Effect of C-Reactive Protein on Lipoprotein(a)-Associated Cardiovascular Risk in Optimally Treated Patients With High-Risk Vascular Disease
Question Can inflammation modulate lipoprotein(a)–associated cardiovascular risk during secondary prevention in optimally treated patients with high-risk vascular disease?
Findings In a prespecified post hoc secondary analysis of the ACCELERATE trial, in patients with established vascular disease who were optimally treated, increasing lipoprotein(a) levels (assessed as either quintiles or continuous logarithmic transformed levels) during treatment were significantly associated with cardiovascular death, myocardial infarction, and stroke only in individuals with high-sensitivity C-reactive protein levels of 2 mg/L or higher during treatment, but not in those with levels less than 2 mg/L. Similar significant associations were identified in time-to-first event rates and survival curves, as well as specifically in the placebo-treated group.
Meaning There is likely to be incremental benefit in lowering lipoprotein(a) levels in optimally treated patients with high-risk vascular disease, which appears to be optimized in patients with concomitant high-sensitivity C-reactive protein levels of 2 mg/L or more.