Treatment with PCSK9 inhibitors reduces the expression of scavenger receptors CD16, CD36 and CD45 in patients with stable coronary artery disease and elevated Lp(a) levels

Q: What is the clinical evidence from this study?

Study design: RCT. Population: Stable coronary artery disease and elevated Lp(a) levels (n=100). Intervention: PCSK9 inhibitor vs. Placebo. Primary outcome: Expression of scavenger receptors CD16+, CD36+, and CD45+ on peripheral blood mononuclear cells (PBMCs) (p=0.046 (CD16+), <0.001 (CD45+), 0.019 (NCM CD36+)).

Q: What does this research mean for the field?

Treatment with PCSK9 inhibitors significantly reduces the expression of scavenger receptors CD16, CD36, and CD45 on peripheral blood mononuclear cells in patients with stable coronary artery disease and elevated Lp(a) levels. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To determine the effect of PCSK9 inhibitor therapy on PBMC scavenger receptor (CD16, CD36, and CD45) expression and their link to lipid levels in stable coronary artery disease patients with elevated Lp(a).

S Ugovsek; A Rehberger Likozar; T Levstek; J Zupan; K Trebusak Podkrajsek; T Trimmel; Mira Brekalo; F Marka; P Hohensinner; W Speidl; P Haider; M Sebestjen

doi:10.1093/eurheartj/ehag785.4134

October 1, 2026European Heart JournalOpen Access

Treatment with PCSK9 inhibitors reduces the expression of scavenger receptors CD16, CD36 and CD45 in patients with stable coronary artery disease and elevated Lp(a) levels

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Key result

PCSK9 inhibitors significantly reduce pro-inflammatory scavenger receptor expression on PBMCs compared to placebo.

P=0.046 (CD16+), <0.001 (CD45+), 0.019 (NCM CD36+)
n=100

Why the study?

Although PCSK9 inhibitors effectively lower lipid concentrations and reduce cardiovascular events, their impact on scavenger receptors CD16+, CD36+, and CD45+ on peripheral blood mononuclear cells remained poorly understood.

Does treatment with PCSK9 inhibitors reduce the expression of scavenger receptors CD16+, CD36+, and CD45+ on peripheral blood mononuclear cells in statin-treated patients with stable coronary artery disease and elevated Lp(a) levels?

Key Points

To determine the effect of PCSK9 inhibitor therapy on PBMC scavenger receptor (CD16, CD36, and CD45) expression and their link to lipid levels in stable coronary artery disease patients with elevated Lp(a).
Randomized, double-blind, placebo-controlled trial including 100 statin-treated patients in stable condition following myocardial infarction with elevated Lp(a) levels.
Participants received either a PCSK9 inhibitor or placebo subcutaneously every two weeks for 6 months.
Biochemical profiles and peripheral blood mononuclear cell (PBMC) surface marker expressions were assessed at baseline and 6 months.
PCSK9 inhibitor therapy significantly decreased PBMCs expressing CD16+ (p=0.046) and CD45+ (p<0.001), as well as non-classical monocytes expressing CD36+ (p=0.019), with no changes observed in intermediate or classical monocytes, or in the placebo group.
Following PCSK9 inhibitor treatment, intermediate monocyte CD36+ expression correlated inversely with changes in Lp(a) (ρ=-0.276, p=0.029), total cholesterol (ρ=-0.306, p=0.014), LDL cholesterol (ρ=-0.276, p=0.027), and apolipoprotein B (ρ=-0.400, p=0.001).
Non-classical monocyte CD36+ expression was also associated with changes in Lp(a) (ρ=-0.252, p=0.046), whereas no significant correlations between monocyte subsets and lipid changes appeared in the placebo arm.

Study Design

Type

RCT (n=100)

Blinding

Double-blind

Randomization

Randomized

Structured PICO

Does treatment with PCSK9 inhibitors reduce the expression of scavenger receptors CD16+, CD36+, and CD45+ on peripheral blood mononuclear cells in statin-treated patients with stable coronary artery disease and elevated Lp(a) levels?

P

Population

100 statin-treated patients in the stable phase after myocardial infarction with elevated Lp(a) levels, followed for 6 months.

I

Intervention

PCSK9 inhibitors every two weeks for 6 months added to statin therapy

C

Comparator

Placebo every two weeks for 6 months added to statin therapy

O

Outcome

Expression of scavenger receptors CD16+, CD36+ and CD45+ on peripheral blood mononuclear cells (PBMCs) after 6 monthssurrogate

Main Result

p-value: p=0.046 (CD16+), <0.001 (CD45+), 0.019 (NCM CD36+)

Implication

PCSK9 inhibitor therapy significantly reduces the expression of pro-atherogenic scavenger receptors (CD16+, CD36+, CD45+) on monocytes in statin-treated patients with stable coronary artery disease and elevated Lp(a), demonstrating an anti-inflammatory cellular effect linked to lipid lowering.

Abstract

Background Atherosclerosis is a chronic inflammatory disease driven by dyslipidemia and activation of immune system. Scavenger receptors CD16+, CD36+ and CD45+ on peripheral blood mononuclear cells (PBMCs) are involved in foam cell formation and endothelial dysfunction, promoting atherosclerosis. Although protein convertase subtilisin/kexin type 9 (PCSK9) inhibitors (PCSK9i) effectively lower lipid concentration and reduce cardiovascular events, their impact on above mentioned scavenger receptors remains poorly understood. Purpose We aimed to examine the impact of PCSK9i treatment on the expression of scavender receptors CD16+, CD36+ and CD45+ on PBMC, and their association with lipoprotein levels in patients with stable coronary disease and significantly elevated lipoprotein (a) (Lp(a)) levels. Methods In randomized, double-blind, placebo-controlled trial we included 100 statin-treated patients in stable phase after myocardial infarction elevated Lp(a) values. The patients received PCSK9i or placebo every two weeks for 6 months. Biochemical and cell analysis at baseline and after 6 months were performed. Results Treatment with PCSK9i significantly decreased concentration of PBMCs expressing CD16+ and CD45+ (p=0.046 and p<0.001, respectively), and non-classical monocytes (NCM) expressing CD36+ (p=0.019), while no differences were observed among classical (CM) or intermediate monocytes (IM) expressing CD36+, neither in the placebo group. After treatment with PCSK9i, expression of IM CD36+ was associated with changes in Lp(a) (ρ=-0.276, p=0.029), total cholesterol (ρ=-0.306, p=0.014), low-density lipoprotein cholesterol (ρ=-0.276, p=0.027) and apolipoprotein B (ρ=-0.400, p=0.001). Additionally, expression of NCM CD36+ was associated with changes in Lp(a) (ρ=-0.252, p=0.046). No significant associations were observed between lipid parameters and monocyte subsets in the placebo group. Conclusion In patients with stable coronary disease and elevated Lp(a) levels, treatment with PCSK9i significantly decreases expression of scavenger receptors CD16+, CD36+ and CD45+ on PBMCs.

Discussion

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Cite This Study

Ugovsek et al. (2026) conducted an RCT in Stable coronary artery disease and elevated Lp(a) levels (n=100). PCSK9 inhibitor vs. Placebo was evaluated on Expression of scavenger receptors CD16+, CD36+, and CD45+ on peripheral blood mononuclear cells (PBMCs) (p=0.046 (CD16+), <0.001 (CD45+), 0.019 (NCM CD36+)).

synapsesocial.com/papers/6ae13d9e043bfbd635332d3b https://doi.org/10.1093/eurheartj/ehag785.4134

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Treatment with PCSK9 inhibitors reduces the expression of scavenger receptors CD16, CD36 and CD45 in patients with stable coronary artery disease and elevated Lp(a) levels

Key Points

Study Design

Structured PICO

Main Result

Implication

Abstract

Discussion

Cite This Study

Treatment with PCSK9 inhibitors reduces the expression of scavenger receptors CD16, CD36 and CD45 in patients with stable coronary artery disease and elevated Lp(a) levels

Key Points

Study Design

Structured PICO

Main Result

Implication

Abstract

Discussion

Cite This Study

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