Important discrepancies between the populations studied might explain these diverging findings, as in our population about 85% of patients were treated with a statin, in contrast to the two populations discussed above. Furthermore, we described for the first time a correlation of IM with LDL-cholesterol. Despite the obvious link between hypercholesterolemia and atherogenesis, many individuals with LDL-levels within the normal range, still develop atherosclerotic disease. This suggests a significant heterogeneity of LDL-particles, as the subfraction of small dense LDL supposedly exhibits enhanced atherogenic potential. Proposed mechanisms include a stronger predisposition for oxidation, lower LDL-receptor affinity and an increased accumulation within the vascular wall. Several cross-sectional and prospective studies have suggested an association of elevated sdLDL levels with the presence of Ibrutinib Src-bcr-Abl inhibitor cardiovascular disease. Recently, it has been shown within the ARIC-study population consisting of 11419 men and women that sdLDL plasma levels were associated with incident coronary heart disease in a model including established risk factors. In our study, sdLDL levels showed a weak correlation with NCM. However, when patients were stratified according to AB1010 tertiles of sdLDL levels, patients in the highest sdLDL tertile show a more pro-inflammatory distribution of monocyte subsets. Additionally, CM levels were lowest in patients in within the highest sdLDL tertile. These findings were independent of BMI, statin dose and hsCRP levels. The latter findings are of importance, as in another study including 166 overweight patients, the correlation between LDL and monocyte subsets was diminished after adjusting for BMI, which remained the only significant regressor for monocyte subset distribution, as detected by multivariate regression analysis. In the I LIKE HOMe study, including 622 apparently healthy volunteers not receiving lipid-lowering therapy, a positive correlation between plasma triglycerides and NCM was demonstrated, as well as a weak negative correlation between plasma HDL and NCM. Again, adjustment for BMI eliminated these correlations. In our study, BMI did not differ between patients according to their sdLDL tertiles and did not influence the association between monocyte subset distribution and sdLDL plasma levels. Several studies have reported conflicting results regarding the effects of statin therapy on monocyte subset distribution. A small observational study in patients after heart transplantation demonstrated that statins depleted both circulating classical and non-classical monocytes. Patients receiving atorvastatin showed a stronger reduction in CM as compared to patients receiving pravastatin, who exhibited a strong decrease in NCM. Another very small study including patients on chronic hemodialysis, demonstrated that simvastatin treatment reduced CD14 expression on circulating human monocytes. Temporal cessation of statin treatment for two weeks in 66 stable CAD patients could not demonstrate an effect on circulating monocyte subset numbers, as demonstrated recently. In a study including approximately 80 hypercholesterolemic patients, fluvastatin treatment combined with diet was compared with diet alone in its effects on monocyte subset distribution. Interestingly, fluvastatin treatment for 1 year lead to a 25% increase of CM as compared to a decrease of 75% of NCM. This is a surprising outcome of a study examining only two subsets of monocytes in patients taking a statin not commonly used anymore; in our study, only 1 patient was treated with fluvastatin.