Endothelial damage in atherosclerosis is characterized by abnormal vascular functionality. Hyperlipidemic patients show alterations in ocular vascularization. However, it is not known whether these alterations are reversible after the lipid profile returns to normal. This study evaluates a rabbit model of hypercholesterolemia, examining the ultrastructural changes in the choroid, and the changes in it after a period of normal blood-cholesterol values induced by a standard diet. Rabbits were divided into three groups: G0, fed a standard diet; G1A, fed a 0.5% cholesterol-enriched diet for 8 months; and G1B, fed a 0.5% cholesterol-enriched diet for 8 months followed by a standard diet for a further 6 months. Eyes were processed for transmission electron microscopy. G1A had a buildup of lipids at the suprachoroidea that compressed the vascular layers, and hypertrophy of endothelial and vascular smooth muscle cells. In G1B there was less lipid accumulation than in G1A, but this was not followed by reversal of the choroidal damage. The suprachoroidea thickness of G1B was still greater than in G0 due to abundant collagen fibers. The intervascular spaces of the choroid had fewer lipids than G1A but more collagen fibers than G0. The large- and medium-sized vessel layers and choriocapillaris were less compressed than in G1A but exhibited basal membrane and endothelial changes similar to those in G1A. Normalization of serum cholesterol levels is not enough to reverse cholesterol-induced vascular damage to the choroid. These choroidal changes could be compatible with a chronic ischemia that could produce retinal degeneration.