1.ATHEROSCLEROSIS & MYOCARDIAL INFARCTION MARYAM JAMILAH BINTI ABDUL HAMID 082013100002 IMS BANGALORE

2. LEARNING OUTCOME Student should be able to give the definition ofatherosclerosis and myocardial infarction. Student should be able to explain the process ofatherosclerosis and myocardial infarction. Student should be able to list the causes ofatherosclerosis and myocardial infarction. 3. ATHEROSCLEROSIS Definition: Hardening of the arteries, and caused by plaque building up in the vessel. Over time the plaque causes thickening of the walls of the artery. Stiffness and a loss of elasticity also result. 4. Endothelial injury Monocytes adhere to endothelial cells & move to subendothelial (intima)Scavenger receptorSuperoxide Nitric oxide Hydrogen peroxide Other oxidants1)highly specific and regulated receptor mediated pathway for LDL uptake macrophages possess high levels of scavenger receptor activity; can bind to a broad range of ligands (non-specific) and mediate the endocytosis of chemically modified LDL in which the lipid components or apo B have been oxidized.Transformed into macrophages LDL + Oxidized LDLVitamin E Ascorbic acid B-Carotene Other Macrophages consumes antioxidants 2)Unlike the LDL receptor, the excess modified (oxidized) scavenger receptor is not downlipoprotein & become foam cells regulated in response to increased Foam cells accumulate, intracellular cholesterol. release growth factors and cytokines; stimulate migration 3)Cholesteryl esters (CE) accumulate of smooth muscle cells from in macrophages and cause their media to intima transformation into foam cells, Smooth muscle cells proliferate, produce collagen & which participate in the formation of take up lipid, potentially atherosclerotic plaque becoming foam cells. 5. Smooth muscle cells proliferate, produce collagen & take up lipid, potentially becoming form cells. Diameter of the lumen Blood become turbulence Activation of clot formation Produce thrombusStop at the line if you are discussing about atherosclerosis, go beyond the line for myocardial infarctionThrombus get calcifiedCalcified thrombus is the atherosclerotic plaque Block the coronary artery/arteries Myocardium not supplied by oxygen Anaerobic glycolysis Lactic acid produce (lactic acidosis), pH 6. Lactic acid produce (lactic acidosis), pH Less ATP production/no ATP production Inefficient contraction of myocardium (heart muscles) Heart muscles supplies by this artery dies Pain at that area Myocardial infarction 7. MYOCARDIAL INFARCTION Definition: Irreversible necrosis of heart muscle secondary to prolonged ischemia 8. Causes of Myocardial Infarction Presence of atherosclerosis. High Lipoprotein (a) in the plasma. 9. Presence of atherosclerosis Presence of atherosclerotic plaque in coronary artery willdecrease the oxygen delivery to the heart. This leads to ischemia of myocardium (cardiac muscle)and lastly causes dead to the myocardium. Degree of blockage of coronary artery: Partially blockage Fully blockage In early stage of atherosclerosis, drugs will be given todilute the plaque in the coronary arteries but in later stage, angioplasty cam be done. However, if the blockage is too much, bypass surgery should be done to create newpathway for the oxygen in red blood cell to be taken by myocardium 10. Lipoprotein (a) in heart disease Present in large quantities in the plasma, isassociated with an increased risk of coronary heart disease. Lp(a) is nearly identical in structure to an LDLparticle. Lp(a) has additional apo(a), that is covalently linkedat a single site to apo B-100. Apo(a) is structurally homologous to 11. Elevated Lp(a) slows the breakdown of blood clotsthat trigger heart attacks because it competes with plasminogen for binding to fibrin. Circulating levels of Lp(a) are determined primarilyby genetics. 12. Factors influencing level of Lp(a) Trans fatty acids have been shown toincrease Lp(a) Estrogen decreases both LDL andLp(a). Niacin reduces Lp(a) and raises HDL. 13. (MI) Type 1 spontaneous MI related to ischemia due to aprimary coronary event such as plaque erosion and/or rupture, fissuring(split), or dissection Type 2 MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension Type 3 sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood Type 4 associated with coronary angioplasty or stents: Type 4a MI associated with percutaneous coronaryintervention (PCI) 14. CONCLUSION Atherosclerosis: Hardening, stiffness and lost of elasticity of the arteries because formation of plaque inside the artery Myocardial infarction:Irreversible necrosis of myocardiumSo, as a human being, we should take optimum amount of lipid. This is because some of the food will cause harm to our body when we take them excessively. 15. REFERENCES Lippincotts Illustrated Reviews: Biochemistry Fifth Edition, Richard A. Harvey, PhD and Denise R. Ferrier, PhD, Lippincott Williams & Wilkins, Philadelphia, USA. http://surgery.about.com/od/beforesurgery/f/Arterioscl erosisAtherosclerosis.htm http://emedicine.medscape.com/article/155919overview https://www.google.com/search?q=fibrilysis&oq=fibrily sis&aqs=chrome..69i57j0l5.5118j0j7&sourceid=chrom e&espv=210&es_sm=93&ie=UTF-8 http://www.heart.org/HEARTORG/Conditions/HeartAtt ack/AboutHeartAttacks/About-HeartAttacks_UCM_002038_Article.jsp