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CLINICAL APPLICATIONS OF ENZYMES: MYOCARDIAL INFARCTION Coronary artery disease is the leading cause of death in the United States and in most western countries. It is caused by lesions ( atherosclerotic plaques – more on these next semester in Biochem 108) in the blood vessels of the heart. Plaques narrow the arterial opening and interfere with blood flow to the heart. When inflamed plaques set in motion the blood clotting cascade, a blood clot forms , the artery is occluded, and blood flow to a portion of the heart muscle stops – this is a heart attack or myocardial infarction . The sequence of metabolic events leading to plaque formation is complex, and we will discuss some of these next semester. For some additional information (if you want), go to: dci/Diseases/Cad/CAD_WhatIs.html There are several well-established risk factors for coronary artery disease (CAD) . High cholesterol levels, hypertension (high blood pressure), and smoking are all risk factors, as are high circulating levels of LDL (low density lipoprotein) and VLDL (very low density lipoprotein). Smoking oxidizes LDL and makes it more likely to accumulate in plaques lining the blood vessels. In addition, the carbon monoxide in cigarette smoke combines with hemoglobin and prevents oxygen from binding; to compensate, the body produces more red blood cells and this makes the blood more viscous and makes the heart work harder to pump the blood. Hypertension exposes the arteries to physical stress which can injure the vessels and also cause cells lining the arteries to multiply abnormally. All of these factors contribute to plaque formation and ultimately to atherosclerosis . Coronary artery disease can result in myocardial infarction (MI) , typically with the formation of a blood clot on the surface of an arterial lesion. The clot either blocks the artery or is carried elsewhere into the coronary system and causes a block there. When this happens, the cells in the heart that are cut off from their oxygen supply begin to die. If an artery is only partially blocked, damage to the heart muscle can be limited by giving the patient oxygen to breathe. In some cases, this can be followed up by treatment with “clot busters” – drugs that break down the clot and allow blood flow to resume. These treatments are effective only if administered early in the course of a MI. For more information on myocardial infarctions (but only if you want), go to: While television shows like ER and Rescue 911 make it seem quite simple to diagnose a heart attack, in fact, many patients experiencing their first MI fall into the low to medium risk category and present with atypical symptoms. This is especially true of women experiencing MIs. Electrocardiograms of the heart often do not show specific changes indicating a heart attack for several days after the attack. In addition, angina (chest pain associated
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This note was uploaded on 03/31/2008 for the course BIOCHEM 107 taught by Professor Toews during the Fall '07 term at UNC.

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