Update in atherothrombotic disease.
Crucial advances in our understanding of the pathogenesis of atherothrombosis, defined as atherosclerosis and its thrombotic complications, have been achieved during the past two decades. The historical hypothesis of pathogenesis ("lipid accumulation") has evolved to integrate several factors contributing to the initiation and evolution of this complex disease. Endothelial dysfunction is considered to be the earliest event in atherogenesis. Inflammation and apoptosis play critical roles in its progression and onset. Tissue factor is postulated to be a central actor in determining plaque thrombogenicity. A hyperreactive state of the blood ("vulnerable blood") may be responsible for one-third of all the acute coronary syndromes. This review will discuss emerging concepts in the pathogenesis of and therapeutic approaches to atherothrombotic disease.
Viles-Gonzalez
Juan F
JF
Cardiovascular Biology Research Laboratory, Zena and Michael A. Wiener Cardiovascular Institute, Box 1030, Mount Sinai School of Medicine, One East 100th Street, New York, NY 10029, USA.
Anand
Sunil X
SX
Valdiviezo
Carolina
C
Zafar
M Urooj
MU
Hutter
Randolf
R
Sanz
Javier
J
Rius
Teresa
T
Poon
Michael
M
Fuster
Valentin
V
Badimon
Juan J
JJ
D000208:Acute Disease; D017209:Apoptosis / Q000502:physiology; D001161:Arteriosclerosis / Q000503:physiopathology*; D004727:Endothelium / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology; D012307:Risk Factors; D013925:Thromboplastin; D013927:Thrombosis / Q000503:physiopathology*
D013925:Thromboplastin