Abstract

Accelerated atherosclerosis, increased cardiovascular morbidity and mortality have been associated with rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Vascular function, clinical and laboratory markers and the effects of anti-TNF therapy were assessed in arthritides. Fifty-three 53 patients including 36 RA patients treated with either etanercept (ETN) or certolizumab pegol and 17 AS patients treated with ETN were included in a 12-month follow-up study. Ultrasonography was performed to determine flow-mediated vasodilation (FMD), common carotid intima-media thickness (ccIMT) and arterial pulse-wave velocity (PWV) in all patients. All assessments were performed at baseline and 6 and 12 months after treatment initiation. A significant improvement of brachial artery FMD was observed after 6 months (p = 0.004). A tendency of FMD improvement was also observed after 12 months (p = 0.065). ccIMT did not change throughout the year. PWV significantly improved after 12 months (p = 0.034). Higher baseline ccIMT (p = 0.009) and PWV (p = 0.038) were associated with clinical non-response (cNR) versus response (cR) to biologics. Multiple analysis confirmed the association of baseline ccIMT with age (p = 0.003) and cNR (p = 0.009), as well as that of baseline PWV with age at diagnosis (p = 0.022) and current chest pain (p = 0.004). Treatment itself determined the 12-month changes in FMD (p = 0.020) and PWV (p = 0.007). In a mixed cohort of RA and AS patients, TNF inhibition improved or stabilized vascular pathophysiology. Inflammation may be associated with FMD, while, among others, cNR may influence vascular function.

Highlights

  • Extended author information available on the last page of the articleArthritides, such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with accelerated, inflammatory atherosclerosis, as well as increased cardiovascular (CV) morbidity and mortality [1,2,3,4]

  • Overt atherosclerosis and increased arterial stiffness are indicated by abnormal endothelium-dependent, flow-mediated vasodilation (FMD) of the brachial artery, common carotid intima-media thickness and carotid plaques, as well as arterial pulse-wave velocity (PWV), respectively [2, 5]

  • Systemic inflammation associated with RA and AS is the major driver of atherosclerosis and CV disease (CVD) in these diseases [1]

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Summary

Introduction

Extended author information available on the last page of the articleArthritides, such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with accelerated, inflammatory atherosclerosis, as well as increased cardiovascular (CV) morbidity and mortality [1,2,3,4]. Overt atherosclerosis and increased arterial stiffness are indicated by abnormal endothelium-dependent, flow-mediated vasodilation (FMD) of the brachial artery, common carotid intima-media thickness (ccIMT) and carotid plaques, as well as arterial pulse-wave velocity (PWV), respectively [2, 5]. These preclinical abnormalities predict the development of subsequent CV events in arthritides [1, 2, 5]. With respect to surrogate markers, anti-TNF biologics may improve or at least stabilize vascular morphology and function including FMD [7, 11,12,13,14,15,16,17], ccIMT [7, 13, 16, 18,19,20] and PWV [7, 21,22,23,24,25]

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