Background and Aims Recent investigations have suggested an interdependence of lipoprotein(a) [Lp(a)]-related risk for cardiovascular disease with background inflammatory burden. The aim the present analysis was to investigate whether high-sensitive C-reactive protein (hsCRP) modulates the association between Lp(a) and coronary heart disease (CHD) in the general population. Methods Data from 71 678 participants from 8 European prospective population-based cohort studies were used (65 661 without/6017 with established CHD at baseline; median follow-up 9.8/13.8 years, respectively). Fine and Gray competing risk-adjusted models were calculated according to accompanying hsCRP concentration (<2 and ≥2 mg/L). Results Among CHD-free individuals, increased Lp(a) levels were associated with incident CHD irrespective of hsCRP concentration: fully adjusted sub-distribution hazard ratios [sHRs (95% confidence interval)] for the highest vs. lowest fifth of Lp(a) distribution were 1.45 (1.23–1.72) and 1.48 (1.23–1.78) for a hsCRP group of <2 and ≥2 mg/L, respectively, with no interaction found between these two biomarkers on CHD risk (Pinteraction = 0.82). In those with established CHD, similar associations were seen only among individuals with hsCRP ≥ 2 mg/L [1.34 (1.03–1.76)], whereas among participants with a hsCRP concentration <2 mg/L, there was no clear association between Lp(a) and future CHD events [1.29 (0.98–1.71)] (highest vs. lowest fifth, fully adjusted models; Pinteraction = 0.024). Conclusions While among CHD-free individuals Lp(a) was significantly associated with incident CHD regardless of hsCRP, in participants with CHD at baseline, Lp(a) was related to recurrent CHD events only in those with residual inflammatory risk. These findings might guide adequate selection of high-risk patients for forthcoming Lp(a)-targeting compounds.

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C 反应蛋白可改变脂蛋白 (a) 相关的冠心病风险：BiomarCaRE 项目

背景和目标 最近的研究表明，脂蛋白(a) [Lp(a)]相关的心血管疾病风险与背景炎症负担之间存在相互依赖性。本分析的目的是调查高敏感 C 反应蛋白 (hsCRP) 是否调节一般人群中 Lp(a) 与冠心病 (CHD) 之间的关联。方法 使用来自 8 项欧洲前瞻性人群队列研究的 71 678 名参与者的数据（65 661 名参与者在基线时没有确诊 CHD，6017 名参与者在基线时确诊为 CHD；中位随访时间分别为 9.8 年/13.8 年）。Fine和Gray竞争风险调整模型根据伴随的hsCRP浓度(＜2和≥2mg/L)进行计算。结果 在无 CHD 的个体中，无论 hsCRP 浓度如何，Lp(a) 水平升高与 CHD 事件相关：Lp(a 最高与最低五分之一的完全调整子分布风险比 [sHR（95% 置信区间）]对于 hsCRP ＜2 和 ≥2 mg/L 组，分布分别为 1.45 (1.23–1.72) 和 1.48 (1.23–1.78)，在这两种生物标志物之间未发现与 CHD 风险相关的相互作用 (Pinteraction = 0.82)。在患有先天性心脏病的患者中，仅在 hsCRP ≥ 2 mg/L [1.34 (1.03–1.76)] 的个体中观察到类似的关联，而在 hsCRP 浓度 <2 mg/L 的参与者中，Lp 与 Lp 之间没有明显的关联。 (a) 和未来的 CHD 事件 [1.29 (0.98–1.71)]（最高与最低五分之一，完全调整模型；Pinteraction = 0.024）。结论 虽然在无 CHD 的个体中，无论 hsCRP 水平如何，Lp(a) 都与 CHD 事件显着相关，但在基线患有 CHD 的参与者中，Lp(a) 仅在那些有残余炎症风险的患者中与复发性 CHD 事件相关。这些发现可能会指导高危患者对即将推出的 Lp(a) 靶向化合物的充分选择。