AtherosclerosisThecharacteristic cellular componentsinatherosclerotic plaques are foam cells,which aretransformed macrophages and smooth muscle cells thathave become filled with cholesteryl estersGlycation of lipoproteins in poorly controlleddiabetes also contributes to foam cell formationArterial hypertension accelerates atherogenesis. It iswell established that appropriate treatment of elevatedblood pressure helps to prevent coronary disease andstroke6
6 The characteristic cellular components in atherosclerotic plaques are foam cells, which are transformed macrophages and smooth muscle cells that have become filled with cholesteryl esters. Glycation of lipoproteins in poorly controlled diabetes also contributes to foam cell formation. Arterial hypertension accelerates atherogenesis. It is well established that appropriate treatment of elevated blood pressure helps to prevent coronary disease and stroke. Atherosclerosis
Atherosclerosis1.Cause(1) Those that contain apolipoprotein (apo) B100 havebeen identified as the vehicles in which cholesterol istransported into the artery wall(2) Low levels of HDL are an independent risk factor forcoronary disease(3) Cigarette smoking is a major risk factor for coronarydisease. It is associated with reduced levels of HDLimpairment of cholesterol retrieval, cytotoxic effectson the endothelium. increased oxidation ofatherogenic lipoproteins, and stimulation ofthrombogenesis
7 Atherosclerosis 1. Cause (1) Those that contain apolipoprotein (apo) B100 have been identified as the vehicles in which cholesterol is transported into the artery wall. (2) Low levels of HDL are an independent risk factor for coronary disease. (3) Cigarette smoking is a major risk factor for coronary disease. It is associated with reduced levels of HDL, impairment of cholesterol retrieval, cytotoxic effects on the endothelium, increased oxidation of atherogenic lipoproteins, and stimulation of thrombogenesis
AtherosclerosisBecause the process of atherogenesis ismultifactorial, therapy should be directed at alltheriskmodifiablefactors,includingatherogenichyperlipidemia.Therefore,thetimely diagnosis and treatment of lipoproteindisorders can be expected to decrease morbidityand mortality due to coronary disease8
8 Because the process of atherogenesis is multifactorial, therapy should be directed at all the modifiable risk factors, including atherogenic hyperlipidemia. Therefore, the timely diagnosis and treatment of lipoprotein disorders can be expected to decrease morbidity and mortality due to coronary disease. Atherosclerosis
LPATHOPHYSIOLOGYOEHYPERLIPOPROTEINEMANormal lipoprotein metabolism1.StructureTGandCEThe major lipoproteins ofplasma areparticles withhydrophobiccoreregionsApoproteincontainingcholesterylestersCholesterol1and triglycerides.Amonolayerofunesterifiedcholesterolandphospholipids surrounds thePhospholipidscore.Specific proteins(apolipoproteins)arelocatedon the surface.9
9 I. PATHOPHYSIOLOGY OF HYPERLIPOPROTEINEMIA Normal lipoprotein metabolism 1. Structure The major lipoproteins of plasma are particles with hydrophobic core regions containing cholesteryl esters and triglycerides. A monolayer of unesterified cholesterol and phospholipids surrounds the core. Specific proteins (apolipoproteins) are located on the surface
TGangCE2.Svnthesis & CatabolismApoproteinCholesterolA. Chylomicrons:PhospholipidChylomicrons, the largest of the lipoproteins, areformed in the intestine and carry triglycerides ofdietary origin. Some cholesteryl esters also appearin the chylomicron core. Phospholipids and freecholesterol-together with newly synthesized apoB48, A-I, A-II and other proteins--form the surfacemonolayer. The chylomicrons transit the thoracicduct to the blood stream10
10 2. Synthesis & Catabolism A. Chylomicrons: Chylomicrons, the largest of the lipoproteins, are formed in the intestine and carry triglycerides of dietary origin. Some cholesteryl esters also appear in the chylomicron core. Phospholipids and free cholesterol—together with newly synthesized apo B48, A-I, A-II and other proteins—form the surface monolayer. The chylomicrons transit the thoracic duct to the blood stream