Background: Lipoprotein(a) Lp(a) is an independent risk factor for cardiovascular disease, but its mechanistic role in abdominal aortic aneurysm (AAA) remains uncertain. Given that inflammation plays a central role in both vascular remodeling and aneurysm progression, we hypothesized that systemic inflammation mediates the relationship between Lp(a) and AAA. Methods: This retrospective study included 468 hospitalized patients between 2022 and 2024, consisting of 148 with AAA and 320 with valvular heart disease as control. Serum Lp(a) levels and routine hematologic indices were measured, and seven derived inflammatory indices (e.g., neutrophil-to-HDL ratio, monocyte-to-HDL ratio, lymphocyte-to-HDL ratio, platelet-to-HDL ratio PHR) were calculated. Mediation analyses adjusted for clinical covariates assessed direct and indirect effects of Lp(a) on AAA. Results: Multivariable logistic regression analysis revealed that both Lp(a) and PHR were independently associated with AAA (Lp(a): OR = 1.002 1.001, 1.003; PHR: OR = 1.006 1.003, 1.006). Mediation analysis showed that only PHR demonstrated a statistically significant mediating effect between Lp(a) and AAA (average causal mediation effect = 0.0002, 0.0000, 0.0004). The total effect of Lp(a) on AAA was 0.0018, with a direct effect of 0.0017 and an indirect effect via PHR of 0.0001. Conclusions: Elevated Lp(a) was independently associated with the presence of AAA, and part of this association was mediated through platelet-related inflammatory activation, as reflected by PHR. This suggests a role for platelet-related inflammation in the underlying mechanism, which may inform future therapeutic strategies.
He et al. (Tue,) studied this question.