Fujimoto Hajime, Yamaguchi Tetsu
Toranomon Hospital.
Nihon Rinsho. 2006 Apr;64(4):611-6.
Acute coronary syndrome is a clinical state induced by the thrombosis following the rupture of unstable atherosclerotic plaque. Atherosclerotic plaque increases its vulnerability by the accumulation of foam cells, inflammation, oxidative stress, and apoptosis of vascular wall cells including macrophage. Inflammation and oxidative stress stimulates macrophages to produce matrix metalloproteinase (MMP), which degrades extracellular matric proteins and causes thinning of the fibrous cap. When the fibrous cap of the plaque tears, thrombogenic lipid core is exposed to blood, and platelets accumulate at the site, resulting in the significant reduction of coronary blood flow. Treatment of acute coronary syndrome patients should be focused on the stabilization of the plaque as well as vasodilatation, oxygen supply, or control of hemodynamics.