Higher Cardiovascular Disease Mortality Research Articles

Mechanism of efferocytosis in atherosclerosis.

Atherosclerosis (AS) is a chronic inflammatory vascular disease that occurs in the intima of large and medium-sized arteries with the immune system's involvement. It is a common pathological basis for high morbidity and mortality of cardiovascular diseases. Abnormal proliferation of apoptotic cells and necrotic cells leads to AS plaque expansion, necrotic core formation, and rupture. In the early stage of AS, macrophages exert an efferocytosis effect to engulf and degrade apoptotic, dead, damaged, or senescent cells by efferocytosis, thus enabling the regulation of the organism. In the early stage of AS, macrophages rely on this effect to slow down the process of AS. However, in the advanced stage of AS, the efferocytosis of macrophages within the plaque is impaired, which leads to the inability of macrophages to promptly remove the apoptotic cells (ACs) from the organism promptly, causing exacerbation of AS. Moreover, upregulation of CD47 expression in AS plaques also protects ACs from phagocytosis by macrophages, resulting in a large amount ofresidual ACs in the plaque, further expanding the necrotic core. In this review, we discussed the molecular mechanisms involved in the process of efferocytosis and how efferocytosis is impaired and regulated during AS, hoping to provide new insights fortreatingAS.

TRIM11 expression levels was downregulated and prevents ferroptosis of cardiomyocyte by Dusp6 in acute myocardial infarction.

Acute myocardial infarction (AMI) is the high incidence rate and mortality of common cardiovascular disease. Herein, we explored the critical role of TRIM11 in AMI and its underlying mechanism. Serum from patients with AMI were collected from our hospital. Mice of model group received angiotensin II. Mice of model + TRIM11 group received with Ang II and TRIM11 vectors. Mice of sham group received normal saline. H9c2 cells were performed transfections using Lipofectamine 2000 (Thermo Fisher Scientific Inc, Shanghai, China), and treated with Ang II. TRIM11 mRNA expression was reduced, was negative correlation with collagen I/III mRNA expression, systolic blood pressure, diastolic blood pressure, left anteroposterior atrial diameter, right atrial diameter, or left ventricular ejection fraction in patient with AMI. TRIM11 mRNA and protein expression were also suppressed. METTL3 regulates TRIM11 methylation to reduce TRIM11 gene stability in model of AMI. TRIM11 gene ameliorated AMI in mice model. TRIM11 gene reduced reactive oxygen species production level of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis of cardiomyocyte in-vitro model. TRIM11 gene reduced ferroptosis by the inhibition of mitochondrial damage of cardiomyocyte in model of AMI. TRIM11 induced Dusp6 protein expression. Bioluminescence imaging showed that TRIM11 virus increased Dusp6 expression in heart tissue of mice model. The inhibition of Dusp6 reduced the effects of TRIM11 on ferroptosis of cardiomyocyte in model of AMI. In conclusion, this study demonstrates that TRIM11 improves AMI by regulating Dusp6 to inhibit ferroptosis of cardiomyocyte, and suggest a novel target for AMI.

Ultra-processed food consumption and mortality among patients with stages I–III colorectal cancer: a prospective cohort study

Ultra-processed foods (UPFs) are emerging as a risk factor for colorectal cancer (CRC), yet how post-diagnostic UPF intake may impact CRC prognosis remains unexplored. Data collected from food frequency questionnaires were used to estimate intakes of total UPFs and UPF subgroups (serving/d) at least 6 months but less than 4 years post-diagnosis among 2498 patients diagnosed with stages I-III CRC within the Nurses' Health Study and Health Professionals Follow-up Study during 1980-2016. Hazard ratios (HR) and 95% confidence intervals (CIs) of all-cause, CRC- and cardiovascular disease (CVD)-specific mortality in association with UPF consumption were estimated using an inverse probability weighted multivariable Cox proportional hazards regression model, adjusted for confounders. The mean (SD) age of patients at diagnosis was 68.5 (9.4) years. A total of 1661 deaths were documented, including 321 from CRC and 335 from CVD. Compared to those in the lowest quintile (median=3.6 servings/d), patients in the highest quintile (median=10 servings/d) of post-diagnostic UPF intake had higher CVD mortality (HR=1.65, 95% CI=1.13-2.40) but not CRC or all-cause mortality. Among UPF subgroups, higher consumption of fats/condiments/sauces was associated with a higher risk of CVD-specific mortality (highest vs. lowest quintile of intake, HR=1.96, 95% CI=1.41-2.73), and higher intake of ice cream/sherbet was associated with an increased risk of CRC-specific mortality (highest vs. lowest quintile, HR=1.86, 95% CI: 1.33-2.61). No statistically significant association was found between UPF subgroups and overall mortality. Higher post-diagnostic intake of total UPFs and fats/condiments/sauces in CRC survivors is associated with higher CVD mortality, and higher ice cream/sherbet intake is linked to higher CRC mortality. US National Institutes of Health and the American Cancer Society.

Higher ratio of plasma omega-6/omega-3 fatty acids is associated with greater risk of all-cause, cancer, and cardiovascular mortality: A population-based cohort study in UK Biobank.

Circulating omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) have been associated with various chronic diseases and mortality, but results are conflicting. Few studies examined the role of omega-6/omega-3 ratio in mortality. We investigated plasma omega-3 and omega-6 PUFAs and their ratio in relation to all-cause and cause-specific mortality in a large prospective cohort, the UK Biobank. Of 85,425 participants who had complete information on circulating PUFAs, 6461 died during follow-up, including 2794 from cancer and 1668 from cardiovascular disease (CVD). Associations were estimated by multivariable Cox proportional hazards regression with adjustment for relevant risk factors. Risk for all three mortality outcomes increased as the ratio of omega-6/omega-3 PUFAs increased (all Ptrend <0.05). Comparing the highest to the lowest quintiles, individuals had 26% (95% CI, 15-38%) higher total mortality, 14% (95% CI, 0-31%) higher cancer mortality, and 31% (95% CI, 10-55%) higher CVD mortality. Moreover, omega-3 and omega-6 PUFAs in plasma were all inversely associated with all-cause, cancer, and CVD mortality, with omega-3 showing stronger effects. Using a population-based cohort in UK Biobank, our study revealed a strong association between the ratio of circulating omega-6/omega-3 PUFAs and the risk of all-cause, cancer, and CVD mortality. Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institute of Health under the award number R35GM143060 (KY). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Higher ratio of plasma omega-6/omega-3 fatty acids is associated with greater risk of all-cause, cancer, and cardiovascular mortality: A population-based cohort study in UK Biobank

Background:Circulating omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) have been associated with various chronic diseases and mortality, but results are conflicting. Few studies examined the role of omega-6/omega-3 ratio in mortality.Methods:We investigated plasma omega-3 and omega-6 PUFAs and their ratio in relation to all-cause and cause-specific mortality in a large prospective cohort, the UK Biobank. Of 85,425 participants who had complete information on circulating PUFAs, 6461 died during follow-up, including 2794 from cancer and 1668 from cardiovascular disease (CVD). Associations were estimated by multivariable Cox proportional hazards regression with adjustment for relevant risk factors.Results:Risk for all three mortality outcomes increased as the ratio of omega-6/omega-3 PUFAs increased (all Ptrend &lt;0.05). Comparing the highest to the lowest quintiles, individuals had 26% (95% CI, 15–38%) higher total mortality, 14% (95% CI, 0–31%) higher cancer mortality, and 31% (95% CI, 10–55%) higher CVD mortality. Moreover, omega-3 and omega-6 PUFAs in plasma were all inversely associated with all-cause, cancer, and CVD mortality, with omega-3 showing stronger effects.Conclusions:Using a population-based cohort in UK Biobank, our study revealed a strong association between the ratio of circulating omega-6/omega-3 PUFAs and the risk of all-cause, cancer, and CVD mortality.Funding:Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institute of Health under the award number R35GM143060 (KY). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Heterogeneity in the risk of cardiovascular disease mortality after the hypertensive disorders of pregnancy across mothers' lifetime reproductive history.

Prior studies on maternal cardiovascular disease (CVD) mortality and hypertensive disorders of pregnancy (HDP) have focused only on a woman's first birth and have not accounted for successive affected pregnancies. The objective of this study is to identify mothers' risk of CVD mortality considering lifetime reproductive history. We used data from the Medical Birth Registry of Norway, the Norwegian Cause of Death Registry, and the Norwegian National Population Register to identify all mothers who gave birth from 1967 to 2020. Our outcome was mothers' CVD death before age 70. The primary exposure was the lifetime history of HDP. The secondary exposure was the order of HDP and gestational age at delivery of pregnancies with HDP. We used Cox regression models to estimate hazard ratio (HR) and 95% confidence interval (CI), adjusting for education, mother's age, and year of last birth. These models were stratified by the lifetime number of births. Among 987,378 mothers, 86,294 had HDP in at least one birth. The highest CVD mortality, relative to mothers without HDP, was among those with a pre-term HDP in their first two births, although this represented 1.0% of mothers with HDP (HR 5.12, 95% CI 2.66, 9.86). Multiparous mothers with term HDP in their first birth only had no increased risk of CVD relative to mothers without HDP (36.9% of all mothers with HDP; HR 1.12, 95% CI 0.95, 1.32). All other mothers with HDP had a 1.5- to 4-fold increased risk of CVD mortality. This study identified heterogeneity in the risk of CVD mortality among mothers with a history of HDP. A third of these mothers are not at higher risk compared to women without HDP, while some less common patterns of HDP history are associated with severe risk of CVD mortality.

Social Determinants of Health and Disparities in Hypertension and Cardiovascular Diseases.

High blood pressure causes over 10 million preventable deaths annually globally. Populations in low- and middle-income countries suffer the most, experiencing increased uncontrolled blood pressure and cardiovascular disease (CVD) deaths. Despite improvements in high-income countries, disparities persist, notably in the United States, where Black individuals face up to 4× higher CVD mortality than White individuals. Social determinants of health encompass complex, multidimensional factors linked to an individual's birthplace, upbringing, activities, residence, workplaces, socioeconomic and environmental structures, and significantly affect health outcomes, including hypertension and CVD. This review explored how social determinants of health drive disparities in hypertension and related CVD morbidity from a socioecological and life course perspective. We present evidence-based strategies, emphasizing interventions tailored to specific community needs and cross-sector collaboration to address health inequalities rooted in social factors, which are key elements toward achieving the United Nations' Sustainable Development Goal 3.4 for reducing premature CVD mortality by 30% by 2030.

Cholesterol paradox in the community-living old adults: is higher better?

To evaluate the associations of lipid indicators and mortality in Beijing Elderly Comprehensive Health Cohort Study. A prospective cohort was conducted based on Beijing Elderly Comprehensive Health Cohort Study with 4499 community older adults. After the baseline survey, the last follow-up was March 31, 2021 with an average 8.13 years of follow-up. Cox proportional hazard model was used to estimate the hazard ratios (HR) with 95% CI for cardiovascular disease (CVD) death and all-cause death in associations with baseline lipid indicators. A total of 4499 participants were recruited, and the mean levels of uric acid, body mass index, systolic blood pressure, diastolic blood pressure, fasting plasma glucose, total cholesterol (TC), triglyceride, and low-density lipoprotein cholesterol (LDL-C) showed an upward trend with the increasing remnant cholesterol (RC) quarters (Ptrend < 0.05), while the downward trend was found in high-density lipoprotein cholesterol (HDL-C). During the total 36,596 person-years follow-up, the CVD mortality and all-cause mortality during an average 8.13 years of follow-up was 3.87% (95% CI: 3.30%-4.43%) and 14.83% (95% CI: 13.79%-15.86%) with 174 CVD death participants and 667 all-cause death participants. After adjusting for confounders, the higher level of TC (HR = 0.854, 95% CI: 0.730-0.997), LDL-C (HR = 0.817, 95% CI: 0.680-0.982) and HDL-C (HR = 0.443, 95% CI: 0.271-0.724) were associated with lower risk of CVD death, and the higher level of HDL-C (HR = 0.637, 95% CI: 0.501-0.810) were associated with lower risk of all-cause death. The higher level of RC (HR = 1.276, 95% CI: 1.010-1.613) increase the risk of CVD death. Compared with the normal lipid group, TC ≥ 6.20 mmol/L group and LDL-C ≥ 4.10 mmol/L group were no longer associated with lower risk of CVD death, while RC ≥ 0.80 mmol/L group was still associated with higher risk of CVD death. In normal lipid group, the higher levels of TC, LDL-C and HDL-C were related with lower CVD death. In community older adults, higher levels of TC and HDL-C were associated with lower CVD mortality in normal lipid reference range. Higher RC was associated with higher CVD mortality, which may be a better lipid indicator for estimating the CVD death risk in older adults.

LncRNA TUG1 as potential novel biomarkerfor prognosis of cardiovascular diseases.

Globally, cardiovascular diseases (CVDs) are among the leading causes of death. In light of the high prevalence and mortality of CVDs, it is imperative to understand the molecules involved in CVD pathogenesis and the signaling pathways that they initiate. This may facilitate the development of more precise and expedient diagnostic techniques, the identification of more effective prognostic moleculesand the identification of potential therapeutic targets. Numerous studies have examined the role of lncRNAs, such as TUG1, in CVD pathogenesis in recent years. According to this review article, TUG1 can be considered a biomarker for predicting the prognosis of CVD.

Social connection and mortality in UK Biobank: a prospective cohort analysis

BackgroundComponents of social connection are associated with mortality, but research examining their independent and combined effects in the same dataset is lacking. This study aimed to examine the independent and combined associations between functional and structural components of social connection and mortality.MethodsAnalysis of 458,146 participants with full data from the UK Biobank cohort linked to mortality registers. Social connection was assessed using two functional (frequency of ability to confide in someone close and often feeling lonely) and three structural (frequency of friends/family visits, weekly group activities, and living alone) component measures. Cox proportional hazard models were used to examine the associations with all-cause and cardiovascular disease (CVD) mortality.ResultsOver a median of 12.6 years (IQR 11.9–13.3) follow-up, 33,135 (7.2%) participants died, including 5112 (1.1%) CVD deaths. All social connection measures were independently associated with both outcomes. Friends/family visit frequencies < monthly were associated with a higher risk of mortality indicating a threshold effect. There were interactions between living alone and friends/family visits and between living alone and weekly group activity. For example, compared with daily friends/family visits-not living alone, there was higher all-cause mortality for daily visits-living alone (HR 1.19 [95% CI 1.12–1.26]), for never having visits-not living alone (1.33 [1.22–1.46]), and for never having visits-living alone (1.77 [1.61–1.95]). Never having friends/family visits whilst living alone potentially counteracted benefits from other components as mortality risks were highest for those reporting both never having visits and living alone regardless of weekly group activity or functional components. When all measures were combined into overall functional and structural components, there was an interaction between components: compared with participants defined as not isolated by both components, those considered isolated by both components had higher CVD mortality (HR 1.63 [1.51–1.76]) than each component alone (functional isolation 1.17 [1.06–1.29]; structural isolation 1.27 [1.18–1.36]).ConclusionsThis work suggests (1) a potential threshold effect for friends/family visits, (2) that those who live alone with additional concurrent markers of structural isolation may represent a high-risk population, (3) that beneficial associations for some types of social connection might not be felt when other types of social connection are absent, and (4) considering both functional and structural components of social connection may help to identify the most isolated in society.

Abstract 18695: C5ORF51/RIMOC1 - A Novel Regulator of Cardiogenesis

Introduction: Adult human cardiomyocytes (CMs) have poor capacity for proliferation and functional recovery after heart attack, thus leading to the high morbidity and mortality of cardiovascular diseases. Thus, there is great need to understand the underlying mechanisms of adult CM turnover and maturation. While screening for modulators of TEAD1, the downstream transcriptional effector of Hippo pathway, my lab identified a novel factor—C5ORF51/RIMOC1—as a potential cardiomyogenic modulator. C5ORF51 (hereinafter referred to as C5x) is a previously uncharacterized protein of nearly unknown function, which appears to play critical roles in the regulation of CM homeostasis and heart size. Hypothesis: C5x is a novel cardiomyogenic regulator which determines CM turnover, maturation, and function. Methods and Results: (1) Ex vivo C5x deletion in mouse neonatal CMs leads to significantly increased percentages of cells in S-G2-M phases, suggesting that C5x mediates CM cell cycle arrest in a cell-autonomous manner; (2) In vivo CM-specific C5x-knockout mouse model shows significantly enhanced CM proliferation in adult mice as well as increased CM endowment and mononuclear diploid populations, indicating that C5x has an essential role in cell replication and division in vivo; (3) With age, C5x-CM-knockout mice develop systolic dysfunction, massive cardiomegaly, late-onset dilated cardiomyopathy, and premature mortality, demonstrating a critical role of C5x in maintaining normal cardiac function; (4) RNA sequencing analysis further reveals that C5x loss-of-function activates fetal gene expression while its gain-of-function suppresses fetal gene expression, suggesting C5x as a gatekeeper of the fetal gene program. Conclusions: C5x is required for CM cell cycle arrest, and its loss results in fetal gene activation leading to a primitive cell state and immature CM expansion.

Association between knee osteoarthritis and mortality: a serial propensity score-matched cohort study

Background/Aims: The association between symptomatic knee osteoarthritis (OA) and higher cardiovascular disease (CVD) mortality is established; however, findings from studies that utilized regression analysis were limited, attributed to the strong association between OA and metabolic risk factors. This study aimed to evaluate the association between knee OA and mortality through propensity score matching.Methods: This was a cohort study including Korean National Health and Nutrition Examination Survey (2010–2013) participants aged ≥ 50 years. By linking the survey data to cause of death data (through 2019) from Statistics Korea, mortality and cause-specific mortality data were obtained. Radiographic knee OA (ROA) was defined as bilateral Kellgren–Lawrence grade ≥ 2. Propensity score matching (1:1) was conducted between asymptomatic ROA, knee pain, and symptomatic ROA groups and normal groups, balancing the confounding factors. Time to death was analyzed using Cox proportional hazard modeling.Results: A higher CVD mortality was observed in the symptomatic ROA group, but not in others; the risk estimates were asymptomatic ROA (hazard ratio [HR] 1.12; 95% confidence interval [CI] 0.77–1.65), knee pain (HR 0.61; 95% CI 0.27–1.38), and symptomatic ROA (HR 1.39; 95% CI 0.89–2.17). No association was found between the all-cause/cancer mortality and other groups.Conclusions: When propensity score matching controls metabolic risk factor imbalances, the association between symptomatic knee OA and higher CVD mortality was weaker compared to results of prior studies that used regression adjustment. The results may be more precise estimates of the total risk of knee OA for mortality in Koreans.

Oridonin attenuates atherosclerosis by inhibiting foam macrophage formation and inflammation through FABP4/PPARγ signalling.

Both lipid accumulation and inflammatory response in lesion macrophages fuel the progression of atherosclerosis, leading to high mortality of cardiovascular disease. A therapeutic strategy concurrently targeting these two risk factors is promising, but still scarce. Oridonin, the bioactive medicinal compound, is known to protect against inflammatory response and lipid dysfunction. However, its effect on atherosclerosis and the underlying molecular mechanism remain elusive. Here, we showed that oridonin attenuated atherosclerosis in hyperlipidemic ApoE knockout mice. Meanwhile, we confirmed the protective effect of oridonin on the oxidized low-density lipoprotein (oxLDL)-induced foam macrophage formation, resulting from increased cholesterol efflux, as well as reduced inflammatory response. Mechanistically, the network pharmacology prediction and further experiments revealed that oridonin dramatically facilitated the expression of peroxisome proliferator-activated receptor gamma (PPARγ), thereby regulating liver X receptor-alpha (LXRα)-induced ATP-binding cassette transporter A1 (ABCA1) expression and nuclear factor NF-kappa-B (NF-κB) translocation. Antagonist of PPARγ reversed the cholesterol accumulation and inflammatory response mediated by oridonin. Besides, RNA sequencing analysis revealed that fatty acid binding protein 4 (FABP4) was altered responding to lipid modulation effect of oridonin. Overexpression of FABP4 inhibited PPARγ activation and blunted the benefit effect of oridonin on foam macrophages. Taken together, oridonin might have potential to protect against atherosclerosis by modulating the formation and inflammatory response in foam macrophages through FABP4/PPARγ signalling.

Impact of hypertriglyceridaemia on cardiovascular mortality according to low-density lipoprotein cholesterol in a 15.6-million population.

The aim of this study was to assess the association between triglyceride (TG) levels and cardiovascular disease (CVD) mortality concerning low-density lipoprotein cholesterol (LDL-C) and age in the general population. From the Korean National Health Insurance Service database, 15 672 028 participants aged 18-99 who underwent routine health examinations were followed up for CVD mortality. Hazard ratios for CVD mortality were calculated using Cox models after adjusting for various confounders. During a mean of 8.8 years of follow-up, 105 174 individuals died of CVD. There was a clear log-linear association between TG and overall CVD mortality down to 50 mg/dL. Each two-fold increase in TG was associated with 1.10-fold (overall CVD), 1.22-fold [ischaemic heart disease (IHD)], 1.24-fold [acute myocardial infarction (AMI)], and 1.10-fold (ischaemic stroke) higher CVD mortality. Haemorrhagic stroke and heart failure were not associated with TG levels. The impact of hypertriglyceridaemia (HTG) on CVD weakened but remained present in persons with LDL-C < 100 mg/dL, in whom each two-fold higher TG was associated with 1.05-fold (overall CVD), 1.12-fold (IHD), 1.15-fold (AMI), and 1.05-fold (ischaemic stroke) higher CVD mortality. The younger population (18-44 years) had stronger associations between TG levels and mortality from overall CVD, IHD, and AMI than the older population. Hypertriglyceridaemia independently raises CVD mortality with lingering risks in young and older individuals with low LDL-C levels, suggesting the importance of management of HTG even with controlled LDL-C.

Late-Night Overeating and All-Cause and Cardiovascular Disease Mortality in Adults Aged ≥ 50: A Cohort Study.

Late-night overeating (LNOE) is closely associated with many health risk factors, but whether LNOE can increase the risk of death remains unknown. Thus, the prospective cohort study aimed to investigate the relationship between LNOE and mortality using data from the National Health and Nutrition Examination Survey. 11,893 participants aged 50 years and older were included in the study. Dietary information was obtained through 24-h dietary recall interviews. Cox regression, subgroup, sensitivity, and restricted cubic spline analyses were used to assess the association between LNOE and mortality. During a median follow-up of 8.3 years, 2,498 deaths occurred. After adjusting for major confounders, compared to the non-late-night eating (NLNE) group, the LNOE group was associated with higher risks of all-cause (HR = 1.47, 95% CI = 1.06-2.04) and cardiovascular disease (CVD) mortality (HR = 2.02, 95% CI = 1.13-3.60). No significant association was found between late-night eating (LNE) and mortality. Subgroup analyses showed that the LNOE group had a greater risk of all-cause and CVD mortality in participants older than 70 years, with alcohol consumption and hypertension and demonstrated an increased risk of all-cause mortality in males and higher CVD mortality in females. The habit of LNOE was an independent risk factor for all-cause and CVD mortality in US adults aged 50 years and older, which was also influenced by age, sex, alcohol consumption, and hypertension.

Common in atherogenesis and carcinogenesis: clonal hematopoiesis

Clonal hematopoiesis is a common age-dependent state accompanied by the expansion of mutant hematopoietic stem cells as a result of somatic mutations and is associated with a high risk of hematopoietic neoplasms and cardiovascular diseases. Clonal hematopoiesis in human ontogenesis occurs asymptomatically, and the fraction of mutant clones can exceed more than 2% of the total pool of circulating nucleated blood cells by age 70. Due to the variability of the accumulation rate of mutant clones, signs of clonal hematopoiesis can be observed at a younger age. Clonal hematopoiesis may act as a benign, precancerous condition and a strong factor for acute cardiovascular events such as myocardial infarction and stroke. Current evidence indicates that somatic mutations in driver genes of clonal hematopoiesis significantly increase the risk of acute conditions such as acute myeloid leukemia and acute myocardial infarction. The high mortality and morbidity of cardiovascular and cancer diseases, and their strong association with clonal hematopoiesis, make it of indeterminate potential worthy of close attention.

Lipid metabolism and rheumatoid arthritis.

As a chronic progressive autoimmune disease, rheumatoid arthritis (RA) is characterized by mainly damaging the synovium of peripheral joints and causing joint destruction and early disability. RA is also associated with a high incidence rate and mortality of cardiovascular disease. Recently, the relationship between lipid metabolism and RA has gradually attracted attention. Plasma lipid changes in RA patients are often detected in clinical tests, the systemic inflammatory status and drug treatment of RA patients can interact with the metabolic level of the body. With the development of lipid metabolomics, the changes of lipid small molecules and potential metabolic pathways have been gradually discovered, which makes the lipid metabolism of RA patients or the systemic changes of lipid metabolism after treatment more and more comprehensive. This article reviews the lipid level of RA patients, as well as the relationship between inflammation, joint destruction, cardiovascular disease, and lipid level. In addition, this review describes the effect of anti-rheumatic drugs or dietary intervention on the lipid profile of RA patients to better understand RA.

Preserved vegetable consumption and its association with mortality among 440,415 people in the China Kadoorie Biobank

BackgroundFresh vegetable consumption has been associated with lower incidence of cardiovascular disease (CVD). However, whether preserved vegetable consumption is linked with CVD and mortality remains unclear. This study aimed to assess the associations of preserved vegetable consumption with all-cause and cause-specific mortality.MethodsA total of 440,415 participants free of major chronic diseases, aged 30–79 years, were enrolled from 10 diverse regions in China between 2004 and 2008 and were followed up for an average of 10 years. Preserved vegetable consumption was assessed using a validated food frequency questionnaire. Cause-specific hazard models with the consideration of competing risk from various deaths were performed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) of mortality.ResultsDuring 4,415,784 person-years of follow-up, we documented 28,625 deaths. After adjustment for major risk factors, preserved vegetable consumption was marginally associated with higher CVD mortality (P = 0.041 for trend and P = 0.025 for non-linearity) but not associated with cancer mortality and total mortality. For specific causes of death, consuming preserved vegetables was associated with higher hemorrhagic stroke mortality. The multivariable-adjusted HRs (95% CIs) of hemorrhagic stroke mortality compared with non-consumers were 1.32 (1.17–1.50) for 1–3 days/week and 1.15 (1.00–1.31) for regular consumers (≥4 days/week) (P = 0.006 for trend and P < 0.001 for non-linearity). In addition, regular preserved vegetable consumption was associated with increased risk of digestive tract cancer mortality [HR (95% CI): 1.13 (1.00–1.28); P = 0.053 for trend] and esophageal cancer mortality [HR (95% CI): 1.45 (1.17–1.81); P = 0.002 for trend].ConclusionsFrequent consumption of preserved vegetables was associated with higher risk of mortality from hemorrhagic stroke and esophageal cancer in China. Our findings suggest limiting preserved vegetable consumption might be protective for premature death from hemorrhagic stroke and digestive tract cancer.

New insight of complement system in the process of vascular calcification

The complement system defences against pathogenic microbes and modulates immune homeostasis by interacting with the innate and adaptive immune systems. Dysregulation, impairment or inadvertent activation of complement system contributes to the pathogenesis of some autoimmune diseases and cardiovascular diseases (CVD). Vascular calcification is the pivotal pathological basis of CVD, and contributes to the high morbidity and mortality of CVD. Increasing evidences indicate that the complement system plays a key role in chronic kidney diseases, atherosclerosis, diabetes mellitus and aging-related diseases, which are closely related with vascular calcification. However, the effect of complement system on vascular calcification is still unclear. In this review, we summarize current evidences about the activation of complement system in vascular calcification. We also describe the complex network of complement system and vascular smooth muscle cells osteogenic transdifferentiation, systemic inflammation, endoplasmic reticulum stress, extracellular matrix remodelling, oxidative stress, apoptosis in vascular calcification. Hence, providing a better understanding of the potential relationship between complement system and vascular calcification, so as to provide a direction for slowing the progression of this burgeoning health concern.

Abstract P570: The Association of Ideal Cardiovascular Health With Self-Reported Health in Black American Women

Introduction: Black American women suffer disproportionately from an increased burden of cardiovascular health (CVH) risk factors, earlier onset of cardiovascular disease (CVD), and higher CVD mortality when compared to their White women. The Partnering in Negating Statistics (P.I.N.S.) for Black Women Initiative is an academic-community-government partnership aimed at uplifting Black women to achieve total health and wellness through the provision of education, access to resources, and partnership in science. Women’s community wellness events have operationalized the P.I.N.S. Initiative mission since 2021, drawing Black women and their families to take part in resources like cardiovascular disease screenings (AHA’s Life’s Simple 7 [LS7] and Life’s Essential 8 [LE8]) and education. The study presented herein examined the association of ideal cardiovascular health (ICH) with self-reported health among Black American women who attended the community wellness events. Methods: Community wellness events focusing on Black women occurred in 2021 and 2022. At these events, a battery of measurements including CVH metrics (blood pressure, glucose, cholesterol, body mass index [BMI], physical activity, smoking, diet and sleep duration) and self-reported health(poor, fair, good, excellent) were collected from participants who chose to participate in biometric screening. The associations between LS7 (range 0-14)/LE8 (range 0-100) with self-reported health were tested using multinomial logistic regression controlling for age, income, and education. Results: One-hundred and twenty-three Black American women with complete LS7 and self-reported health data were included in the analysis 2021 and 2022, of those 63 of participants in 2022 had LE8 data. The mean age of participants was 50 (SD 14), 66%, 23%, 7% and 2% were employed, retired, unemployed and students, 76% and 15%, were enrolled in private insurance, Medicaid/Medicare and 15% had no insurance. Sixty-nine percent had educational attainment ≥ college. In fully adjusted analyses, a 1-unit increase (range 4-13) in LS7 was associated with a 34% lower odds of fair vs. excellent self-reported health (OR 0.66, 95%CI: 0.46, 0.96,p=0.0281). A 1-unit increase in LE8 (range 38-91) was associated with a 13% lower odds of fair vs. excellent self-reported health (OR 0.87, 95%CI: 0.78, 0.98, p=0.0258). Conclusion: Attainment of higher ICH was associated with lower odds of fair vs. excellent self-reported health among Black American women. This finding is important in community-based health interventions and clinical trial recruitment in historically underrepresented populations including Black women, as individuals who appropriately recognize their health status may be more likely to engage in clinical and community-based research to improve health.