Figure 1.

Apo B lipoprotein response‐to‐retention model of atherosclerosis initiation and progression. High plasma concentrations of apo B lipoproteins (LDL, IDL, VLDL, chylomicron remnants, Lp(a)) increase entry into intima and retention. Apo B lipoproteins bind to proteoglycans and begin aggregating, a process that accelerates once plaque begins. Retention is influenced by particle composition and diet, among other factors. Retention leads to a maladaptive cellular response leading to increased inflammation, fibrosis, and necrosis. The lipid/necrotic core forms when normal phagocytotic processes and efferocytosis are overwhelmed by continued retention and accumulation of “toxic” apo B lipoproteins. Plaque rupture or erosion can lead to formation of overlying thrombus, which can precipitate an acute clinical event. Apo indicates Apolipoprotein; IDL, intermediate lipoprotein; LDL, low‐density lipoprotein; Lp(a), Lipoprotein (a); VLDL, very‐low‐density lipoprotein.