Atherosclerosis is not accelerated in rheumatoid arthritis of low activity or remission, regardless of antirheumatic treatment modalities.
RA associates with increased cardiovascular disease (CVD) morbidity and mortality due to accelerated atherosclerosis, attributed to both classical risk factors and chronic inflammation. The aim of this study was to test the hypothesis that effective disease control over 3 years modifies acceleration of atherosclerosis in RA.



Consecutive, non-diabetic RA patients previously examined by ultrasonography for subclinical atherosclerosis were re-evaluated after 3.2 (0.2) years, provided that they were in remission/low disease activity (DAS28 <3.2) for at least 75% of this period. Patients (n = 139) were demographically matched with 139 non-diabetic, non-RA control individuals studied in parallel.



Patients and controls (mean age of 56 years at baseline) had a comparable burden of classical CVD risk factors. Patients' pulse wave velocity (reflecting arterial stiffness) changed by 0.07 m/s/year and left carotid intima-media thickness (reflecting wall hypertrophy) increased by 0.009 mm/year; formation of new atheromatic plaques in carotid and/or femoral arterial beds occurred in 22%. Multivariate analysis after correcting for all classical CVD risk factors and anti-hypertensive/lipid-lowering therapies demonstrated no significant differences between patients and controls in any of the subclinical atherosclerosis indices. Changes in all atherosclerosis indices from baseline to end of follow-up were comparable between those 56 patients treated with biologic DMARDs and their demographically matched patients treated with synthetic DMARDs.



Effective disease control may abrogate any RA-specific effect on the progression of atherosclerosis regardless of treatment. Whether early and sustained RA control translates to the CVD outcomes expected in the general population should be examined in prospective studies.
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
Aikaterini
A
Arida
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
Athanasios D
AD
Protogerou
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
George
G
Konstantonis
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
Kalliopi
K
Fragiadaki
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
George D
GD
Kitas
Rheumatology Unit, 1st Department of Propaedeutic Internal Medicine, Laikon Hospital, National and Kapodistrian Univeristy of Athens.|Joint Academic Rheumatology Program, National and Kapodistrian University of Athens, Medical School, Greece.
Petros P
PP
Sfikakis
D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications* / Q000188:drug therapy; D050197:Atherosclerosis / Q000209:etiology*; D001685:Biological Factors / Q000627:therapeutic use; D002340:Carotid Artery Diseases / Q000209:etiology; D059168:Carotid Intima-Media Thickness; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005263:Femoral Artery; D006801:Humans; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000209:etiology; D011239:Prednisolone / Q000627:therapeutic use; D059289:Vascular Stiffness
D018501:Antirheumatic Agents; D001685:Biological Factors; D011239:Prednisolone; D008727:Methotrexate
arterial stiffness; atheromatic plaques; atheromatosis; atherosclerosis; biologic therapies; cardiovascular disease; intima–media thickness; progression; pulse wave velocity; rheumatoid arthritis