title: Rheumatoid arthritis is sufficient to cause atheromatosis but not arterial stiffness or hypertrophy in the absence of classical cardiovascular risk factors.
abstract: Rheumatoid arthritis (RA) associates with increased cardiovascular disease (CVD) mortality thought to be due to accelerated arterial disease. Different components of arterial disease, namely, atheromatosis, arteriosclerosis, and arterial wall hypertrophy, are differentially affected by classical CVD risk factors, which are highly prevalent in these patients. We hypothesized that RA disease per se may also differentially affect these components. Of 267 consecutive RA patients, we selected specifically those who were free of established CVD and CVD risk factors (18 %); of them, 41 patients (36 women, 49 ± 13 years) could be matched effectively 1:1 for age and gender to healthy controls. Atheromatosis was assessed by the presence of carotid and/or femoral artery plaques, arteriosclerosis by pulse wave velocity and local wall elasticity, and arterial hypertrophy by intima-media thickness and cross-sectional area. More patients had atheromatic plaques than controls (29 vs. 12 %, p = 0.039), and multiarterial atheromatosis was more prevalent in RA (22 vs. 2 %, p = 0.026). Accelerated atheromatosis was not associated with rheumatoid factor, or anti-cyclic citrullinated peptide (CCP) autoantibody status. Plaque burden in patients with less than 5 years disease duration (aged 41 ± 13 years) was comparable to their matched controls. In contrast, all indices of arterial stiffness and hypertrophy were similar between controls and RA patients, even in those with long-standing disease. RA per se is sufficient to cause atheromatosis in the absence of classical CVD risk factors, but has minimal, if any, effect on arteriosclerosis and arterial wall hypertrophy.
authors.affiliation: First Department of Propaedeutic Internal Medicine, Laikon Hospital, Athens University Medical School, Ag Thoma, 17, 11527, Athens, Greece.
authors.forename: Aikaterini
authors.initials: A
authors.lastname: Arida
authors.forename: Evi
authors.initials: E
authors.lastname: Zampeli
authors.forename: George
authors.initials: G
authors.lastname: Konstantonis
authors.forename: Kalliope
authors.initials: K
authors.lastname: Fragiadaki
authors.forename: George D
authors.initials: GD
authors.lastname: Kitas
authors.forename: Athanasios D
authors.initials: AD
authors.lastname: Protogerou
authors.forename: Petros P
authors.initials: PP
authors.lastname: Sfikakis
mesh_terms: D000328:Adult; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000453:epidemiology* / Q000276:immunology; D050197:Atherosclerosis / Q000453:epidemiology; D002318:Cardiovascular Diseases / Q000453:epidemiology; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000453:epidemiology*; D059168:Carotid Intima-Media Thickness; D016022:Case-Control Studies; D015984:Causality; D004548:Elasticity; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging; D006801:Humans; D006984:Hypertrophy; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000276:immunology; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000453:epidemiology*; D063177:Pulse Wave Analysis; D012217:Rheumatoid Factor / Q000276:immunology; D012720:Severity of Illness Index; D066253:Vascular Remodeling; D059289:Vascular Stiffness
chemical_list: D018501:Antirheumatic Agents; D010456:Peptides, Cyclic; C487763:cyclic citrullinated peptide; D012217:Rheumatoid Factor