Stabilization of atherosclerotic plaques: an update

Vulnerable plaquesThe majority of coronary thrombi ( 75%) is caused by plaque rupture. 1,2Prototype of the rupture-prone plaque contains a large, soft, lipid-rich necrotic core with a thin and inflamed fibrous cap, so-called thin-cap fibroatheroma (TCFA) (Figure 1). 3,4Other common features include expansive remodelling, large plaque size, plaque haemorrhage, neovascularization, adventitial inflammation, and 'spotty' calcifications. 4Thin-cap fibroatheroma caps are usually ,65 mm thick. 4Figure 2 summarizes factors contributing to the formation of vulnerable plaques.No distinct morphological features have been identified for the erosion-prone plaques, but they are usually rarely associated with expansive remodelling, scarcely calcified, and contain only limited inflammation. 2,5 Inflammatory cells, cytokines, chemokines, and growth factorsVulnerable plaques contain monocytes, macrophages, and T-cells.Of the T-cells, CD4+ T-helper (Th) cells are the most prominent. 6-cells can differentiate into a Th1 phenotype, which secretes and responds to IFN-g or a Th2 phenotype, which secretes and responds to IL-4, IL-10, and IL-13 (Figure 3).T-cells promote the vulnerability of plaques through their effects on macrophages.Similarly, there are two main plaque macrophage phenotypes: pro-inflammatory M1 macrophages (IFN-g-induced) and anti-inflammatory or regulatory M2 macrophages (IL-4/IL-13-induced). 7 Cytokines and chemokines important for regulating inflammatory and immune responses are listed in Supplementary material online,