Introduction
Lipoprotein (
a
) [Lp(
a
)] is a risk factor for coronary artery disease (CAD). To the best of our knowledge, this is the first study addressing the relationship between Lp(
a
) and platelet reactivity in primary and secondary prevention.
Methods
Lp(
a
) was evaluated in 396 individuals with (82.3%) and without (17.7%) obstructive CAD. The population was divided into two groups according to Lp(
a
) concentrations with a cutoff value of 50 mg/dL. The primary objective was to evaluate the association between Lp(
a
) and adenosine diphosphate (ADP)-induced platelet reactivity using the VerifyNow™ P2Y
12
assay. Platelet reactivity was also induced by arachidonic acid and collagen–epinephrine (C-EPI) and assessed by Multiplate™, platelet function analyzer™ 100 (PFA-100), and light transmission aggregometry (LTA) assays. Secondary objectives included the assessment of the primary endpoint in individuals with or without CAD.
Results
Overall, 294 (74.2%) individuals had Lp(
a
) < 50 mg/dL [median (IQR) 13.2 (5.8–27.9) mg/dL] and 102 (25.8%) had Lp(
a
) ≥ 50 mg/dL [82.5 (67.6–114.5) mg/dL],
P
< 0.001. Univariate analysis in the entire population revealed no differences in ADP-induced platelet reactivity between individuals with Lp(
a
) ≥ 50 mg/dL (249.4 ± 43.8 PRU) versus Lp(
a
) < 50 mg/dL (243.1 ± 52.2 PRU),
P
= 0.277. Similar findings were present in individuals with (
P
= 0.228) and without (
P
= 0.669) CAD, and regardless of the agonist used or method of analysis (all
P
> 0.05). Finally, multivariable analysis did not show a significant association between ADP-induced platelet reactivity and Lp(
a
) ≥ 50 mg/dL [adjusted OR = 1.00 [(95% CI 0.99–1.01),
P
= 0.590].
Conclusion
In individuals with or without CAD, Lp(
a
) ≥ 50 mg/dL was not associated with higher platelet reactivity.
Electronic supplementary material
The online version of this article (10.1007/s12325-020-01483-y) contains supplementary material, which is available to authorized users.