Subclinical peripheral arterial disease in rheumatoid arthritis.
OBJECTIVE
Rheumatoid arthritis (RA) is associated with accelerated atherosclerosis in the carotid arteries, but little is known about the magnitude of this process in peripheral arteries. Assessing preclinical atherosclerosis in both arterial beds in RA might provide additional prognostic value during risk stratification for primary prevention. Therefore in the present structural study we examined femoral versus carotid subclinical atherosclerosis in RA and controls.


METHODS
Intima-media thickness (IMT) and atheromatous plaque presence and vulnerability in femoral versus carotid arteries were examined in 80 RA patients without overt cardiovascular disease or diabetes and 80 controls matched 1:1 for age, gender and traditional cardiovascular disease risk factors.


RESULTS
Femoral IMT and plaque prevalence were increased in RA than controls (p=0.001 and 0.008, respectively). These increases remained significant after adjustment for potentially confounding factors that differed between groups, such as C-reactive protein and HDL-cholesterol serum levels, and statin use. Femoral plaque vulnerability did not differ between RA and controls. The presence of RA was found to be an independent predictor of increased femoral IMT (p=0.004), after adjustment for traditional cardiovascular risk factors, C-reactive protein and treatment with angiotensin converting enzyme inhibitors and statins. Femoral plaques were less frequent than carotid plaques in RA patients (22.5% vs 45.0% respectively, p=0.003) and in contrast to carotid plaques were independent of age and glucose levels.


CONCLUSIONS
Subclinical peripheral atherosclerosis in RA is more advanced than in controls. Prospective studies are required to confirm that RA is an independent risk factor for peripheral arterial disease.
Stamatelopoulos
Kimon S
KS
Vascular Laboratory, Department of Clinical Therapeutics, Alexandra Hospital, 80, Vassilissis Sofias Ave, PO Box 11528, Athens, Greece. stamatelopoulosk@yahoo.gr
Kitas
George D
GD
Papamichael
Christos M
CM
Kyrkou
Katerina
K
Zampeli
Evangelia
E
Fragiadaki
Kalliopi
K
Panoulas
Vasileios F
VF
Mavrikakis
Myron
M
Sfikakis
Petros P
PP
D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000453:epidemiology*; D058070:Asymptomatic Diseases; D050197:Atherosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000453:epidemiology*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002340:Carotid Artery Diseases / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000453:epidemiology*; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D005263:Femoral Artery / Q000000981:diagnostic imaging; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D058729:Peripheral Arterial Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000453:epidemiology*; D015995:Prevalence; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D014463:Ultrasonography
D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein