3. Smoking: Endothelial damage, CO↑ -PDGF↑, SMCn →mediaproliferation ,emigration2)LDLoxidation → Ox-LDL中4. Diabetes and hyperinsulimemia:Hyperglycemia - LDL glycolate ox-LDL→hypertriglyceride2Hyperinsulimemia 一→ SMC↑、HDLI
3. Smoking: ① Endothelial damage, CO↑ PDGF↑, SMC proliferation , emigration →media ② LDL oxidation ox-LDL 4. Diabetes and hyperinsulimemia: ① Hyperglycemia LDL glycolate ox-LDL hypertriglyceride ② Hyperinsulimemia SMC↑、HDL↓
5.Heredity: 200genesHDL-receptor gene mutation-→familyhypercholesterolemia6. Age and sex:()Age: age↑-→AS factors changesarterial wall proliferative change(2) Sex: estrogen → HDLpostmenopausal female =male
5. Heredity: 200genes HDL-receptor gene mutation→ family hypercholesterolemia 6. Age and sex： (1) Age: age↑→AS factors changes arterial wall proliferative change (2) Sex: estrogen → HDL postmenopausal female = male
7. Others:Obesity , stressful life type , hypoxia , dietlack of Vit. C,infection of bacteria ,virus8. Lack of exercise :9. Intake of alcohol :Protective role for moderate intake ofalcohol:HDLA large amount of intake of alcohol:hypertension, cerebral hemorrhage
7. Others: Obesity , stressful life type , hypoxia , diet lack of Vit. C , infection of bacteria , virus 8. Lack of exercise : 9. Intake of alcohol : Protective role for moderate intake of alcohol : HDL A large amount of intake of alcohol: hypertension, cerebral hemorrhage
70-e1560199650-IMenWomen40-81cC830-54820-一32281015OBPSystolic120160160160160160160Cholesterol220220260260260260260HDL-C50505035353535+++DiabetesCigarettes++Figure 12-11Estimated lO-year risk of coronary heart diseaseaccording to yariouscombinations of risk factorlevels.From Kannel WB,et al:An updateoncoronary riskfactors.MedClinNorthAm79:951,1995.)
(二)Pathogenesis1. Response to injury hypothesis :(1) Chronic endothelial injury(2)Insudation ofLDLintovessel wall(3)Modification of lipoprotein by oxidatin(4) Adhesion of blood monocyte to the EC(5)Adhesionofplatelet(6)Activated platelet,macrophage releasefactors(7)Proliferation of SMC in the intima andaccumulation of extracellular matrix(collagen(8)Enhanced accumulation of lipid intracellularlyand extracellularly
(二) Pathogenesis 1. Response to injury hypothesis : (1) Chronic endothelial injury (2) Insudation of LDL into vessel wall (3) Modification of lipoprotein by oxidatin (4) Adhesion of blood monocyte to the EC (5) Adhesion of platelet (6) Activated platelet , macrophage release factors (7) Proliferation of SMC in the intima and accumulation of extracellular matrix(collagen) (8) Enhanced accumulation of lipid intracellularly and extracellularly