Intracoronary monocyte expression pattern and HDL subfractions after non-ST elevation myocardial infarction

Aims: Coronary artery disease (CAD) is described as a range of clinical conditions including myocardial infarction (MI) and unstable angina. Lipid and apolipoprotein profiles together with the study of cholesterol deposit and efflux serve to identify novel pre and post infarct scenarios for the treatment of these patients. In (non-ST elevation myocardial infarction) NSTEMI patients, we analysed both systemic and intracoronary serum ability to accept cholesterol as well as cholesterol efflux capacity (CEC) of monocytes in terms of expression of genes involved in the reverse cholesterol transport (RCT). Methods and results: While HDL-C quantity was similar between systemic and coronary arterial blood, in 21 NSTEMI patients we observed a significant reduction of the pre beta-HDL fraction and the levels of Apolipoproteins AI, AII, B and E in coronary versus systemic serum. These data are complemented with the observed reduction of CEC. On the contrary, compared to systemic arterial monocytes, in coronary microenvironment of NSTEMI patients after myocardial infarction, the monocytes exhibited a higher mRNA expression of nuclear receptor LXR alpha and its targets ABCA1 and APOE, which drive cholesterol efflux capacity. Conclusion: In this cross-sectional study we observe that in the immediate post infarction period, there is a spontaneous bona fide ligand-induced activation of the LXR driven cholesterol efflux capacity of intracoronary monocytes to overcome the reduced serum ability to accept cholesterol and to inhibit the post-infarction pro-inflammatory local microenvironment.

Automated summary

The study observed differences in cholesterol acceptability and efflux capacity in serum and monocytes of NSTEMI patients, indicating potential mechanisms for post-infarction treatment. The activation of LXR-driven cholesterol efflux capacity in intracoronary monocytes post-infarction may help overcome reduced serum cholesterol acceptance and inhibit local inflammation.