Key result
Higher Lp(a) is linked to greater arachidonic acid-induced platelet aggregation without statins or antiplatelets.
Why the study?
The physiological effect of Lp(a) on platelet activity is unclear, and few studies have evaluated this relationship without the confounding effects of statins or antiplatelet agents.
Is Lp(a) independently associated with platelet aggregation in subjects not taking statins or antiplatelet drugs?
Cross-Sectional (n=92)
No
Is Lp(a) independently associated with platelet aggregation in subjects not taking statins or antiplatelet drugs?
Effect estimate: β 0.023
p-value: p=0.027
Lp(a) is positively associated with platelet aggregation independent of Lp-PLA2, providing a potential mechanistic explanation for its atherothrombotic effects.
Lp(a) association with platelet aggregation is hypothesis-generating; leaves open mechanistic role and need for prospective validation.
The physiological effect of Lp(a) on platelet activity is unclear. Previous studies explored the relationship between Lp(a) and platelet aggregation in patients taking statins and antiplatelet agents, but few was conducted in individuals without the bias of those drugs that either influence Lp(a) or platelet activity. The aim of this study was to assess the relationship between Lp(a) levels and platelet aggregation in subjects not taking statins or antiplatelet drugs. A hospital-based cross-sectional study was conducted to investigate the independent contribution of Lp(a) to platelet activity by controlling the effects of potential confounding factors including lipoprotein-associated phospholipase A2 [Lp-PLA2]. Blood samples were collected from 92 subjects without statins or antiplatelet agents from the Second Xiangya Hospital. The univariate correlation analysis showed a significant correlation between AA-induced average aggregation rate [AAR] and ApoB (r = 0.324, P = 0.002), ApoA1 (r = 0.252, P = 0.015), Lp(a) (r = 0.370, P < 0.001), Lp-PLA2 (r = 0.233, P = 0.025) and platelet counts [PLT] (r = 0.389, P < 0.001). Multivariate regression analysis suggested that Lp(a) contributed independently to AA-induced average aggregation rate (β = 0.023, P = 0.027) after controlling for the effects of ApoB, Lp-PLA2 and platelet counts. Lp(a) is positively associated with platelet aggregation independent of Lp-PLA2, which may partly account for the atherothrombotic effect of Lp(a).
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Liu et al. (2022) conducted a cross-sectional in Subjects without statins or antiplatelet agents (n=92). Lp(a) was evaluated on AA-induced average aggregation rate (β 0.023, p=0.027). Plasma Lp(a) levels were independently and positively associated with arachidonic acid-induced platelet aggregation (β = 0.023, P = 0.027) in subjects not taking statins or antiplatelet agents.
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