Atherosclerosis and myocardial infarction

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Atherosclerosis and myocardial infarction

  1. 1. ATHEROSCLEROSIS & MYOCARDIAL INFARCTION MARYAM JAMILAH BINTI ABDUL HAMID 082013100002 IMS BANGALORE
  2. 2. LEARNING OUTCOME  Student should be able to give the definition of atherosclerosis and myocardial infarction.  Student should be able to explain the process of atherosclerosis and myocardial infarction.  Student should be able to list the causes of atherosclerosis and myocardial infarction.
  3. 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. 4. Endothelial injury Monocytes adhere to endothelial cells & move to subendothelial (intima) Scavenger receptor Superoxide Nitric oxide Hydrogen peroxide Other oxidants 1)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 LDL Vitamin 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. 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 thrombus Stop at the line if you are discussing about atherosclerosis, go beyond the line for myocardial infarction Thrombus get calcified Calcified thrombus is the atherosclerotic plaque Block the coronary artery/arteries Myocardium not supplied by oxygen Anaerobic glycolysis Lactic acid produce (lactic acidosis), pH
  6. 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. 7. MYOCARDIAL INFARCTION Definition: Irreversible necrosis of heart muscle secondary to prolonged ischemia
  8. 8. Causes of Myocardial Infarction  Presence of atherosclerosis.  High Lipoprotein (a) in the plasma.
  9. 9. Presence of atherosclerosis  Presence of atherosclerotic plaque in coronary artery will decrease 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 to dilute 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 new pathway for the oxygen in red blood cell to be taken by myocardium
  10. 10. Lipoprotein (a) in heart disease  Present in large quantities in the plasma, is associated with an increased risk of coronary heart disease.  Lp(a) is nearly identical in structure to an LDL particle.  Lp(a) has additional apo(a), that is covalently linked at a single site to apo B-100.  Apo(a) is structurally homologous to
  11. 11.  Elevated Lp(a) slows the breakdown of blood clots that trigger heart attacks because it competes with plasminogen for binding to fibrin.  Circulating levels of Lp(a) are determined primarily by genetics.
  12. 12. Factors influencing level of Lp(a)  Trans fatty acids have been shown to increase Lp(a)  Estrogen decreases both LDL and Lp(a).  Niacin reduces Lp(a) and raises HDL.
  13. 13. (MI)  Type 1 – spontaneous MI related to ischemia due to a primary 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 coronary intervention (PCI)
  14. 14. CONCLUSION Atherosclerosis: Hardening, stiffness and lost of elasticity of the arteries because formation of plaque inside the artery Myocardial infarction: Irreversible necrosis of myocardium ―So, 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. 15. REFERENCES  Lippincott’s 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

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