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Results for “CARDIOVASCULAR DISEASES”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 19 records
All sourcesNASA NTRSDOE OSTI
DOE OSTI2018

A cross-disciplinary evaluation of evidence for multipollutant effects on cardiovascular disease

Highlights: • Efficiencies may be gained using a multipollutant context to regulate air pollutants. • We perform an evaluation of multipollutant effects on cardiovascular disease CVD. • effect of combined exposure than either PM or O{sub 3} exposure alone. • Heterogeneous results were observed across disciplines for other two-pollutant combinations: PM and CO, NO{sub 2} and PM{sub 10}, O{sub 3} and NO{sub 2}, CO and O{sub 3}. The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and individuals are exposed to more than one pollutant at a time.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2018

Lipidomic insight into cardiovascular diseases

Highlights: • Update on current lipidomic research in cardiovascular diseases. • Lipidomic research's discovery of novel lipid species correlated with cardiovascular risks. • Potential of lipidomics to identify biomarker lipid molecules that predict future cardiovascular events in young patients. Cardiovascular disease is a primary cause of mortality worldwide. Therefore, it is of major interest to identify sensitive molecular markers that predict cardiovascular events and point to therapeutic strategies that will increase lifespans. Dysregulated lipid metabolism is recognized as an established risk factor in cardiovascular diseases. However, it is still largely unknown which specific lipid molecular species reflect cardiovascular risk. In addition, understanding the whole lipidome signature in vascular pathophysiology is challenging. Recent advancements of mass-spectrometry allow researchers to detect each individual lipid species from unbiased small samples. In this review, we update the current research on lipidomic approaches in cardiovascular diseases.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2018

Urinary tungsten and incident cardiovascular disease in the Strong Heart Study: An interaction with urinary molybdenum

Highlights: • Baseline urinary tungsten levels were not associated with cardiovascular disease incidence. • Elevated urinary tungsten was associated with cardiovascular disease in the presence of low urinary molybdenum. • The association between tungsten and cardiovascular disease was inverse at higher molybdenum levels. • Molybdenum may modify the association between tungsten and incident cardiovascular disease. Tungsten (W) interferes with molybdenum (Mo) binding sites and has been associated with prevalent cardiovascular disease (CVD). We evaluated if (1) W exposure is prospectively associated with incident CVD and (2) the association between urinary W levels and incident CVD is modified by urinary Mo levels.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2018

Ecological analysis of associations between groundwater quality and hypertension and cardiovascular disease in rural Saskatchewan, Canada using Bayesian hierarchical models and administrative health data

Highlights: • Hardness and magnesium were associated with decreased risk of cardiovascular disease. • Arsenic concentrations were not associated with the risk of cardiovascular disease. • Summarized water health standards were not associated with cardiovascular disease. Associations between groundwater quality and the prevalence of hypertension and ischemic heart disease were investigated in rural areas of the Canadian province of Saskatchewan. The partially ecological study was analyzed using Bayesian hierarchical models to account for spatial variability in risk. Exposure measures and health outcomes were estimated based on previously collected water quality surveillance data from public water supplies and private wells and administrative health data. Water quality exposures for each study region were estimated by applying geostatistical techniques to arsenic concentrations and principal component (PC) scores. The PC scores summarized groups of parameters measuring either health standards or aesthetic objectives described by the province. Generalized linear mixed models with a log link assessed associations between water quality and observed count of health outcomes relative to the expected value. The Bayesian models contained uncorrelated and spatially correlated random effects for each geographic region. Effect estimates were controlled for sex and age by stratification of case and expected case counts, for smoking by inclusion of sex- and age-specific prevalence of chronic obstructive pulmonary disease as a surrogate covariate, and for education and income by use of census data. There was no evidence for associations between groundwater arsenic concentrations in public or private water supplies and increased risk of hypertension or cardiovascular disease. An increase in the second aesthetic objectives PC score from public supplies was associated with a protective effect against ischemic heart disease. This PC value summarized hardness and magnesium Similarly, an increase in the second aesthetic objectives PC in private supplies was associated with decreased prevalence of hypertension. The results of this study are consistent with others demonstrating a relationship between elevated hardness and magnesium concentrations in drinking water and reduced risk of hypertension and cardiovascular disease. Further investigation is warranted with individual exposure history, particularly with respect to the potential beneficial effect of hard water on the prevalence of hypertension and cardiovascular disease.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2018

Projections for temperature-related years of life lost from cardiovascular diseases in the elderly in a Chinese city with typical subtropical climate

Highlights: • First evidence on temperature-related cardiovascular diseases’ YLL in the elderly. • An important dual problem of climate change and aging was investigated. • Adaptation of the population to global warming was taken into consideration. • Heat-related YLL will increase tremendously even considering 30% adaptation. Extreme temperature is an important risk factor for cardiovascular diseases, and the elderly are particularly vulnerable to temperature variation. Global warming and the increasingly aging population are two major global challenges for human health; thus, an urgent need exists to project the temperature-related cardiovascular disease burden regarding both of the aforementioned factors. We aimed to the project temperature-related burden of cardiovascular diseases using years of life lost (YLL) in the elderly in a Chinese city with typical subtropical climate.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2017

Cadmium exposure is associated with soluble urokinase plasminogen activator receptor, a circulating marker of inflammation and future cardiovascular disease

Background: Diet and smoking are the main sources of cadmium exposure in the general population. Cadmium increases the risk of cardiovascular diseases, and experimental studies show that it induces inflammation. Blood cadmium levels are associated with macrophages in human atherosclerotic plaques. Soluble urokinase-type plasminogen activator receptor (suPAR) is an emerging biomarker for cardiovascular events related to inflammation and atherosclerotic plaques. The aim was to examine whether blood cadmium levels are associated with circulating suPAR and other markers of inflammation. Methods: A population sample of 4648 Swedish middle-aged women and men was examined cross-sectionally in 1991–1994. Plasma suPAR was assessed by ELISA, leukocytes were measured by standard methods, and blood cadmium was analysed by inductively coupled plasma mass spectrometry. Prevalent cardiovascular disease, ultrasound-assessed carotid plaque occurrence, and several possible confounding factors were recorded. Results: After full adjustment for risk factors and confounding variables, a 3-fold increase in blood cadmium was associated with an 10.9% increase in suPAR concentration (p<0.001). In never-smokers, a 3-fold increase in blood cadmium was associated with a 3.7% increase in suPAR concentration (p<0.01) after full adjustment. Blood cadmium was not associated with C-reactive protein, white blood cell count and Lp-PLA2 but with neutrophil/lymphocyte ratio in one of two statistical models. Conclusions: Exposure to cadmium was associated with increased plasma suPAR in the general population, independently of smoking and cardiovascular disease. These results imply that cadmium is a possible cause for raised levels of this inflammatory marker. - Highlights: • Cadmium is a toxic proinflammatory, proatherosclerotic metal. • Soluble urokinase-type plasminogen activator receptor (suPAR) in plasma is a promising proinflammatory marker of atherosclerosis. • Blood cadmium and plasma suPAR were measured in a cohort of 4648 Swedish men and women. • Blood cadmium was positively associated with plasma suPAR, also in never smokers.

60 APPLIED LIFE SCIENCES↗
DOE OSTI2016

Cardiovascular Disease Risk in a Large, Population-Based Cohort of Breast Cancer Survivors

Purpose: To conduct a large, population-based study on cardiovascular disease (CVD) in breast cancer (BC) survivors treated in 1989 or later. Methods and Materials: A large, population-based cohort comprising 70,230 surgically treated stage I to III BC patients diagnosed before age 75 years between 1989 and 2005 was linked with population-based registries for CVD. Cardiovascular disease risks were compared with the general population, and within the cohort using competing risk analyses. Results: Compared with the general Dutch population, BC patients had a slightly lower CVD mortality risk (standardized mortality ratio 0.92, 95% confidence interval [CI] 0.88-0.97). Only death due to valvular heart disease was more frequent (standardized mortality ratio 1.28, 95% CI 1.08-1.52). Left-sided radiation therapy after mastectomy increased the risk of any cardiovascular event compared with both surgery alone (subdistribution hazard ratio (sHR) 1.23, 95% CI 1.11-1.36) and right-sided radiation therapy (sHR 1.19, 95% CI 1.04-1.36). Radiation-associated risks were found for not only ischemic heart disease, but also for valvular heart disease and congestive heart failure (CHF). Risks were more pronounced in patients aged <50 years at BC diagnosis (sHR 1.48, 95% CI 1.07-2.04 for left- vs right-sided radiation therapy after mastectomy). Left- versus right-sided radiation therapy after wide local excision did not increase the risk of all CVD combined, yet an increased ischemic heart disease risk was found (sHR 1.14, 95% CI 1.01-1.28). Analyses including detailed radiation therapy information showed an increased CVD risk for left-sided chest wall irradiation alone, left-sided breast irradiation alone, and internal mammary chain field irradiation, all compared with right-sided breast irradiation alone. Compared with patients not treated with chemotherapy, chemotherapy used ≥1997 (ie, anthracyline-based chemotherapy) increased the risk of CHF (sHR 1.35, 95% CI 1.00-1.83). Conclusion: Radiation therapy regimens used in BC treatment between 1989 and 2005 increased the risk of CVD, and anthracycline-based chemotherapy regimens increased the risk of CHF.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2023

Targeted curation of the gut microbial gene content modulating human cardiovascular disease

Despite the promise of the gut microbiome to predict human health, few studies expose the molecular-scale processes underpinning such forecasts. We mined over 200,000 gut-derived genomes from cultivated and uncultivated microbial lineages to inventory the gut microorganisms and their gene content that control trimethylamine-induced cardiovascular disease. We assigned an atherosclerotic profile to the 6,341 microbial genomes that encoded metabolisms associated with heart disease, creating the Methylated Amine Gene Inventory of Catabolism database (MAGICdb). From microbiome gene expression data sets, we demonstrate that MAGICdb enhanced the recovery of disease-relevant genes and identified the most active microorganisms, unveiling future therapeutic targets. From the feces of healthy and diseased subjects, we show that MAGICdb predicted cardiovascular disease status as effectively as traditional lipid blood tests. This functional microbiome catalog is a public, exploitable resource, designed to enable a new era of microbiota-based therapeutics and diagnostics

metatranscriptomics↗
DOE OSTI2018

Systemic inflammatory markers associated with cardiovascular disease and acute and chronic exposure to fine particulate matter air pollution (PM2.5) among US NHANES adults with metabolic syndrome

Highlights: • A cross sectional study of the effect of PM{sub 2.5} AP on inflammatory biomarkers among NHANES participants was conducted. • Participants’ Census tract of residence was linked to USEPA downscaler modeled air pollution for the continental US. • Goal was the assessment of susceptibility of adults with metabolic syndrome to PM2.5 exposure and levels of CRP and WBC. • There was a significant effect of PM2.5 at lag day 0; a 10 µg/m3 rise was associated with a 10.1% increase in CRP level. • There were no significant associations with CRP or WBC for those without metabolic syndrome. There has been no investigation to date of adults with metabolic syndrome examining the association of short and long-term exposure to fine particulate matter (PM{sub 2.5}) air pollution with cardiovascular-disease related inflammatory marker (WBC and CRP) levels in a nationally representative sample. The goal of this study is to assess the susceptibility of adults with metabolic syndrome to PM{sub 2.5} exposure as suggested by increased cardiovascular-disease related inflammatory marker levels.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2019

New Insights in the Control of Low-Density Lipoprotein Cholesterol to Prevent Cardiovascular Disease

Purpose of Review: Low-density lipoprotein cholesterol (LDL-C) is one major cause of cardiovascular disease (CVD). In this review, we discuss current developments in the understanding of LDL-C as lifelong risk factor, treatment targets, and emerging approaches to reduce cardiovascular risk by lowering LDL-C. Recent Findings: Recent evidence underscores the importance of LDL-C lowering in CVD prevention by mechanisms that increase the hepatic clearance of apolipoprotein B-containing lipoproteins from the plasma. Mendelian randomization studies provided evidence on both safety and efficacy of lower LDL-C in the long term. For young individuals, metrics other than 10-year CVD risk are required. Despite this evidence, LDL-C treatment target attainment is poor. Novel approaches are therefore needed. These include individualized strategies and new LDL-C-lowering pharmaceuticals. Summary: Early, long-term treatment with LDL-C-lowering therapies has the potential to markedly reduce CVD incidence and progression. Future research should aim to identify patient characteristics that enable physicians to tailor therapy to each individual patient.

62 RADIOLOGY AND NUCLEAR MEDICINE↗
DOE OSTI2018

Whole blood mercury and the risk of cardiovascular disease among the Greenlandic population

Highlights: • The Greenlandic Inuit have very high levels of whole blood mercury. • Whole blood mercury was not associated with incident CVD in Greenland. • CVD was associated with traditional risk factors such as HbA{sub 1c} and physical activity. Studies have found mercury to be associated with cardiovascular disease (CVD), however, primarily in populations with low exposure. The highest levels, and variations in the levels, of whole blood mercury (WBM) worldwide have been found in Greenland. We prospectively assessed the association between WBM and the risk of developing CVD in the Greenlandic population.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2024

Simulated Microgravity Alters Gene Regulation Linked to Immunity and Cardiovascular Disease

Microgravity exposure induces a cephalad fluid shift and an overall reduction in physical activity levels which can lead to cardiovascular deconditioning in the absence of countermeasures. Future spaceflight missions will expose crew to extended periods of microgravity among other stressors, the effects of which on cardiovascular health are not fully known. In this study, we determined cardiac responses to extended microgravity exposure using the rat hindlimb unloading (HU) model. We hypothesized that exposure to prolonged simulated microgravity and subsequent recovery would lead to increased oxidative damage and altered expression of genes involved in the oxidative response. To test this hypothesis, we examined hearts of male (three and nine months of age) and female (3 months of age) Long–Evans rats that underwent HU for various durations up to 90 days and reambulated up to 90 days post-HU. Results indicate sex-dependent changes in oxidative damage marker 8-hydroxydeoxyguanosine (8-OHdG) and antioxidant gene expression in left ventricular tissue. Three-month-old females displayed elevated 8-OHdG levels after 14 days of HU while age-matched males did not. In nine-month-old males, there were no differences in 8-OHdG levels between HU and normally loaded control males at any of the timepoints tested following HU. RNAseq analysis of left ventricular tissue from nine-month-old males after 14 days of HU revealed upregulation of pathways involved in pro-inflammatory signaling, immune cell activation and differential expression of genes associated with cardiovascular disease progression. Taken together, these findings provide a rationale for targeting antioxidant and immune pathways and that sex differences should be taken into account in the development of countermeasures to maintain cardiovascular health in space.

Genetics & Heredity↗
DOE OSTI2018

Projection of temperature-related mortality due to cardiovascular disease in beijing under different climate change, population, and adaptation scenarios

Highlights: • The population change can bring 5 times growth to temperature-related CVD deaths. • Increase of heat-related CVD deaths is higher than decrease of cold-related ones. • The adaptation to climate change may cause more temperature-related CVD deaths. Human health faces unprecedented challenges caused by climate change. Thus, studies of the effect of temperature change on total mortality have been conducted in numerous countries. However, few of those studies focused on temperature-related mortality due to cardiovascular disease (CVD) or considered future population changes and adaptation to climate change. We present herein a projection of temperature-related mortality due to CVD under different climate change, population, and adaptation scenarios in Beijing, a megacity in China. To this end, 19 global circulation models (GCMs), 3 representative concentration pathways (RCPs), 3 socioeconomic pathways, together with generalized linear models and distributed lag non-linear models, were used to project future temperature-related CVD mortality during periods centered around the years 2050 and 2070. The number of temperature-related CVD deaths in Beijing is projected to increase by 3.5–10.2% under different RCP scenarios compared with that during the baseline period. Using the same GCM, the future daily maximum temperatures projected using the RCP2.6, RCP4.5, and RCP8.5 scenarios showed a gradually increasing trend. When population change is considered, the annual rate of increase in temperature-related CVD deaths was up to fivefold greater than that under no-population-change scenarios. The decrease in the number of cold-related deaths did not compensate for the increase in that of heat-related deaths, leading to a general increase in the number of temperature-related deaths due to CVD in Beijing. In addition, adaptation to climate change may enhance rather than ameliorate the effect of climate change, as the increase in cold-related CVD mortality greater than the decrease in heat-related CVD mortality in the adaptation scenarios will result in an increase in the total number of temperature-related CVD mortalities.

54 ENVIRONMENTAL SCIENCES↗
DOE OSTI2019

An Overview of Genomic Biomarker Use in Cardiovascular Disease Clinical Trials

Clinical trial designs targeting patient subgroups with certain genetic characteristics may enhance the efficiency of developing drugs for cardiovascular disease ( CVD ). To evaluate the extent to which genetic knowledge translates to the CVD pipeline, we analyzed how genomic biomarkers are utilized in trials. Phase II and III trial protocols for investigational new drugs for CVD and risk factors were evaluated for prospective and exploratory genomic biomarker use; drug targets were evaluated for the presence of evidence that genetic variations can impact CVD risk or drug response. We identified 134 programs (73 unique drug targets) and 147 clinical trials. Less than 1% ( n = 1/147) trials used a genomic biomarker prospectively for in‐trial enrichment despite 32% ( n = 23/73) of the drug targets having evidence of genetic variations. Additionally, 46% ( n = 68/147) of the trials specified exploratory biomarker use. The results highlight an opportunity for more targeted CVD drug development by leveraging genomic biomarker knowledge.

Adeniyi, Oluseyi↗
DOE OSTI2022

Simulated Night- Shift Schedule Disrupts the Plasma Lipidome and Reveals Early Markers of Cardiovascular Disease Risk

Introduction: The circadian system coordinates daily rhythms in lipid metabolism, storage and utilization. Disruptions of internal circadian rhythms due to altered sleep/wake schedules, such as in night-shift work, have been implicated in increased risk of cardiovascular disease and metabolic disorders. To determine the impact of a night-shift schedule on the human blood plasma lipidome, an in-laboratory simulated shift work study was conducted. Methods: Fourteen healthy young adults were assigned to 3 days of either a simulated day or night-shift schedule, followed by a 24-h constant routine protocol with fixed environmental conditions, hourly isocaloric snacks, and constant wakefulness to investigate endogenous circadian rhythms. Blood plasma samples collected at 3-h intervals were subjected to untargeted lipidomics analysis. Results: More than 400 lipids were identified and quantified across 21 subclasses. Focusing on lipids with low between-subject variation per shift condition, alterations in the circulating plasma lipidome revealed generally increased mean triglyceride levels and decreased mean phospholipid levels after night-shift relative to day-shift. The circadian rhythms of triglycerides containing odd chain fatty acids peaked earlier during constant routine after night-shift. Regardless of shift condition, triglycerides tended to either peak or be depleted at 16:30 h, with chain-specific differences associated with the direction of change. Discussion: The simulated night-shift schedule was associated with altered temporal patterns in the lipidome. This may be premorbid to the elevated cardiovascular risk that has been found epidemiologically in night-shift workers.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2022

Quantile-Specific Heritability of Inflammatory and Oxidative Stress Biomarkers Linked to Cardiovascular Disease

Purpose: Heritability (h 2 , the proportion of the phenotypic variance attributable to additive genetic effects) is traditionally assumed to be constant throughout the distribution of the phenotype. However, the heritabilities of circulating C-reactive protein, interleukin-6, plasminogen activator inhibitor type-1 (PAI-1), and monocyte chemoattractant protein-1 (MCP-1) concentrations depend upon whether the phenotype is high or low relative to their distributions (quantile-dependent expressivity), which may account for apparent gene–environment interactions. Whether the heritabilities of other inflammatory biomarkers linked to cardiovascular disease are quantile-dependent remain to be determined. Patients and Methods: Quantile-specific offspring-parent (β OP ) and full-sib regression slopes (β FS ) were estimated by applying quantile regression to the age- and sex-adjusted phenotypes of families surveyed as part of the Framingham Heart Study. Quantile-specific heritabilities were calculated as: h 2 =2β OP /(1+r spouse ) and h 2 ={(1+8r spouse β FS ) 0.5 – 1}/(2r spouse ). Results: Heritability (h 2 ± SE) of lipoprotein-associated phospholipase A2 (Lp-PLA 2 ) mass concentrations increased from 0.11 ± 0.03 at the 10 th percentile, 0.08 ± 0.03 at the 25 th , 0.12 ± 0.03 at the 50 th , 0.20 ± 0.04 at the 75 th , and 0.26 ± 0.06 at the 90 th percentile, or 0.0023 ± 0.0006 per each one-percent increase in the phenotype distribution (P linear trend = 0.0004). Similarly, h 2 increased 0.0029 ± 0.0011 (P linear trend = 0.01) for sP-selectin, 0.0032 ± 0.0009 (P linear trend = 0.0001) for soluble intercellular adhesion molecule 1 (sICAM-1), and 0.0026 ± 0.0006 for tumor necrosis factor receptor 2 (TNFR2) (P linear trend = 5.0 × 10 -6 ) per each one-percent increase in their distributions when estimated from β OP . Osteoprotegerin and soluble ST2 heritability also increased significantly with increasing percentiles of their distributions when estimated from β FS . Lp-PLA 2 activity, CD40 ligand, TNFα, interleukin-18, and myeloperoxidase heritability showed no significant quantile-dependence. Conclusion: The heritabilities of circulating Lp-PLA 2 -mass, sP-selectin, sICAM-1, TNFR2, osteoprotegerin and soluble ST2 concentrations are quantile-dependent, which may contribute to purported genetic modulations of: 1) sP-selectin’s relationships to venous thrombosis, pulmonary hypertension, type 2 diabetes and atorvastatin treatment; 2) sICAM-I’s relationships to brain abscess and atorvastatin treatment; and 3) Lp-PLA 2 ’s relationships to myocardial infarction and preeclampsia.

60 APPLIED LIFE SCIENCES↗