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AtherosclerosisAtherosclerosis Atherosclerotic Cardiovascular Disease (ASCVD) Smooth m. proliferation Endothelial injury Lipids (cholesterol) Pathogenesis of atherosclerosis 1 Normal Artery Structure Lipoprotein particle 2 XX 60,00060,000 xx 180,000180,000 Robert Hamilton, Ph.D. EM: Negative staining Cardiovascular Research Inst., UCSF 3 The cholesterol in LDL accounts for ©Medscape approx. 70% of the plasma cholesterol Arteriosclerosis (Hardening of the arteries) Arterial wall thickening + loss of elasticity Monckeberg medial Arteriolosclerosis Atherosclerosis calcific sclerosis hyaline hyperplastic ¾Age 50 -small arteries/arterioles -aorta & branches + ¾Radiologic calcif. -hyaline type / hyperplastic coronary arteries ¾Lumen intact -hypertension / diabetes -ASCVD causes 38% of ¾Clinically insignif. all deaths in N. America 4 ATHEROSCLEROSIS: response-to-injury model Atherosclerosis is a chronic inflammatory response of the arterial wall to endothelial injury. 1. Chronic endothelial injury 2. Accumulation of lipoproteins (LDL mainly) basic tenets 3. Monocyte adhesion to endothelium 4. Platelet adhesion 5. Factors releasedÆSMC recruitment 6. SMC proliferation and ECM production 7. Lipid accumulation: extracellular/mac-SMC Risk Factors for Atherosclerosis •Hyperlipidemia •Smoking •Hypertension •Turbulence •Genetics 5 Endothelial injury Early Chronic—repetitive injury non- denuding endothelial dysfunction -cig. smoke toxins -homocysteine -?? Infectious agents -cytokinesÆgenes for Endothelial injury Early Chronic—repetitive injury non- denuding endothelial dysfunction -cig. smoke toxins 1. Hemodynamic -homocysteine disturbances -?? Infectious agents (turbulence) 2. Hypercholesterolemia 3. Inflammation 6 Endothelial injury Early Chronic—repetitive injury non- denuding endothelial dysfunction IEM -cig. smoke toxins 1. Hemodynamic -homocysteine disturbances -?? Infectious agents (turbulence) 2. Hypercholesterolemia Smooth muscle proliferation: 3. Inflammation - proliferative & synthetic phenotype in intimal SMC’s (vs. SMC in media) - growth factors: PDGF, FGF, TGFα Pathogenic sequence of atherosclerotic lesions 7 Normal aorta Fatty streak Atheromatous plaque (fibrofatty plaque) Complicated plaque 8 Fatty Streaks Atheromatous plaque (fibrofatty atheroma; plaque; atheroma) 9 Complicated plaque: ulcerated/thrombus Aneurysm 10 Thrombus in aneurysm ATHEROSCLEROSIS: Vessel involvement: desc. order 5 circle of Willis vessels 4 internal carotid a’s Ao 2 Cor. A’s 1 abd. aorta 3 popliteal a’s 11 Development of the smooth muscle cap Atherosclerostic Plaque Structure 12 AA IELIEL MM ECEC 13 14 15 16 17 18 Natural history of atherosclerosis Robbins 8/e Atherosclerosis (AS): Summary 1. AS is an intima-based lesion with a fibrous cap and atheromatous (gruel-like) core 2. Constituents: SMC’s, ECM, inflamm., lipid, necrotic debris 3. Endothelial injury + inflammation drive AS: risk factors influence EC dysfunction, SMC recruitment and activation 4. AS plaque complications: rupture—thrombosis—hemorrhage— embolization 5. Rx: risk factor recognition + reduction 19.

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Report on the Cooperative Study of Intracranial Aneurysms And
Report on the Cooperative Study of Intracranial Aneurysms and Subarachnoid Hemorrhage SECTION VIII, Part I Results of the Treatment of Intracranial Aneurysms by Occlusion of the Carotid Artery in the Neck HIRO NISHIOKA, M.D.* Introduction In a late postoperative study of retinal artery CCLUSION of the cervical portion of the pressures in 13 patients with carotid liga- carotid artery has been employed tion, Christiansson '6~ found eight patients O since 1885 as a definitive treatment who had maintained pressure drops of 20 per for intracranial aneurysm. The resultant re- cent or more over a period of from 1 to 13 duction of intra-arterial pressure is expected years. The observation that there was stasis to reduce the likelihood of subsequent of blood within the aneuwsmal sac after hemorrhage. The alteration of blood flow carotid occlusion was made at angiography characteristics within the aneurysmal sac by Eeker and Riemenschneider '51. During may encourage thrombosis with organization digital carotid occlusion, they found that and fibrosis, which would strengthen the wall Diodrast remained within the sac for over a or obliterate the sac. That pressure can be minute, and, in the same patient, angiog- reduced effectively in the internal carotid raphy performed one week after partial artery by proximal internal or common ca- occlusion of the common carotid by a tan- rotid occlusion has been substantiated amply talum clip showed no filling of the aneurysm. by the works of many authors. However, Aneurysms may decrease visibly in size or pressure reductions distal to the bifurcation become progressively thrombosed after ca- of the internal carotid artery following ca- rotid ligation.
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Peripheral Arterial Disease
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The Pathobiology of the Saccular Cerebral Artery Aneurysm Rupture
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Pvd-Vs-Pad.Pdf
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