Aortic stenosis
Severe aortic stenosis patients have 35% higher Lp(a) and more lysis-prone fibrin clots, linking Lp(a) to a prothrombotic phenotype in 138 patients (Atherosclerosis 2022)
Original title: Apolipoproteins and lipoprotein(a) as factors modulating fibrin clot properties in patients with severe aortic stenosis
In 138 patients with isolated severe aortic stenosis (AS) compared with matched controls without AS, the authors measured serum apolipoproteins, oxidised LDL, and Lp(a), alongside plasma fibrin clot permeability and lysis using three assays. AS patients had 34.9% higher Lp(a) and 25.9% higher apoA-I, alongside less compact fibrin clots (13.3% lower and 53.2% lower maximal absorbance on two assays, 28.3% higher permeability) that were more susceptible to lysis (17.9% lower Lys50) than controls. After adjusting for confounders including statin use, LDL cholesterol and apoB were inversely associated with clot permeability, while apoC-II and apoC-III were linked to clot density measures explaining 56-64% of their variability; only one clot-lysis assay (CLT2018) was associated with Lp(a) itself. Multiple regression identified apoC-III, apoB, apoA-I, apoE, kidney function and oxidised LDL as predictors of hypofibrinolysis. The findings show apolipoproteins, including Lp(a), contribute to a prothrombotic fibrin clot phenotype in severe aortic stenosis.
Original abstract
Background And Aims: Large amounts of clot-bound lipoproteins were reported in proteomic analysis of plasma clot but their impact on fibrin clot properties is unknown. We investigated a contribution of lipid profile and apolipoproteins (apo) to the prothrombotic plasma fibrin clot phenotype in patients with aortic stenosis (AS).
Methods: In 138 patients with isolated severe AS, we determined serum apoA-I, A-II, B, C-II, C-III, E, oxidized low-density lipoprotein (OxLDL) and lipoprotein(a) concentrations. Plasma fibrin clot permeability (Ks), maximal absorbance (MaxAbsCLT2018 and MaxAbsLys50), and fibrinolytic capacity were studied using 3 plasma-based lysis assays (CLT2018, CLT, and Lys50), and compared with well-matched patients without AS (control group).
Results: After adjustment for confounding factors, including statin use, only low-density lipoprotein cholesterol (LDL-C) and apoB levels were inversely associated with Ks. Triglycerides, apoC-II, and C-III were associated with MaxAbsCLT2018 and MaxAbsLys50, explaining 56-64% of their variability. CLT2018 and CLT showed associations with total cholesterol, LDL-C, triglycerides, and OxLDL as well as with apoB, C-II, C-III, and E. ApoA-I, C-II, and C-III but not serum lipids were associated with Lys50. Only CLT2018 was associated with lipoprotein(a). ApoC-III, B, A-I, and E along with estimated glomerular filtration rate and OxLDL predicted hypofibrinolysis in multiple regression analysis. AS patients had higher lipoprotein(a) (+34.9%) and apoA-I (+25.9%) levels and less compact fibrin clots (-13.3% lower MaxAbsCLT2018, -53.2% lower MaxAbsLys50, and +28.3% higher Ks) displaying higher susceptibility to lysis (-17.9% lower Lys50) in comparison with control group.
Conclusions: Apolipoproteins and OxLDL contribute to prothrombotic fibrin clot phenotype in severe AS. Moreover, apolipoproteins better than serum lipids predicted hypofibrinolysis, which provides additional argument for a role of elevated lipoproteins in the prothrombotic state.
aortic stenosismechanismsthrombosis
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.