How Common Is Residual Inflammatory Risk?
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After initiating aggressive statin therapy, high-risk atherosclerosis patients can be classified as having residual cholesterol risk (on-treatment low-density lipoprotein cholesterol [LDLC] ≥70 mg/dL), residual inflammatory risk (on-treatment high-sensitivity C-reactive protein [hsCRP] ≥2 mg/L), both conditions, or neither. In contemporary lipid-lowering trials, there are roughly twice as many individuals in whom the principle unmet clinical need is residual inflammatory risk as compared with residual cholesterol risk. As such, continued translational investigation into inflammatory mediators of plaque initiation, progression, and rupture is crucial for the vascular biology community and ultimately for patient care.
A critical principle of personalized medicine is to provide the right therapy to the right patient at the right time. Yet, in the treatment of chronic atherosclerosis, statin therapy has proven so effective that all patients should be aggressively treated for life, typically with high-intensity regimens.1
Addressing the problem of residual risk after statin therapy has proven complex as differing biological processes drive recurrent events in different patients. On the one hand, individuals treated with statins who, nonetheless, have persistently elevated levels of atherogenic lipoproteins represent a group with residual cholesterol risk where additional lipid-lowering therapies, including PCSK9 (proprotein convertase subtilisin-kexin type 9) inhibition, are likely to prove effective. On the other hand, the majority of patients treated with a higher intensity statins will achieve 50% to 85% reductions in LDLC and apolipoprotein B.2,3 For these individuals in whom cholesterol is no longer the primary problem, the translational research community has …