Figure 6.

Drug effect. The mechanistic rationale for plaque changes based on drug action. Left: baseline characteristics of plaque burden show levels of stenosis, localized wall remodeling, calcification, lipid-rich necrotic core, and intraplaque hemorrhage. Upper right: without the administration of drug, the natural history of the plaque demonstrates increases associated with generally elevated levels of triglycerides, manifesting as high and sometimes increasing levels of saturated fatty acids, APOCIII, and cholesterol. This results in morphological measures and a proportional occupancy of low-attenuating components such as LRNC and IPH. In addition, the distance between lumen and LRNC, the cap thickness, decreases, with a net migration to less stable characteristics. Lower right: with icosapent ethyl, serum levels of these lipid species drop, causing reductions in features that contribute to instability, migrating the plaques to acquire more stable characteristics.