The Impact of Atorvastatin Treatment on the Distribution of Low-Density Lipoprotein Subfractions and the Level of Vitamin D in Patients After Acute Myocardial Infarction: Preliminary Findings

Abstract

Clinical trial results indicate that statin therapy aimed at normalising the lipid profile can prevent and reduce the risk of cardiovascular events. Both LDL and HDL consist of several subfractions, with only the smallest and densest subfractions being the most atherogenic. We examine the effect of Atorvastatin treatment not only on basic lipid profile parameters but also atherogenic lipoprotein subfractions and 25(OH)D levels in patients after the first acute myocardial infarction. The study population had not previously received lipid-lowering medications. Serum 25(OH)D concentration was determined by direct competitive immunochemiluminescent assays. Lipoprotein subfractions, including VLDL, IDL-C, IDL-B, and IDL-A, as well as LDL1, LDL2 (large LDL), and LDL3-7 (sdLDL), were measured in serum (Lipoprint^® system). Almost all patients had 25(OH)D deficiency. Atorvastatin primarily reduced strongly atherogenic sdLDL and decreased the less atherogenic large LDL subfractions. A statistically significant reduction in VLDL cholesterol and IDL fractions was also observed. Analysing LDL subfractions provides a more detailed insight into lipid metabolism and enables the identification of patients with a more atherogenic phenotype. LDL subfractions may thus become not only more accurate prognostic biomarkers but also targets for lipid-lowering therapy. Vitamin D deficiency is associated with atherogenic dyslipidaemia, particularly high levels of sdLDL.

Keywords: 25(OH)D; acute myocardial infarction; atorvastatin; lipid profile; lipoprotein subfractions; triglyceride-rich lipoproteins.

Figure 1

Vitamin D concentrations pre- and post-Atorvastatin treatment. The results of vitamin D concentrations for all patients are presented as mean ± standard deviation.

Figure 2

Changes in LDL subfractions pre- and post-Atorvastatin treatment (model lipid electrophoresis for one representative patient). (a) Pre-intervention: predominantly phenotype B (not indicative of type A—the presence of small, dense LDL), with atherogenic LDL3-7 subfractions (in red) and large, less atherogenic subfractions LDL1-2 (in yellow). (b) Post-intervention: LDL phenotype A, with marked reduction in atherogenic LDL subfractions (mainly large LDL), LDL3-7 (in red), and large, less atherogenic subfractions LDL1-2 (in yellow).

Figure 3

Atherogenic lipoprotein concentrations pre- and post-Atorvastatin treatment. The results of atherogenic lipoprotein concentrations for all patients are presented as mean ± standard deviation.