Accumulation of atherogenic lipoproteins in the arterial intima is a key event in the development of atherosclerosis. The likelihood of increased lipoprotein accumulation in the intima increases with increasing influx: arterial influx of lipoproteins is increased by increased arterial wall permeability, increased lipoprotein concentration in plasma, and by high blood pressure. On entrance into the arterial intima, lipoproteins can either efflux as intact particles, be retained in the intima, or be degraded by intimal cells. Increased degradation as well as increased retention of lipoproteins in the intima have both been associated with increased development of atherosclerosis. Therefore, low rates of efflux of intact particles, as appears to be the case for large particles like VLDL, IDL, and possibly lipoprotein (a) could potentially promote atherosclerosis.