Clinica chimica acta; international journal of clinical chemistry · 2026
Combined effect of elevated lipoprotein (a) and high-sensitivity C-reactive protein on the risk of coronary heart disease.
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Yang Longwei, Sun Junxiang, Zhuang Qian, Zhao Xianghai, Chen Yanchun, Wei Pengfei, Xie Hankun, Liu Jiahui, Yang Song, Shen Chong
Аннотация
BACKGROUND: Elevated lipoprotein (a) [Lp(a)] is linked to increased coronary heart disease (CHD) risk in Europeans with systemic inflammation, whereas evidence in other populations is limited. This study examined the combined effects of elevated Lp(a) and high-sensitivity C-reactive protein (hsCRP) on CHD risk in Chinese populations.
METHODS: The prospective cohort included 4128 participants followed for a median of 14.16 years. Lp(a) and hsCRP were stratified into age- and sex-specific tertiles based on Generalized Additive Models for Location, Scale and Shape (GAMLSS) analysis. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CHD risk and their interactions. Sensitivity analyses used clinical cut-offs, median splits, continuous modelling, and competing risk models. Population attributable fraction (PAF) quantified risk.
RESULTS: Lp(a) was not independently associated with CHD in the overall population. In the highest hsCRP tertile, medium and high Lp(a) tertiles showed increased CHD risk, with adjusted HRs (95% CIs) of 1.837 (1.052-3.206) and 2.021 (1.174-3.481), respectively (Ptrend = 0.014), explaining 37.986% of the CHD burden in that stratum. Joint analysis revealed significant associations only when using maximally selected rank statistics to identify optimal cut-points, with the dual-high group exhibiting the highest risk (HR = 1.626, P = 0.003). Additive and multiplicative interactions were significant for the tertile, optimal, and median cut-points (all P < 0.050). Sensitivity analyses confirmed the robustness.
CONCLUSION: The impact of high Lp(a) levels on CHD risk is contingent upon elevated hsCRP, suggesting that hyperinflammation drives the pathogenic effect of Lp(a) in CHD development.
METHODS: The prospective cohort included 4128 participants followed for a median of 14.16 years. Lp(a) and hsCRP were stratified into age- and sex-specific tertiles based on Generalized Additive Models for Location, Scale and Shape (GAMLSS) analysis. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) for CHD risk and their interactions. Sensitivity analyses used clinical cut-offs, median splits, continuous modelling, and competing risk models. Population attributable fraction (PAF) quantified risk.
RESULTS: Lp(a) was not independently associated with CHD in the overall population. In the highest hsCRP tertile, medium and high Lp(a) tertiles showed increased CHD risk, with adjusted HRs (95% CIs) of 1.837 (1.052-3.206) and 2.021 (1.174-3.481), respectively (Ptrend = 0.014), explaining 37.986% of the CHD burden in that stratum. Joint analysis revealed significant associations only when using maximally selected rank statistics to identify optimal cut-points, with the dual-high group exhibiting the highest risk (HR = 1.626, P = 0.003). Additive and multiplicative interactions were significant for the tertile, optimal, and median cut-points (all P < 0.050). Sensitivity analyses confirmed the robustness.
CONCLUSION: The impact of high Lp(a) levels on CHD risk is contingent upon elevated hsCRP, suggesting that hyperinflammation drives the pathogenic effect of Lp(a) in CHD development.