Journal articles on the topic 'Sle, Oxidative stress, Fibrinogen, Cardiovascular risk'
To see the other types of publications on this topic, follow the link: Sle, Oxidative stress, Fibrinogen, Cardiovascular risk.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 33 journal articles for your research on the topic 'Sle, Oxidative stress, Fibrinogen, Cardiovascular risk.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Segal, BM, W. Thomas, X. Zhu, A. Diebes, G. McElvain, E. Baechler, and M. Gross. "Oxidative stress and fatigue in systemic lupus erythematosus." Lupus 21, no. 9 (April 16, 2012): 984–92. http://dx.doi.org/10.1177/0961203312444772.
Full textAbstract:
Objective: The objective of this study is to investigate the relationship of oxidative stress to fatigue in systemic lupus erythematosus (SLE). Methods: Patients with a confirmed diagnosis of SLE by ACR criteria and healthy controls completed validated questionnaires to assess depression and fatigue. Fatigue was measured with the Fatigue Severity Scale (FSS) and the Profile of Fatigue (Prof-F). Visual analogue scales (VAS) were also used to assess fatigue and pain. Depression was measured with the Center for Epidemiologic Studies Depression Scale (CES-D). Plasma F2-isoprostane was measured with gas chromatography/mass spectroscopy to assess oxidative stress. Evaluation included medical record review, physical exam and calculation of body mass index (BMI), disease activity (SLEDAI) and damage (SLICC) in the SLE patients. Results: Seventy-one SLE patients with low disease activity (mean SLEDAI = 1.62 standard error (SE) 0.37, range 0–8) were compared to 51 controls. Fatigue-limiting physical activity (defined as FSS ≥ 4) was present in 56% of patients and 12% of controls. F2-isoprostane was higher in SLE patients with fatigue compared to not-fatigued SLE subjects ( p = .0076) who were otherwise similar in ethnicity, disease activity and cardiovascular risk factors. Plasma F2-isoprostane was strongly correlated with FSS and Profile of Somatic Fatigue (Prof-S) ( p < .0001), VAS fatigue ( p = .005), CES-D ( p = .008) and with BMI ( p = .0001.) In a multivariate model, F2-isoprostane was a significant predictor of FSS after adjustment for age, BMI, pain and depression ( p = .0002). Conclusion: Fatigue in SLE patients with low disease activity is associated with increased F2-isoprostane. F2-isoprostane could provide a useful biomarker to explore mitochondrial function and the regulation of oxidative pathways in patients with SLE in whom fatigue is a debilitating symptom.
2
Ruiz-Limon, Patricia, Nuria Barbarroja, Carlos Perez-Sanchez, Maria Angeles Aguirre, Maria Laura Bertolaccini, Munther A. Khamashta, Antonio Rodriguez-Ariza, et al. "Atherosclerosis and cardiovascular disease in systemic lupus erythematosus: effects of in vivo statin treatment." Annals of the Rheumatic Diseases 74, no. 7 (March 21, 2014): 1450–58. http://dx.doi.org/10.1136/annrheumdis-2013-204351.
Full textAbstract:
ObjectiveStatins may have beneficial vascular effects in systemic lupus erythematosus (SLE) beyond their cholesterol-lowering action, although the mechanisms involved are not completely understood. We investigated potential mechanisms involved in the efficacy of fluvastatin in preventing atherothrombosis in SLE.MethodsEighty-five patients with SLE and 62 healthy donors were included in the study. Selected patients (n=27) received 20 mg/day fluvastatin for 1 month. Blood samples were obtained before the start and at the end of treatment. Monocytes from five patients were treated in vitro with fluvastatin.ResultsIncreased prothrombotic and inflammatory variables were found in patients with SLE. SLE monocytes displayed altered mitochondrial membrane potential and increased oxidative stress. Correlation and association analyses demonstrated a complex interplay among autoimmunity, oxidative stress, inflammation and increased risk of atherothrombosis in SLE. Fluvastatin treatment of patients for 1 month reduced the SLE Disease Activity Index and lipid levels, oxidative status and vascular inflammation. Array studies on monocytes demonstrated differential expression in 799 genes after fluvastatin treatment. Novel target genes and pathways modulated by fluvastatin were uncovered, including gene networks involved in cholesterol and lipid metabolism, inflammation, oxidative stress and mitochondrial activity. Electron microscopy analysis showed increased density volume of mitochondria in monocytes from fluvastatin-treated patients, who also displayed higher expression of genes involved in mitochondrial biogenesis. In vitro treatment of SLE monocytes confirmed the results obtained in the in vivo study.ConclusionsOur overall data suggest that fluvastatin improves the impairment of a redox-sensitive pathway involved in processes that collectively orchestrate the pathophysiology of atherothrombosis in SLE.
3
Baniamerian, H., F. Bahrehmand, A. Vaisi-Raygani, Z. Rahimi, and T. Pourmotabbed. "Angiotensin type 1 receptor A1166C polymorphism and systemic lupus erythematosus: correlation with cellular immunity and oxidative stress markers." Lupus 26, no. 14 (May 22, 2017): 1534–39. http://dx.doi.org/10.1177/0961203317711008.
Full textAbstract:
Angiotensin II, one of the rennin–angiotensin system components, is important in the cardiovascular hemodynamic and plays an important role in the development of cardiovascular disease in systemic lupus erythematosus (SLE) patients. The angiotensin II, through interaction with angiotensin II type 1 receptor (AGTR1), promotes proliferation, inflammation and fibrosis. The single nucleotide polymorphism of the AGTR1 (dbSNP: rs5186) gene can be associated with development and progression of SLE disease. The aims of this study were to compare the frequency of AGTR1 rs5186 in SLE patients with healthy individuals and to evaluate possible association between AGTR1 A1166C gene polymorphism and serum level of lipids, neopterin and malondialdehyde in SLE patients from a population of West Iran. One hundred SLE patients and 98 healthy subjects were studied. The AGTR1 A1166C polymorphism was detected by polymerase chain reaction– restriction fragment length polymorphism method and the serum lipid profile was obtained by enzymatic method. Neopterin and malondialdehyde were detected using high-performance liquid chromatography. We did not detect significant association between AGTR1 A1166C polymorphism and the risk of SLE. The levels of triglyceride (225 ± 118 mg/dl), neopterin (30 ± 24 nmol/l) and malondialdehyde (25 ± 9.6 nmol/l) in SLE patients were significantly higher than those in control subjects (139 ± 56 mg/dl, p = 0.03, 6.4 ± 2, p = 0.03, 9.4 ± 2.5 nmol/l, p = 0.01, respectively). Individuals with AGTR1 AC + CC genotype had higher levels of total cholesterol and malondialdehyde compared with those with AGTR1 AA genotype. SLE patients with either AGTR1 AA or AGTR1AC + CC genotype had significantly higher malondialdehyde or neopterin levels compared with the corresponding control subjects. In conclusion, although the present study did not find any association between AGTR1 A1166C polymorphism and the risk of SLE, the presence of this polymorphism was associated with higher levels of malondialdehyde and higher concentration of neopterin in patients.
4
Khaliq, Shagufta, Mudassar Ali Roomi, Shaheena Naz, Komal Iqbal, Muhammad Imran Ashraf, and Muniza Saeed. "Obstructive Sleep Apnea and Cardiovascular Risk Markers (Fibrinogen & Gamma Glutamyl Transferase) in Obese Males." Pakistan Journal of Medical and Health Sciences 15, no. 12 (December 10, 2021): 3312–14. http://dx.doi.org/10.53350/pjmhs2115123312.
Full textAbstract:
Aim: To determine and compare gamma glutamyl transferase (GGT) and fibrinogen among obese males with and without obstructive sleep apnea (OSA). Second objective was to investigate correlation between blood pressure and GGT. Methodology: Sixty-four obese males aged 20-45 years with BMI > 25kg/m2 were included by convenience sampling. The study was conducted, after obtaining ethical approval from IRB, at the Department of Physiology, Post Graduate Medical Institute, Lahore from August 2014 to May 2015. Participants having acute or chronic inflammatory conditions were excluded. Participants were screened for OSA by Berlin and STOP BANG questionnaires. Diagnosis of OSA was made by overnight portable pulse oximetry. The participants were divided into two groups. Group I had 32 obese males with OSA. Group II contained 32 obese males without OSA. After an overnight fasting of 10-12 hours blood samples were drawn. Serum fibrinogen and GGT were measured by spectrophotometer. The data was analyzed using SPSS-22. Quantitative variables were compared between the two groups by Mann-Whitney U test. Spearman correlation was used to correlate blood pressure and GGT among the participants. Results: Fibrinogen was significantly raised (p=0.015) in obese males with OSA. Systolic blood pressure (p=0.003), diastolic blood pressure (p=0.001) and mean arterial blood pressure (p<0.001) showed strong positive correlation with GGT in obese males with OSA. Conclusion: Proinflammatory, procoagulant and proatherogenic marker fibrinogen levels were significantly raised in obese otherwise healthy males with OSA. Oxidative stress marker GGT showed strong positive correlation with blood pressure in obese males with OSA. Keywords: Fibrinogen, gamma glutamyl transferase, inflammation, obstructive sleep apnea, oxidative stress
5
Ryan, Michael J. "Young Investigator Award Lecture of the APS Water and Electrolyte Homeostasis Section, 2008: The pathophysiology of hypertension in systemic lupus erythematosus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1258—R1267. http://dx.doi.org/10.1152/ajpregu.90864.2008.
Full textAbstract:
Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects women during their reproductive years. Although SLE can affect any organ system, the kidneys are prominently involved in the form of immune complex glomerulonephritis. In addition, in women with SLE, risk for the development of cardiovascular disease is dramatically increased. Hypertension is a major risk factor for cardiovascular disease and is highly prevalent in women with SLE. Nevertheless, there has been little exploration of the pathophysiological mechanisms that promote SLE hypertension. This review discusses the role of several mechanisms, with an emphasis on the kidney, in SLE hypertension. These mechanisms include the renin-angiotensin system, endothelin, oxidative stress, sex steroids, metabolic changes, peroxisome proliferator-activated receptor-γ, and, perhaps most importantly, chronic inflammation and cytokines. Growing evidence suggests a link between chronic inflammation and hypertension. Therefore, elucidation of mechanisms that promote SLE hypertension may be of significant value not only for patients with SLE, but also for a better understanding of the basis for essential hypertension.
6
Floris, Alberto, Matteo Piga, Arduino Aleksander Mangoni, Alessandra Bortoluzzi, Gian Luca Erre, and Alberto Cauli. "Protective Effects of Hydroxychloroquine against Accelerated Atherosclerosis in Systemic Lupus Erythematosus." Mediators of Inflammation 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/3424136.
Full textAbstract:
Cardiovascular (CV) morbidity and mortality are a challenge in management of patients with systemic lupus erythematosus (SLE). Higher risk of CV disease in SLE patients is mostly related to accelerated atherosclerosis. Nevertheless, high prevalence of traditional cardiovascular risk factors in SLE patients does not fully explain the increased CV risk. Despite the pathological bases of accelerated atherosclerosis are not fully understood, it is thought that this process is driven by the complex interplay between SLE and atherosclerosis pathogenesis. Hydroxychloroquine (HCQ) is a cornerstone in treatment of SLE patients and has been thought to exert a broad spectrum of beneficial effects on disease activity, prevention of damage accrual, and mortality. Furthermore, HCQ is thought to protect against accelerated atherosclerosis targeting toll-like receptor signaling, cytokine production, T-cell and monocyte activation, oxidative stress, and endothelial dysfunction. HCQ was also described to have beneficial effects on traditional CV risk factors, such as dyslipidemia and diabetes. In conclusion, despite lacking randomized controlled trials unambiguously proving the protection of HCQ against accelerated atherosclerosis and incidence of CV events in SLE patients, evidence analyzed in this review is in favor of its beneficial effect.
7
Sciatti, Edoardo, Ilaria Cavazzana, Enrico Vizzardi, Ivano Bonadei, Micaela Fredi, Mara Taraborelli, Romina Ferizi, Marco Metra, Angela Tincani, and Franco Franceschini. "Systemic Lupus Erythematosus and Endothelial Dysfunction: A Close Relationship." Current Rheumatology Reviews 15, no. 3 (July 31, 2019): 177–88. http://dx.doi.org/10.2174/1573397115666181126105318.
Full textAbstract:
Background: Accelerated atherosclerosis, responsible for premature cardiovascular disease, has been estimated to develop or progress in 10% of systemic lupus erythematosus (SLE) patients each year and to be 6-fold more frequent in SLE compared with the general population. The mechanisms underlying accelerated atherosclerosis in SLE are complex and involve classical and “non-classical” cardiovascular risk factors. Subclinical and disseminated atherosclerosis is associated with endothelial dysfunction and arterial stiffness. Objective: The aim of this review is to analyze the association between SLE and endothelial dysfunction. Results and Conclusion: Different mechanisms have been proposed to explain the prevalence of endothelial dysfunction in SLE, which are briefly reported in this review: impaired clearance of apoptotic cells, oxidative stress markers, B cell activation with different circulating autoantibodies, different subtypes of T lymphocytes, cytokine cascade. Several studies and meta-analyses show a significant trend towards a prevalence of subclinical accelerated atherosclerosis in patients with SLE compared with healthy controls, since childhood. Based on general considerations, we suggest a multidisciplinary management to assess endothelial dysfunction at the diagnosis of the disease and to periodically search for and treat the traditional cardiovascular risk factors. Prospective studies are needed to confirm the benefits of this management.
8
Harjai, Kishore J. "Potential New Cardiovascular Risk Factors: Left Ventricular Hypertrophy, Homocysteine, Lipoprotein(a), Triglycerides, Oxidative Stress, and Fibrinogen." Annals of Internal Medicine 131, no. 5 (September 7, 1999): 376. http://dx.doi.org/10.7326/0003-4819-131-5-199909070-00009.
Full text
9
Kostopoulou, Myrto, Dionysis Nikolopoulos, Ioannis Parodis, and George Bertsias. "Cardiovascular Disease in Systemic Lupus Erythematosus: Recent Data on Epidemiology, Risk Factors and Prevention." Current Vascular Pharmacology 18, no. 6 (September 17, 2020): 549–65. http://dx.doi.org/10.2174/1570161118666191227101636.
Full textAbstract:
Systemic Lupus Erythematosus (SLE) is associated with increased risk for accelerated atherosclerosis and cardiovascular (CV) events including coronary heart disease, cerebrovascular and peripheral artery disease. CV events occur both early and late during the disease course, with younger patients being at much higher risk than age-matched counterparts. The risk cannot be fully accounted for by the increased prevalence of traditional atherosclerotic factors and may be due to pathophysiologic intermediates such as type I interferons and other inflammatory cytokines, oxidative stress, activated granulocytes and production of extracellular chromatin traps, antiphospholipid and other autoantibodies causing dysfunction of lipoproteins, altogether resulting in endothelial injury and pro-atherogenic dyslipidaemia. These mechanisms may be further aggravated by chronic intake of prednisone (even at doses <7.5 mg/day), whereas immunomodulatory drugs, especially hydroxychloroquine, may exert antiatherogenic properties. To date, there is a paucity of randomized studies regarding the effectiveness of preventative strategies and pharmacological interventions specifically in patients with SLE. Nevertheless, both the European League Against Rheumatism recommendations and extrapolated evidence from the general population emphasize that SLE patients should undergo regular monitoring for atherosclerotic risk factors and calculation of the 10-year CV risk. Risk stratification should include diseaserelated factors and accordingly, general (lifestyle modifications/smoking cessation, antihypertensive and statin treatment, low-dose aspirin in selected cases) and SLE-specific (control of disease activity, minimization of glucocorticoids, use of hydroxychloroquine) preventive measures be applied as appropriate. Further studies will be required regarding the use of non-invasive tools and biomarkers for CV assessment and of risk-lowering strategies tailored to SLE.
10
Taylor, Erin B., and Michael J. Ryan. "Understanding mechanisms of hypertension in systemic lupus erythematosus." Therapeutic Advances in Cardiovascular Disease 11, no. 1 (July 31, 2016): 20–32. http://dx.doi.org/10.1177/1753944716637807.
Full textAbstract:
Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder that predominately affects women of reproductive age. Hypertension is an important cardiovascular risk factor that is prevalent in this patient population. Despite the high incidence of hypertension in women with SLE, the pathophysiological mechanisms underlying the development of hypertension remain poorly understood. This review will focus on disease-related factors, including inflammation, autoantibodies, and sex hormones that may contribute to hypertension in patients with SLE. In addition, we will highlight studies performed by our laboratory using the female NZBWF1 (F1 hybrid of New Zealand Black and New Zealand White strains) mouse model, a spontaneous model of SLE that mimics human disease and develops hypertension and renal injury. Specifically, using female NZBWF1 mice, we have demonstrated that multiple factors contribute to the pathogenesis of hypertension, including the inflammatory cytokine, tumor necrosis factor (TNF)-α, oxidative stress, as well as B-cell hyperactivity and autoantibody production.
11
Binti, Nabila Nawar, Nourin Ferdausi, Md Eahsanul Karim Anik, and Laila Noor Islam. "Association of albumin, fibrinogen, and modified proteins with acute coronary syndrome." PLOS ONE 17, no. 7 (July 26, 2022): e0271882. http://dx.doi.org/10.1371/journal.pone.0271882.
Full textAbstract:
Acute coronary syndrome (ACS) comprises a pathophysiological spectrum of cardiovascular diseases related to atherosclerotic coronary plaque erosion. Oxidative stress and inflammation play pivotal roles in the development and progression of atherosclerosis, which affects circulatory proteins, including albumin and fibrinogen, thereby causing an imbalance in albumin to globulin and fibrinogen to albumin ratios. This study aimed to assess the effect of oxidative stress on circulatory proteins, correlate these parameters, and investigate their significance in patients with ACS. In this case-control study, the major blood proteins in patients with ACS and a control group were evaluated using standard methods. Out of 70 ACS cases, 75.7% had ST-elevation myocardial infarction (STEMI), 18.6% had non-STEMI, and 5.7% had unstable angina. The mean cardiac troponin I level in patients was 12.42 ng/mL. The patients demonstrated a significantly reduced level of human serum albumin (HSA), 3.81 ± 0.99 g/dL, compared to controls, 5.33 ± 0.66 g/dL. The albumin to globulin ratio (AGR) was significantly depressed in patients while their mean fibrinogen level and the fibrinogen to albumin ratio (FAR) were significantly higher. Multivariate logistic regression analysis showed that albumin and fibrinogen were significantly associated with the risk of ACS, showing the potential of these parameters to be used for risk assessment of ACS. The ischemia modified albumin (IMA) and protein carbonyls were significantly higher in patients which showed significant positive correlations with FAR. Albumin, IMA and protein carbonyls were found to have high diagnostic sensitivity and specificity for ACS. Overall, these circulatory and modified proteins in ACS patients, particularly lower HSA, AGR, and higher IMA and protein carbonyls may help assess risk.
12
Lopez-Pedrera, Chary, Nuria Barbarroja, Alejandra Mª Patiño-Trives, Maria Luque-Tévar, Carmen Torres-Granados, Mª Angeles Aguirre-Zamorano, Eduardo Collantes-Estevez, and Carlos Pérez-Sánchez. "Role of microRNAs in the Development of Cardiovascular Disease in Systemic Autoimmune Disorders." International Journal of Molecular Sciences 21, no. 6 (March 16, 2020): 2012. http://dx.doi.org/10.3390/ijms21062012.
Full textAbstract:
Rheumatoid Arthritis (RA), Systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) are the systemic autoimmune diseases (SADs) most associated with an increased risk of developing cardiovascular (CV) events. Cardiovascular disease (CVD) in SADs results from a complex interaction between traditional CV-risk factors, immune deregulation and disease activity. Oxidative stress, dyslipidemia, endothelial dysfunction, inflammatory/prothrombotic mediators (cytokines/chemokines, adipokines, proteases, adhesion-receptors, NETosis-derived-products, and intracellular-signaling molecules) have been implicated in these vascular pathologies. Genetic and genomic analyses further allowed the identification of signatures explaining the pro-atherothrombotic profiles in RA, SLE and APS. However, gene modulation has left significant gaps in our understanding of CV co-morbidities in SADs. MicroRNAs (miRNAs) are emerging as key post-transcriptional regulators of a suite of signaling pathways and pathophysiological effects. Abnormalities in high number of miRNA and their associated functions have been described in several SADs, suggesting their involvement in the development of atherosclerosis and thrombosis in the setting of RA, SLE and APS. This review focusses on recent insights into the potential role of miRNAs both, as clinical biomarkers of atherosclerosis and thrombosis in SADs, and as therapeutic targets in the regulation of the most influential processes that govern those disorders, highlighting the potential diagnostic and therapeutic properties of miRNAs in the management of CVD.
13
Michelucci, Elena, Silvia Rocchiccioli, Melania Gaggini, Rudina Ndreu, Sergio Berti, and Cristina Vassalle. "Ceramides and Cardiovascular Risk Factors, Inflammatory Parameters and Left Ventricular Function in AMI Patients." Biomedicines 10, no. 2 (February 11, 2022): 429. http://dx.doi.org/10.3390/biomedicines10020429.
Full textAbstract:
Background: Ceramides, biologically active lipids correlated to oxidative stress and inflammation, have been associated with adverse outcomes in acute myocardial infarction (AMI). The purpose of this study was to assess the association between ceramides/ratios included in the CERT1 score and increased cardiovascular (CV) risk, inflammatory and left ventricular function parameters in AMI. Methods: high performance liquid chromatography-tandem mass spectrometry was used to identify Cer(d18:1/16:0), Cer(d18:1/18:0), and Cer(d18:1/24:1) levels and their ratios to Cer(d18:1/24:0), in 123 AMI patients (FTGM coronary unit, Massa, Italy). Results: Cer(d18:1/16:0): higher in female patients (<0.05), in patients with dyslipidemia (<0.05), and it directly and significantly correlated with aging, brain natriuretic peptide-BNP, erythrocyte sedimentation rate-ESR and fibrinogen. Cer(d18:1/18:0): higher in females (<0.01) and patients with dyslipidemia (<0.01), and increased according to the number of CV risk factors (considering hypertension, dyslipidemia and diabetes). Moreover, it significantly correlated with BNP, troponin at admission, ESR, C reactive protein-CRP, and fibrinogen. Cer(d18:1/24:1): significantly correlated with aging, BNP, fibrinogen and neutrophils. Cer(d18:1/16:0)/Cer(d18:1/24:0): higher in female patients (<0.05), and in patients with higher wall motion score index-WMSI (>1.7; ≤0.05), and in those with multivessel disease (<0.05). Moreover, it significantly correlated with aging, BNP, CRP, ESR, neutrophil-to-lymphocyte ratio-NRL, and fibrinogen. Cer(d18:1/18:0)/Cer(d18:1/24:0): higher in female patients (<0.001), and increased according to age. Moreover, it was higher in patients with lower left ventricular ejection fraction (<35%, ≤0.01), higher WMSI (>1.7, <0.05), and in those with multivessel disease (0.13 ± 0.06 vs. 0.10 ± 0.05 µM, <0.05), and correlates with BNP, ESR, CRP, fibrinogen and neutrophils, platelets, NLR, and troponin at admission. Multiple regression analysis showed that Cer(d18:1/16:0)/Cer(d18:1/24:0) and Cer(d18:1/18:0)/Cer(d18:1/24:0) remained as independent determinants for WMSI after multivariate adjustment (Std coeff 0.17, T-value 1.9, ≤0.05; 0.21, 2.6, <0.05, respectively). Conclusion: Distinct ceramide species are associated with CV risk, inflammation and disease severity in AMI. Thus, a detailed analysis of ceramides may help to better understand CV pathobiology and suggest these new biomarkers as possible risk predictors and pharmacological targets in AMI patients.
14
Hozawa, Atsushi, David R. Jacobs, Michael W. Steffes, Myron D. Gross, Lyn M. Steffen, and Duk-Hee Lee. "Relationships of Circulating Carotenoid Concentrations with Several Markers of Inflammation, Oxidative Stress, and Endothelial Dysfunction: The Coronary Artery Risk Development in Young Adults (CARDIA)/Young Adult Longitudinal Trends in Antioxidants (YALTA) Study." Clinical Chemistry 53, no. 3 (March 1, 2007): 447–55. http://dx.doi.org/10.1373/clinchem.2006.074930.
Full textAbstract:
Abstract Background: Serum carotenoid concentrations relate inversely to cardiovascular disease incidence. To clarify the effect of carotenoids on atherosclerotic risk factors, we examined the association of circulating carotenoids with inflammation, oxidative stress, endothelial dysfunction, and smoking. Methods: Black and white men and women in the Coronary Artery Risk Development in Young Adults study, ages 18 to 30 years at recruitment (1985–1986) from 4 US cities, were investigated over 15 years. We included 2048 to 4580 participants in analyses of the sum of serum α-carotene, β-carotene, zeaxanthin/lutein, and β-cryptoxanthin concentrations and of lycopene at year 0 and at year 7. Results: The year 0 sum of 4 carotenoids was inversely associated (all P <0.05) with year 0 leukocyte count (slope per sum carotenoid SD, −0.17); year 7 fibrinogen (slope, −0.10); year 7 and year 15 C-reactive protein (slope, −0.12 and −0.09); and year 15 F2-isoprostanes (slope, −13.0), soluble P-selectin (slope, −0.48), and soluble intercellular adhesion molecule-1 (sICAM1; slope, −5.1). Leukocyte counts and sICAM1 and F2-isoprostane concentrations had stronger associations in smokers than in nonsmokers, and sICAM1 concentrations were higher in the highest carotenoid quartile in smokers than in the lowest carotenoid quartile in nonsmokers. Superoxide dismutase was positively associated with the sum of 4 carotenoids (slope, 0.12; P <0.01). Lycopene was inversely associated only with sICAM1. The year 7 carotenoid associations with these markers were mostly similar to those at year 0. Conclusions: Circulating serum carotenoids were associated, some interactively with smoking, in apparently beneficial directions with markers of inflammation, oxidative stress, and endothelial dysfunction.
15
Dounousi, Evangelia, Constantinos Tellis, Paraskevi Pavlakou, Anila Duni, Vasillios Liakopoulos, Patrick B. Mark, Aikaterini Papagianni, and Alexandros D. Tselepis. "Association between PCSK9 Levels and Markers of Inflammation, Oxidative Stress, and Endothelial Dysfunction in a Population of Nondialysis Chronic Kidney Disease Patients." Oxidative Medicine and Cellular Longevity 2021 (July 20, 2021): 1–8. http://dx.doi.org/10.1155/2021/6677012.
Full textAbstract:
Proprotein convertase subtilisin/kexin 9 (PCSK9) plays an important role in lipid metabolism while available literature regarding its involvement in the pathogenesis of atherosclerosis and in the expression of genes associated with apoptosis and inflammation is constantly increasing. Patients with chronic kidney disease (CKD) experience disproportionately increased cardiovascular morbidity and mortality due to dyslipidemia, accelerated atherosclerosis, inflammation, oxidative stress, and other risk factors. In the present cross-sectional study, we investigated the possible association of serum PCSK9 levels with markers of inflammation, oxidative stress, and endothelial damage in patients with CKD. Patients and Methods. Ninety-two patients with CKD stages II-ΙV (eGFR CKD-EPI 47.3 ± 25.7 ml/min/1.73 m2, mean age 66 years, 51 men) were included in the study. Plasma PCSK9 levels were correlated with comorbidities (arterial hypertension, diabetes mellitus, and history of cardiovascular disease), renal function indices (eGFR, proteinuria–UPR/24 h), lipid parameters (LDL-cholesterol, HDL-cholesterol, triglycerides, Lp(a), APO-A1, and APO-B), and soluble biomarkers of inflammation, oxidative stress, and endothelial damage (hs-CRP, fibrinogen, 8-epiPGF2a, ox-LDL, IL-6, TNF-α, sICAM-1, and sVCAM-1). Results. The mean plasma value of PCSK9 was 278.1 ng/ml. PCSK9 levels showed direct correlation with serum triglycerides ( p = 0.03 ), Lp(a) ( p = 0.01 ), and sICAM-1 levels ( p = 0.03 ). There was no significant correlation between PCSK9 levels and indices of the renal function, other lipid profile parameters, inflammatory markers, or comorbidities. Multiple regression analysis showed a significant effect of Lp(a) on PCSK9 levels, and for each unit of higher Lp(a), an increase by 3.082 is expected (95% CI: 0.935-5.228, p = 0.006 ). At the same time, patients receiving statins are expected to have on average 63.8 ng/ml higher PCSK9 values compared to patients not receiving statins (95% CI: 14.6-113.5, p = 0.012 ). Conclusion. Plasma levels of PCSK9 in nondialysis CKD patients are correlated with endothelial dysfunction and lipid metabolism parameters. Statin intake increases PCSK9 levels significantly in this patient population. PCSK9 levels are not correlated with the severity of kidney disease. Major prospective studies are necessary to investigate the role of PCSK9 in the atherosclerotic cardiovascular outcome in CKD.
16
Ferdous, Zannatul, Sumaya Beegam, Nur E. Zaaba, Ozaz Elzaki, Saeed Tariq, Yaser E. Greish, Badreldin H. Ali, and Abderrahim Nemmar. "Exacerbation of Thrombotic Responses to Silver Nanoparticles in Hypertensive Mouse Model." Oxidative Medicine and Cellular Longevity 2022 (January 15, 2022): 1–10. http://dx.doi.org/10.1155/2022/2079630.
Full textAbstract:
With advent of nanotechnology, silver nanoparticles, AgNPs owing majorly to their antibacterial properties, are used widely in food industry and biomedical applications implying human exposure by various routes including inhalation. Several reports have suggested AgNPs induced pathophysiological effects in a cardiovascular system. However, cardiovascular diseases such as hypertension may interfere with AgNPs-induced response, yet majority of them are understudied. The aim of this work was to evaluate the thrombotic complications in response to polyethylene glycol- (PEG-) coated AgNPs using an experimental hypertensive (HT) mouse model. Saline (control) or PEG-AgNPs (0.5 mg/kg) were intratracheally (i.t.) instilled four times, i.e., on days 7, 14, 21, and 28 post-angiotensin II-induced HT, or vehicle (saline) infusion. On day 29, various parameters were assessed including thrombosis in pial arterioles and venules, platelet aggregation in whole blood in vitro, plasma markers of coagulation, and fibrinolysis and systemic oxidative stress. Pulmonary exposure to PEG-AgNPs in HT mice induced an aggravation of in vivo thrombosis in pial arterioles and venules compared to normotensive (NT) mice exposed to PEG-AgNPs or HT mice given saline. The prothrombin time, activated partial thromboplastin time, and platelet aggregation in vitro were exacerbated after exposure to PEG-AgNPs in HT mice compared with either NT mice exposed to nanoparticles or HT mice exposed to saline. Elevated concentrations of fibrinogen, plasminogen activator inhibitor-1, and von Willebrand factor were seen after the exposure to PEG-AgNPs in HT mice compared with either PEG-AgNPs exposed NT mice or HT mice given with saline. Likewise, the plasma levels of superoxide dismutase and nitric oxide were augmented by PEG-AgNPs in HT mice compared with either NT mice exposed to nanoparticles or HT mice exposed to saline. Collectively, these results demonstrate that PEG-AgNPs can potentially exacerbate the in vivo and in vitro procoagulatory and oxidative stress effect in HT mice and suggest that population with hypertension are at higher risk of the toxicity of PEG-AgNPs.
17
Katicheva, A. V., N. A. Brazhenko, O. N. Brazhenko, A. G. Chuikova, S. G. Zheleznyak, N. V. Tsygan, and A. V. Nikolau. "Assesment of premarure death in patients with pulmonary tuberculosis and chronic obstructive pulmonary disease." Bulletin of the Russian Military Medical Academy 22, no. 2 (June 15, 2020): 19–22. http://dx.doi.org/10.17816/brmma50039.
Full textAbstract:
The risk of developing cardiovascular pathology and premature death from it in patients with pulmonary tuberculosis in combination with chronic obstructive pulmonary disease is assessed. It has been established that more than 80% of patients with pulmonary tuberculosis are regular tobacco users. Chronic tobacco intoxication leads to the formation of chronic obstructive pulmonary disease, affecting the course of the tuberculosis process. In patients with tuberculosis on the background of smoking and chronic obstructive pulmonary disease, pronounced clinical manifestations of the disease are determined, which are accompanied by a common tuberculosis process, decomposition in the lung tissue and bacterial excretion. Patients suffering from comorbid pathology revealed deep disturbances in the homeostatic balance of the body and changes in the reactivity of the body. Changes in the proteinogram were determined, with the predominance of g - и -2 fractions, an increase in C-reactive protein and fibrinogen, which confirms a pronounced systemic inflammatory response. The pathological state of homeostatic equilibrium of the body is accompanied by the development of hypoxemia, oxidative stress, systemic inflammation, endothelial dysfunction and dyslipidemia. In a third of patients, changes in the lipid profile are determined against the background of a lack of body weight, which is an unfavorable prognostic sign during chronic obstructive pulmonary disease. Such phenomena contribute to the development of multifocal atherogenesis, systemic arterial hypertension, cardiac remodeling and the rapid development of cardiovascular pathology. In patients with comorbidity, changes in the electrocardiogram are characterized by remodeling of the myocardium, a change in the position of the electrical axis of the heart, overload of the right heart, hypertrophy of the left heart. These patients are characterized by a decrease in exercise tolerance, a moderate and high risk of developing cardiovascular complications and premature death from them. Identified changes are predictors of early disability and premature death of patients with tuberculosis, contribute to a decrease in the quality and life expectancy of patients.
18
Haziza, Christelle, Guillaume de La Bourdonnaye, Andrea Donelli, Dimitra Skiada, Valerie Poux, Rolf Weitkunat, Gizelle Baker, Patrick Picavet, and Frank Lüdicke. "Favorable Changes in Biomarkers of Potential Harm to Reduce the Adverse Health Effects of Smoking in Smokers Switching to the Menthol Tobacco Heating System 2.2 for 3 Months (Part 2)." Nicotine & Tobacco Research 22, no. 4 (May 24, 2019): 549–59. http://dx.doi.org/10.1093/ntr/ntz084.
Full textAbstract:
Abstract Introduction Tobacco Heating System (THS) 2.2, a candidate modified-risk tobacco product, aims at offering an alternative to cigarettes for smokers while substantially reducing the exposure to harmful and potentially harmful constituents found in cigarette smoke. Methods One hundred and sixty healthy adult US smokers participated in this randomized, three-arm parallel group, controlled clinical study. Subjects were randomized in a 2:1:1 ratio to menthol Tobacco Heating System 2.2 (mTHS), menthol cigarette, or smoking abstinence for 5 days in confinement and 86 subsequent ambulatory days. Endpoints included biomarkers of exposure to harmful and potentially harmful constituents (reported in our co-publication, Part 1) and biomarkers of potential harm (BOPH). Results Compliance (protocol and allocated product exposure) was 51% and 18% in the mTHS and smoking abstinence arms, respectively, on day 90. Nonetheless, favorable changes in BOPHs of lipid metabolism (total cholesterol and high- and low-density cholesterol), endothelial dysfunction (soluble intercellular adhesion molecule-1), oxidative stress (8-epi-prostaglandin F2α), and cardiovascular risk factors (eg, high-sensitivity C-reactive protein) were observed in the mTHS group. Favorable effects in other BOPHs, including ones related to platelet activation (11-dehydrothromboxane B2) and metabolic syndrome (glucose), were more pronounced in normal weight subjects. Conclusions The results suggest that the reduced exposure demonstrated when switching to mTHS is associated with overall improvements in BOPHs, which are indicative of pathomechanistic pathways underlying the development of smoking-related diseases, with some stronger effects in normal weight subjects. Implications Switching to mTHS was associated with favorable changes for some BOPHs indicative of biological pathway alterations (eg, oxidative stress and endothelial dysfunction). The results suggest that switching to mTHS has the potential to reduce the adverse health effects of smoking and ultimately the risk of smoking-related diseases. Switching to mTHS for 90 days led to reductions in a number of biomarkers of exposure in smokers, relative to those who continued smoking cigarettes, which were close to those observed when stopping smoking (reported in our co-publication, Part 1). Initial findings suggest reduced levels of 8-epi-prostaglandin F2α and intercellular adhesion molecule 1, when switching to mTHS for 90 days. These changes are comparable to what is observed upon smoking cessation. In normal weight subjects, additional favorable changes were seen in 11-dehydrothromboxane B2, fibrinogen, homocysteine, hs-CRP, percentage of predicted forced expiratory volume in 1 second, systolic blood pressure, diastolic blood pressure, glucose, high-density lipoprotein, apolipoprotein A1, and triglycerides. Trial registration NCT01989156.
19
Triginer, L., I. Carrión Barberà, L. Tío, T. C. Salman Monte, C. Pérez, L. Polino, A. Ribes, J. Llorente Onaindia, and J. Monfort. "AB1460 ACCUMULATED ADVANCED GLYCATION ENDPRODUCTS ARE SIGNIFICANTLY HIGHER IN PATIENTS WITH IMMUNE-MEDIATED INFLAMMATORY DISEASES THAN IN HEALTHY POPULATION." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1835.3–1836. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4893.
Full textAbstract:
BackgroundAdvanced glycation endproducts (AGEs) are the result of non-enzymatic glycation of proteins, lipids or nucleic acids. In circumstances characterized by increased oxidative and carbonyl stress, such as chronic inflammation, AGEs can be formed more rapidly1, generating reactive oxygen species and activating inflammatory signaling cascades through their chief signaling receptor (commonly abbreviated as RAGE)2. This positive feedback of inflammation can play a role in the etiology of immune-mediated inflammatory diseases, more specifically in rheumatoid arthritis (RA), ankylosing spondylitis (AS) and systemic lupus erythematosus (SLE).ObjectivesTo investigate whether the accumulated concentrations of AGEs in patients with SLE, RA or AS are significantly higher than in healthy patients.MethodsOne hundred thirteen consecutive patients fulfilling ACR/EULAR criteria for RA, 60 patients fulfilling ASAS/OMERACT MRI criteria for AS, 97 patients fulfilling ACR/SLICC criteria for SLE and 527 sex-matched healthy controls were recruited.in cross-sectional study. Exclusion criteria were pregnancy, diabetes mellitus, corticosteroid treatment ≥ 20mg/day and malignant neoplasm. Accumulated AGEs were non-invasively measured by skin autofluorescence (Age Reader Mu Connect, Diagnostics Technologies B.V) and demographic and clinical data were collected. AGEs comparisons between patients and controls were performed by multiple linear regression analysis adjusted by confunders, previously described in literature (age, smoking habit and cardiovascular risk-factors). Age was centered at 55 years.ResultsTable 1 shows some descriptive characteristics of our cohorts. AGEs adjusted mean was significantly increased in SLE patients compared with matched controls (95% CI [2.27, 2.76] vs [1.66, 1.89], p<0.0001), RA patients and controls (95% CI [2.41, 2.61] vs [1.68, 1.88], p<0.0001) and AS patients and controls (95% CI [2.03, 2.6] vs [1.66, 1.93], p<0.0001). In all 3 models, AGEs were also significantly positive correlated with smoking habit measured by packs per year (p<0.001) and age (p<0.0001).Table 1.Descriptive characteristics of the cohortsSLERAASPatientsControlsPatientsControlsPatientsControlsN=96N=189N=113N=240N=60N=99AGEs2.57 (0.65)1.98 (0.45)2.59 (0.58)2.00 (0.42)2.26 (0.46)1.90 (0.46)Age51.0 [43.0;61.0]56.0 [52.0;62.0]58.0 [54.0;65.0]61.0 [56.0;66.0]47.5 [41.0;55.0]53.0 [49.0;57.0]SmokerNo76 (79.2%)133 (70.4%)86 (76.1%)196 (81.7%)42 (70.0%)58 (58.6%)Yes20 (20.8%)56 (29.6%)27 (23.9%)44 (18.3%)18 (30.0%)41 (41.4%)Packs/year0.00 [0.00;10.8]2.50 [0.00;18.8]2.50 [0.00;18.0]0.00 [0.00;12.6]0.00 [0.00;7.88]14.9 [2.00;30.6]HypertensionNo74 (77.1%)116 (61.4%)77 (68.1%)146 (60.8%)53 (88.3%)75 (75.8%)Yes22 (22.9%)73 (38.6%)36 (31.9%)94 (39.2%)7 (11.7%)24 (24.2%)ObesityNo80 (83.3%)128 (67.7%)86 (76.1%)163 (67.9%)51 (85.0%)81 (81.8%)Yes16 (16.7%)61 (32.3%)27 (23.9%)77 (32.1%)9 (15.0%)18 (18.2%)DyslipidemiaNo85 (88.5%)104 (55.0%)79 (69.9%)108 (45.0%)51 (85.0%)55 (55.6%)Yes11 (11.5%)85 (45.0%)34 (30.1%)132 (55.0%)9 (15.0%)44 (44.4%)Continuous normal: mean (SD); Continuous non-normal: median [IQR]; Categorical: absolute (relative frequency)ConclusionAccumulated AGEs in all 3 pathologies are significantly higher than in the healthy controls. The different means of AGEs in each of the diseases, being higher in SLE and lower in AS, may suggest a different participation of AGEs in the immune-mediated mechanisms of each pathology.References[1]K. de Leeuw, R. Graaff et al., Accumulation of advanced glycation endproducts in patients with systemic lupus erythematosus, Rheumatology, Volume 46, Issue 10, October 2007, Pg 1551–1556.[2]Yan S., Ramasamy R. & Schmidt A. Mechanisms of Disease: advanced glycation end-products and their receptor in inflammation and diabetes complications. Nat Rev Endocrinol4, 285–293 (2008).Disclosure of InterestsNone declared
20
Petrov, Ye Ye, Yu G. Burmak, T. A. Ivanytska, I. A. Pogoryelova, and L. B. Nyemchenko. "Сharacteristics of Some Hemostasis System Indices in Patients with Compensated Chronic Cor Pulmonale of Broncho-Pulmonary Genesis and Peculiarities of Their Changes in Conditions of Comorbidity with Stable Coronary Heart Disease." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 8, no. 1 (February 27, 2023): 140–45. http://dx.doi.org/10.26693/jmbs08.01.140.
Full textAbstract:
The purpose of the study was to research and analyze the peculiarities of changes of some hemostasis system indices and define their possible role in the formation of a vascular lesion in the patients with compensated chronic cor pulmolale of broncho-pulmonary genesis in conditions of its comorbidity with stable coronary heart disease. Materials and methods. The retrospective study and analysis of hemostasis system indices (platelet count, thrombin time, prothrombin time, antithrombin – III, plasma tolerance to heparin, plasmin lysis, fibrinogen, soluble fibrin) in 64 patients with chronic obstructive pulmonary disease and compensated chronic cor pulmonale (29 female, 35 male, mean age – 54.6 ± 2.3) were carried out. 32 patients with the isolated pathology formed the comparative group whereas 32 patients with the comorbid coronary heart disease (exertional angina, functional class II-III, postinfarction or aterosclerotic cardiosclerosis) built the main group. The obtained research results of the patients of the main and comparative groups were compared both in groups and with the indices of practically healthy individuals (n = 15) of the same gender and age. Results and discussion. The obtained results indicated the presence of a significant increase of coagulation potential (the changes of indices of platelets, fibrinogen, plasma tolerance to heparin, antithrombin – III, and soluble fibrin) and activation of fibrinolysis system (thrombin time) and, simultaneous, its more pronounced depression (plasmin lysis) and increase of prothrombin time in case of presence of comorbid coronary heart disease in the patients with chronic cor pulmonale in conditions of chronic inflammatory process. Comorbidity promoted to the formation of disbalance of systemic correlation hemocoagulation and fibrinolysis. Our results confirm to a certain extent the following ideas of scientists: there are hypercoagulation and “exhaustion of the anticoagulant system potential” in case of combination of coronary heart disease and chronic obstructive pulmonary disease; hypercoagulation together with the oxidative stress and chronic systemic inflammation are general pathogenic mechanisms of chronic obstructive pulmonary disease and cardiovascular diseases, particularly of the coronary heart disease. Conclusion. The analysis of the changes of the hemostasis system indices in patients with compensated chronic cor pulmonale of broncho-pulmonary genesis indicates the presence of an increase of coagulation potential; the most significant changes with suppression of fibrinolytic activity are typical of the patients with comorbid coronary heart disease. The peculiarities of the hemostasis system changes in the patients with compensated chronic cor pulmonale of broncho-pulmonary genesis should be considered as a marker of the increased risk of the thrombogenic vascular complications. It should be taken into account for treatment-diagnostic strategy formation
21
Petrov, Ye Ye, Yu G. Burmak, S. I. Treumova, T. A. Ivanytska, and T. A. Savchuk. "The Peculiarities of Some Indices of Hemostasis System Changes in the Patients with Chronic Cor Pulmonale of Broncho-Pulmonary Genesis during Decompensation Stage and in Conditions of its Comorbidity with Hypertensive Disease." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 1 (March 22, 2022): 144–49. http://dx.doi.org/10.26693/jmbs07.01.144.
Full textAbstract:
The purpose of the study is to research and analyze the peculiarities of some indices of hemostasis system changes and define their possible role in the formation of a vascular lesion in the patients with chronic cor pulmolale of broncho-pulmonary genesis during decompensating stage and in conditions of its comorbidity with hypertensive disease. Materials and methods. The retrospective study and analysis of indices of hemostasis system (platelet count, thrombin time, prothrombin time, antithrombin - III, plasma tolerance to heparin, plasmin lysis, fibrinogen, soluble fibrin) in 96 patients with chronic obstructive pulmonary disease and decompensated chronic cor pulmolale with signs of circulatory insufficiency of the 2nd stage (female – 34, male – 62, mean age – 57.5±1.2) were carried out. 32 patients with the isolated pathology formed the comparative group whereas 64 patients with the comorbid hypertensive disease of the 2nd stage, of the 2nd degree of arterial hypertension, built the main group. The obtained research results of the patients of the main and comparative groups were compared both in groups and with the indices of practically healthy individuals (n = 15) of the same gender and age. Results and discussion. The obtained results indicated to a certain extent the presence of a significant increase of coagulation potential, an increase of fibrinolysis system activity and the disorder of “external way” of blood coagulation. It doesn’t exclude the change of procoagulant factors content/activity and can be considered as a result of their intensive using. The foregoing changes were the most significant (it concerns all indices) in the patients with chronic cor pulmolale and comorbid hypertensive disease. Our results confirm to a certain extent the following idea of scientists. Hypercoagulation and activation of the platelets together with the chronic systemic inflammation and oxidative stress are general pathogenic mechanisms of chronic obstructive pulmonary disease and cardiovascular diseases, particularly of the arterial hypertension. It is reflected clearly as a very important constituent part of “mutual burden” syndrome in case of a comorbid course. Conclusion. The peculiarity of the hemostasis system changes in patients with decompensated chronic cor pulmolale of broncho-pulmonary genesis is an increase of its coagulation potential; the most significant its manifestations with activation and simultaneous suppression of fibrinolytic activity are typical of the patients with the comorbid hypertensive disease (it can be considered as manifestations of the chronic disseminated intervascular coagulation syndrome). The increased coagulation potential of a hemostasis system in the patients with decompensated chronic cor pulmolale of broncho-pumonary genesis should be considered as a marker of the risk of the thrombogenic vascular complications development; it is necessary to carry out the periodical monitoring of its indices with the purpose of prevention of the development of cardiovascular events both in the isolated course of chronic cor pulmolale and in the conditions of comorbidity with hypertensive disease
22
Stokes, Andrew, Anna E. Wilson, Wubin Xie, Olusola A. Orimoloye, Jessica L. Fetterman, Andrew P. Defilippis, Rachel J. Keith, et al. "Abstract 17095: Association of Cigarette and Electronic Cigarette Use Behaviors With Levels of Inflammatory and Oxidative Stress Biomarkers Among United States Adults, Path 2013-2014." Circulation 142, Suppl_3 (November 17, 2020). http://dx.doi.org/10.1161/circ.142.suppl_3.17095.
Full textAbstract:
Introduction: Electronic cigarette (e-cigarette) use has increased rapidly in recent years; however, the cardiovascular risks of e-cigarettes remain unclear. Using data from the Population Assessment of Tobacco and Health Survey, this study assesses the cross-sectional association of cigarette and e-cigarette use behaviors with markers of inflammation (high-sensitivity C-reactive protein [hsCRP], soluble intercellular adhesion molecule [sICAM], interleukin-6 [IL-6], fibrinogen), oxidative stress (8-isoprostane [F2PG2a]), and nicotine exposure (cotinine). Methods: We analyzed data from adults (18+ years) who provided urine and blood specimens at wave 1 (2013-2014). Biomarkers were examined as continuous and categorical variables using the clinical cut points of ≥3 mg/L for hsCRP >10 ng/mL for cotinine, and the upper quartiles of fibrinogen (≥381mg/dL), IL-6 (≥2.32 pg/mL), sICAM (≥288.77 ng/mL), and 8-isoprostane (≥788 pg/mL). Progressively adjusted negative binomial and generalized structural equation models were used, as well as sensitivity checks to assess the robustness of associations. Results: Of the 7,019 participants (58.6% non-users, 1.8% current vapers, 29.7% current smokers, 9.9% dual users), 67.2% had ≥1 high inflammatory or oxidative stress marker. Current vapers had increased risk of high hsCRP (IRR 1.28; 95% CI,1.02-1.59) and sICAM (IRR 2.01; 95% CI,1.42-2.85) compared to non-users. Relative to current smokers, current vapers who were former smokers had lower risk of having ≥1 high inflammatory or oxidative stress marker (IRR 0.80; 95% CI,0.69-0.94). Dual users had higher levels of all 5 inflammatory and oxidative stress markers compared to never smokers in both continuous and categorical models, with similar levels compared to current smokers. Current smokers and dual users had higher levels of cotinine compared to exclusive vapers. Conclusions: This study suggests that current vapers may have lower levels of inflammatory and oxidative stress markers compared to current smokers, but only after complete cessation of combustible cigarettes. Our findings strengthen the need for longitudinal studies investigating the association of vaping with markers of cardiovascular risk, particularly among dual users.
23
Bostan, Cem, Aysem Kaya, and Zerrin Yigit. "Differences Between Morbid Obesity With Metabolic Syndrome and Overweight Turkish Adult Participants in Multiple Atherosclerotic Cardiovascular Disease Risk Factors." Angiology, November 4, 2020, 000331972097016. http://dx.doi.org/10.1177/0003319720970161.
Full textAbstract:
Obesity and metabolic syndrome (MetS) are public health problems and are increasing globally. We assessed the differences in lipid profiles through lipid testing, thrombotic and inflammatory parameters, and oxidative stress indexes between overweight and obese patients with MetS in a Turkish adult population. We included 100 obese (body mass index [BMI] >30 kg/m2) patients with MetS (66 women, 34 men, mean age 54.0 ± 10.1 years) and 15 overweight (BMI 25-30 kg/m2) individuals (11 women, 4 men, mean age 50.2 ± 14.5 years) as controls. The group with MetS had significantly higher levels of glycaemia, uric acid, high-sensitivity C-reactive protein, homocysteine, fibrinogen, total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, small dense LDL, oxidized LDL, apolipoprotein B (Apo B), lipoprotein (a), small and intermediate high-density lipoprotein (HDL) particles, oxidative stress index, and significantly lower levels of HDL-cholesterol (HDL-C), Apo A, and large HDL particles. In conclusion, obesity with MetS increase atherogenic dyslipidemia and thrombotic, inflammatory and oxidative stress biomarkers. Furthermore, obesity with MetS decreases protective mechanisms of atherosclerosis. We should at least try to prevent overweight individuals from becoming obese with MetS.
24
Pasupuleti, Pullaiah, M. M. Suchitra, Aparna R. Bitla, and Alok Sachan. "Attenuation of Oxidative Stress, Interleukin-6, High-Sensitivity C-Reactive Protein, Plasminogen Activator Inhibitor-1, and Fibrinogen with Oral Vitamin D Supplementation for Six Months in Patients with Type 2 Diabetes Mellitus having Vitamin D Deficiency." Journal of Laboratory Physicians, December 31, 2021. http://dx.doi.org/10.1055/s-0041-1742285.
Full textAbstract:
Abstract Objectives Type 2 diabetes mellitus (T2DM) associated with oxidative stress and inflammation causes endothelial dysfunction, which promotes cardiovascular risk. Vitamin D with its pleiotropic effect is said to protect against cardiovascular risk. However, with vitamin D deficiency being more prevalent in T2DM, the cardiovascular risk may get compounded. Materials and Methods An interventional study was conducted on 100 patients with T2DM having vitamin D deficiency (vitamin D < 20 ng/mL), who were given oral supplementation of 2,000 IU/day of vitamin D for a period of 6 months. Serum vitamin D, biomarkers of oxidative stress, malondialdehyde (MDA), oxidized LDL (OxLDL), ferric reducing ability of plasma (FRAP), biomarkers of inflammation, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), and fibrinogen were measured at baseline and at the end of the third and sixth month of vitamin D supplementation. Statistical Analysis Repeated measures analysis of variance (ANOVA) was applied for comparison between baseline and third- and sixth-month data after vitamin D supplementation. Linear regression by generalized estimating equations (GEE), which grouped repeated measures for each subject and accounted for correlations that may occur from multiple observations within subjects, was applied. Results Serum vitamin D levels reached normal levels with a significant decrease in OxLDL, hsCRP, IL-6, PAI-1, and fibrinogen levels, with a significant increase in FRAP (p = 0.001) levels at the end of 6 months of vitamin D supplementation. These changes were observed even after correction with glycemic control (HbA1c). However, a significant decrease in MDA was observed only at the end of the sixth month of vitamin D supplementation. Vitamin D levels showed a significant negative association with Ox-LDL, Hs-CRP, IL-6, PAI-1, and fibrinogen, even after adjusting for BMI and statin use (p = 0.001). Conclusion Supplementation of vitamin D for a period of 6 months in patients with T2DM having vitamin D deficiency is beneficial in the attenuation of oxidative stress and inflammation.
25
Rezk-Hanna, Mary, Umme Shefa Warda, Andrew C. Stokes, Jessica Fetterman, Jian Li, Paul M. Macey, Muhammad Darawad, et al. "Associations of Smokeless Tobacco Use With Cardiovascular Disease Risk: Insights From the Population Assessment of Tobacco and Health Study." Nicotine & Tobacco Research, January 6, 2022. http://dx.doi.org/10.1093/ntr/ntab258.
Full textAbstract:
Abstract Introduction Cigarette smoking is strongly associated with the development of cardiovascular disease (CVD). However, evidence is limited as to whether smokeless tobacco (ST) use is associated with CVD. Aims and Methods Using data from 4347 adults in the Population Assessment of Tobacco and Health Study (2013–2014), we compared geometric mean concentrations of CVD-related harm biomarkers and biomarkers of exposure among exclusive ST users and exclusive cigarette smokers—in relation to recent nicotine exposure—and never tobacco users, adjusting for age, sex, race/ethnicity, income, body mass index, and CVD. Biomarker levels among exclusive ST users who were former established cigarette smokers were compared with exclusive cigarette smokers. Results Compared with cigarette smokers, ST users had significantly higher concentrations of total nicotine equivalents (TNE) but lower concentrations of inflammatory (high-sensitivity C-reactive protein, interleukin-6, intercellular adhesion molecule, fibrinogen) and oxidative stress (8-isoprostane) biomarkers (all p < .05). Biomarker levels among ST users were similar to never smokers. ST users who were former cigarette smokers had lower levels of inflammatory and oxidative stress biomarkers and biomarkers of exposure (cadmium, lead, 1-hydroxypyrene, acrylonitrile, and acrolein), compared with cigarettes smokers (p < .05), despite having higher TNE levels (p < .05). Among cigarette smokers, but not among ST users, inflammatory biomarkers and TNE were highly correlated. Conclusions ST use is not associated with increases in biomarkers of CVD-related harm and exposure, compared with never smokers, despite exposure to nicotine at levels higher than those observed among cigarette smokers. These findings support the concept that increases in CVD risk among cigarette smokers is caused primarily by constituents of tobacco smoke other than nicotine. Implications Despite having higher levels of nicotine and compared with exclusive cigarette smokers, exclusive ST users (including those who were former cigarette smokers) had significantly lower concentrations of inflammatory and oxidative stress biomarkers, comparable to levels observed among never tobacco users. These findings suggest that increases in CVD risk among cigarette smokers is caused primarily by tobacco constituents other than nicotine and that switching to ST is likely associated with lower CVD risk.
26
Mahajan, Sahil, Heemani Dave, Santosh Bothe, Debarshikar Mahpatra, Sandeep Sonawane, Sanjay Kshirsagar, and Santosh Chhajed. "Objective Monitoring of Cardiovascular Biomarkers using Artificial Intelligence (AI)." Asian Journal of Pharmaceutical Research, August 12, 2022, 229–34. http://dx.doi.org/10.52711/2231-5691.2022.00038.
Full textAbstract:
Different CVDs (CVD) are the leading wreak of mortality and disability worldwide. The pathology of CVD is complex; multiple biological pathways have been involved. Biomarkers act as a measure of usual or pathogenic biological processes. They play a significant part in the definition, prognostication, and decision-making with respect to the treatment of cardiovascular events. Inthis article, we had summarized key biomarkers which are essential to predict CVDs. We had studied prevalence, pattern of expression of biomarkers (salivary, inflammatory, oxidative stress, chemokines, antioxidants, genetic, etc.), its measurable impact, benefits of early detection and its scope. A considerable number of deaths due to cardiovascular diseases (CVDs) can be attributed to tobacco smoking and it rises the precarious of deathfrom coronary heart disease and cerebrovascular diseases. Cytokines which is categorized into pro inflammatory and anti-inflammatory take part in as biomarkers in CHD, MI, HF. Troponin, growth differentiation factor-15(GDF-15), C-reactive protein, fibrinogen, uric acid diagnose MI and CAD. Matrix Metalloproteins, Cell Adhesion Molecules, Myeloperoxidase, Oxidative stress biomarkers, Incendiary biomarkers are useful to predict the risk of UA, MI, and HF. Increased Endothelin-1, Natriuretic peptides, copeptin, ST-2, Galectin-3, mid-regional-pro-adrenomedullin, catecholamines are used to prognosticate Heart failure. Modern technologies like Artificial Intelligence (AI), Biosensor and high-speed data communication made it possible to collect the high-resolution data in real time. The high-resolution data can be analyzed with advance Machine Learning (ML) algorithms, it will not only help to discover the disease patterns but also an real-time and objective monitoring of bio-signals can help to discover the unknown patterns linked with CVD.
27
Rezk-hanna, Mary, Umme Warda, Mary-Lynn Brecht, and Neal L. Benowitz. "Abstract 11103: Associations of Smokeless Tobacco Use with Cardiovascular Disease Risk: Insights from the Population Assessment of Tobacco and Health Study." Circulation 144, Suppl_1 (November 16, 2021). http://dx.doi.org/10.1161/circ.144.suppl_1.11103.
Full textAbstract:
Introduction: Combustible tobacco smoking is strongly associated with the development of cardiovascular disease (CVD). However, evidence is limited as to whether smokeless tobacco (ST) use is associated with CVD. Methods: Using data from 4347 adults in the Population Assessment of Tobacco and Health Study (2013-2014), we compared geometric mean concentrations of CVD-related harm biomarkers and biomarkers of exposure among current exclusive ST product users and exclusive cigarette smokers—in relation to nicotine exposure—and never tobacco users, adjusting for age, sex, race/ethnicity, income, BMI and CVD. Biomarker levels among exclusive ST users who were former established cigarette smokers were examined and compared to levels among exclusive cigarette smokers. Results: Compared to cigarette smokers, ST users had significantly higher concentrations of total nicotine equivalents (TNE) but lower concentrations of inflammatory (high-sensitivity C-Reactive-Protein, interleukin-6, intercellular adhesion molecule, fibrinogen) and oxidative stress (8-isoprostane) biomarkers (all P<0.05). Biomarker levels among ST users were similar to never smokers. Exclusive ST users who were former cigarette smokers had lower levels of inflammatory and oxidative stress biomarkers and biomarkers of exposure (including cadmium, lead, 1-hydroxypyrene, acrylonitrile and acrolein), compared to cigarettes smokers (p<0.05), despite having higher TNE levels (P<0.05). In cigarette smokers, but not among ST users, inflammatory biomarkers and TNE were highly correlated. Conclusions: ST use is not associated with increases in biomarkers of CVD-related harm and exposure, compared to never smokers, despite exposure to nicotine at levels higher than those observed among cigarette smokers. These findings support the concept that increases in CVD risk among cigarette smokers is caused primarily by constituents of tobacco smoke other than nicotine.
28
Mukherjee, Rishav, Soumya Sarathi Mondal, Rishav Sanghai, Subhendu Bikash Naiya, Lamsaka Lyngdoh, and Raja Bhattacharya. "Carotid Intima Media Thickness as a Marker of Atherosclerotic Burden in Patients with Systemic Lupus Erythematosus: A Cross-sectional Study from a Tertiary Care Centre of Eastern India." JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH, 2023. http://dx.doi.org/10.7860/jcdr/2023/59731.17395.
Full textAbstract:
Introduction: Systemic Lupus Erythematosus (SLE) patients have an increased burden of atherosclerosis leading to adverse Cardiovascular (CV) events. Alterations in endothelial function, dysregulated immune system and increased oxidative stress are implicated in their development and progression. Carotid artery ultrasound is recommended to assess and follow progression of subclinical atherosclerosis and correlate with traditional/non traditional CV risk factors in SLE. Aim: To study the correlation between Carotid Intima Media Thickness (CIMT), traditional/non traditional CV risk factors in SLE. Materials and Methods: The hospital-based, descriptive, cross-sectional study was conducted in the Department of Internal Medicine, Medical College Kolkata, Kolkata, West Bengal, India, from April 2019 to August 2020. Patients with SLE, diagnosed by Systemic Lupus International Collaborating Clinics (SLICC) 2012 criteria, aged >12 years, irrespective of therapy status, were recruited by consecutive sampling. Subjects were classified as Lupus Nephritis (LN) and Lupus without Nephritis (LWN). Demographic data, parameters to define SLE (SLICC 2012 criteria), blood parameters like lipid profile, fasting plasma glucose, anti-Double stranded Deoxyribose Nucleic Acid antibody (anti-dsDNA Ab), C3/C4 levels, 24 hour urine protein values, haemoglobin, C-reactive Protein (CRP), serum homocysteine and Carotid Intima Media thickness as measured by Ultrasonography (USG) doppler study, duration of disease and medication history were considered as study variables. Statistical analysis was done by using Z-test, t-test, Analysis of variance (ANOVA), Chi-square test (for categorical data) and other non parametric statistical tests and correlation tests wherever applicable. A p-value <0.05 was considered to be statistically significant. Results: Fifty five SLE patients were studied. Subgroup analysis was performed between LN (n=36) and LWN (n=19). The mean age of the study subjects was 33 years with mean disease duration of 4.6 years. LN patients had longer disease duration, younger age of disease onset and longer duration of steroid usage. The mean systolic Blood Pressure (BP) was significantly higher in LN subgroup. Framingham Risk Scores (FRS) was positively correlated with duration of SLE disease and Systemic Lupus Erythematosus Disease Activity Index (SLEDAI-2K) scores and duration of steroid therapy. The mean CIMT of the study population is 0.91 mm with 10.9% plaque prevalence whereas, mean CIMT of the LN subgroup and LWN subgroup was 1.02±0.27 mm and 0.86±0.3 mm, respectively; however no statistically significant difference in CIMT was observed between two subgroups. CIMT positively correlated with anti-dsDNA Ab levels, FRSs, anaemia, SLE Disease activity scores, 24 hour urine protein, duration of steroid usage, serum creatinine and CRP. No correlation between CIMT and age of subjects, Fasting Plasma Glucose (FPG), Triglycerides (TG) serum homocysteine was observed. Conclusion: Systemic lupus erythematous patients have a high atherosclerosis burden and are at increased risk of adverse CV events. LN patients, early age of lupus onset, longer disease duration with prolonged steroid therapy, significant proteinuria, higher anti-dsDNA Ab levels and hypocomplementemia were observed to have higher mean CIMT and plaque formation.
29
Ntounousi, Evangelia, Konstantinos Tellis, Paraskevi Pavlakou, Anila Duni, Vassilios Liakopoulos, Aikaterini Papagianni, and Alexandros Tselepis. "MO474PCSK9 LEVELS AND MARKERS OF INFLAMMATION, OXIDATIVE STRESS AND ENDOTHELIAL DYSFUNCTION IN A POPULATION OF NON-DIALYSIS CHRONIC KIDNEY DISEASE PATIENTS: IS THERE AN ASSOCIATION?" Nephrology Dialysis Transplantation 36, Supplement_1 (May 1, 2021). http://dx.doi.org/10.1093/ndt/gfab090.0036.
Full textAbstract:
Abstract Background and Aims Proprotein convertase subtilisin / kexin 9 (PCSK9) plays an important role in lipid metabolism while available literature regarding its involvement in the pathogenesis of atherosclerosis and in the expression of genes associated with apoptosis and inflammation is constantly increasing. Patients with chronic kidney disease (CKD) experience disproportionately increased cardiovascular morbidity and mortality due to dyslipidemia, accelerated atherosclerosis, inflammation, oxidative stress and other risk factors. In the present cross-sectional study, we investigated the possible association of serum PCSK9 levels with markers of inflammation, oxidative stress and endothelial damage in patients with CKD. Method Ninety-two patients with CKD stage II-ΙV (eGRF CKD-EPI 47.3 ±25.7ml/min/1,73m2, mean age 66 years, 51 men) were included. Plasma PCSK9 levels were correlated with comorbidities (arterial hypertension; diabetes mellitus, history of cardiovascular disease), renal function indices (eGFR, proteinuria – UPR/24h), lipid parameters (LDL-cholesterol, HDL-cholesterol, triglycerides, Lp (a), APO-A1, APO-B), as well as soluble biomarkers of inflammation, oxidative stress and endothelial damage (hs-CRP, fibrinogen, 8-epiPGF2a, ox-LDL, IL-6, TNF-α, sICAM-1, sVCAM-1). Results The mean plasma value of PCSK9 was 278.1ng/ml. PCSK9 levels showed direct correlation with serum triglycerides (p = 0.03), Lp(a) (p = 0.01), and sICAM-1 levels (p = 0.03). There was no significant correlation between PCSK9 levels and indices of renal function, other lipid profile parameters, inflammatory markers or co-morbidities. Multiple regression analysis showed a significant effect of the Lp(a) on PCSK9 levels, for each unit of higher Lp(a), an increase by 3.082 is expected (95% CI: 0.935 - 5.228, p=0.006). At the same time, patients receiving statins are expected to have on average 63.8ng/ml higher PCSK9 values compared to patients not receiving statins (95% CI: 14.6 - 113.5 p=0.012). Conclusion Plasma levels of PCSK9 in non-dialysis CKD patients are correlated with endothelial dysfunction and lipid metabolism parameters. Statin intake increases PCSK9 levels significantly in this patient population. PCSK9 levels are not correlated with the severity of kidney disease. Major prospective studies are necessary to investigate the role of PCSK9 in the atherosclerotic cardiovascular outcome in CKD
30
Pereira, A., M. Mendonca, J. A. Sousa, F. Mendonca, M. Neto, R. Rodrigues, A. C. Sousa, et al. "P4459The influence of the polymorphism BUD13-ZNF259 rs964184 on coronary disease according to age." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz745.0856.
Full textAbstract:
Abstract A recent GWAS study found a significant association between the BUD13-ZNF259 rs964184 polymorphism, dyslipidemia and the onset of coronary disease (CAD). This variant encoding zinc finger protein (ZPR1) interacts with the receptor tyrosine kinase at cellular level, increasing oxidative stress, inflammatory response and atherogenesis. There are no studies of the effect of this variant on the Portuguese population. Objective Investigate the association of BUD13-ZNF259 rs964184 with dyslipidemia and its impact on CAD risk. Evaluate its impact in different age groups of our population. Methods A case-control study was performed with 3050 subjects (1619 coronary patients with 53.3±8 years; 78.9% male and 1431 controls with 52.8±8 years; 76.6% male) from the GENEMACOR study population. Traditional risk factors (smoking, dyslipidemia, diabetes, family history, hypertension, body mass index, alcohol consumption, physical inactivity) and others considered new, such as creatinine clearance, pulse wave velocity, homocysteine, fibrinogen, lipoprotein (a), APOB and PCR (hs) were investigated. BUD13-ZNF259 variant was genotyped and analyzed using the dominant model (CG + GG vs. CC). Bivariate and multivariate analyzes (logistic regression) were used to estimate the ORs and 95% CI, after adjusting for potential confounding factors, in 3 different age groups (<45; 45–55; >55). Results BUD13-ZNF259 polymorphism presented an independent and significant risk of CAD (OR=1.58; 95% CI: 1.07–2.32; p=0.019) only in the group of young coronary patients <45 years (n=482 patients), as well as dyslipidemia (OR=2.04; 95% CI: 1.26–3.31; p=0.003). After binary logistic regression entering with the interaction between dyslipidemia and the dominant model ZNF259 (CG + GG vs. CC), we verified an association with CAD risk (OR= 1.78; 95% CI: 1.08–2.95; p=0.025). Conclusion BUD13-ZNF259 rs964184 variant showed a significant risk for the onset of CAD in the young population (<45 years). The impact of the interaction of ZPR1 protein with tyrosine kinase (Syk) at the cellular level seems to be more relevant in young patients. This aspect may represent a possible prophylactic and therapeutic target, especially in coronary disease in young people.
31
Shoamanesh, Ashkan, Sarah R. Preis, Alexa S. Beiser, Carlos S. Kase, Philip A. Wolf, Emelia J. Benjamin, Jose R. Romero, and Sudha Seshadri. "Abstract W MP55: Inflammatory Biomarkers and Incident Stroke in the Framingham Offspring Study." Stroke 45, suppl_1 (February 2014). http://dx.doi.org/10.1161/str.45.suppl_1.wmp55.
Full textAbstract:
Background: Inflammatory cascades are believed to be involved in pathogenesis of small vessel disease and atherothrombosis. We related a comprehensive panel of inflammatory biomarkers to risk of incident ischemic stroke (IS) in a community-dwelling sample Methods: Stroke-free Framingham Offspring attending exam cycle 7 (1998-2001) had multiple serum inflammatory biomarkers measured. Fourteen biomarkers representing various components of the inflammatory cascade, including systemic inflammation (C-reactive protein [CRP], interleukin-6, monocyte chemotactic protein 1, tumor necrosis factor-α, tumor necrosis factor receptor 2 [TNFr2], osteoprotegerin and fibrinogen), vascular inflammation (intercellular adhesion molecule-1, CD40 ligand, P-selectin, lipoprotein-associated phospholipase A2 mass and activity, total homocysteine [tHcy] and vascular endothelial growth factor [VEGF]) and oxidative stress (myeloperoxidase) were selected. Cox proportional hazard models were used to relate individual biomarkers to risk of incident IS. Model A included age and sex. Model B additionally adjusted for systolic blood pressure, hypertension treatment, current smoking, diabetes, cardiovascular disease, and atrial fibrillation. Hazard ratios (HR) are presented as per 1 SD increment. Results: In 3224 participants (age: 61±9 years, 54% women), 98 experienced incident IS (mean follow-up of 9.8 [±2.2] years). In Model A, log-CRP (HR: 1.28 [95%CI 1.04-1.56]), log-TNFR2 (HR: 1.33 [95%CI 1.09-1.63]), tHcy (HR: 1.32 [95%CI 1.11-1.58]) and VEGF (HR: 1.25 [95%CI 1.07-1.46]) were associated with risk of incident IS. All associations, except for CRP, remained significant in Model B {log-TNFR2 (1.24 [1.02-1.51]), tHcy (1.20 [1.01-1.43]), VEGF (1.21 [1.04-1.42]) and CRP (1.13 [0.92-1.40])}. Addition of these 4 biomarkers to the clinical Framingham Stroke Risk Profile score improved stroke risk prediction (net reclassification improvement: 0.34; p<0.05 using boundaryless models). Conclusions: Higher levels of four biomarkers: CRP, tHcy, TNFR2 and VEGF increased risk of incident ischemic stroke. Further research is required to confirm their utility in improving stroke risk prediction, and explore their role as potential therapeutic targets.
32
Petrucci, G., L. Viti, M. Sacco, D. Hatem, S. Lancellotti, A. Rizzi, F. Zaccardi, et al. "Effect of low-dose rivaroxaban with low-dose aspirin vs low-dose aspirin on platelet and oxidative biomarkers: a randomized study in diabetes patients with stable peripheral or coronary artery disease." European Heart Journal 43, Supplement_2 (October 1, 2022). http://dx.doi.org/10.1093/eurheartj/ehac544.2719.
Full textAbstract:
Abstract Background Rivaroxaban (Riva), a direct FXa inhibitor, at 2.5 mg twice-daily (bid) combined with low-dose aspirin (ASA, 100 mg once daily-od) reduced major vascular events vs. ASA alone in subjects with stable coronary artery (CAD) or symptomatic peripheral artery disease (PAD). Whether this benefit is due to the anticoagulant effect or additional FXa-mediated effects through the platelet and endothelial cell thrombin receptors is unknown. Type 2 diabetes mellitus (T2DM) is characterized by high platelet activation and oxidative stress that may contribute to increased cardiovascular risk. Purpose We investigated the effects of Riva (2.5 mg bid) + ASA (100 mg od) vs. ASA (100 mg od) alone on platelet and oxidative biomarkers in subjects with T2DM and stable vascular disease (stable CAD, symptomatic PAD and/or significant carotid stenosis). Methods In this randomized, open-label, cross-over trial, patients were randomized to continue ASA for 4 weeks and then add Riva for 4 weeks, or add Riva in the first 4 weeks and then continue with ASA alone for 4 weeks. Primary endpoints were: in vivo platelet activation and lipid peroxidation, assessed by the urinary excretion of 11-dehydro-TXB2 (TXM) and 8-iso-PGF2alpha (ISOP), respectively. Secondary endpoints included: routine coagulation tests, D-dimer, thrombin generation, serum TXB2, and Riva plasma concentrations. Results Seventy-6 subjects (10 females) were recruited: age 68±7 years (mean±SD); BMI 27.1±3.5 kg/m2; fasting glucose 129±31 mg/dL; HbA1c 6.8±0.9%; serum creatinine 1±0.25 mg/dL; LDL-cholesterol 77±31 mg/dL. Two patients dropped out: one for benign, self-limiting hematuria, one for unwillingness to continue, 8 subjects are completing the study leaving 66 who completed the 8-week randomized treatment and showed no sequence effect. Urinary TXM and ISOP were significantly reduced by Riva+ASA vs. ASA alone: TXM was 260 [195–398] vs. 335 [225–441] pg/mg creatinine and ISOP 722 [601–991] vs. 827 [648–1350] pg/mg creatinine (median [IQR]) on Riva+ASA vs. ASA alone, respectively (p<0.001 for paired samples). Riva plasma concentrations were 48±1.9 ng/ml at peak and 21±1.4 ng/ml at trough. The velocity of thrombin formation significantly decreased with Riva+ASA vs. ASA alone (velocity index, 46±3% vs. 83±3%; peak-height, 66±2% vs. 83±1%, respectively). aPTT levels were slightly but significantly prolonged by Riva vs. ASA alone (44±1 vs. 39±1 sec). Serum TXB2, D-dimer, von Willebrand factor, PT, fibrinogen and endogenous thrombin potential values were similar between treatments. Conclusions In ASA-treated subjects with T2DM and stable vascular disease, the addition of very low-dose Riva restrained incompletely-suppressed lipid peroxidation and platelet activation and modified the kinetics of thrombin formation. These changes may contribute to the beneficial effects of the Riva+ASA combination. Funding Acknowledgement Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Investigator-initiated study funded by Bayer AG
33
Cernaro, Valeria, Vincenzo Calabrese, Saverio Loddo, Roberta Corsaro, Vincenzo Macaione, Valentina Teresa Ferlazzo, Rosalia Maria Cigala, et al. "MO139INDOLE-3-ACETIC ACID CORRELATES WITH MONOCYTE TO HIGH-DENSITY LIPOPROTEIN (HDL) RATIO (MHR) IN CHRONIC KIDNEY DISEASE (CKD) PATIENTS AND MAY BE EFFICIENTLY REMOVED BY ACETATE-FREE BIOFILTRATION." Nephrology Dialysis Transplantation 36, Supplement_1 (May 1, 2021). http://dx.doi.org/10.1093/ndt/gfab092.0017.
Full textAbstract:
Abstract Background and Aims Indole-3-acetic acid (IAA, also called auxin) is a protein-bound indolic uremic toxin deriving from tryptophan metabolism by the intestinal bacteria. Previous studies have shown that increased IAA is associated with enhanced tissue factor synthesis in endothelial and peripheral blood mononuclear cells, oxidative stress and endothelial inflammation with resulting higher risk of thrombotic events and both cardiovascular and all-cause mortality. An emerging biomarker of cardiovascular disease is the monocyte to high-density lipoprotein (HDL) ratio (MHR). Its prognostic value is related to the ability of monocytes to release several cytokines involved in inflammation and atherogenesis and to the protective role of HDL through removal of cholesterol from peripheral tissues and suppression of both monocyte progenitor cell proliferation and differentiation and monocyte activation. In this single-centre cross-sectional observational study, we investigated the potential association of IAA with MHR and other markers of cardiovascular risk in a cohort of patients with CKD and evaluated the effect of a single midweek dialysis session with AFB (Acetate-free Biofiltration) technique on IAA serum concentrations. Method We enrolled 61 non-dialysis CKD adult patients and 6 dialysis patients treated with AFB technique. IAA levels were measured using an enzyme-linked immunosorbent assay (ELISA) kit (Cat. number abx150354; Abbexa Ltd, Cambridge, UK). Post-dialysis IAA levels were corrected for haemoconcentration. Results In the whole cohort of 67 patients, IAA was directly related to creatinine (ρ = 0.247; P = 0.0441), potassium (r = 0.2871; P = 0.0185), Ca x P product (ρ = 0.256; P = 0.0365) and MHR (ρ = 0.321; P = 0.0082). After adjustment for creatinine, the correlation between IAA and potassium became not significant (r = 0.1968; P = 0.1133). Stratifying patients according to the history of cardiovascular disease, in the 40 patients with previous cardiovascular events IAA levels correlated significantly with uric acid (r = 0.3952; P = 0.0116) and MHR (ρ = 0.380; P = 0.0157). In the remaining 27 patients without history of cardiovascular disease, IAA only correlated with potassium (r = 0.3912; P=0.0481) and, though borderline significantly, with creatinine (ρ = 0.349; P = 0.0805). To assess whether IAA would independently predict MHR values, we evaluated potential correlations of MHR with risk factors for cardiovascular disease. MHR was related with fibrinogen (ρ = 0.426; P = 0.0010), arterial hypertension (ρ = 0.274; P = 0.0251), C-reactive protein (ρ = 0.332; P = 0.0061), gender (ρ = -0.375; P = 0.0017; 0 = male, 1 = female), and CKD stage (ρ = 0.260; P = 0.0337). A multiple regression analysis identified IAA as an independent predictor of MHR. Lastly, IAA levels were higher in dialysis patients compared to non-dialysis CKD patients (97.44 ± 21.58 versus 65.08 ± 24.38 ng/ml respectively; P = 0.0026) and it was significantly removed by a single AFB session (97.44 ± 21.58 versus 54.59 ± 21.74 ng/ml; P = 0.0028) with a reduction ratio of 43.80 ± 17.47%. Conclusion This study shows a statistically significant association between IAA and MHR. Based on previous experimental studies, such relationship could be explained by the activation of the transcription factor aryl hydrocarbon receptor. Indeed, IAA is a potent ligand of aryl hydrocarbon receptor and the latter has proinflammatory and proatherogenic activities and can reduce HDL levels. Moreover, AFB efficiently removes IAA during a single dialysis session. Prospective studies with appropriate sample size and sufficiently long period of observation are required to evaluate if decreasing IAA levels, through targeted therapeutic strategies in non dialysis CKD patients or by optimization of dialysis techniques and prescriptions in patients receiving renal replacement therapy, may reduce MHR levels and cardiovascular events and improve clinical outcomes and survival.