scholarly journals O3C.1 Silica exposure in swedish iron foundries and biological markers of inflammation and coagulation in blood

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A25.2-A25
Author(s):  
Lena Andersson ◽  
Ing-Liss Bryngelsson ◽  
Håkan Westberg

BackgroundWork-related exposure to silica is a health hazard worldwide causing i.e. silicosis. Inflammation is known to be a cause of cardiovascular diseases and some studies have presented elevated cardiovascular disease mortality in relation to silica exposure. The aim of this study was to investigate the relationship between inhalation of exposure to silica in Swedish iron foundries and markers of inflammation and coagulation in blood.MethodsPersonal sampling of respirable dust and silica was performed for 85 subjects in three Swedish iron foundries. Stationary measurements were used to study concentrations of respirable dust and silica, inhalable and total dust, PM10 and PM2.5, the particle surface area and the particle number concentrations. The markers of inflammation analyzed were, interleukins (IL-1β, IL-6, IL-8, IL-10 and IL-12), C-reactive protein, serum amyloid A (SAA), and markers of coagulation fibrinogen, factor VIII (FVIII), von Willebrand factor, and d-dimer were measured in plasma or serum. The sampling was performed on the second or third day of a working week following a work free weekend, and additional sampling on the fourth or fifth day.The personal and stationary measurement data were categorized into three classes to introduce high contrast with a minimum of 10 workers in each group. A mixed model analysis adjusted for sex, age, smoking, infections, blood group, sampling day and BMI was used.ResultsFor personal sampling the average 8 hour time-weighted average air concentration of respirable dust were 0.85 mg/m3 and respirable silica 0.052 mg/m3. For the high exposure group, statistically significant increased levels of SAA, fibrinogen and FVIII were determined for some exposure measures.ConclusionsThis study may indicate an increased risk of cardiovascular disease when observing relations between particle exposure and inflammatory markers.

2019 ◽  
Vol 20 (9) ◽  
pp. 2154 ◽  
Author(s):  
Mercurio ◽  
Lobasso ◽  
Barbieri ◽  
Parrella ◽  
Ciervo ◽  
...  

Background and aim: Systemic lupus erythematosus (SLE) is associated with increased risk of cardiovascular disease (CVD). Among many mechanisms, accelerated atherosclerosis, endothelial dysfunction, and hypercoagulability play a main role. Here, we investigate whether inflammatory, serological and clinical markers of SLE determine and correlate with arterial stiffness in SLE patients. Materials and methods: Routine blood samples, inflammatory mediators, specific antibodies, and 24 h proteinuria were measured in 43 SLE patients and 43 age and sex-matched controls using routine laboratory assays. We also assessed arterial stiffness by measuring radial artery applanation tonometry-derived augmentation index (AI), normalized AI (AIx@75), aortic pulse pressure, central systolic, diastolic and peripheral blood pressure. Results: SLE patients showed a significantly greater arterial stiffness vs. controls, as demonstrated by the significantly higher AIx@75 and aortic pulse pressure. Interestingly, regression analysis showed that age, systolic pulse pressure, inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), daily dose of glucocorticoids, and cumulative organ damage positively correlated with arterial stiffness. Conclusions: SLE patients show increased arterial stiffness which correlates with markers of inflammation, that is involved in early alterations in arterial walls. Applanation tonometry can be used to screen SLE patients for subclinical vascular damage to implement prevention strategies for CVD.


2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1585.2-1585
Author(s):  
N. Garg ◽  
A. Syngle ◽  
D. Gera ◽  
S. Kaur

Background:Systemic sclerosis (SSc) patients have an increased risk for atherosclerotic cardiovascular disease (CVD), possibly mediated by inflammatory and fibrotic mechanisms1. However, pathogenesis of accelerated atherosclerosis in SSc remains to be elucidated. Endothelial dysfunction is the key initial event in atherosclerosis. Predictors for rapid evolution of cardiovascular complications would be highly desirable for CV risk stratification. This study aims to assess endothelial function and atherosclerosis in SSc, in context of markers of inflammation and vascular function in SSc patients.Objectives:To assess endothelial function and atherosclerosis in SSc in context of markers of inflammation and vascular function in SSc patients.Methods:A cross-sectional study was performed in 20 SSc patients meeting the 2013 European League Against Rheumatism (EULAR) and American College of Rheumatology (ACR) classification criteria and 18 healthy controls matched for age and sex. Flow-mediated dilatation (FMD) assessed by AngioDefender and CIMT measured ultrasonographically. Disease-specific measures included: Disease duration, Modified Rodnan Skin Score (mRSS), EUSTAR activity score in SSc. We also assayed markers of inflammation, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), proinflammatory cytokines (interleukin IL-1, IL-6, and IL-17), and endothelial dysfunction including lipids, serum nitrite and TBARS (marker of oxidative stress). Quality of life measured by Scleroderma Health Assessment Questionnaire (SHAQ).Results:FMD is significantly lower in SSc patients compared with controls (6.13±0.35% vs. 9.12±0.25%, p≤0.05). CIMT is significantly higher in SSc patients compared with controls (0.071±0.04cm vs. 0.035±0.02cm p≤0.05). Compared with controls, SSc patients had significantly (p≤0.05) elevated mRSS, EUSTAR score, ESR, CRP, IL-1, IL-6, IL-17, nitrite, TBARS and SHAQ whereas HDL levels are significantly reduced in SSc compared with controls (p≤0.05). In SSc, FMD inversely correlated with EUSTAR score, mRSS, IL-6 (Fig. 1A), serum nitrite (Fig. 1B), TBARS (Fig. 1C) and CIMT (Fig. 1D). CIMT positively correlated with age (Fig. 2A), disease duration, CRP (Fig. 2B) and IL-17 (Fig. 2C) and inversely correlated with HDL (Fig. 2D) (p< 0.05).Conclusion:In the present study, FMD and CIMT are impaired in SSc, indicating endothelial dysfunction and accelerated atherosclerosis, respectively. EUSTAR score, mRSS, IL-6, serum nitrite, CIMT and TBARS predicted endothelial dysfunction. Age, disease duration, CRP, IL-17, HDL and impaired FMD predicted accelerated atherosclerosis. SSc-related inflammatory mechanisms (IL-6, IL-17) and markers of vascular function (CRP, serum nitrite and TBARS) may all be involved in the development of vascular disease in SSc. Cytokine-triggered inflammation mediated by nitrite and TBARS is associated with endothelial dysfunction and accelerated atherosclerosis in SSc. These markers would possibly serve as predictors of endothelial dysfunction and atherosclerosis and more importantly therapeutic targets to prevent premature atherosclerosis and cardiovascular disease in SSc.References:[1]Pagkopoulou E, Poutakidou M, Garyfallos A, Kitas G, Dimitroulas T. Cardiovascular risk in systemic sclerosis: Micro- and Macro-vascular involvement. Indian Journal of Rheumatology 2017;12:S211-7.Acknowledgments:NoneDisclosure of Interests:None declared


2018 ◽  
Vol 25 (35) ◽  
pp. 4507-4517 ◽  
Author(s):  
Mauro Rigato ◽  
Gian Paolo Fadini

Background: Circulating progenitor cells (CPCs) and endothelial progenitor cells (EPCs) are immature cells involved in vascular repair and related to many aspects of macro and microvascular disease. <p> Objective: We aimed to review studies reporting the prognostic role of CPCs/EPCs measurement on development of cardiovascular disease and microangiopathy. <p> Methods and Results: We reviewed the English language literature for prospective observational studies reporting the future development of cardiovascular disease or microangiopathy in patients having a baseline determination of CPCs/EPCs. We retrieved 34 studied reporting on cardiovascular outcomes and 2 studies reporting on microvascular outcomes. Overall, a reduced baseline level of CPCs/EPCs was associated with a significant increased risk of cardiovascular events, all-cause death, and onset/progression of microangiopathy. The most predictive phenotypes were CD34+ and CD34+CD133+. The main limitation was related to the high heterogeneity among studies in terms of patient characteristics and cell phenotypes. <p> Conclusion: The present review shows that a reduced level of circulating progenitor cells is a risk factor for the development of future cardiovascular events and death. In addition, low CPCs/EPCs levels predict the onset or worsening of microalbuminuria and retinopathy in diabetic patients.


2020 ◽  
Vol 26 (43) ◽  
pp. 5617-5627
Author(s):  
Mirjana Stojković ◽  
Miloš Žarković

The prevalence of subclinical hypothyroidism (SH) is 3-10%. The prevalence of subclinical hyperthyroidism (SHr) is 0.7-9.7%. Thyroid hormones affect cardiac electrophysiology, contractility, and vasculature. SH is associated with an increased risk of coronary heart disease (CHD), especially in subjects under 65. SHr seems to be associated with a slightly increased risk of CHD and an increase in CHD-related mortality. Both SH and SHr carry an increased risk of developing heart failure (HF), especially in those under 65. Both SH and SHr are associated with worse prognoses in patients with existing HF. SH is probably not associated with atrial fibrillation (AF). SHr, low normal thyroid-stimulating hormone (TSH) and high normal free thyroxine (FT4) are all associated with the increased risk of AF. An association between endothelial dysfunction and SH seems to exist. Data regarding the influence of SHr on the peripheral vascular system are conflicting. SH is a risk factor for stroke in subjects under 65. SHr does not increase the risk of stroke. Both SH and SHr have an unfavourable effect on cardiovascular disease (CVD) and all-cause mortality. There is a U-shaped curve of mortality in relation to TSH concentrations. A major factor that modifies the relation between subclinical thyroid disease (SCTD) and mortality is age. SH increases blood pressure (BP). SHr has no significant effect on BP. Lipids are increased in patients with SH. In SHr, high-density lipoprotein cholesterol and lipoprotein( a) are increased. SCTD should be treated when TSH is over 10 mU/l or under 0.1 mU/l. Treatment indications are less clear when TSH is between normal limits and 0.1 or 10 mU/L. The current state of knowledge supports the understanding of SCTD’s role as a risk factor for CVD development. Age is a significant confounding factor, probably due to age-associated changes in the TSH reference levels.


2019 ◽  
Vol 17 (3) ◽  
pp. 298-306 ◽  
Author(s):  
Charalambos Vlachopoulos ◽  
Dimitrios Terentes-Printzios ◽  
Konstantinos Aznaouridis ◽  
Nikolaos Ioakeimidis ◽  
Panagiotis Xaplanteris ◽  
...  

Background: Recent data advocate adoption of a more intensive treatment strategy for management of blood pressure (BP). </P><P> Objective: We investigated whether the overall effects of the Systolic Blood Pressure Intervention Trial (SPRINT) are applicable to cardiovascular disease (CVD) patients. </P><P> Methods: In a post hoc analysis we analyzed data from SPRINT that randomly assigned 9361 individuals to a systolic BP (SBP) target of <120 mmHg (intensive treatment) or <140 mmHg (standard treatment). 1562 patients had clinically evident CVD (age=70.3±9.3 years, 24% females) at study entry and were followed for 3.1 years. Further, we assessed the effect of low (<150 mmHg) baseline SBP on outcome. </P><P> Results: In CVD patients, there was no benefit from the intensive treatment regarding all endpoints, except for a marginally significant benefit on all-cause mortality (hazard ratio [HR]: 0.67; 95% confidence interval [CI], 0.45 to 1.00; p=0.0509). Further, while there was no increase in serious adverse events (SAE) in the intensive group, there was increased risk for study-related SAE, acute renal failure and electrolyte abnormalities. In patients with low baseline SBP there was a beneficial effect on allcause mortality (HR: 0.56; 95% CI: 0.33 to 0.96; p=0.033), but with greater stroke incidence (HR: 2.94; 95% CI: 1.04 to 8.29; p=0.042). </P><P> Conclusion: We confirm the beneficial effect of the intensive strategy in SPRINT study on all-cause mortality and the harmful effect on specific adverse outcomes in patients with CVD. However, in patients with low baseline SBP stroke may increase.


2020 ◽  
Vol 18 (5) ◽  
pp. 473-487 ◽  
Author(s):  
Charalampos Papagoras ◽  
Paraskevi V. Voulgari ◽  
Alexandros A. Drosos

The spondyloarthritides are a group of chronic systemic inflammatory joint diseases, the main types being ankylosing spondylitis (AS) and psoriatic arthritis (PsA). Evidence accumulating during the last decades suggests that patients with AS or PsA carry an increased risk for cardiovascular disease and cardiovascular death. This risk appears to be mediated by systemic inflammation over and above classical cardiovascular risk factors. The excess cardiovascular risk in those patients has been formally acknowledged by scientific organizations, which have called physicians’ attention to the matter. The application by Rheumatologists of new effective anti-rheumatic treatments and treat-to-target strategies seems to benefit patients from a cardiovascular point of view, as well. However, more data are needed in order to verify whether anti-rheumatic treatments do have an effect on cardiovascular risk and whether there are differences among them in this regard. Most importantly, a higher level of awareness of the cardiovascular risk is needed among patients and healthcare providers, better tools to recognize at-risk patients and, ultimately, commitment to address in parallel both the musculoskeletal and the cardiovascular aspect of the disease.


2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
E Leiter ◽  
K L Greenberg ◽  
M Donchin ◽  
O Keidar ◽  
S Siemiatycki ◽  
...  

Abstract Background Women from low socio-economic, culturally insular populations are at increased risk for cardiovascular disease (CVD). The ultra-Orthodox Jewish (UOJ) community in Israel is a difficult to access, rapidly growing low socio-economic, insular minority with numerous obstacles to health. The current study investigates CVD-related risk factors (RF) in a sample of OUJ women, comparing sample characteristics with the general population. Addressing the questions, 'Are UOJ women at increased risk for CVD?', 'Which RFs should be addressed beyond the general population's?', this study can inform public health initiatives (PHI) for this and similar populations. Methods Self-administered questionnaires completed by a cluster randomized sample of 239 women from a UOJ community included demographics, fruit, vegetables, and sweetened drink consumption, secondhand smoke exposure, physical activity (PA) engagement, and BMI. Population statistics utilized for comparison of demographic and cardiovascular risk factors were obtained from government-sponsored national surveys. Results Compared with the general population, UOJ women were less likely to consume 5 fruits and vegetables a day (12.7% vs. 24.3%, p&lt;.001) and more likely to consume &gt; 5 cups of sweetened beverages a day (18.6% vs. 12.6%, p=.019). UOJ women also reported less secondhand smoke exposure (7.2% vs. 51.4%, p&lt;.001) and higher rates of PA recommendation adherence (60.1% vs. 25.6%, p&lt;.0001) than the general population. Obesity was higher in UOJ women (24.3% vs. 16.1%, p&lt;.0001). Conclusions This study suggests that PHIs in this population target healthy weight maintenance, nutrition, and PA. As a consequence of this study, the first CVD prevention intervention has been implemented in this population, targeting the identified RFs. Utilizing a mixed methods and community-based participatory approach, this innovative 3-year intervention reached over 2,000 individuals. Key messages This study identified nutrition risk behaviors and high levels of obesity in a difficult to access, minority population. This study informed the planning and implementation of a community-based PHI.


BMC Medicine ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Min Gao ◽  
Susan A. Jebb ◽  
Paul Aveyard ◽  
Gina L. Ambrosini ◽  
Aurora Perez-Cornago ◽  
...  

Abstract Background Traditionally, studies investigating diet and health associations have focused on single nutrients. However, key nutrients co-exist in many common foods, and studies focusing solely on individual nutrients may obscure their combined effects on cardiovascular disease (CVD) and all-cause mortality. We aimed to identify food-based dietary patterns which operate through excess energy intake and explain high variability in energy density, free sugars, saturated fat, and fiber intakes and to investigate their association with total and fatal CVD and all-cause mortality. Methods Detailed dietary data was collected using a 24-h online dietary assessment on two or more occasions (n = 116,806). We used reduced rank regression to derive dietary patterns explaining the maximum variance. Multivariable Cox-proportional hazards models were used to investigate prospective associations with all-cause mortality and fatal and non-fatal CVD. Results Over an average of 4.9 years of follow-up, 4245 cases of total CVD, 838 cases of fatal CVD, and 3629 cases of all-cause mortality occurred. Two dietary patterns were retained that jointly explained 63% of variation in energy density, free sugars, saturated fat, and fiber intakes in total. The main dietary pattern was characterized by high intakes of chocolate and confectionery, butter and low-fiber bread, and low intakes of fresh fruit and vegetables. There was a positive linear association between the dietary pattern and total CVD [hazard ratio (HR) per z-score 1.07, 95% confidence interval (CI) 1.04–1.09; HRtotal CVD 1.40, 95% CI 1.31–1.50, and HRall-cause mortality 1.37, 95% CI 1.27–1.47 in highest quintile]. A second dietary pattern was characterized by a higher intakes of sugar-sweetened beverages, fruit juice, and table sugar/preserves. There was a non-linear association with total CVD risk and all-cause mortality, with increased risk in the highest quintile [HRtotal CVD 1.14, 95% CI 1.07–1.22; HRall-cause mortality 1.11, 95% CI 1.03–1.19]. Conclusions We identified dietary patterns which are associated with increased risk of CVD and all-cause mortality. These results help identify specific foods and beverages which are major contributors to unhealthy dietary patterns and provide evidence to underpin food-based dietary advice to reduce health risks.


2021 ◽  
Vol 14 ◽  
pp. 117954412110287
Author(s):  
Mir Sohail Fazeli ◽  
Vadim Khaychuk ◽  
Keith Wittstock ◽  
Boris Breznen ◽  
Grace Crocket ◽  
...  

Objective: To scope the current published evidence on cardiovascular risk factors in rheumatoid arthritis (RA) focusing on the role of autoantibodies and the effect of antirheumatic agents. Methods: Two reviews were conducted in parallel: A targeted literature review (TLR) describing the risk factors associated with cardiovascular disease (CVD) in RA patients; and a systematic literature review (SLR) identifying and characterizing the association between autoantibody status and CVD risk in RA. A narrative synthesis of the evidence was carried out. Results: A total of 69 publications (49 in the TLR and 20 in the SLR) were included in the qualitative evidence synthesis. The most prevalent topic related to CVD risks in RA was inflammation as a shared mechanism behind both RA morbidity and atherosclerotic processes. Published evidence indicated that most of RA patients already had significant CV pathologies at the time of diagnosis, suggesting subclinical CVD may be developing before patients become symptomatic. Four types of autoantibodies (rheumatoid factor, anti-citrullinated peptide antibodies, anti-phospholipid autoantibodies, anti-lipoprotein autoantibodies) showed increased risk of specific cardiovascular events, such as higher risk of cardiovascular death in rheumatoid factor positive patients and higher risk of thrombosis in anti-phospholipid autoantibody positive patients. Conclusion: Autoantibodies appear to increase CVD risk; however, the magnitude of the increase and the types of CVD outcomes affected are still unclear. Prospective studies with larger populations are required to further understand and quantify the association, including the causal pathway, between specific risk factors and CVD outcomes in RA patients.


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