Atherogenesis In Patients Research Articles

Lipoprotein(a) is a predictor of atherogenesis in patients with COPD

Lipoprotein(a) is a predictor of atherogenesis in patients with COPD

Associations between serological biomarkers and subclinical atherosclerosis in patients with rheumatoid arthritis after 11 years of follow-up.

To investigate the relationship between biomarkers known to be involved in both chronic inflammation and subclinical atherosclerosis, as measured by carotid intima media thickness (cIMT), in patients with RA compared to controls. Between 2000 and 2004, all patients under 60 years of age with newly diagnosed RA in the northern region of Sweden were invited to participate in this study. Measurements of cIMT were undertaken at inclusion (T0), after five years of follow-up (T5) and after eleven years of follow-up (T11). Patients were clinically assessed and blood was drawn for analysis of biomarkers. In patients with RA (n=54), linear regression models showed that cIMT at T11 was associated with levels of GDF-15 at T5 and T11, but not with baseline levels. GDF-15 was strongly associated with age. At T11, mean level of GDF-15 was elevated compared to controls. Levels of adiponectin, MCP-1, cathepsin S, endoglin and IL-6 were higher in patients with RA compared to controls, but showed no association with cIMT. In multivariable linear regression models with cIMT at T11 as dependent variable, change in GDF-15 from T0 to T11 was associated to an increase in cIMT at T11. Adjusting for systolic blood pressure and age respectively rendered this association statistically non-significant,CONCLUSIONS: Among these patients with RA GDF-15 was associated to cIMT after 11 years of follow-up. GDF-15 should be a biomarker of interest in future research, to further understand its role in the accelerated atherogenesis in patients with RA.

The effect of antioxidant therapy on some pathogenetic factors of primary open-angle glaucoma

The study analyzes the vascular remodulation, antioxidant and antihypoxic effects of the drug Mexidol in patients with PAOG. The study included 78 patients with POAG of the early (n=43) and advanced stage (n=35) with average age of 67.8±1.5 years. The main study group consisted of 47 patients who received Mexidol in addition to local hypotensive treatment; 31 patients comprised the control group. In the comparison groups, the degree of ED was determined by the results of reactive hyperemia test, patients' blood plasma was analyzed for levels of stable nitric oxide metabolite (nitrite NO2-) and endothelin-1 (ET-1). General assessment of oxidative stress was carried out by high-performance liquid chromatography. Functional activity of the retina was studied using an electroretinograph and static computer perimetry performed according to the standard technique. The following changes are observed in patients of the main group using Mexidol: the index of oscillatory potentials significantly increases, peak latency decreases, perimeter indices show positive trends, vascular endothelial function improves according to reactive hyperemia test, concentration of vasoconstrictor mediator ET-1 in blood plasma decreases and of nitrite (NO2-) increases moderately, the coefficient of bioeffective vasotonic activity decreases, the level of glutathione peroxidase increases (p<0.05 compared to the baseline value), the level of malonyldialdehyde decreases, lipid metabolism improves (reduction in total cholesterol, low-density lipoprotein-cholesterol, triglycerides, decrease in the Atherogenic Index compared to the initial level). The drug Mexidol proved to be an effective endothelial protector, a powerful antioxidant and antihypoxant, contributed to deceleration of atherogenesis in patients with POAG.

Urine transferrin as an early endothelial dysfunction marker in type 2 diabetic patients without nephropathy: a case control study

BackgroundAlbumin, along with other proteins, is abnormally eliminated via the urine during early stages of diabetic nephropathy. Moreover, endothelial dysfunction (ED) accompanying early diabetic nephropathy may develop even before microalbuminuria is detectable. Transferrin has a molecular weight comparable to albumin, whereas transferrinuria and microalbuminuria in a 24-h urine sample may comparably reflect early diabetic nephropathy. Whereas transferrin metabolism is related with ED during very early diabetic nephropathy has not been elucidated yet. This case–control study aimed to evaluate the relation between ED and urine transferrin, even before early diabetic nephropathy is present.MethodsPatients were enrolled from two study sites in Mexico City: Ticomán General Hospital (healthy controls); and a Specialized Clinic for the Management of the Diabetic Patient (cases). All patients provided written informed consent. The primary endpoint was the correlation between urinary transferrin concentration and ED measured in type 2 diabetic patients without albuminuria. ED was evaluated by ultrasonographic validated measurements, which included carotid intima-media thickness (CIMT) and flow mediated dilation (FMD). Plasma biomarkers included glycated hemoglobin, creatinine, cholesterol and triglycerides, as well as urine albumin, transferrin and evidence of urinary tract infection.ResultsSixty patients with type 2 Diabetes Mellitus (t2DM; n = 30) or without t2DM (n = 30), both negative for microalbuminuria, were recruited. The group with t2DM were older, with higher values of HbA1c and higher ED. This group also showed significant differences in urine transferrin and urine/plasma transferrin ratio, as compared with healthy controls (14.4 vs. 18.7 mg/mL, p = 0.04, and 74.2 vs. 49.5; p = 0.01; respectively). Moreover, urine transferrin correlated with higher CIMT values (r = 0.37, p = 0.04), being particularly significant for t2DM population. CIMT also correlated with time from t2DM diagnosis (r = 0.48, p < 0.001) and HbA1c (r = 0.48; p < 0.001).ConclusionUrine transferrin correlated with subclinical atherogenesis in patients with t2DM without renal failure, suggesting its potential to identify cardiovascular risk in patients at very early nephropathy stage without microalbuminuria.

Порівняльна характеристика факторів атероґенезу в пацієнтів із симптомним і асимптомним перебігом атеросклеротичних каротидних стенозів

To study a comparative assessment of risk factors for atherogenesis in patients with different clinical manifestations of carotid atherosclerotic stenosis. The study included 106 patients (men — 74, women — 32) aged 39 to 79 years (mean age 62.6 ± 0.9), which devided to 3 clinical groups: Group I — 35 patients with acute atherothrombotic stroke with ipsilateral carotid stenosis, group II — 41 patients after acute cerebrovascular events and carotid endarterectomy, group III — 30 patients with asymptomatic atherosclerotic carotid stenosis and the control group, which consisted of 20 relatively healthy individuals. The degree of stenosis of the internal carotid arteries was highest (&gt; 70 %) in the group of patients who underwent carotid endarterectomy. In addition in this group was prevalence younger men, compared with the group of asymptomatic stenosis and women (p = 0.00300), there was an older age of patients and moderate stenosis of 50–69 % (p = 0.00647). In patients with stenotic atherosclerosis of the internal carotid artery, there was a significant increase in the level of Lp-PLA2 compared with the control. This confirms that Lp-PLA2 can be considered as a marker of carotid atherosclerosis and influence the development of ischemic stroke. The highest level of Lp-PLA2 was observed in the clinical group of patients who underwent carotid endarterectomy after ischemic stroke and there was a tendency to a more significant increase in total cholesterol. This suggests a more aggressive course of the atherosclerotic process in patients in this group.

ATHEROGENIC INDEX OF PLASMA (AIP): A MARKER OF RISK FOR ISCHEMIC STROKE

Background Atherogenic Index of Plasma (AIP) has been shown as a good surrogate marker for early atherogenesis in patients with cardiovascular disease. Atherosclerosis has been implicated in the pathogenesis of cerebrovascular disease and its leading comorbidities such as hypertension, diabetes, obesity and smoking. This study aims to determine the possibility of Atherogenic Index of Plasma as a marker of risk for ischemic stroke, to determine its relationship to hypertension, diabetes, obesity and smoking as well as its relationship to carotid artery stenosis and intracranial stenosis. Methods and Results This is a cross-sectional analytic study done in a tertiary hospital. A total of 64 patients (45 males and 19 females) diagnosed with acute or subacute ischemic stroke were included in the study. History of hypertension, diabetes and dyslipidemia were recorded. Lipid profile (Total cholesterol, Triglycerides, High Density Lipoprotein and Low Density Lipoprotein), Body Mass Index, presence and severity of intracranial stenosis on MRA and presence of carotid artery stenosis and carotid intima-media thickness were recorded. Atherogenic Index of Plasma was positively correlated with total cholesterol [r(62) = .300, p=.016], triglycerides [r(62) = .760, p=.000], smoking [p=.05], and is negatively correlated with HDL [r(62)=-.572, p=.000] and age [r(62)=-.311, p=.012]. AIP did not show any correlation with hypertension, diabetes, intracranial stenosis, carotid artery stenosis and intima-media thickness. Conclusion Atherogenic index of plasma showed positive association with other lipid parameters consistent with findings in literature. No significant association was seen with other comorbidities which was probably influenced by the selected population of the study. Still, AIP shows a potential as a surrogate marker for early atherogenesis which is an important mechanism for ischemic strokes.

Senescent Phenotype Induced by p90RSK-NRF2 Signaling Sensitizes Monocytes and Macrophages to Oxidative Stress in HIV-Positive Individuals

The incidence of cardiovascular disease is higher in HIV-positive (HIV+) patients than it is in the average population, and combination antiretroviral therapy (cART) is a recognized risk factor for cardiovascular disease. However, the molecular mechanisms that link cART and cardiovascular disease are currently unknown. Our study explores the role of the activation of p90RSK, a reactive oxygen species-sensitive kinase, in engendering senescent phenotype in macrophages and accelerating atherogenesis in patients undergoing cART. Peripheral whole blood from cART-treated HIV+ individuals and nontreated HIV-negative individuals was treated with H2O2 (200 µmol/L) for 4 minutes, and p90RSK activity in CD14+ monocytes was measured. Plaque formation in the carotids was also analyzed in these individuals. Macrophage senescence was determined by evaluating their efferocytotic ability, antioxidation-related molecule expression, telomere length, and inflammatory gene expression. The involvement of p90RSK-NRF2 signaling in cART-induced senescence was assessed by p90RSK-specific inhibitor (FMK-MEA) or dominant-negative p90RSK (DN-p90RSK) and NRF2 activator (NRF2A). Further, the severity of atherosclerosis was determined in myeloid cell-specific wild-type and DN-p90RSK transgenic mice. Monocytes from HIV+ patients exhibited higher levels of p90RSK activity and were also more sensitive to reactive oxygen species than monocytes from HIV-negative individuals. A multiple linear regression analysis involving cART, Reynolds cardiovascular risk score, and basal p90RSK activity revealed that cART and basal p90RSK activity were the 2 significant determinants of plaque formation. Many of the antiretroviral drugs individually activated p90RSK, which simultaneously triggered all components of the macrophage senescent phenotype. cART inhibited antioxidant response element reporter activity via ERK5 S496 phosphorylation. NRF2A reversed the H2O2-induced overactivation of p90RSK in cART-treated macrophages by countering the induction of senescent phenotype. Last, the data obtained from our gain- or loss-of-function mice conclusively showed the crucial role of p90RSK in inducing senescent phenotype in macrophages and atherogenesis. cART increased monocyte/macrophage sensitivity to reactive oxygen species- in HIV+ individuals by suppressing NRF2-ARE activity via p90RSK-mediated ERK5 S496 phosphorylation, which coordinately elicited senescent phenotypes and proinflammatory responses. As such, our report underscores the importance of p90RSK regulation in monocytes/macrophages as a viable biomarker and therapeutic target for preventing cardiovascular disease, especially in HIV+ patients treated with cART.

Dysfunctional high density lipoprotein failed to rescue the function of oxidized low density lipoprotein-treated endothelial progenitor cells: a novel index for the prediction of HDL functionality

Lipid metabolic disorders play critical roles in atherogenesis. Traditionally, it has been suggested that reduced high density lipoprotein (HDL) levels might be an important morbidity indicator for cardiovascular diseases. Therefore, it has been argued that therapeutically raising HDL levels may reduce atherogenesis in patients with dyslipidemia. However, recent clinical trials to elevate serum HDL levels by pharmacologic approaches failed to demonstrate clinical efficacy. Thus, to investigate the functionality of HDL and to explore the possible clinical relevance as well as to define an effective indicator that can represent HDL function may provide another key and reference to disclose the clinical treatment of dyslipidemia. We analyzed the association between the data of dichlorofluorescein assay (assay the functionality of HDL), the effect of HDL on oxidized low density lipoprotein (oxLDL)-stimulated endothelial progenitor cells (EPCs) in vitro, levels of circulating EPCs, and ex vitro EPC colony forming units of each case, we defined the indicator (relative HDL index (RHDL index) = dichlorofluorescein assay result of each subject/dichlorofluorescein assay reading of our young healthy controls) that may represent functionality of HDL. HDL from healthy adults protected oxLDL-treated EPCs by modulating p38 mitogen-activated protein kinase and Rho activation and by promoting nitric oxide production. HDL from subject with RHDL index ≧2 also failed to restore the functionality of oxLDL-treated EPCs via cell-signaling pathways in vitro. The RHDL index significantly correlated with patients' circulating EPC number or EPC colony forming units ex vivo. In conclusions, we explored the RHDL index as a score to predict a patient's EPC functions in vivo and ex vitro.

Selection of genes with transcriptional activity in peripheral blood mononuclear cells and associated with atheroprotective effect of HDL in patients with coronary artery disease

Aim: To identify the cluster of genes with transcriptional activity in peripheral blood mononuclear cells and related to HDL metabolism and atherogenesis in patients with CAD.

Oxidative burden in familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is a genetic disorder characterized by high serum levels of low-density lipoprotein cholesterol (LDL-c). FH is characterized by accelerated development of atherosclerosis and represents the most frequent hereditary cause of premature coronary heart disease. Mutations of the LDL receptor gene are the genetic signature of FH, resulting in abnormal levels of circulating LDLs. Moreover, FH promotes the generation of reactive oxygen species (ROS) which is another key mechanism involved in atherosclerosis development and progression. The aim of this narrative review is to update the current knowledge on the pathophysiological mechanisms linking FH to ROS generation and their detrimental impact on atherosclerotic pathophysiology. With this purpose, we reviewed experimental and clinical data on the association between FH and OS and the functional role of OS as a promoter of inflammation and atherosclerosis. In this regard, oxidant species such as oxidized LDL, malondialdehyde, ROS, and isoprostanes emerged as leading mediators of the oxidative injury in FH. In conclusion, targeting oxidative stress may be a promising therapeutic strategy to reduce atherogenesis in patients with FH.

Adventitial tertiary lymphoid organ classification in human atherosclerosis.

Atherosclerosis is a chronic inflammatory disease of the arterial wall. Adjacent to lamina intima lesion progression, a cellular compound develops in the lamina adventitia, defined as tertiary lymphoid organs (TLO) in mice. But in human system, it remains unknown whether these adventitial cellular accumulations represent these highly organized immunological structures. In this study, we investigated whether the adventitial cellular compounds represent TLOs in 72 human coronary artery samples by immunoenzyme staining. The study showed that the adventitial cellular compound partly represented TLOs in human coronary arteries affected by atherogenesis in patients suffering from ischemic heart disease (56%) or a fatal myocardial infarction (100%), but not dilated cardiomyopathy. In addition, we established a classification for human TLOs, stage I-III, and showed that all stages were present in diseased coronary arteries. The stage of TLOs highly correlated with lesion size as well as plaque instability and rupture, and all patients with a myocardial infarction had stage III. Additionally, there were cellular infiltration and destruction of the lamina media, which were restricted to TLOs next to ruptured plaques in patients with a fatal myocardial infarction. TLOs are present in patients with a coronary artery disease and highly correlated with lesion size, plaque instability, and rupture. Further studies are needed to investigate whether TLOs might be a specific diagnostic and drug target to modify plaque instability/rupture.

Subclinical atherogenesis in patients with mild psoriasis: A role for IL-6?

A link of psoriasis with subclinical atherosclerosis has been postulated and cytokine network might intermediate this association. Few data are available in patients with mild psoriasis. We evaluated carotid intima-media thickness (cIMT) in drug-free psoriatic individuals and controls. In parallel, we searched for associations of cIMT with disease activity indexes and serum interleukins (IL) in psoriatic patients. An experienced radiologist performed the cIMT analyses. Cytokine concentrations were assessed by flow cytometry. Disease activity was evaluated based on psoriasis area and severity index (PASI) as well as body surface area (BSA). Sixty-five (65) patients and 64 controls were studied. Mean age of patients (50.9 years) did not differ from controls (p=0.362). A low PASI and BSA (< 10) prevailed (69.2% and 56.9%, respectively). Median levels of IL-12p70, TNF-α, IL-1β and IL-10 were significantly lower in cases than in controls (adjusted p<0.05), while IL-6 and IL-8 medians did not differ between groups (adjusted p>0.05). Smoking habit and diabetes mellitus predominated in cases (p=0.002). An altered cIMT (≥ 0.9 mm) was more frequent in cases than in controls (23.8% versus 8.5%, adjusted p=0.045). Mean cIMT was higher in cases with a borderline significance (p=0.057). cIMT scores did not correlate to PASI (rs=0.066; p=0.250) or BSA (rs=0.175; p=0.185), but did correlate significantly with serum IL-6 (rs=0.26; p=0.005). Subclinical atherosclerosis was more frequent in patients with mild psoriasis than controls. cIMT in psoriatic individuals correlated with serum IL-6, pointing to an eventual proatherogenic role of IL-6 in these patients. Newer studies should clarify the connection of atherogenesis with cytokines in psoriasis.

The role of oxidized low-density lipoproteins and autoantibodies to them in atherogenesis in patients with coronary atherosclerosis

The role of oxidized low-density lipoproteins and autoantibodies to them in atherogenesis in patients with coronary atherosclerosis

Protein factors of oxidative stress and atherogenesis in patients with arterial hypertension

Protein factors of oxidative stress and atherogenesis in patients with arterial hypertension

Anti-TNF-α therapy improves insulin sensitivity in non-diabetic patients with psoriasis: a 6-month prospective study.

Psoriasis is a chronic inflammatory disease associated with increased risk of cardiovascular death. Several studies have shown a beneficial effect of anti-TNF-α therapy on the mechanisms associated with accelerated atherogenesis in patients with inflammatory arthritis, including an improvement of insulin sensitivity. In this study, we aimed to determine for the first time whether the anti-TNF-α monoclonal antibody adalimumab may improve insulin sensitivity in non-diabetic patients with psoriasis. Prospective study on a series of consecutive non-diabetic patients with moderate to severe psoriasis seen at the Dermatology Division of Hospital Universitario Marques de Valdecilla (Northern Spain) who completed 6months of therapy with adalimumab (80mg at week 0 followed by 40mg every other week, starting 1week after the initial dose). Patients with chronic kidney disease, hypertension or body mass index≥35kg/m(2) were excluded. Metabolic and clinical evaluation including assessment of insulin sensitivity using the Quantitative Insulin Sensitivity Check Index (QUICKI) was performed at the onset of the treatment (time 0) and at month 6. Twenty-nine patients (52% women; 38.6±10.7years) with moderate to severe psoriasis [body surface area (BSA) 37.9±16.3%], Psoriasis Area and Severity Index [(PASI) 18.9±7.8] were assessed. Statistically significant improvement (P=0.008) of insulin sensitivity was observed after 6months of adalimumab therapy (QUICKI at time 0: 0.35±0.04 vs. 0.37±0.04 at month 6). Significant improvement of erythrocyte sedimentation rate, ultrasensitive C-reactive protein, BSA, PASI, Nail Psoriasis Severity Index, physician global assessment and psoriatic arthritis screening and evaluation questionnaire was also observed at month 6 (P<0.05 for each variable). Our results support a beneficial effect of the anti-TNF-α blockade on the mechanisms associated with accelerated atherogenesis in patients with psoriasis.

Recombinant domain V of β2-glycoprotein I inhibits the formation of atherogenic oxLDL/β2-glycoprotein I complexes.

β2-glycoprotein I (β2-GPI) is a plasma protein that interacts with oxidized low-density lipoproteins (oxLDL) via β2-GPI domain V to form oxLDL/β2-GPI complexes, potential autoantigens promoting atherogenesis in patients with antiphospholipid syndrome (APS). Such a interaction would expose β2-GPI domain I or/and IV, structures recognized by anti-β2-GPI autoantibodies. IgG immune complexes with oxLDL/β2-GPI complexes can interact with macrophages via Fcγ receptor, causing oxLDL/β2-GPI endocytosis and foam cell formation, contributing to atherosclerosis. Here, we use recombinant domain V to study the interaction between oxLDL and β2-GPI and hypothesized that domain V would interfere with this interaction thereby reducing oxLDL macrophage uptake and foam cell formation. The β2-GPI domain V sequence was expressed by using the Pichia pastoris expression system to obtain recombinant domain V of β2-GPI (P.rβ2-GPI DV). ELISA tests demonstrated that P.rβ2-GPI DV interacted with oxLDL via 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), a negatively charged lipid moiety of oxLDL. The ω-carboxyl residue of oxLig-1 is required for the interaction. Serologic tests showed a significant increase in oxLDL and oxLDL/β2-GPI levels in patients with APS (p < 0.05 compared to controls). P.rβ2-GPI DV was able to bind oxLDL in high affinity and competitively inhibited native β2-GPI (nβ2-GPI) binding to free oxLDL as well as to oxLDL from the oxLDL/β2-GPI complexes. These observations suggest that P.rβ2-GPI DV may be used to inhibit the formation of the oxLDL/β2-GPI complexes, a potential approach for reducing foam cell development and mitigating atherogenesis in patients with APS. The present work provides a new effective strategy to prevent the progression of atherothrombotic vascular complications in APS patients.

AB0353 Independent Paradoxically Inverse Associations of Retinol Binding Protein 4 with Metabolic Risk and Endothelial Activation in the Absence of A Retinol Binding Protein 4 – Atherosclerosis Relationship in Rheumatoid Arthritis

BackgroundWhereas retinol binding protein 4 (RBP) enhances metabolic risk and atherogenesis in non-rheumatoid arthritis (RA) subjects (1,2), its role in atherogenesis in patients with RA is currently unknown.ObjectivesWe investigated the...

Human monoclonal Fab and human plasma antibodies to carbamyl‐epitopes cross‐react with malondialdehyde‐adducts

Oxidized low-density lipoprotein (OxLDL) plays a crucial role in the development of atherosclerosis. Carbamylated LDL has been suggested to promote atherogenesis in patients with chronic kidney disease. Here we observed that plasma IgG and IgM antibodies to carbamylated epitopes were associated with IgG and IgM antibodies to oxidation-specific epitopes (ρ = 0·65-0·86, P < 0·001) in healthy adults, suggesting a cross-reaction between antibodies recognizing carbamyl-epitopes and malondialdehyde (MDA)/malondialdehyde acetaldehyde (MAA) -adducts. We used a phage display technique to clone a human Fab antibody that bound to carbamylated LDL and other carbamylated proteins. Anti-carbamyl-Fab (Fab106) cross-reacted with oxidation-specific epitopes, especially with MDA-LDL and MAA-LDL. We showed that Fab106 bound to apoptotic Jurkat cells known to contain these oxidation-specific epitopes, and the binding was competed with soluble carbamylated and MDA-/MAA-modified LDL and BSA. In addition, Fab106 was able to block the uptake of carbamyl-LDL and MDA-LDL by macrophages and stained mouse atherosclerotic lesions. The observed cross-reaction between carbamylated and MDA-/MAA-modified LDL and its contribution to enhanced atherogenesis in uraemic patients require further investigation.

Low level of inflammatory marker in hyperhomocysteinemic patients on statin therapy

Inflammatory processes including increased activation of chemokines play an important role in atherogenesis. Patients with hyperhomocysteinemia have increased risk for cardiovascular events that potentially involve enhanced inflammation. Statins may have anti-inflammatory actions at least partly independent on their lipid-lowering effects. In the present study we examined the association between statins and chemokine levels in patients with hyperhomocysteinemia. Our major findings were (i) patients with hyperhomocysteinemia on statin treatment (n = 14) have significantly lower plasma levels of the CXC chemokine epithelial neutrophil activating peptide (ENA)-78 compared to hyperhomocysteinemic patients not on statin treatment (n = 8). In fact, levels of ENA-78 in statin-treated patients did not differ from those of healthy controls (n = 17); (ii) plasma levels of ENA-78 and growth-related oncogene (GRO)α correlated with levels of LDL-cholesterol and homocysteine; (iii) in contrast, plasma levels of the CC chemokine monocyte chemoattractant peptide (MCP)-1 were similar between statin-users, non-statin users and controls, and did not correlate with levels of LDL-cholesterol or homocysteine; and (iv) in vitro studies showed that simvastatin significantly reduced release of ENA-78, GROα and MCP-1 from peripheral blood mononuclear cells in healthy controls (n = 7) in a concentration-dependent manner, without affecting release of RANTES. Our data may suggest that ENA-78 and GROα may be involved in the inflammatory arm of atherogenesis in patients with elevated risk of cardiovascular disease, with potential down-regulatory effect of statins.

SAT0043 Potential Determinants of Atherogenesis in Patients with Rheumatoid Arthritis from Two Population Groups

BackgroundThe very early steps in atherosclerosis comprise adhesion of monocytes to the endothelium and monocyte transmigration through the endothelial barrier into the intima. These processes are effectuated by adhesion molecules...