Different inflammatory pathways underlying cardiovascular risk in secondary prevention
Abstract
This commentary refers to ‘ Targeted proteomics improves cardiovascular risk prediction in secondary prevention ’ , by N.S. Nurmohamed et al ., https://doi.org/10.1093/ eurheartj/ehac055 and the discussion piece ‘ Targeted proteomics improves cardiovascular risk prediction in secondary prevention: the impact of statin treatment? ’ , by P. Giral, https://doi.org/10.1093/eurheartj/ehac329. Giral raises two questions regarding our recently published manu-script ‘ Targeted proteomics improves cardiovascular risk prediction in secondary prevention ’ . 1 First, he notes that there could be a bias introduced by the use of statin therapy which is known to lower C-reactive protein (CRP). Secondly, he questions why lipid lowering therapy (LLT) use was not present in the clinical risk model which was used as comparison to the protein model. In the exploratory analysis of our study, we assessed in fl ammatory pathways by dividing patients into high or low residual in fl ammatory risk pro fi les based on baseline CRP levels. Patients from the Second Manifestations of ARTerial disease (SMART) were divided in a high CRP ( > 2 mg/L) and low CRP ( ≤ 2 mg/L) group. Since statins reduce CRP, Giral questions whether statin use could have introduced a bias in the exploratory analysis. Therefore, we compared the frequency of statin use in patients with high and low CRP. There were slightly more statin users in the low CRP group (67%) than in the high CRP group (59%) in
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