Key result
Definite FH is linked to ~34% higher Lp-PLA2 levels versus non-definite FH despite therapy.
Why the study?
Familial hypercholesterolemia is associated with accelerated atherosclerosis and increased cardiovascular risk, but circulating biomarkers of inflammation and atherosclerosis across clinical diagnostic strata require evaluation.
Do patients with definite FH have higher circulating biomarkers of inflammation and atherosclerosis compared to non-definite FH despite maximally tolerated lipid-lowering therapy?
Cross-Sectional (n=80)
No
Do patients with definite FH have higher circulating biomarkers of inflammation and atherosclerosis compared to non-definite FH despite maximally tolerated lipid-lowering therapy?
Absolute Event Rate: 62.2% vs 46.5%
p-value: p=0.03
Patients with definite familial hypercholesterolemia exhibit persistently higher circulating Lp-PLA2 and TNF-α concentrations despite maximally tolerated lipid-lowering therapy, suggesting ongoing activation of specific inflammatory pathways.
May signal residual inflammatory risk in definite FH on therapy; hypothesis-generating for targeted anti-inflammatory trials.
Background: Familial hypercholesterolemia (FH) is associated with accelerated atherosclerosis and an increased risk of cardiovascular disease. Aims: To evaluate circulating biomarkers of inflammation and atherosclerosis in patients with clinically suspected FH stratified according to the Dutch Lipid Clinic Network (DLCN) criteria. Methods: This cross-sectional study included 80 patients (mean age, 53.4 [13.2] years; 58% women) receiving maximally tolerated lipid-lowering therapy (statins ± ezetimibe). Serum concentrations of lipoprotein-associated phospholipase A2 (Lp-PLA2), tumor necrosis factor-α (TNF-α), apolipoprotein B (ApoB), oxidized low-density lipoprotein (oxLDL), and monocyte chemoattractant protein-1 (MCP-1) were measured. Participants were classified as definite FH (DLCN score > 8; n = 45) or non-definite FH (DLCN score ≤ 8; n = 35). Biomarker concentrations were analyzed according to the above subgroups and sex. Results: Patients with definite FH had significantly higher serum Lp-PLA2 concentrations (62.2 [33.8] vs. 46.5 [19.9] ng/mL; p = 0.03) and TNF-α concentrations (6.94 [4.53] vs. 4.51 [2.93] pg/mL; p = 0.02) compared to non-definite FH, whereas ApoB, oxLDL, and MCP-1 concentrations did not differ significantly between the subgroups. Women had significantly higher TNF-α concentrations compared to men (6.57 [4.74] vs. 4.60 [2.20] pg/mL; p = 0.04) with no differences among other cytokines. Conclusions: Patients with definite FH exhibited persistently higher circulating Lp-PLA2 and TNF-α concentrations despite maximally tolerated lipid-lowering therapy, suggesting ongoing activation of specific inflammatory pathways. These findings support further investigation of Lp-PLA2 and TNF-α as candidate biomarkers for cardiovascular risk assessment in FH.
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Brzóska-Ritter et al. (2026) conducted a cross-sectional in Familial hypercholesterolemia (n=80). Definite familial hypercholesterolemia (DLCN score > 8) vs. Non-definite familial hypercholesterolemia (DLCN score ≤ 8) was evaluated on Serum Lp-PLA2 concentration (ng/mL) (p=0.03). Patients with definite familial hypercholesterolemia exhibited significantly higher serum Lp-PLA2 and TNF-α concentrations compared to those with non-definite FH despite lipid-lowering therapy.
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