Abstract

BACKGROUND: Inconsistent data have suggested an interaction between Lp(a) and hs-CRP levels, putting patients with concomitant elevation at the greatest risk for atherosclerotic cardiovascular events. To date, the association between Lp(a), systemic inflammation as measured by hs-CRP, and coronary plaque phenotype has not been unraveled. METHODS: Among consecutive asymptomatic patients evaluated for primary prevention of coronary artery disease, we explored the associations between Lp(a), hs-CRP and coronary atherosclerosis using atherosclerosis imaging-quantitative coronary CT angiography (AI-QCT; Cleerly Labs, Cleerly Inc., Denver,CO). The associations between Lp(a), hs-CRP and the AI-QCT outcomes defined as percent atheroma volume (PAV) as well as percent low-density non-calcified plaque volume (LD-NCPV) were assessed using multivariable linear regression adjusted for clinical risk factors. RESULTS: The mean age of the 373 included patients was 56.2 ± 8.9 years, 71.6% were male, and 54.2% was on statin therapy. Mean±SD LDL-C was 106 ± 41 mg/dl, median (IQR) Lp(a) was 31 (11, 89) nmol/L, while median hs-CRP levels were 0.8 (0.4, 1.8) mg/L. In the multivariable-adjusted analysis, Lp(a) levels were significantly associated with an increase in PAV (0.367 increase in PAV per 100 nmol/l increase in Lp(a), p=0.026) and percent LD-NCPV (0.018 increase in PAV per 100 nmol/l increase in Lp(a), p=0.031). However, there was no effect of adding hs-CRP to the models (p=0.446), and we observed no direct relationship between hs-CRP and PAV (p=0.446) or percent LD-NCPV (0.871). Table 1. CONCLUSIONS: Lp(a) is associated with low-density non-calcified plaque and total coronary plaque burden. The current study found no impact of hs-CRP on these associations, nor were hs-CRP levels associated with plaque burden.

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