Macrophage Heterogeneity of Culprit Coronary Plaques in Patients With Acute Myocardial Infarction or Stable Angina

Abstract

We investigated the polarization states of macrophages in coronary atherectomy tissues retrieved from patients with acute myocardial infarction (AMI, n = 52) or stable angina pectoris (SAP, n = 22). The specimens were analyzed immunohistochemically using antibodies specific to CD11c (M1 marker), CD206 (M2 marker), and to markers of endothelial cells, macrophages, and smooth muscle cells. Baseline characteristics were similar in the 2 groups. The proportion of areas immunopositive for a smooth muscle actin was similar, but those positive for CD31 and CD68 were larger in the AMI group compared with the SAP group. In addition, AMI had significantly greater areas immunopositive for CD11c (P = .007) than did SAP, but CD206 (P = .102) positivity was not different in the 2 groups. In conclusion, M1 macrophage infiltration, not M2 macrophage infiltration, was increased in culprit plaques of patients with AMI. Macrophage heterogeneity may therefore be related to plaque instability. Macrophages are heterogeneous and can exist as either proinflammatory (M1) or anti-inflammatory (M2) types.1-5 M1 macrophages primarily secrete proinflammatory cytokines, thus amplifying the inflammation. In contrast, M2 macrophages secrete anti-inflammatory cytokines, damping the inflammatory responses. Therefore, tipping the balance toward pro- or anti-inflammatory types may affect plaque stability. However, the relationship between macrophage heterogeneity and plaque instability remains uncertain. We investigated the phenotypic heterogeneity of macrophages in coronary atherectomy tissues obtained from patients with acute myocardial infarction (AMI) or stable angina pectoris (SAP) and examined the relationship between their expression levels and clinical manifestations.