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It remains unclear if the developmental trajectories of a specific inflammatory biomarker during the acute phase of ST-elevation myocardial infarction (STEMI) provide outcome prediction. By applying latent class growth modeling (LCGM), we identified three distinctive trajectories of CD14++CD16+ monocytes using serial flow cytometry assays from day 1 to day 7 of symptom onset in 96 de novo STEMI patients underwent primary percutaneous coronary intervention. Membership in the high-hump-shaped trajectory (16.8%) independently predicted adverse cardiovascular outcomes during a median follow-up of 2.5 years. Moreover, inclusion of CD14++CD16+ monocyte trajectories significantly improved area under the curve (AUC) when added to left ventricular ejection fraction-based prediction model (ΔAUC = 0.093, P = 0.013). Therefore, CD14++CD16+ monocyte trajectories during STEMI hospitalization are a novel risk factor for post-STEMI adverse outcomes. These results provide the first proof-of-principle evidence in support of the risk stratification role of LCGM-based longitudinal modeling of specific inflammatory markers during acute STEMI.

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To detect the development of monocytes and proliferative macrophages in atherosclerosis of ApoE −/− mice, we randomly assigned 84 ApoE −/− mice fed western diet or chow diet. On weeks 2, 4, 6, 8, 10, and 12 after fed high-fat diet or normal chow diet, animals were euthanized (n = 7 for each group at each time point). Flow cytometry methods were used to analyze the proportions of circulation monocyte subsets. The macrophage and proliferative macrophage accumulation within atherosclerotic plaques was estimated by confocal florescence microscopy. Plasma levels of total cholesterol and triglyceride were measured by ELISA kit. The plaques of aortic sinus were stained with Oil Red O. The percent of Ly6C hi circulation monocyte, the density of proliferation macrophage, the total plasma cholesterol and triglyceride levels, the lesion area of ApoE −/− mice were consistently elevated in chow diet throughout the trial. The total plasma cholesterol and triglyceride levels, the lesion area were elevated in western diet group with age, and they were always higher than the chow diet group. The Ly6C hi monocytes and proliferative macrophages reached a plateau at 8 weeks and 6 weeks; despite continued high-triglyceride high-cholesterol diet the percent did not significantly change. Interestingly, the density of macrophage did not change significantly over age in western and chow diet groups. Our results provide a dynamic view of Ly6C hi monocyte subset, the density of macrophage and proliferation macrophage change during the development and progression of atherosclerosis, which is relevant for designing new treatment strategies targeting mononuclear phagocytes in this model.