3 coronary artery disease MI.pdf - CARDIOVASCULAR DISEASE-major cause of death disability-950,000 die each year 40 before reaching a hospital Coronary

3 coronary artery disease MI.pdf - CARDIOVASCULAR...

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1 CARDIOVASCULAR DISEASE -major cause of death & disability -950,000 die each year, 40% before reaching a hospital Coronary Artery Disease CAD affects the arteries that provide blood, oxygen, & nutrients to the myocardium Mostly results from coronary artherosclerosis
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2 ATHEROSCLEROSIS Atherosclerosis- - a disease of the arterial intima affecting elastic large & medium sized arteries -is characterized by intimal plaques (lipid core covered by a fibrous cap) that obstructs the lumen, weakens the wall and may lead to atheroembolism. The disease starts in childhood, but only produces symptoms in middle age or later. Leads to infarcts of heart, brain, gut, limbs; aortic aneurysms and sudden cardiac death. Hardening of arteries (arteriosclerosis)- the progressive narrowing and hardening of the arteries over time Schematic diagram of the arterial wall
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3 ATHEROSCLEROSIS- RISK FACTORS .
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4 HYPOTHESES - The response-to-injury -The response-to- lipoprotein retention -Oxidative modification The three hypotheses share common elements: - LDL uptake - inflammation
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5 Endothelial and smooth muscle cell activation by inflammation
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6 INITIATION OF ATHEROSCLEROSIS- ENDOTELIAL DYSFUNCTION 1. Accumulation of extracellular lipid - Lipoproteins are captured and retained by binding to proteoglycans in the intima - Bound lipoproteins are susceptible to oxidative or chemical modifications 2. Leukocyte recruitment and accumulation - Adhesion molecule expression leukocyte adhesion to endothelium diapedesis - Production of chemoattractants directed migration of leukocytes
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7 FATTY STREAK Atheroma Progression 3. Intracellular lipid accumulation - Once within the arterial intima, monocytes take up lipid via 'scavenger' receptors to become foam cells - Cytokines such as CSF-1 stimulate macrophage proliferation
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8 THE ADVANCED, COMPLICATED LESION OF ATHEROSCLEROSIS 4. Smooth muscle cell migration, proliferation - Medial smooth muscle cells change phenotype and become susceptible to chemoattractants (eg PDGF) which induce their migration into the intima. - Once within the intima, these phenotypically altered smooth muscle cells are stimulated to proliferate by other cytokine/growth factors .
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9 UNSTABLE FIBROUS PLAQUES IN ATHEROSCLEROSIS 5. Extracellular matrix synthesis - Intimal smooth muscle cells are induced to synthesise ECM proteins incl collagens I and III, proteoglycans - Matrix degrading enzymes aid SMC migration and matrix turnover required for arterial remodelling
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13 RECOMMENDED BLOOD LIPIDS [mg/dl] LDL < 100 →Optimal 100- 129 → Near optimal 130- 159 → Borderline 160- 189→ High ≥ 190 → Very High Total Cholesterol < 200 → Desirable 200- 239 → Borderline ≥ 240 → High HDL < 40 → Low ≥ 60 → High Serum Triglycerides < 150 → normal 150- 199 → Borderline 200- 499 → High ≥ 500 → Very High
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14 GENETIC CAUSES OF DYSLIPIDEMIA raised or abnormal levels of lipids and/or lipoproteins in the blood Disease Lipid Profile Prevalen ce Etiology Primary Hypercholesterolemia Familial Hypercholesterolemia  LDL 1:500 (+/- ) LDL Receptor
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  • Fall '19
  • Krzysztof Okoń

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