[Relation between gene polymorphism and acute coronary syndrome].
The acute coronary syndrome, consisting of myocardial infarction and unstable angina, is the most important manifestation of coronary disease and is characterized by atherosclerotic plaque disruption and coronary thrombosis. In the coronary vessel wall, this process contains abnormalities of extracellular matrix, fibrinolytic system, endothelial function, and, possibly, vascular inflammation. Potentially thousands of genes are relevant to this apparently complex disease. Although many risk factors are intercorrelated, raising the possibility of a higher level of genetic control by a small number of master genes that control fundamental physiological systems. Such genes are likely to be relevant to the combined processes of plaque instability and coronary thrombosis.
Igase
Michiya
M
Department of Geriatric Medicine, Ehime University School of Medicine.
Miki
Tetsuro
T
D000789:Angina, Unstable / Q000235:genetics*; D050197:Atherosclerosis / Q000235:genetics / Q000473:pathology; D017630:Connexins / Q000235:genetics; D003328:Coronary Thrombosis / Q000235:genetics; D037501:Galectin 2 / Q000235:genetics; D006801:Humans; D008233:Lymphotoxin-alpha / Q000235:genetics; D020782:Matrix Metalloproteinases / Q000235:genetics; D009203:Myocardial Infarction / Q000235:genetics*; D052250:Nitric Oxide Synthase Type III / Q000235:genetics; D017395:Plasminogen Activator Inhibitor 1; D011110:Polymorphism, Genetic; D013577:Syndrome; D000097006:Gap Junction alpha-4 Protein
D017630:Connexins; D037501:Galectin 2; D008233:Lymphotoxin-alpha; D020782:Matrix Metalloproteinases; D052250:Nitric Oxide Synthase Type III; D017395:Plasminogen Activator Inhibitor 1; D000097006:Gap Junction alpha-4 Protein; C051321:SERPINE1 protein, human; C496314:NOS3 protein, human