TY - JOUR
TI - Cardiovascular risk in rheumatoid arthritis and mechanistic links: From pathophysiology to treatment
AU - Fragoulis, G.E.
AU - Panayotidis, I.
AU - Nikiphorou, E.
JO - Current Vascular Pharmacology
PY - 2020
VL - 18
TODO - 5
SP - 431-446
PB - Bentham Science Publishers
SN - 1570-1611
TODO - 10.2174/1570161117666190619143842
TODO - abatacept;  cyclic citrullinated peptide antibody;  cytokine;  glucocorticoid;  hydroxychloroquine;  intercellular adhesion molecule 1;  Janus kinase inhibitor;  leflunomide;  lipid;  metalloproteinase;  methotrexate;  nonsteroid antiinflammatory agent;  rituximab;  salazosulfapyridine;  tocilizumab;  tumor necrosis factor;  tumor necrosis factor inhibitor;  vascular cell adhesion molecule 1;  antiinflammatory agent;  antirheumatic agent, atherosclerosis;  cardiovascular disease;  cardiovascular risk;  diabetes mellitus;  dyslipidemia;  endothelial dysfunction;  foam cell;  genetics;  hypertension;  inflammation;  macrophage;  metabolic syndrome X;  obesity;  pathophysiology;  plaque forming cell;  Review;  rheumatoid arthritis;  smoking;  smooth muscle cell;  T lymphocyte;  animal;  cardiovascular disease;  cardiovascular system;  comorbidity;  drug effect;  human;  immunology;  inflammation;  lifestyle;  pathophysiology;  rheumatoid arthritis;  risk assessment, Animals;  Anti-Inflammatory Agents;  Antirheumatic Agents;  Arthritis, Rheumatoid;  Cardiovascular Diseases;  Cardiovascular System;  Comorbidity;  Heart Disease Risk Factors;  Humans;  Inflammation;  Life Style;  Risk Assessment
TODO - Rheumatoid arthritis (RA) is an autoimmune inflammatory arthritis. Inflammation, however, can spread beyond the joints to involve other organs. During the past few years, it has been well recog-nized that RA associates with increased risk for cardiovascular (CV) disease (CVD) compared with the general population. This seems to be due not only to the increased occurrence in RA of classical CVD risk factors and comorbidities like smoking, obesity, hypertension, diabetes, metabolic syndrome, and others but also to the inflammatory burden that RA itself carries. This is not unexpected given the strong links between inflammation and atherosclerosis and CVD. It has been shown that inflammatory cytoki-nes which are present in abundance in RA play a significant role in every step of plaque formation and rupture. Most of the therapeutic regimes used in RA treatment seem to offer significant benefits to that end. However, more studies are needed to clarify the effect of these drugs on various parameters, including the lipid profile. Of note, although pharmacological intervention significantly helps reduce the inflammatory burden and therefore the CVD risk, control of the so-called classical risk factors is equally important. Herein, we review the current evidence for the underlying pathogenic mechanisms linking inflammation with CVD in the context of RA and reflect on the possible impact of treatments used in RA. © 2020 Bentham Science Publishers.
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