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Peri-procedural myocardial injury, which is associated with worse long-term clinical outcome, is a common complication related to inflammatory pathogenetic mechanisms. Monocytes and macrophages play key roles in the initiation and progression of atherosclerosis. Recent studies have demonstrated that monocytes in human peripheral blood are heterogeneous, including CD14+CD16- monocytes and CD14+CD16+ monocytes. Several lines of evidence suggested that CD14+CD16+ monocytes might contribute to the accelerated atherosclerosis. In view of the heightened appreciation of the heterogeneity of circulating monocytes, we hypothesized that an up-shifting subset of CD14+CD16+ monocytes might be induced by percutaneous coronary intervention (PCI), which subsequently leads to peri-procedural myocardial injury. Moreover, statins loading before PCI could exert anti-inflammatory effects partly by modulating monocyte phenotype and thus prevent peri-procedural myocardial injury.

The role of monocyte phenotype switching in peri-procedural myocardial injury and its involvement in statin therapy