Dysfunctional ECs promote leukocyte adhesion and migration, which is a critical component in the initiation and progression of atherosclerotic lesion development.1, 2 Patients with MI had higher VCAM‐1 expression on coronary artery ECs which would promote monocyte adhesion and infiltration into the vessel wall.34 Our study showed that the EMPs upregulated the expression of MCP‐1 and CCR‐5, the well‐known signals which promote monocyte adhesion to ECs, was dependent on the IL‐1β and NF‐кB signal pathways. This evidence concerns the gene CCR5 and myocardial infarction.