeline. Individual-level exposures to fine particulate with an aerodynamic diameter <2.5 μm (PM2.5), particulate matter with an aerodynamic diameter of less than 10 μm (PM10), and black carbon (BC) were estimated using a validated 1-km resolution spatiotemporal model. Results from generalized additive and linear mixed-effects models indicated that each interquartile range (IQR) increase in 1-year PM2.5, PM10, and BC exposure was associated with significant elevations in FAI across all vessels, such as increases of 7.57, 8.72, and 2.35 HU in the right coronary artery, respectively. Furthermore, longitudinal analysis revealed that IQR increases in pollutants corresponded to accelerated annual FAI progression. These associations were notably stronger among participants with hypertension, diabetes, or a history of smoking. In conclusion, among patients with suspected coronary artery disease, long-term exposure to PM is intrinsically linked to localized and progressive coronary inflammation. These findings provide a proximal toxicological link between ambient pollution and coronary pathophysiology, underscoring the urgency of integrating environmental determinants into cardiovascular risk assessment and prevention strategies for vulnerable populations.

Atherosclerotic cardiovascular disease (ASCVD), the primary cause of mortality worldwide, is distinguished by the development of atherosclerotic plaques due to lipid accumulation in the artery wall, ultimately resulting in a range of severe cardiovascular and cerebrovascular complications. In recent years, aggregation-induced emission luminogens (AIEgens), which possess the advantages of fluorescence enhancement in aggregated states, exceptional photostability, and finely tunable biocompatibility, have emerged as a promising candidate for the diagnosis and treatment of ASCVD. This review systematically summarizes the research advancements of AIEgens in ASCVD over the past five years, mainly including the properties of AIEgens and the design for ASCVD management, the application of AIEgens in ASCVD biomarkers sensing, imaging and treatment of ASCVD. Additionally, the existing challenges of AIEgens in ASCVD are discussed, and the prospects are also proposed.

Acute mountain sickness (AMS) is a major health issue for lowlanders when they ascend rapidly to altitudes above 2500 m. Thyroid hormones are essential for adaptive responses to the hypoxic environment of high altitude. However, there is limited evidence regarding the association between thyroid function and the prevalence of AMS. This study included 70 healthy euthyroid Chinese lowlanders who ascended from Beijing (44 m above sea level) to Lhasa (3650 m above sea level) by aircraft (flight time, approximately 5 h). The dataset was divided into a training set (80%) and a validation set (20%) for the development and validation of a prediction model. Thyroid hormones, demographic data and blood biochemical data were measured in the week before the ascent. The subjects in the training set were divided into an AMS group and a non‐AMS group based on the 2018 Lake Louise Acute Mountain Sickness Scale score. Thyroid hormones and thyroid hormone sensitivity indices were compared between the groups. Multivariable logistic regression analysis revealed that a higher baseline total triiodothyronine (TT3) level (odds ratio (OR) 2.474, 95% confidence interval (CI) 1.083–5.653) and a higher free triiodothyronine/free thyroxine (FT3/FT4) ratio (OR 3.427; 95% CI 1.266–9.280) were independent risk factors for development of AMS. The receiver‐operating characteristic and calibration curves showed that the model had good predictive ability and consistency in both the training and validation sets. In China, euthyroid lowlanders with a higher TT3 level or FT3/FT4 ratio are more susceptible to AMS after exposure to high altitudes.

Current diagnostic technique in direct identification of multi-site plaques and simultaneous assessment of plaque vulnerability remains a challenge, which is crucial for indicating the risk of atherosclerotic cardiovascular diseases (ASCVD). Herein, an osteopontin (OPN)-specific nanoprobe (OPN Ab-Au/FeNiPO4@ICG) with both multiple spectra optoacoustic tomography (MSOT) and computed tomography (CT) imaging, is constructed successfully realizing systemic screening of vulnerable plaque. OPN Ab-Au/FeNiPO4@ICG nanoprobe specifically targeted OPN-overexpressed foam cells and recognized the vulnerable plaque at the molecular level. In AS mice, CT imaging exhibits that OPN Ab-Au/FeNiPO4@ICG nanoprobe effectively avoid interference from calcification and accurately visualized AS plaque. MSOT functional imaging results reveals that after the injection of OPN Ab-Au/FeNiPO4@ICG nanoprobe, the carotid plaque exhibited a much higher MSOT signal than the aortic arch plaque (P = 0.0291). Further pathological analysis displays that the carotid plaque possessed a much higher vulnerability score (P = 0.0247), in agreement with the MSOT signals. More importantly, the linear regression analysis confirms the high correlation between the MSOT signals and plaque vulnerability with R = 0.7095 (P = 0.0216), demonstrating the potential of the proposed nanoprobe in systematic evaluation of plaque vulnerability. This work employs the dual-model nanoprobe strategy for both plaque localization and vulnerability assessment, greatly advancing the accurate diagnosis of ASCVD.

心血管疾病(cardiovascular disease,CVD)是全世界死亡的主要原因.研究表明表观遗传修饰在CVD的进展中起着重要作用.在几种已知的RNA修饰中,N6-甲基腺苷(N6-methyladenosine,m6A)RNA甲基化修饰是研究最多的RNA表观转录组修饰,该过程是动态的、可逆的,在mRNA代谢和各种生物活动中起着至关重要的作用.在这篇综述中,我们描述了 m6A甲基化的作用机制,总结了 m6A甲基化在CVD中的作用,包括动脉粥样硬化、心肌梗死、心力衰竭和糖尿病相关CVD等.m6A甲基化及其调控因子有望成为CVD的治疗靶点.

Heart failure with preserved ejection fraction (HFpEF) accounts for almost half of all heart failure (HF) cases worldwide. Unfortunately, its incidence is expected to continue to rise, and effective therapy to improve clinical outcomes is lacking. Numerous efforts currently directed towards the pathophysiology of human HFpEF are uncovering signal transduction pathways and novel therapeutic targets. The nitric oxide-cyclic guanosine phosphate-protein kinase G (NO-cGMP-PKG) axis has been described as an important regulator of cardiac function. Suppression of the NO-cGMP-PKG signalling pathway is involved in the progression of HFpEF. Therefore, the NO-cGMP-PKG signalling pathway is a potential therapeutic target for HFpEF. In this review, we aim to explore the mechanism of NO-cGMP-PKG in the progression of HFpEF and to summarize potential therapeutic drugs that target this signalling pathway.

Cardiac fibrosis, a significant pathological alteration following myocardial infarction (MI), remains enigmatic with respect to the role of cardiac endothelial cells (ECs). To elucidate the proteomic shifts in cardiac ECs accompanying MI-induced cardiac fibrosis, a standard MI mice model was established through ligation of the left anterior descending branch. Following 14 days of effective modeling, we isolated primary ECs from the hearts of both sham and MI models utilizing the CD31 microbeads sorting technique. Quantitative proteomics and bioinformatics methodologies, including tandem mass spectrometry, were employed to discern proteomic alterations in the primary endothelial cells of the experimental groups. Comprehensive analyses, including Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, functional enrichment analysis, and functional enrichment cluster analysis, revealed an up-regulation of proteins associated with extracellular matrix-receptor interaction pathway in cardiac fibrosis post-MI. Subsequent Western blot analysis confirmed the up-regulation of specific proteins involved in this pathway, namely collagen type VI alpha 2 (Col6α2), vitronectin (Vtn), and integrin beta (Itgβ). We conclude that the expression levels of Col6α2, Vtn, and Itgβ in primary ECs during the early stage of cardiac fibrosis, 14 days post-MI, were significantly elevated compared to the sham group (P < 0.05). This observation suggests that ECM-receptor interaction could potentially influence the progression of cardiac fibrosis following MI.

随着全球老龄化加剧,钙化性主动脉瓣膜疾病(calcified aortic valve disease,CAVD)已成为继冠心病、高血压之后的第三大心血管疾病.以往认为CAVD是一种退行性病变,但最新的研究提示该病的进展是一个主动的、可调节的过程.CAVD的具体发病机制仍不明确,考虑到瓣膜钙化是多种分子及机制共同参与的复杂过程,本文就主动脉瓣钙化的发病机制及抗钙化的研究进展作一综述.

Abstract Aims Takotsubo syndrome (TTS) is an acute reversible cardiac dysfunction that may occur during the peri‐operative period and among patients with serious illness. We aimed to evaluate the clinical characteristics, peri‐operative management, and prognosis of peri‐operative TTS (pTTS) and explore the factors associated with pTTS. Methods We conducted a retrospective nested case–control study using the database of patients who underwent in‐hospital non‐cardiac surgeries between January 2017 and December 2020 in Peking University Third hospital. Cases were adult patients diagnosed TTS at discharge who were matched with four controls based on operative types. Multivariable conditional logistic regression was used to identified the factors associated with pTTS. The area under the curve (AUC) was used to evaluate the diagnostic efficacy. Results Among the 128 536 patients underwent non‐cardiac surgery, 20 patients with pTTS and 80 patients without were enrolled in this study. The incidence of pTTS was about 0.016% in our centre. The median age of patients with pTTS was 52.5 (38.25, 76.25) years, although 90% of them were female. Fifty per cent (9 cases) of female patients were pre‐menopausal. Caesarean section has the highest proportion of pTTS (30% of the pTTS cases) with the incidence of caesarean section‐related pTTS of 0.06% in our centre. A high prevalence of non‐apical ballooning pattern of regional wall motion abnormality (seven cases, 35%) and a high mortality (two cases, 10%) were observed. Left ventricular ejection fraction (LVEF) of patients with pTTS was significantly decreased (41.7 ± 8.8%). In the acute phase, supportive treatments aiming to reduce life‐threatening complications were main treatment strategies. After receiving systematic treatment, significant improvements were observed in LVEF (63.1 ± 13.5%), with median recovery time of LVEF of 7.48 days. Leucocyte count [odds ratio (OR): 4.59; 95% confidence interval (CI): 1.10–19.15], haemoglobin (HGB) (OR: 10.52; 95% CI: 1.04–106.36), and the revised cardiac risk index (RCRI) score (OR: 6.30; 95% CI: 1.05–37.88) were the factors significantly associated with pTTS. The RCRI score performed poorly in the prediction of pTTS (AUC: 0.630; 95% CI: 0.525–0.735). After adding leucocyte count and HGB into the RCRI score, the AUC was significantly improved (AUC: 0.768; 95% CI: 0.671–0.865; P = 0.001). Conclusions Patients with pTTS have some differences compared with common TTS, including higher proportion of pre‐menopausal female, higher prevalence during caesarean section, higher prevalence of non‐apical ballooning pattern of regional wall motion abnormality, and higher mortality. The RCRI score performed poorly in the evaluation of pTTS. Adding HGB and leucocyte count into the RCRI score could significantly improve its predictive performance.

ω-3多不饱和脂肪酸(omega-3 polyunsaturated fatty acids,ω-3PUFAs)是从甲基碳起第1个双键位于第3碳与第4碳之间且含有多个双键的脂肪酸,人体自身无法产生,多来自植物种子及深海鱼类,因而归为必需脂肪酸.心力衰竭(简称心衰)指各种原因导致的心功能下降,以肺、体循环淤血为主要临床表现的综合征,是心脏疾病发展的终末阶段.其病因众多,病理生理机制复杂.近年来,尽管已有大量的临床试验及基础研究报道,但ω-3PUFAs对心衰的作用仍具有较大争议.本文总结了有关ω-3PUFAs和心衰的最新研究进展,试对其治疗心衰的研究作一综述.

AIMS:Evidence on the impacts of traffic-related air pollution (TRAP) on ST-segment elevation myocardial infarction (STEMI) events is limited. We aimed to assess the acute effects of TRAP exposure on the clinical onset of STEMI and related cardiac impairments. METHODS AND RESULTS:We recruited patients who were admitted for STEMI and underwent primary percutaneous coronary intervention at Peking University Third Hospital between 2014 and 2020. Indicators relevant to cardiac impairments were measured. Concomitantly, hourly concentrations of traffic pollutants were monitored throughout the study period, including fine particulate matter, black carbon (BC), particles in size ranges of 5-560 nm, oxides of nitrogen (NOX), nitrogen dioxide, and carbon monoxide. The mean (SD) age of participants was 62.4 (12.5) years. Daily average (range) concentrations of ambient BC and NOX were 3.9 (0.1-25.0) μg/m3 and 90.8 (16.6-371.7) μg/m3. Significant increases in STEMI risks of 5.9% (95% CI: 0.1, 12.0) to 21.9% (95% CI: 6.0, 40.2) were associated with interquartile range increases in exposure to TRAP within a few hours. These changes were accompanied by significant elevations in cardiac troponin T levels of 6.9% (95% CI: 0.2, 14.1) to 41.7% (95% CI: 21.2, 65.6), as well as reductions in left ventricular ejection fraction of 1.5% (95% CI: 0.1, 2.9) to 3.7% (95% CI: 0.8, 6.4). Furthermore, the associations were attenuated in participants living in areas with higher residential greenness levels. CONCLUSIONS:Our findings extend current understanding that short-term exposure to higher levels of traffic pollution was associated with increased STEMI risks and exacerbated cardiac impairments, and provide evidence on traffic pollution control priority for protecting vulnerable populations who are at greater risks of cardiovascular events.

BackgroundMajor adverse cardiovascular events (MACEs) represent a significant reason of morbidity and mortality in non-cardiac surgery during perioperative period. The prevention of perioperative MACEs has always been one of the hotspots in the research field. Current existing models have not been validated in Chinese population, and have become increasingly unable to adapt to current clinical needs. ObjectivesTo establish and validate several simple bedside tools for predicting MACEs during perioperative period of non-cardiac surgery in Chinese hospitalized patients. DesignWe used a nested case-control study to establish our prediction models. A nomogram along with a risk score were developed using logistic regression analysis. An internal cohort was used to evaluate the performance of discrimination and calibration of these predictive models including the revised cardiac risk index (RCRI) score recommended by current guidelines. SettingPeking University Third Hospital between January 2010 and December 2020. PatientsTwo hundred and fifty three patients with MACEs and 1,012 patients without were included in the training set from January 2010 to December 2019 while 38,897 patients were included in the validation set from January 2020 and December 2020, of whom 112 patients had MACEs. Main Outcome MeasuresThe MACEs included the composite outcomes of cardiac death, non-fatal myocardial infarction, non-fatal congestive cardiac failure or hemodynamically significant ventricular arrhythmia, and Takotsubo cardiomyopathy. ResultsSeven predictors, including Hemoglobin, CARDIAC diseases, Aspartate aminotransferase (AST), high Blood pressure, Leukocyte count, general Anesthesia, and Diabetes mellitus (HASBLAD), were selected in the final model. The nomogram and HASBLAD score all achieved satisfactory prediction performance in the training set (C statistic, 0.781 vs. 0.768) and the validation set (C statistic, 0.865 vs. 0.843). Good calibration was observed for the probability of MACEs in the training set and the validation set. The two predictive models both had excellent discrimination that performed better than RCRI in the validation set (C statistic, 0.660, P < 0.05 vs. nomogram and HASBLAD score). ConclusionThe nomogram and HASBLAD score could be useful bedside tools for predicting perioperative MACEs of non-cardiac surgery in Chinese hospitalized patients.

近年来,新型口服降糖药物钠-葡萄糖共转运蛋白2抑制剂(SGLT2i)在2型糖尿病患者心血管获益方面涌现出大量证据,多项临床试验显示SGLT2i可以显著降低2型糖尿病患者心血管死亡风险和心力衰竭住院率,其中达格列净被证实对非糖尿病的心力衰竭患者同样具有心血管保护作用.目前针对SGLT2i心血管获益机制方面的研究已取得部分进展,本文将从容量调节学说、改善血管内皮功能、改善心肌能量代谢、改善心室重构和调节全身代谢等5个方面阐述SGLT2i心血管获益的机制.

微小RNA(microRNA)是一种长度介于15～23个核苷酸的非编码RNA分子,在生物体内拥有复杂的调控机制,包括心血管系统在内的全身多种疾病均可导致microRNA表达水平的改变,其同时在疾病的病理生理进展和转归中发挥不可或缺的作用.临床中持续的心房颤动患者,左心房直径明显扩大,长期的心房颤动维持状态易致心房结构重构.心房纤维化(atrial fibrosis)不但是心房结构性重构的标志性改变,更是心房颤动产生和维持的基础.MicroRNA可通过多种途径调控心房纤维化的进程,维持与平衡心房组织的代谢活动.本篇综述中,我们将从microRNA的角度来探讨心房纤维化的病理生理机制,归纳microRNA对心房纤维化的作用靶点与相关信号通路.

Purpose: Trimethylamine N-oxide (TMAO) is recently the main risk factor for coronary heart disease (CHD). Plasma lipid levels are conventionally used to predict coronary risk, but the correlation between TMAO and plasma lipid levels in unstable angina pectoris (UAP) was unclear. Our objective was to compare the plasma level of TMAO to lipoprotein ratios and conventional lipid parameters in UAP patients. Methods: A total of 114 control participants and 184 UAP patients were enrolled. Demographic characteristics were collected. Plasma levels of TMAO and lipid in all patients were measured and analyzed. The receiver operating characteristic analysis (ROC), univariate, and multivariate logistic regression analyses were carried out to examine the relationship between TMAO, lipoprotein ratios, conventional lipid parameters, and UAP. Results: The plasma levels of TMAO were remarkably increased in UAP patients (3.28 ± 1.97 µM) compared with control participants (1.52 ± 0.59 µM, P < 0.01). TMAO was significantly correlated with lipid levels in UAP patients. The ROC, univariate and multivariate logistic regression analysis both showed that the TMAO significantly increased the risk for occurrence of UAP. Conclusions: Our data indicate that the TMAO is superior to lipoprotein ratios and conventional lipid parameters in predicting occurrence of UAP.

Whereas emergency cardiopulmonary bypass has become widely used in the adult population for refractory cardiac arrest,1 there are no reported cases of its use in a pediatric patient. We report a case of an adolescent with corrected complex congenital heart disease who survived medically refractory ventricular arrhythmias by being placed on cardiopulmonary bypass.

Background Our previous study demonstrated that the expression of miR-16 was downregulated in the cell and animal models of atherosclerosis (AS), a main contributor to coronary artery disease (CAD). Overexpression of miR-16 inhibited the formation of foam cells by exerting anti-inflammatory roles. These findings indicated miR-16 may be an anti-atherogenic and CAD miRNA. The goal of this study was to further validate the expression of miR-16 in CAD patients and explore its therapeutic roles in an AS animal model. Methods A total of 40 CAD patients and 40 non-CAD people were prospectively registered in our study. The AS model was established in ApoE-/- mice fed a high-fat diet. The model mice were randomly treated with miR-16 agomiR (n = 10) or miR-negative control (n = 10). Hematoxylin-eosin staining was conducted for histopathological examination in thoracic aorta samples. ELISA and immunohistochemistry were performed to determine the expression levels of inflammatory factors (IL-6, TNF-α, MCP-1, IL-1β, IL-10, and TGF-β). qRT-PCR and western blotting were carried out to detect the mRNA and protein expression levels of PDCD4, miR-16, and mitogen-activated protein kinase pathway-related genes. Results Compared with the normal control, miR-16 was downregulated in the plasma and peripheral blood mononuclear cell of CAD patients, and its expression level was negatively associated with IL-6 and the severity of CAD evaluated by the Gensini score, but positively related with IL-10. Injection of miR-16 agomiR in ApoE-/- mice reduced the formation of atherosclerotic plaque and suppressed the accumulation of proinflammatory factors (IL-6, TNF-α, MCP-1, and IL-1β) in the plasma and tissues but promoted the secretion of anti-inflammatory factors (IL-10 and TGF-β). Mechanism analysis showed overexpression of miR-16 might downregulate target mRNA PDCD4 and then activate p38 and ERK1/2, but inactivate the JNK pathway. Conclusions Our findings suggest miR-16 may be a potential diagnostic biomarker and therapeutic target for atherosclerotic CAD.

PURPOSE:Atrial fibrillation (AF) is one of the most commonly sustained arrhythmias in clinical practice. Long non-coding RNAs (lncRNAs) are gene regulatory elements involved in the development of several diseases. We aimed to explore the expression characteristics of lncRNAs associated with AF.METHODS:We randomly assigned 12 adult healthy mongrel dogs into a control group and an atrial pacing group. Atrial pacing stimulation was performed at a high frequency of 500 beats per min for 14 consecutive days in the atrial pacing group. HE and Masson staining were used to detect rapid atrial pacing induced atrial fibrosis. Total RNA extraction was performed on dog atrial tissues and was used for high-throughput sequencing of lncRNAs.RESULTS:A total of 10,310 lncRNAs were detected, and 33 differentially expressed lncRNAs were screened. Among them, 19 lncRNAs were upregulated in the atrial pacing group, and 14 lncRNAs were downregulated. Gene Ontology (GO) classification, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and interaction networks showed that AF-related lncRNAs participate in the regulation of AF in diverse biological processes, cellular components, molecular functions, signaling pathways, and complex interactions with miRNAs and mRNAs. Five differentially expressed lncRNAs were selected for RT-PCR validation, and the verification results were consistent with the results of lncRNA sequencing.CONCLUSIONS:In summary, our study enhances our understanding of the biological functions of AF-related lncRNAs by screening and analyzing differentially expressed lncRNAs, and the results help to enrich the theoretical basis for the treatment of atrial fibrillation.