Abstract
Chronic total occlusion (CTO) is probably caused by thrombus and lipid-rich cholesterol esters that are replaced over time by collagen and calcium deposition. Experimental models showed endothelial cell necrosis in response to vessel ligation, whereas more recent models suggest that the endothelium might retain viability guiding the subsequent development of CTO, including CTO neo-revascularization, which occurs within the lumen and in various layers of the vessel wall, by the release of paracrine substances. It is uncertain whether after CTO recanalization the recovery of anterograde reverses endothelial dysfunction, thus promoting vasodilation and positive remodeling.