Endothelial Dysfunction In Cardiovascular Diseases: Therapeutic Implications After Coronary Angioplasty.

Restenosis remains the principal limitation of coronary angioplasty; its main mechanisms are neointimal hyperplasia and vascular remodeling. The endothelium destroyed at angioplasty will progressively recover the denuded zone. However, dysfunction of this neo-endothelium persists for quite a period and may participate in restenosis by influencing these two components (hyperplasia and remodeling). Several therapeutic strategies are under evaluation to try and accelerate the regeneration of the endothelium and make it functional more rapidly. Increasing available nitric oxide (NO) decreases the hyperplasia and improves endothelial function. Growth factors accelerate the endothelial regeneration and improves its function: the effect on hyperplasia depends on the growth factor used. The angiotensin converting enzyme inhibitors decrease hyperplasia by improving endothelial function. These therapeutic strategies merit evaluation in the clinical setting.