| Literature DB >> 12466705 |
Abstract
A recent shift in the clinical paradigm of acute coronary syndromes led to a burst of activity in developing animal models related to plaque vulnerability. In the present review, animal models of spontaneous and induced plaque rupture, thrombosis, and hemorrhage and "vulnerability endpoints" in conventional models of atherosclerosis are discussed. These endpoints include readouts related to biomechanical properties of the plaques, collagen turnover, underlying inflammation, and lipid accumulation. Challenges in model validation are emphasized. Development of new animal models and new tools of monitoring plaque vulnerability will facilitate design of plaque-stabilizing therapies.Entities:
Mesh:
Year: 2002 PMID: 12466705 DOI: 10.1097/00001573-200211000-00008
Source DB: PubMed Journal: Curr Opin Cardiol ISSN: 0268-4705 Impact factor: 2.161