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Results Following infliximab infusion, a rapid increase in the percentage of endothelial‐dependent vasodilatation was found in all patients (mean ± SD 9.4 ± 5.5% 2 days postinfusion compared with 2.8 ± 2.5% 2 days before infusion). However, values returned to baseline by 4 weeks after infusion. There were no differences in the percentage of endothelial‐independent vasodilatation prior to and after infusion. A decrease in the individual disease activity score for each patient was observed at day 7 postinfusion ( P = 0.02). Seven consecutive patients (5 women and 2 men; age range 25–73 years, median 41 years) that fulfilled the 1987 American College of Rheumatology (formerly American Rheumatism Association) classification criteria for RA ( ) were studied. They were recruited from the outpatient rheumatology clinic of the Hospital Xeral‐Calde, Lugo, in northwest Spain. Because the purpose of this study was to assess endothelial function in long‐term infliximab‐treated RA patients, we set the following inclusion criteria: patients must have been seen by the same rheumatologist (MAG‐G) over a period of 1 month; patients must have been treated with infliximab for at least 1 year; patients must currently be receiving infliximab every 8 weeks; patients must currently be receiving 1 or more disease‐modifying antirheumatic drug (DMARD); patients must be nonsmokers or had stopped smoking at least 5 years previously.

Exclusion criteria were as follows: patients with diabetes mellitus and patients who had suffered cardiovascular or cerebrovascular events. Three of the 7 patients were being treated with infliximab 3 mg/kg intravenously every 8 weeks. The other 4 required 5 mg/kg every 8 weeks because of disease severity. Besides nonsteroidal antiinflammatory drugs, all had received treatment with low doses of prednisone immediately after disease diagnosis (range 3–13 years, median 5 years). All had started treatment with prednisone 5 mg twice daily. In all patients, treatment with a DMARD was initiated when a diagnosis of RA was made. When endothelial function was evaluated, all patients were being treated with MTX (range 15–25 mg/week).

One patient had a history of hypertension. However, appropriate control of her blood pressure was achieved following treatment with angiotensin‐converting enzyme inhibitor therapy. None of them were being treated with statin lipid‐lowering drugs at the time of the study. None had ever used nitrates or were taking estrogens. Concomitant medication was not changed during the period of study. All but 1 were positive for rheumatoid factor.

Informed consent was obtained from all cases. The local institutional review committee approved the study protocol. Study protocol. Endothelial‐dependent (postischemia) and independent (postnitroglycerin) vasodilatation were measured by brachial ultrasonography. Brachial artery diameter and flow were determined as previously described (, ). A B‐mode scan of the right brachial artery in a longitudinal section was performed in supine patients using a 7.5‐MHz phased‐array transducer on a Hewlett Packard SONOS 5500 system (McMinnville, OR).

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The anterior and posterior media–intima interfaces were used to define artery diameter. This was calculated as the average of measurements during 4 cardiac cycles at end‐diastole. The forearm blood pressure cuff was inflated on the ipsilateral wrist to 150 mm Hg above resting systolic blood pressure for 5 minutes.

The endothelial‐dependent vasodilatation was measured for 60 seconds after cuff release. To assess endothelial‐independent vasodilatation, 400 μg of sublingual nitroglycerin was given. Vasodilatation was measured 4 minutes after nitroglycerin intake. In all cases, a cardiologist (CG‐J) analyzed ultrasound data offline and he was blind to the clinical information and study date. Endothelial‐dependent and independent vasodilatation were evaluated 2 days before infliximab infusion (day –2) and at days 2, 7, and 28 postinfliximab infusion.

In each patient, the Disease Activity Score in 28 joints (DAS28) ( ) was assessed prior to infliximab infusion (day 0) and at days 7 and 28 postinfusion. C‐reactive protein (CRP) was determined at day 0 and at days 2, 7, and 28 after infusion of the drug. Erythrocyte sedimentation rate (ESR), total cholesterol, high‐density lipoprotein (HDL) cholesterol, low‐density lipoprotein (LDL) cholesterol, and triglycerides were determined prior to infusion at day 0, and at days 7 and 28 after infusion. RESULTS Following infusion of the drug, a dramatic and rapid increase in the percentage of endothelial‐dependent vasodilatation was found (Figure ). In all patients, percentages of endothelial‐dependent vasodilatation at day 2 after infusion (mean ± SD 9.4 ± 5.5%, range 2.5–17.4%) were greater than those observed 2 days before infusion (mean ± SD 2.8 ± 2.5%, range –1.1–5.2%). At day 7 postinfusion, the percentage of endothelial‐dependent vasodilatation in all these patients was greater than before infusion at day –2 ( P = 0.02).