predictor in their RA cohort, but they did not describe relationships of these factors to the 5% of patients with extremely low lipid levels in their analysis. Furthermore, elevation of the erythrocyte sedimentation rate conferred the greatest hazards, likely interacting with lipid parameter point estimates, and the authors acknowledge that the lack of time-linked lipid and inflammation data is a key limitation. Although other investigators have also described complicated relationships between RA, lipid levels, and CVD-related events (5), the standard of care according to most guidelines for adults (6) supports lipid testing more frequently than every 5 years in patients with CVD risk factors. Therefore, we submit that cholesterol assessment remains important in at-risk patients with RA. We doubt that anyone would disagree that patients with high LDL cholesterol levels and RA should receive statin therapy, but the initiation of statin therapy may depend on whether a patient receives lipid screening. As such, screening remains a critical step in the overall process of preventing adverse cardiovascular events in patients with RA. We agree with Strandberg and colleagues that future research could delineate time-dependent relationships between lipids and inflammation from the time of RA onset. We suggest that the debate should not curb efforts to address modifiable CVD risk factors in patients with RA. In addition to the conclusion by Strandberg et al that statin use is too infrequent in RA, we add that lipid testing is inadequate in RA patients, and that CVD prevention should reflect the current standard of care.
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