Mechanisms of plaque rupture: mechanical and biologic interactions.
Atherosclerotic vascular disease is the most common cause of morbidity and mortality in developed countries, and the world-wide importance of acute vascular syndromes is increasing. Acute events are usually triggered by the development of plaque disruption and subsequent thrombus formation. Histological studies have established specific structural features common among unstable plaques. The plaque has to bear remarkably increased mechanical stress at particular regions, and weakening of the extracellular matrix at these sites leads to fibrous cap rupture. The biologic factors that cause weakening of the plaque at these high stress locations are now emerging. Understanding the interplay of plaque architecture, mechanical properties and matrix biology is critical in the future development of therapies to stabilize lesions.
Arroyo
L H
LH
Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Lee
R T
RT
D000818:Animals; D001158:Arteries / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001696:Biomechanical Phenomena; D003324:Coronary Artery Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005109:Extracellular Matrix / Q000378:metabolism / Q000473:pathology; D006801:Humans; D050356:Lipid Metabolism; D008666:Metalloendopeptidases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D009203:Myocardial Infarction / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology
D008666:Metalloendopeptidases