Cardiovascular Disease Death Research Articles

ET1 acts as a potential plasma biomarker and therapeutic target in deep venous thrombosis rat model.

Deep venous thrombosis (DVT) is the third leading cause of death in cardiovascular disease, following heart attacks and strokes. Early diagnosis and intervention are crucial for effective DVT therapy. We aim to investigate whether endothelin-1 (ET-1) could serve as an early diagnostic marker or a potential therapeutic target in a DVT rat model. CCK8 assay, invasion assay, and flow cytometry were used to detect the proliferation, migration and apoptosis of HUVECs, respectively. Elisa assay was used to detect ET-1 and coagulation factor VII in cell supernatant and rat?s plasma. Western blot was used to detect antioxidant signaling protein. Inferior vena cava stenosis was used to construct the DVT rat model. Lentivirus mediated overexpression of ET-1 in HUVECs impaired the cell proliferation and migration, increased cell apoptosis, inhibited the antioxidant signaling pathway proteins expression (e.g., NQO1, GCLC, Nrf-2), and upregulated coagulation factor VII. Furthermore, overexpression of ET-1 further impaired antioxidant signaling pathway protein in response to H2O2 treatment. However, lentivirus mediated ET-1 knockdown and BQ123 (an ET-1 inhibitor), showed the opposite results with ET-1 overexpression. We then established a DVT rat model by inferior vena cava stenosis. The stenosis induced early expression of ET-1 and coagulation factor VII in plasma at day 1 and restore their level at day 10. BQ123 could downregulate the coagulation factor VII to ameliorate the stenosis effects. Our findings suggest that ET-1 might serve as an early diagnostic marker for DVT rat model and a potential therapeutic target for treating DVT.

Estimating the short-term effect of PM2.5 on the mortality of cardiovascular diseases based on instrumental variables

BackgroundPM2.5 can induce and aggravate the occurrence and development of cardiovascular diseases (CVDs). The objective of our study is to estimate the causal effect of PM2.5 on mortality rates associated with CVDs using the instrumental variables (IVs) method.MethodsWe extracted daily meteorological, PM2.5 and CVDs death data from 2016 to 2020 in Binzhou. Subsequently, we employed the general additive model (GAM), two-stage predictor substitution (2SPS), and control function (CFN) to analyze the association between PM2.5 and daily CVDs mortality.ResultsThe 2SPS estimated the association between PM2.5 and daily CVDs mortality as 1.14% (95% CI: 1.04%, 1.14%) for every 10 µg/m3 increase in PM2.5. Meanwhile, the CFN estimated this association to be 1.05% (95% CI: 1.02%, 1.10%). The GAM estimated it as 0.85% (95% CI: 0.77%, 1.05%). PM2.5 also exhibited a statistically significant effect on the mortality rate of patients with ischaemic heart disease, myocardial infarction, or cerebrovascular accidents (P < 0.05). However, no significant association was observed between PM2.5 and hypertension.ConclusionPM2.5 was significantly associated with daily CVDs deaths (excluding hypertension). The estimates from the IVs method were slightly higher than those from the GAM. Previous studies based on GAM may have underestimated the impact of PM2.5 on CVDs.

Life’s Essential 8 and Incident Cardiovascular Disease in U.S. Women With Breast Cancer

BackgroundRelationships between lifestyle risk factors and cardiovascular disease (CVD) risk in women with breast cancer (BC) are underexplored. ObjectivesTo evaluate the incidence of CVD in relation to the Life’s Essential 8 (LE8) score among women with BC. MethodsData from the Women’s Health Initiative were utilized. The primary exposure was the LE8 score assessed prior to BC diagnosis. The LE8 score was stratified into low (0-59), moderate (60-79), and high (80-100) cardiovascular health (CVH). The primary endpoint was a composite of incident CVD events, which included coronary heart disease, defined as myocardial infarction along with coronary revascularization, CVD death, and stroke. We calculated the cumulative incidence of CVD and estimated hazard ratios. ResultsAmong 7,165 participants, the median age was 70.1 years at BC diagnosis. The mean LE8 score was 62.0 ± 12.2. Over a median follow-up period of 6 years, 490 composite CVD events occurred. The risk of CVD events was highest for low CVH compared with moderate and high CVH. Compared with low CVH, the hazard ratio for incident CVD was 0.57 (95% CI: 0.46-0.69) for moderate CVH and 0.34 (95% CI: 0.20-0.59) for high CVH. LE8, in conjunction with age, provided a C-statistic of 0.74 for the composite risk of CVD. ConclusionsHigher LE8 scores were associated with a lower risk of incident CVD among women with BC in the United States.

Association of Urinary Glyphosate with All-Cause Mortality and Cardiovascular Mortality among Adults in NHANES 2013-2018: Role of Alkaline Phosphatase.

Glyphosate is the most widely used herbicide in the world. This study aimed to evaluate the relationships among urinary glyphosate, all-cause mortality and cardiovascular diseases (CVD)-related mortality in the general US population of adults, and to determine the role of alkaline phosphatase (ALP), an inflammation marker that is associated with glyphosate exposure, in these relationships. Subjects from the National Health and Nutrition Examination Survey (NHANES) 2013-2018 cycles were included. Survey-weighted Cox regression analysis was applied to estimate the relationship of glyphosate with overall and CVD mortalities. Restricted cubic spline (RCS) analysis was utilized to detect the linearity of associations. The intermediary role of ALP was explored by mediation analysis. Our results found consistent and positive associations of glyphosate with all-cause mortality (HR: 1.29, 95%CI: 1.05-1.59) and CVD mortality (HR: 1.32, 95%CI: 1.02-1.70). RCS curves further validated linear and positive dose-dependent relationships between glyphosate and mortality-related outcomes. Moreover, serum ALP was identified as a mediator in these associations and explained 12.1% and 14.0% of the total associations between glyphosate and all-cause death and CVD death risk, respectively. Our study indicated that glyphosate was associated with increased all-cause and CVD mortality in humans. Increased ALP may play an essential role in these associations.

Systematic Review and Meta-Analysis of the Incidence of Chronic Kidney Disease After Pediatric Critical Illness.

Survivors of pediatric critical illnesses are at risk of significant long-term organ sequelae. Chronic kidney disease (CKD) is a complication of critical illness (and ICU interventions) associated with growth impairment, cardiovascular disease, and early death. Our objective was to synthesize the evidence on the incidence of CKD among survivors of pediatric critical illness. MEDLINE, Embase, Cumulative Index to Nursing and Allied Health Literature, and Cochrane Register of Controlled Trials from inception to February 2024. Observational studies reporting the incidence of de novo CKD among survivors of pediatric critical illness. Two reviewers independently extracted data on study design, setting, population, demographics, diagnostic criteria, and outcome. Meta-analysis was used to describe the incidence of CKD among survivors, risk of bias (RoB) assessed using the Joanna Briggs Institute Tool, and strength and reliability of evidence assessed with GRADE (Grading of Recommendations, Assessment, Development, and Evaluations). CKD was quantified as an estimated glomerular filtration rate (eGFR) less than 90 mL/min/1.73 m2 (outcome 1), eGFR less than 60 mL/min/1.73 m2 (outcome 2), and end-stage renal disease (ESRD) as eGFR less than 15 mL/min per 1.73 m2 (outcome 3). Twelve studies (3642 patients) met selection criteria and reported at least one measure of CKD. The median duration of follow-up was 2, 3.6, and 5 years, respectively, for outcomes 1, 2, and 3. For each threshold, the pooled estimate of CKD incidence was 24% (95% CI, 16-32%) for eGFR less than 90, 14% (95% CI, 6-23%) less than 60, and 4% (95% CI, 0-7%) for ESRD. The overall quality assessment indicated a moderate RoB. Among a heterogenous population of pediatric critical illness survivors, an important minority of survivors developed CKD or ESRD. This study highlights the importance of diagnostic criteria for reporting, a greater focus on postcritical care surveillance and follow-up to identify those with CKD. Further study would facilitate the delineation of high-risk groups and strategies for improved outcomes.

Bivalirudin versus heparin in patients undergoing percutaneous coronary intervention in acute coronary syndromes.

Data on outcomes between unfractionated heparin and bivalirudin anticoagulation during percutaneous coronary intervention (PCI) in acute coronary syndromes (ACS) remains inconclusive. We aimed to systematically analyze PCI outcomes comparing unfractionated heparin and bivalirudin. We systematically searched Ovid MEDLINE, Ovid Embase, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science from database inception in 1966 through January 2024 for studies evaluating PCI outcomes comparing unfractionated heparin and bivalirudin. Two investigators independently reviewed data. Conflicts were resolved through consensus. Random-effects meta-analyses were used. Ten prospective trials were identified that enrolled 42,253 individuals who presented with an acute coronary syndrome. Our analysis found that heparin when compared to bivalirudin was associated with an increased risk of trial-based definition of major bleeding (RR 1.68, 95% CI 1.29-2.20), non-access site complications (RR 4.6, 95% CI 1.75-12.09), TIMI major bleeding (RR 1.70, 95% CI 1.20-2.41), major bleeding risks (RR 1.87, 95% CI 1.49-2.36), cardiovascular disease death (RR 1.26, 95% CI 1.02-1.57), and thrombocytopenia (RR 1.67, 95% CI 1.07-2.62). There were no statistically significant differences between heparin and bivalirudin for all-cause mortality, MACE, stroke, reinfarction, target vessel revascularization, acute or stent thrombosis. The present meta-analysis demonstrates bivalirudin reduces major bleeding when used for anticoagulation during PCI in patients with acute coronary syndromes and is not associated with an increased risk of stent thrombosis or MACE.

Single-Ancestry versus Multi-Ancestry Polygenic Risk Scores for CKD in Black American Populations.

Chronic kidney disease (CKD) is a risk factor for cardiovascular disease and early death. Recently, polygenic risk scores (PRS) have been developed to quantify risk for CKD. However, African ancestry populations are underrepresented in both CKD genetic studies and PRS development overall. Moreover, European-ancestry derived PRS demonstrate diminished predictive performance in African ancestry populations. This study aimed to develop a PRS for CKD in Black Americans. We obtained score weights from a meta-analysis of genome-wide association studies (GWAS) for estimated glomerular filtration rate (eGFR) in the Million Veteran Program (MVP) and Reasons for Geographic and Racial Differences in Stroke (REGARDS) Study to develop an eGFR PRS. We optimized the PRS risk model in a cohort of Participants from the Hypertension Genetic Epidemiology Network (HyperGEN). Validation was performed in subsets of Black participants of the Trans-Omics in Precision Medicine (TOPMed) Consortium and Genetics of Hypertension Associated Treatment (GenHAT) Study. The prevalence of CKD-defined as stage 3 or higher-was associated with the PRS as a continuous predictor (OR[95% CI]:1.35[1.08,1.68]) and in a threshold-dependent manner. Further, including APOL1 risk status-a putative variant for CKD with higher prevalence among those of sub-Saharan African descent-improved the score's accuracy. PRS associations were robust to sensitivity analyses accounting for traditional CKD risk factors, as well as CKD classification based on prior eGFR equations. Compared with previously published PRS, the predictive performance of our PRS was comparable to a European-ancestry derived PRS for kidney traits. However, both single-ancestry PRS were less predictive than multi-ancestry derived PRS. In this study, we developed a PRS that was significantly associated with CKD with improved predictive accuracy when including APOL1 risk status. However, PRS generated from multi-ancestry populations outperformed single-ancestry PRS in our study.

Spatio-temporal patterns of excess mortality from non-COVID causes of death in the United States, march-December 2020.

Objectives To estimate the burden of excess mortality from 17 underlying causes of death between March-December 2020 in the United States, and to compare trends in excess deaths from non-COVID causes vs. from COVID-19. Methods Using time series models, we estimated monthly counts of all-cause and cause-specific excess deaths. We stratified by geographic region and compared temporal trends in excess deaths from non-COVID causes to trends in deaths attributed to COVID-19. Results Of approximately 500,000 excess deaths, 70% were attributed to COVID-19. We observed increases in several underlying causes of death, ranging from a 3% increase in kidney disease deaths to a 24% increase in homicides, as well as decreases in deaths from cancer (-0.3%), influenza and pneumonia (-2%), chronic lower respiratory disease (-3%), and suicide (-7%). Trends in excess deaths from cardiovascular disease, diabetes, and Alzheimer's disease closely mirrored trends in deaths from COVID-19. Trends in excess liver disease, homicide, suicide, and motor vehicle accident deaths were negatively correlated with trends in deaths from COVID-19. There was wide regional variation in excess death rates for some causes of death, including a disproportionate increase in homicide and motor vehicle accident deaths in the Great Lakes, and a sustained reduction in cancer deaths in the Mideast and New England. Conclusions Increases in cardiovascular disease, diabetes, and Alzheimer's disease deaths from March-December 2020 likely reflect healthcare system disruptions or acute complications of COVID-19. Excess deaths from homicide and liver disease are more likely to reflect social and economic effects of the emerging pandemic, or other separate causes.

Long-term association of remnant cholesterol with all-cause and cardiovascular disease mortality: a nationally representative cohort study.

Despite reducing low-density lipoprotein cholesterol (LDL-C) to the normal range, residual cardiovascular risk remain. Remnant cholesterol (RC) exerts a potential residual risk for cardiovascular disease (CVD) prevention, and the long-term longitudinal association between RC and mortality has yet to be well elucidated. This study examined a nationally representative sample of 13,383 adults aged 20 years or older (mean age 45.7 and 52% women) who participated in the NHANES III (from1988 to1994). Causes of death were ascertained by linkage to death records through December 31, 2019. The relations of RC with all-cause and CVD mortality were tested using weighted Cox proportional hazard models. Through a median follow-up of 26.6 years, 5,044 deaths were reported, comprising 1,741 deaths of CVD [1,409 deaths of ischemic heart disease (IHD) and 332 deaths of stroke] and 1,126 of cancer. Compared to those with RC <14.26 mg/dl (lowest quartile), participants with RC ≥29.80 mg/dl (highest quartile) had multivariable-adjusted HRs of 1.23 (95% CI: 1.07-1.42) for all-cause mortality, 1.22 (95% CI: 0.97-1.53) for CVD mortality, and 1.32 (95% CI: 1.03-1.69) for IHD mortality, and 0.89 (95% CI: 0.55-1.43) for stroke mortality, and 1.17 (95% CI 0.90-1.52) for cancer mortality. We observed that elevated RC levels increased CVD risk and IHD mortality despite LDL-C being in the normal range. Elevated blood RC was associated with an increased long-term risk of all-cause, CVD, and IHD mortality. These associations were independent of socioeconomic factors, lifestyles, and history of diseases, and remained robust across the LDL-C stratum. Measuring RC levels might favor clinical assessment of early CVD risk. Further investigation is needed to elucidate the optimal range of RC levels for cardiovascular disease health in the general population.

Associations of metabolic changes and polygenic risk scores with cardiovascular outcomes and all-cause mortality across BMI categories: a prospective cohort study

BackgroundAssociations between metabolic status and metabolic changes with the risk of cardiovascular outcomes have been reported. However, the role of genetic susceptibility underlying these associations remains unexplored. We aimed to examine how metabolic status, metabolic transitions, and genetic susceptibility collectively impact cardiovascular outcomes and all-cause mortality across diverse body mass index (BMI) categories.MethodsIn our analysis of the UK Biobank, we included a total of 481,576 participants (mean age: 56.55; male: 45.9%) at baseline. Metabolically healthy (MH) status was defined by the presence of < 3 abnormal components (waist circumstance, blood pressure, blood glucose, triglycerides, and high-density lipoprotein cholesterol). Normal weight, overweight, and obesity were defined as 18.5 ≤ BMI < 25 kg/m2, 25 ≤ BMI < 30 kg/m2, and BMI ≥ 30 kg/m2, respectively. Genetic predisposition was estimated using the polygenic risk score (PRS). Cox regressions were performed to evaluate the associations of metabolic status, metabolic transitions, and PRS with cardiovascular outcomes and all-cause mortality across BMI categories.ResultsDuring a median follow-up of 14.38 years, 31,883 (7.3%) all-cause deaths, 8133 (1.8%) cardiovascular disease (CVD) deaths, and 67,260 (14.8%) CVD cases were documented. Among those with a high PRS, individuals classified as metabolically healthy overweight had the lowest risk of all-cause mortality (hazard ratios [HR] 0.70; 95% confidence interval [CI] 0.65, 0.76) and CVD mortality (HR 0.57; 95% CI 0.50, 0.64) compared to those who were metabolically unhealthy obesity, with the beneficial associations appearing to be greater in the moderate and low PRS groups. Individuals who were metabolically healthy normal weight had the lowest risk of CVD morbidity (HR 0.54; 95% CI 0.51, 0.57). Furthermore, the inverse associations of metabolic status and PRS with cardiovascular outcomes and all-cause mortality across BMI categories were more pronounced among individuals younger than 65 years (Pinteraction < 0.05). Additionally, the combined protective effects of metabolic transitions and PRS on these outcomes among BMI categories were observed.ConclusionsMH status and a low PRS are associated with a lower risk of adverse cardiovascular outcomes and all-cause mortality across all BMI categories. This protective effect is particularly pronounced in individuals younger than 65 years. Further research is required to confirm these findings in diverse populations and to investigate the underlying mechanisms involved.Graphical abstract

Associations between Supper Timing and Mortality from Cardiovascular Disease among People with and without Hypertension.

Less is known about the impact of supper time on cardiovascular disease (CVD) risk among hypertensives and nonhypertensives. We aimed to explore this issue in a cohort study. We analyzed the data of 72,658 participants (15,386 hypertensives and 57,272 nonhypertensives) aged 40-79 years without a history of CVD at baseline (1988-1990) under the Japan Collaborative Cohort study. Supper time was assessed based on self-reported questionnaires categorized as before 17:00, between 17:00 and 20:00, after 20:00, irregular supper time, and reference supper time (17:00-20:00). Hazard ratios (HRs) and 95% confidence intervals (95% CI) of CVD mortality were calculated according to supper time after adjustment for potential confounders, stratified by hypertensive status and age group (＜65 and ≥ 65 years). During a median of 19.4 years of follow-up, 4,850 CVD deaths were recorded. Compared with the reference time, the risk of CVD mortality was higher for irregular supper time for the total population, either hypertensives or nonhypertensives, more specifically hypertensives aged ≥ 65 years; the multivariable HR (95% CI) of CVD mortality in the total population was 1.28 (1.11-1.50, P＜0.01). The supper time of ＞20:00 tended to be associated with the higher risk only for hypertensives; the multivariable HR was 1.39 (0.98-1.96, P=0.06). Irregular supper time was associated with an increased risk of CVD mortality. Supper timing could be a surrogate marker for CVD risk.

Adherence to cardio-protective medications and cardiovascular disease in adults with type 1 diabetes

AimsWe estimated overall refill adherence to all antihypertensive [AHT] and/or lipid-lowering drugs in the treatment regimen and its association with cardiovascular disease (CVD) in adults with type 1 diabetes, taking kidney disease into account. MethodsThis Finnish Diabetic Nephropathy Study involved 1,558 adults with type 1 diabetes who had purchased AHT and/or lipid-lowering drugs within ± 0.5 year from baseline and were followed until their first CVD event, death, or end of 2015. Proportion of days covered (PDC) method was used to calculate adherence. The adherence was classified as good (≥80 %), intermediate (≥50 and <80%) or poor (<50%). ResultsMedian adherence rate was 74% (IQR 63–84 %). Both good (OR 0.55 [95% CI 0.33, 0.92], P=0.02) and intermediate (0.47 [0.29, 0.77], P=0.003) adherence were associated with lower odds of CVD, compared to poor adherence. Moreover, the higher the adherence percentage point in those with moderate albuminuria, the lower was the odds for CVD (0.81 [0.67, 0.98], P=0.03, per 10 unit increase in adherence). ConclusionsIn adults with type 1 diabetes, refill adherence of 50% or more to cardio-protective medications is associated with lower odds of incident CVD. Our findings highlight the relevance of going beyond prescribing protective CVD drugs, ensuring, and improving medication adherence matters.

Effects of ankylosing spondylitis on cardiovascular disease: aMendelian randomization study.

Accumulating evidence suggests that patients with ankylosing spondylitis (AS) have an elevated risk for cardiovascular disease (CVD) and cardiovascular death, however, whether AS has causal effects on the risk of CVD is unclear.Two-sample Mendelian randomization (MR) was utilizedto examine the probable causal link between them. Summary statistics from publicly released genome-wide association studies (GWAS) was used to perform MR analyses. Genetically predicted AS was selected as the exposure variable from published GWAS meta-analyses. CVD was adopted as the outcome variable. The inverse variant weighted method was employed to obtain the casual estimates. The robustness of the results was also examined by evaluating the pleiotropy and heterogeneity of single-nucleotide polymorphisms. According to MR analyses, genetic susceptibility to AS was associated with a high risk of heart failure and ischemic stroke, while negativelygenetic susceptibility was found between AS and peripheral atherosclerosis. No statistical relationship was found between AS and venous thromboembolism, atrial fibrillation, coronary atherosclerosis, and valvular heart disease. Sensitivity analysis showed no evidence of horizontal pleiotropy or heterogeneity. The present study suggests that AS exerts causal effects on the risk of CVD, including heart failure, ischemic stroke, and peripheral atherosclerosis.

Associations of short-term changes in obesity indices with all-cause mortality and cardiovascular disease.

This study aimed to investigate how short-term changes (1-, 3-, and 5-year) in obesity measures affect mortality and cardiovascular disease (CVD) risk. We analyzed longitudinal data from the MJ Health Centre (n = 43,304 for the 1-year study; 24,295 for the 3-year study; 16,138 for the 5-year study) with median follow-up periods of 15.8, 13.9, and 12.3 years, respectively. Associations of short-term obesity indices changes with mortality and Framingham Risk Score changes were explored using time-dependent coefficient Cox regression models, restricted cubic splines, and multivariable linear regression models. All-cause mortality was negatively associated with short-term weight and BMI changes, with greater reductions causing poorer outcomes. Compared with stable groups, short-term reduced weight and BMI were associated with greater risks of all-cause mortality and CVD-specific mortality (5-year study only). Also, either 1- and 3-year reducedor 3-year increased waist circumference and waist to height ratio were related to higher all-cause and CVD deaths than stable groups, respectively. Nonlinear relationships indicated lower cutoff values for short-term changes in obesity indices in predicting all-cause mortality. Decreased obesity indices significantly improved CVD profiles. Short-term changes in obesity indices show complex mortality risks, urging personalized approaches beyond a simple weight loss focus.

Community Pharmacists Identification of Gaps in Care - Statin Utilization for Primary Prevention.

Background: Statins are a highly effective lipid-lowering therapy associated with significant reductions in atherosclerotic cardiovascular disease (ASCVD) events and death. Despite these benefits, statins are underutilized. Pharmacist-led interventions to increase statin prescribing are effective. To our knowledge, no prior studies implemented a comprehensive cardiovascular risk assessment utilizing point-of-care (POC) testing in community pharmacies. Objectives: The primary objective was to determine if community pharmacists can be utilized to identify gaps in care regarding appropriate use of statin therapy for prevention of ASCVD events in HPSAs. Secondary objectives were to assess public interest in ASCVD risk assessment and statin prescribing by the pharmacist, and to identify factors associated with statin gaps in care. Methods: A cross-sectional study was conducted at three independent community pharmacies. Participants were identified based on age and medication history and were scheduled at their pharmacy to receive a comprehensive ASCVD risk screening consisting of POC measurement of a complete lipid panel, blood glucose or A1C, and blood pressure. Participants were informed of their statin candidacy at the screening. Participants completed a survey regarding perceptions of the services provided and opinions of statin prescribing by pharmacists. Results: Of the 57 participants, 43 (75.4%) were possible statin candidates. Most indicated trusting their pharmacist to prescribe a cholesterol-lowering medication and felt insurance should pay for these screenings. Conclusion: ASCVD risk assessment conducted within the community pharmacy setting for can be utilized to identify treatment gaps in status use. Participants indicated trusting pharmacists to provide this service and found the service valuable.

Assessment of essential and toxic trace element levels in erythrocytes of hemodialysis patients with end-stage renal disease

BackgroundChronic kidney disease (CKD) is a global public health problem, resulting in end-stage kidney disease, cardiovascular disease, and premature death. AimThe aim of the study was to determine the profile of essential and toxic trace elements in erythrocytes of patients with end-stage renal disease (ESRD) and their relationship with selected anthropometric and biochemical parameters. MethodsThe present study compared the profiles of trace elements, including toxic sub-stances, in the erythrocytes of 80 hemodialysis patients with CKD with 40 healthy subjects. All patients had stage 5 CKD. The levels of Cd and Pb were determined by graphite furnace atomic absorption spectrometry and levels of Fe, Mn, Zn, Cu Cr, Ni, and Li by inductively coupled plasma atomic emission spectrometry. ResultsThe ESRD patients demonstrated significantly lower Fe and Zn concentrations and significantly higher Mn and Li and toxic Pb and Cd concentrations in erythrocytes compared to those of the healthy controls. Negative correlations were observed, among others, between the concentrations of Cu, Li, and creatinine; Cu and phosphates; Mn, Pb, and transferrin saturation while positive correlations were noted between Cu, Cr, and transferrin and Pb, Cr, and the normalized protein catabolism rate. ConclusionsThe higher concentrations of toxic elements present in the erythrocytes of CKD patients might have resulted from the reduced ability of the kidneys to excrete them. Moreover, differences in the concentrations of essential elements (Fe, Mn, Zn) between the two groups indicated that their resorption in the kidneys of CKD patients was impaired. Patients with CKD might benefit from interventions intended to reduce high, toxic concentrations of Pb and Cd and Li and Mn as an alternative supportive treatment. Iron and zinc supplementation should be a component for the treatment of anemia in CKD patients.

Impact of COVID-19 and Non-COVID-19 Hospitalized Pneumonia on Longer-Term Cardiovascular Mortality in People With Type 2 Diabetes: ANationwide Prospective Cohort Study From Scotland.

In this study we examine whether hospitalized coronavirus disease 2019 (COVID-19) pneumonia increases long-term cardiovascular mortality more than other hospitalized pneumonias in people with type 2 diabetes and aim to quantify the relative cardiovascular disease (CVD) mortality risks associated with COVID-19 versus non-COVID-19 pneumonia. With use of the SCI-Diabetes register, two cohorts were identified: individuals with type 2 diabetes in 2016 and at the 2020 pandemic onset. Hospital and death records were linked for determination of pneumonia exposure and CVD deaths. Poisson regression estimated rate ratios (RRs) for CVD death associated with both pneumonia types, with adjustment for confounders. Median follow-up durations were 1,461 days (2016 cohort) and 700 days (2020 cohort). The adjusted RR for CVD death following non-COVID-19 pneumonia was 5.51 (95% CI 5.31-5.71) prepandemic and 7.3 (6.86-7.76) during the pandemic. For COVID-19 pneumonia, the RR was 9.13 (8.55-9.75). Beyond 30 days post pneumonia, the RRs converged, to 4.24 (3.90-4.60) for non-COVID-19 and 3.35 (3.00-3.74) for COVID-19 pneumonia, consistent even with exclusion of prior CVD cases. Hospitalized pneumonia, irrespective of causal agent, marks an increased risk for CVD death immediately and over the long-term. COVID-19 pneumonia poses a higher CVD death risk than other pneumonias in the short-term, but this distinction diminishes over time. These insights underscore the need for including pneumonia in CVD risk assessments, with particular attention to the acute impact of COVID-19 pneumonia.

Associations of vitamin D status with all-cause and cause-specific mortality in long-term prescription opioid users.

This study aimed to investigate the association between serum 25-hydroxyvitamin D (25(OH)D) concentrations and mortality in long-term prescription opioid users. The study included 1856 long-term prescription opioid users from the National Health and Nutrition Examination Survey (NHANES, 2001-2018). Mortality status were determined by matching with the National Death Index (NDI) records until December 31, 2019. Multivariable Cox proportional hazard models were constructed to assess the association. Over a median follow-up period of 7.75 years, there were 443 cases of all-cause mortality, including 135 cardiovascular disease (CVD) deaths and 94 cancer deaths. After multivariable adjustment, participants with serum 25(OH)D concentrations within 50.00 to <75.00 nmol/L and ≥ 75 nmol/L had a lower risk of all-cause mortality, with hazard ratios (HRs) of 0.50 (95% confidence interval [CI] 0.29, 0.86) and 0.54 (95% CI 0.32, 0.90), respectively. Nevertheless, no significant association was found between serum 25(OH)D concentrations and the risk of CVD or cancer mortality. The RCS analysis revealed a non-linear association of serum 25(OH)D concentration with all-cause mortality (p for non-linear = 0.01). Per 1-unit increment in those with serum 25(OH)D concentrations <62.17 nmol/L corresponded to a 2% reduction in the risk of all-cause mortality (95% CI 0.97, 1.00), but not changed significantly when 25(OH)D concentrations ≥62.17 nmol/L. In conclusion, a non-linear association existed between serum 25(OH)D concentrations and all-cause mortality in long-term prescription opioid users. Maintaining serum 25(OH)D concentrations ≥62.17 nmol/L may be beneficial in preventing all-cause mortality in this population.

457-P: Association of System Inflammation Index with Risk of Cardiovascular Mortality among Individuals with Type 2 Diabetes

Introduction &amp; Objective: This study aimed to examine the associations of system inflammation index, including system inflammation response index (SIRI) and system immune-inflammation index (SII), with cardiovascular mortality in adults with type 2 diabetes (T2D). Methods: This analysis included 2,954 individuals from the National Health and Nutrition Examination Survey (NHANES) 1999-2010. Cardiovascular mortality was ascertained by linkage to National Death Index (NDI) records through 31 December 2019. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: During an average of 12.4 years of follow-up, 248 cardiovascular disease (CVD) deaths occurred. After multivariate adjustment, per one-unit increment in SIRI was significantly associated with a 16% higher risk of cardiovascular mortality (P &amp;lt;0.0001) in a dose-response manner (P non-linear = 0.26). However, the association between SII and CVD deaths exhibits a J-shaped relationship (P non-linear = 0.03) and When extreme level of SII was compared, the multivariate-adjusted HR was 1.81 (95% CI 1.11, 2.95) for CVD deaths (P trend = 0.017). Conclusion: Higher SIRI and very high SII were linearly associated with elevated risk of cardiovascular mortality among individuals with T2D. Disclosure H. Li: None. W. Guo: None. Y. Li: None. T. Zeng: None. W. Kong: None. Funding National Natural Science Foundation of China (Grant No. 81974107); Bethune-Merck Diabetes Research Foundation (Grant No. G-X-2019-056);

Virtual Expansion of the YMCA's Blood Pressure Self-Monitoring (BPSM) Program: Using Telehealth to Adapt an Evidence-Based Program to Reach Rural Communities in South Carolina.

Disparities in cardiovascular disease prevalence and death exist among South Carolina's rural residents. Blood pressure self-monitoring (BPSM), where individuals measure their own blood pressure outside of the clinical environment, coupled with additional support, is an evidence-based, cost-effective strategy that is underutilized at large. The YMCA's BPSM program is an evidence-based, 4-month program that includes 2 individualized office hours with a Healthy Heart Ambassador and 4 nutrition education sessions per month. Participants are provided with a blood pressure cuff and notebook to track their blood pressure at home in between sessions. The SC Department of Health and Environmental Control partnered with the SC Alliance of YMCAs to expand the YMCA's BPSM program virtually. The traditional program was adapted to allow for virtual participant encounters. To target rural communities, partnerships were leveraged or established with rural health centers, federally qualified health centers, free medical clinics, and other state health department regions for participant referrals into the program. A developmental evaluation design was utilized to monitor the virtual adaptation of the YMCA's BPSM program from April 2021 to May 2023. At the end of the project, 10 referral sources were identified to refer participants to the program. In total, 253 participants were referred to the program, 126 participants enrolled into the program, and 52 participants completed the program. Completers of the virtual program were successful in improving their blood pressure. Successes of the virtual program were not without challenges. Lessons learned from the virtual expansion of this program included ensuring participants' readiness to engage in a 4-month program, assessing participants' digital literacy, and considering broadband access in rural areas. Improvements in blood pressure and the program's reach demonstrate merit in continuing to scale the virtual adaptation of this program; however, contextual and structural factors should be considered.