Neointima and arterial injury: dogs, rats, pigs, and more.

Animal models have generated conflicting data regarding human restenosis. Many of these discrepancies can be explained on the basis of experimental methodology, or on improper extensions of animal data to human trials. However, fundamental differences clearly exist in neointimal formation across species. These relate not only to the quantity of neointima, but also to the histopathology as neointima forms. In order to design effective strategies against restenosis, the aggregate knowledge from all animal models must be carefully examined and integrated. The pathophysiology of neointimal formation across species must also be better understood in a unified form. Limitations of the existing animal models, and their relationship to human coronary disease and its treatment by percutaneous interventions, remain poorly understood. A solution to restenosis must lie in a detailed understanding of the events causing neointimal thickening, vascular remodelling, cellular proliferation, and matrix formation. Once the contribution of each is understood, interventions can be strategically planned, demonstrated in animal models, and successfully translated to human therapy.