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Atherosclerosis and Atherothrombosis PowerPoint Presentation

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Description : Check out this medical presentation on Atherosclerosis, which is titled "Atherosclerosis & Atherothrombosis", to know about atherosclerosis, a chronic multifocal immuno-inflammatory fibroproliferative disease affecting large and middle-sized arteries, mainly induced by lipids accumulation.

Tags : Atherosclerosis, Atherothrombosis, chronic multifocal immuno-inflammatory fibroproliferative disease, large, middle-sized, arteries, lipids accumulation

Published on : Jun 02, 2021 | Views : 1949 | Downloads : 2

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Slide 1-

Atherosclerosis & Atherothrombosis Dr. Taras V. Chendey, MD, PhD Chair of Hospital Therapy
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Definition Atherosclerosis is chronic multifocal immuno-inflammatory fibroproliferative disease affecting large and middle-sized arteries, mainly induced by lipids accumulation Word “atherosclerosis” comes from Greek “atheros” – porridge, paste and “sclerosis” - hardening
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Atherosclerosis is a substrate for CVD – MI and stroke, and responsible for the 2/3 of deaths among adults in Ukraine. There are approx. 50 000 MIs and 110 000 strokes in Ukraine annually
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Etiology & Risk Factors Exact etiology is unknown Unmodifiable risk factors Age (men ≥45 yrs, women ≥ 55 yrs) Male gender. Men are at grater risk than premenopausal women, because of the protective effects of endogenous estrogens. Family history of premature coronary heart disease (<55 yrs for 1st-degree male relative, <65 yrs for 1st-degree female relative) – many genes involved
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Modifiable risk factors Hyperlipidemia The presence of hyperlipidemia is the strongest risk factor for atherosclerosis in persons younger than 45 years of age. Both primary and secondary hyperlipidemia increase the risk. Cigarette smoking Hypertension High blood pressure produces mechanical stress on the vessel endothelium. It is a major risk factor for atherosclerosis in all age groups and may be as important or more important than hypercholesterolemia after the age of 45 years. Diabetes mellitus Diabetes elevates blood lipid levels and otherwise increases the risk of atherosclerosis. Obesity (incl. abdominal obesity)
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There are a number of other less well-established risk factors for atherosclerosis, including: High serum homocysteine levels Homocysteine is derived from the metabolism of dietary methionine Homocysteine inhibits elements of the anticoagulant cascade and is associated with endothelial damage. Clinical trial showed no benefit of homocysteine lowering in regards of CV outcomes Elevated serum C-reactive protein It may increase the likelihood of thrombus formation; Inflammation marker; hsCRP >2.0 mg/dL is associated with adverse CV outcomes. Some drugs (statins) decrease hsCRP independently of their main action Infectious agents The presence of some organisms (Chlamydia pneumoniae, herpesvirus hominis, cytomegalovirus) in atheromatous lesions has been demonstrated by immunocytochemistry, but no cause-and-effect relationship has been established. The organisms may play a role in atherosclerotic development by initiating and enhancing the inflammatory response.
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Total CV risk assessment total CVR is a probability of MI or CV death during next 10 (30) years
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http://www.mdcalc.com/framingham-coronary-heart-disease-risk-score/
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Causes of Secondary Hyperlipidemia Diet Hypothyroidism Nephrotic syndrome Anorexia nervosa Obstructive liver disease Obesity Diabetes mellitus Pregnancy Obstructive liver disease Acute heaptitis Systemic lupus erythematousus AIDS (protease inhibitors)
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Hereditary Causes of Hyperlipidemia Familial Hypercholesterolemia Codominant genetic disorder, coccurs in heterozygous form Occurs in 1 in 500 individuals Mutation in LDL receptor, resulting in elevated levels of LDL at birth and throughout life High risk for atherosclerosis, tendon xanthomas (75% of patients), tuberous xanthomas and xanthelasmas of eyes. Familial Combined Hyperlipidemia Autosomal dominant Increased secretions of VLDLs Dysbetalipoproteinemia Affects 1 in 10,000 Results in apo E2, a binding-defective form of apoE (which usually plays important role in catabolism of chylomicron and VLDL) Increased risk for atherosclerosis, peripheral vascular disease Tuberous xanthomas, striae palmaris
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Doi H et al. Circulation 2000;102:670-676 Colome C et al. Atherosclerosis 2000;149:295-302 Cockerill GW et al. Arterioscler Thromb Vasc Biol 1995;15:1987-1994 HDL LDL Chylomicrons, VLDL, and their catabolic remnants > 30 nm 20–22 nm Potentially pro-inflammatory 9–15 nm Potentially anti-inflammatory Lipoprotein Classes
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The Role of Lipoproteins in Atherogenesis HDL Liver Oxidative modification of LDL LDL + VLDL Cholesterol excreted High plasma LDL LDL infiltration into intima + Macrophages Foam cells Fatty streak Advanced fibrocalcific lesion Endothelial injury Adherence of platelets Release of PDGF Other growth factors LCAT APO-A1 APO-A1=Apolipoprotein A1, HDL=High density lipoprotein, LCAT=Lecithin cholesterol acyltransferase, LDL=Low density lipoprotein, PDGF=Platelet-derived growth factor, VLDL=Very low density lipoprotein
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3.7 2.9 2.2 1.7 1.3 1.0 40 70 100 130 160 190 Relative Risk for Coronary Heart Disease (Log Scale) LDL-Cholesterol (mg/dL) Grundy S et al. Circulation 2004;110:227-39 CHD Risk According to LDL-C Level CHD=Coronary heart disease, LDL-C=Low-density lipoprotein cholesterol
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Fridrecksen’s classification of hyperlipidemias
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Checking lipids Nonfasting lipid panel measures HDL and total cholesterol Fasting lipid panel Measures HDL, total cholesterol and triglycerides LDL cholesterol is calculated (Friedwald’s formula): LDL cholesterol = total cholesterol – (HDL + triglycerides/2.2) – valid only for TG levels up to 4.5 mmol/l
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Pathology and pathogenesis The lesions associated with atherosclerosis are of three types: The fatty streak The fibrous atheromatous plaque Complicated lesion The latter two are responsible for the clinically significant manifestations of the disease.
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Modern theory of atherosclerosis Multifactor theory: Structural and functional injury of vascular endothelium; Response to injury of immune cells and smooth muscle cells; The role of lipoproteins in initiation and progression of lesions; The role of growth factors and cytokines; The role of repeated thrombosis in lesions progression. As a result of all presented above atherosclerosis can be defined as vicious inflammatory process.
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Clinical Classification of Atherosclerosis Pre-clinical (asymptomatic) period Clinical period Ischemic stage Necrotic stage Sclerotic stage
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Clinical Manifestations The clinical manifestations of atherosclerosis depend on the vessels involved and the extent of vessel obstruction. Atherosclerotic lesions produce their effects through: narrowing of the vessel and production of ischemia; sudden vessel obstruction caused by plaque hemorrhage or rupture; thrombosis and formation of emboli resulting from damage to the vessel endothelium; In larger vessels such as the aorta, the important complications are those of thrombus formation and weakening of the vessel wall. In medium-size arteries such as the coronary and cerebral arteries, ischemia and infarction caused by vessel occlusion are more common. Although atherosclerosis can affect any organ or tissue, the arteries supplying the heart, brain, kidneys, lower extremities, and small intestine are most frequently involved.
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Clinical manifestations of Atherosclerotic Vascular Disease
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Diagnostic Approaches in Atherosclerosis Gold standard of diagnosis – angiography (X-ray, CT or MRI techniques) Electron-beam CT – “coronary calcium score” – assessment for total plaque burden Doppler ulstrasound – used to detect renal or carotid lesions, assessment of intima-media thickness (useful marker of a/s). IVUS – unique information on plaque structure, volume and area Angioscopy – mostly used in scientific studies
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IVUS image
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Prevention of Atherosclerosis and its Complications Dietary modification: restriction of cholesterol (<200 mg/day), sat. and trans-fats; DASH-type eating plan; dietary sodium restriction. TG elevation: restriction of plain carbohydrates, total fat and total calories; refrain from alcohol Body mass decrease and increase aerobic physical activity help to increase HDL-C, blood pressure and insulin sensitivity Smoking cessation. Quitting halves CVR. Smoking cessation decreases mortality after MI and CABG Hypertension treatment. More pronounced decrease in stroke (~40%) than in MI (~10-20%) Control of diabetes. Strict glycemic control doesn’t seem to affect CVR, but lipid-lowering therapy is more beneficial in diabetics Low-dose aspirin (75-100 mg/day) is indicated in patients at high risk. It acts as antiaggregant and prevents clot formation on the plaque
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Therapies to Lower LDL-C Soluble fiber Soy protein Stanol esters Dietary Adjuncts Ezetimibe Cholesterol absorption inhibitor Cholestyramine Colesevelam Colestipol Guarrem Bile acid sequestrants Atorvastatin (Liprimar) Fluvastatin Lovastatin (generic) Pravastatin Rosuvastatin (Crestor) Simvastatin (Zocor) 3-Hydroxy-3-Methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors [Statins] Drug(s) Class Nicotinic acid Niacin
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HDL-C=High-density lipoprotein cholesterol, LDL-C=Low-density lipoprotein cholesterol, TC=Total cholesterol, TG=Triglycerides *Daily dose of 40mg of each drug, excluding rosuvastatin Cholesterol Management Pharmacotherapy
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HMG-CoA Reductase Inhibitor Trials: Chronology Study Population: Primary prevention Acute coronary syndromes Chronic Coronary heart disease
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Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm (ASCOT-LLA) Sever PS et al. Lancet. 2003;361:1149-1158 0 1 2 3 4 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 Atorvastatin 90 mg/dl* Placebo 126 mg/dl* P=0.0005 Cumulative incidence of MI and fatal CHD (%) Follow-up (yr) 36% RRR *Post-treatment LDL-C level CHD=Coronary heart disease, RR=Relative risk HMG-CoA Reductase Inhibitor: Primary Prevention 10,305 patients with HTN randomized to atorvastatin (10 mg) or placebo for 5 years Statins provide significant benefit in moderate- to high-risk individuals by lowering LDL-C levels below current goals
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O’Keefe JH Jr et al. JACC 2004;43:2142-6 –1 10 0 2 4 6 8 Statin Placebo WOSCOPS AFCAPS LDL cholesterol (mg/dL) 55 195 175 155 135 115 95 75 CHD event rate (%) WOSCOPS ASCOT AFCAPS ASCOT P=0.0019 Relationship between LDL-C Levels and Event Rates in Primary Prevention Statin Trials HMG-CoA Reductase Inhibitor: Primary Prevention AFCAPS= Air Force/Texas Coronary Atherosclerosis Prevention Study, ASCOT= Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm, WOSCOPS= West of Scotland Coronary Prevention Study
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LaRosa JC et al. NEJM 2005;352:1425-1435 CARE=Cholesterol and Recurrent Events Trial, HPS=Heart Protection Study, LIPID=Long-term Intervention with Pravastatin in Ischaemic Disease; 4S=Scandinavian Simvastatin Survival Study, TNT=Treating to New Targets 30 25 20 15 10 5 0 0 70 90 110 130 150 170 190 210 LDL-C (mg/dL) TNT (atorvastatin 80 mg/d) TNT (atorvastatin 10 mg/d) HPS CARE LIPID LIPID CARE HPS Event (%) 4S 4S Statin Placebo Relationship between LDL-C Levels and Event Rates in Secondary Prevention Statin Trials of Patients with Stable CHD HMG-CoA Reductase Inhibitor: Secondary Prevention LDL-C=Low density lipoprotein cholesterol
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elevated hepatic transaminases Dose-dependent phenomenon that is usually reversible myalgias, myopathy, rhabdomyolysis Kashani A et al. Circulation 2006;114:2788-97 *The rate of myalgias leading to discontinuation of atorvastatin in the TNT trial was 4.8% and 4.7% in the 80 mg and 10 mg arms, respectively. Hepatocyte Skeletal myocyte HMG-CoA Reductase Inhibitor: Adverse Effects
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Invasive treatment: angioplasty, stenting and bypass grafting