Improve microvascular dysfunction and RA, reduce cardiovascular risk, with antirheumatics

April 25, 2010

Microvascular dysfunction correlates with systemic inflammation, which plays a key role in cardiovascular disease (CVD) as well as in rheumatoid arthritis (RA). In patients who have active RA, microvascular dysfunction improves in those who respond to antirheumatic treatment; aggressive control of RA disease activity helps avoid further joint damage and disability and may reduce CVD risk.

Microvascular dysfunction correlates with systemic inflammation, which plays a key role in cardiovascular disease (CVD) as well as in rheumatoid arthritis (RA). In patients who have active RA, microvascular dysfunction improves in those who respond to antirheumatic treatment; aggressive control of RA disease activity helps avoid further joint damage and disability and may reduce CVD risk.

Galarraga and associates examined the microvascular effects of treatment with an anti–tumor necrosis factor α (TNF-α) agent (etanercept or adalimumab) or methotrexate in 51 patients who had RA but no CVD. Drug effects were monitored by periodically assessing RA disease activity, inflammation, and skin microvascular responses (iontophoresis with acetylcholine and sodium nitroprusside).

The patients who responded to antirheumatic therapy showed improvement in both the acetylcholine and sodium nitroprusside vascular responses between baseline and all follow-up visits (2 and 4 months). Measurements of disease activity and inflammation also improved significantly, especially among patients receiving an anti–TNF-α drug. Among nonresponders, perfusion measurements did not change appreciably, even though the number of swollen joints declined.

The authors noted that because the anti–TNF-α drugs show the best anti-inflammatory effect and CV risk occurs early after the diagnosis, they should be assessed in early RA.