Atherosclerosis In Rheumatic Diseases Research Articles

Autoimmune and angiogenic biomarkers in autoimmune atherosclerosis

Several inflammatory, proteolytic, angiogenic and bone-associated factors play a role in the development of autoimmune, accelerated atherosclerosis in rheumatic diseases. Some of these may serve as biomarkers of vascular pathology and may be useful in the follow-up of vascular damage and outcome. Multi-biomarker profiles rather than a single markers would likely be optimal in this respect.

Oxidized low density lipoproteins: The bridge between atherosclerosis and autoimmunity. Possible implications in accelerated atherosclerosis and for immune intervention in autoimmune rheumatic disorders.

Atherosclerotic vasculopathy is a multifactorial process causing vessels damage and cardiovascular diseases, the leading causes of death worldwide. Atherosclerotic plaque is the asymptomatic primary, elementary, lesion of atherosclerotic vasculopathy. Accumulation of the oxidized low-density lipoprotein (oxLDL) at sub endothelial sites is now recognized as one of the major trigger events in plaque formation. The concomitant presence at the plaque site of cells belonging to either natural or adaptive immunity, the detection of autoantibodies to oxLDL, the cross-reactivity of oxLDL with anti-phospholipid antibodies, in addition to the clinical evidence of increased rates of cardiovascular events in several rheumatic diseases, has stimulated intensive research to define interconnections between the immune system and traditional risk factors at the molecular levels in order to explain accelerated atherosclerosis. Here, we critically review the results of previous and recent studies, which have disclosed molecules of both innate or adaptive immunity involved in atherosclerosis, focusing primarily on B cells and autoantibodies, where data are more consolidated. Particular attention has also been paid to molecules that may be predictive markers of atherosclerosis progression and can be potential targets for immune intervention to delay the atherosclerotic process. The latter include CD20 antigen, molecules involved in the BAFF-BAFF receptor axis, inflammatory molecules and modified LDL. The successful results of a recent randomized controlled clinical trial targeting inflammasome with anti-IL1β monoclonal antibody in non-autoimmune conditions, prove that specific immunotherapy can be a promising and effective strategy to control atherosclerosis in rheumatic diseases as well.

Usefulness of measuring common carotid intima-media thickness: Ultrasound diagnosis of sub-clinical atherosclerosis in rheumatic diseases. A literature review

Abstract Introduction Patients with rheumatic diseases have an increased cardiovascular risk due to systemic inflammation and endothelial dysfunction, which promotes accelerated atherosclerosis. One way to measure cardiovascular risk, is through the carotid intima-media thickness which is an inexpensive and non-invasive predictor of cardiovascular events. Objective To examine the evidence to determine the usefulness of ultrasound in the diagnosis of sub-clinical atherosclerosis in rheumatic diseases assessed by carotid intima-media thickness (IMT). Material and methods A systematic literature search was performed, using electronic databases of PubMed, for articles published from January 2005 to May 2015, with no language restriction. Observational cohort studies that assessed the prevalence of sub-clinical atherosclerosis using the IMT were included. Results A total of 56 studies were identified for analysis, with almost all (95.7%) reporting an increased IMT in relation to the control group. Conclusions Patients with rheumatic diseases have an increased cardiovascular risk assessed using IMT. This measurement, assessed by carotid ultrasound, may help detect the risk of sub-clinical cardiovascular disease in these populations, allowing to establish a therapeutic strategy to reduce the risk of morbidity and mortality in these patients.

Medición del grosor de la íntima-media carotídea: utilidad y diagnóstico ecográfico de aterosclerosis subclínica en enfermedades reumáticas. Revisión de la literatura

IntroductionPatients with rheumatic diseases have an increased cardiovascular risk due to systemic inflammation and endothelial dysfunction, which promotes accelerated atherosclerosis. One way to measure cardiovascular risk, is through the carotid intima-media thickness which is an inexpensive and non-invasive predictor of cardiovascular events. ObjectiveTo examine the evidence to determine the usefulness of ultrasound in the diagnosis of sub-clinical atherosclerosis in rheumatic diseases assessed by carotid intima-media thickness (IMT). Material and methodsA systematic literature search was performed, using electronic databases of PubMed, for articles published from January 2005 to May 2015, with no language restriction. Observational cohort studies that assessed the prevalence of sub-clinical atherosclerosis using the IMT were included. ResultsA total of 56 studies were identified for analysis, with almost all (95.7%) reporting an increased IMT in relation to the control group. ConclusionsPatients with rheumatic diseases have an increased cardiovascular risk assessed using IMT. This measurement, assessed by carotid ultrasound, may help detect the risk of sub-clinical cardiovascular disease in these populations, allowing to establish a therapeutic strategy to reduce the risk of morbidity and mortality in these patients.

The Rationale for Comparative Studies of Accelerated Atherosclerosis in Rheumatic Diseases

The inflammatory pathogenesis of atherosclerosis is now well-established, owing to in vitro and in vivo studies and the application of high sensitivity assays for C-reactive protein (CRP) in the general population and specific groups at risk for cardiovascular disease (CVD). In view of the complexity of inflammation-induced atherosclerosis, the rationale for comparative studies of atherogenesis in rheumatic diseases with diverse inflammatory pathogenesis seems obvious; they are human in vivo models to study inflammatory mechanisms involved in atherosclerosis and the impact of treatment. Factors implicated in atherogenesis in systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), familial Mediterranean fever (FMF) and Behçet's disease (BD) are discussed in this review. Evidence suggests that enhanced atherosclerosis causes premature cardiovascular events in the autoimmune disease, SLE, and the "high-grade" inflammatory rheumatic disease, RA. Preliminary data suggest that enhanced atherogenesis may accompany FMF in the absence of sufficient suppression of inflammation by colchicine. In the setting of BD, the role of atherosclerosis in the premature manifestation of coronary pathology has not been confirmed; coronary vasculitis and aneurysms appear to constitute the basis of myocardial infarction (MI) in BD. A variety of established and novel risk factors are believed to influence enhanced atherogenesis in rheumatic diseases. Antiphospholipid antibodies are thought to be intimately involved in atherogenesis in SLE and to a lesser extend in RA. CRP may play a more universal role in all rheumatic diseases. The application of high resolution ultrasound of peripheral arteries and other non-invasive techniques may allow targeted use of statins, ACE inhibitors, antiplatelet agents and other cardioprotective drugs in patients with rheumatic diseases, but this needs to be evaluated specifically in prospective studies.

The Rationale for Comparative Studies of Accelerated Atherosclerosis in Rheumatic Diseases

The Rationale for Comparative Studies of Accelerated Atherosclerosis in Rheumatic Diseases

Atherosclerosis in Autoimmune Rheumatic Diseases—Mechanisms and Clinical Findings

Atherosclerosis is one of the major entities leading to morbidity and mortality in the western world. It is known now that atherosclerosis cannot be explained merely by the presence of the Framingham traditional risk factors and that autoimmunity takes a significant role in its pathogenesis. It is also known that individuals with autoimmune diseases demonstrate increased incidence of cardiovascular manifestations and subclinical atherosclerotic disease. The mechanisms for the assumed accelerated atherosclerosis in diseases such as systemic lupus erythematosus, rheumatoid arthritis, antiphospholipid syndrome, and systemic sclerosis include the classical risk factors, but may also be due to chronic inflammatory processes and immune dysregulation. Autoantibodies, autoantigens, pro-inflammatory cytokines, and infectious agents play a role in that process. Involvement of autoimmunity in the pathogenesis of accelerated atherosclerosis in rheumatic diseases and the common pathway that leads to this condition may lead to significant change in prevention of treatment.

Immunologic reactants in the pathogenesis of atherosclerosis in rheumatic diseases

Immunologic reactants in the pathogenesis of atherosclerosis in rheumatic diseases