IndexAbstractIntroductionConclusionReferencesAbstractCoronary heart disease is a condition caused by decreased blood flow to the heart muscle due to atherosclerotic plaque and the deposition of various substances that lead to narrowing of the coronary arteries, plaque or even clotting is due to obesity, unhealthy lifestyle and even genetic factors, this decrease in blood supply can cause myocardial infarction or heart attack which can lead to the death of an area of ​​the heart, this damage is irreversible and some morphological changes occur and a scar is formed. The most dangerous part are the complications that can result such as decreased cardiac output and inability of the heart to pump enough blood to the body (heart failure), difficulty breathing, pericarditis, cardiac rupture, ventricular fibrillation, septal defects and aneurysm. Treatment is based on avoiding smoking, sugars, carbonated drinks, alcohol and fats in the diet, regular exercise and fat loss. Also using beta blockers, aspirin, nitroglycerin, and cholesterol medications to dilate the arteries and improve blood flow to the heart, even surgery if necessary such as stent replacement and coronary bypass. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get Original Essay IntroductionIschemic heart disease, also known as coronary artery disease/heart disease, is a disease or condition caused by narrowing of the coronary arteries causing a reduction in blood and therefore oxygen being delivered to the heart muscle causing chest pain known as angina pectoris , which can even lead to a heart attack. Additionally, some people may have silent ischemia, without angina, which can lead to a sudden (unprecedented) heart attack. Purpose of this work: to discuss the causes or etiology of ischemic heart disease, as well as risk factors, clinical presentations, characteristics of myocardial infarction, complications related to myocardial necrosis. The causes and risk factors of ischemic heart disease include: The buildup of atherosclerotic plaque in the walls of the coronary arteries that supply the heart and other parts of the body. Cholesterol also settles on other substances that build up plaque and cause narrowing of arteries and obstruction of blood flow, as shown in the illustrative figure below. Other controllable causes/risk factors such as: Smoking and high blood pressure as they cause damage to the endothelium of the arteries and contribute to plaque accumulation and blood clotting. High cholesterol levels also contribute to plaque formation. In addition to age, obesity, diabetes (high blood sugar), stress, anxiety and alcohol consumption. Family and genetic history. Coronary heart disease causing disorders (risk factors) can be hereditary as genetics influence the strength of blood vessels and even communications of heart cells and specific proteins, so the body deals with cholesterol and processes it in a way different and therefore affects the risk of developing plaques, ischemia diseases and heart attacks. Genetics pass from parents to children in the form of deoxyribonucleic acid (DNA) through sperm and egg, and genes are copied in every cell. So, if a family member has a heart disease condition, this gives more reason for family members to check the integrity of their cardiovascular system. Clinical presentations: are often not the same in men and women. It is probably chest pain as a stable conditionangina, heart failure and acute coronary syndrome or perhaps even sudden cardiac arrest. The symptoms are barely hidden and the only presentation is an abnormal cardiac EKG or echocardiogram coincidentally ordered for another reason. Acute myocardial infarction as ischemic heart disease is also sometimes diagnosed when a patient presents with chest pain and acute infarction due to thrombosis and arterial occlusion. Dyspnea or difficulty breathing also occurs and is called the equivalent of angina. The mechanism is probably the same as angina, but the central evaluation of afferent stimuli is not the same. So dyssponia is often associated with angina as difficulty breathing is accompanied by chest pain. Dyspnea is also associated with left ventricular ischemia resulting in pulmonary venous congestion causing pulmonary edema. The association between presentation of dyspnea, fatigue and edema occurs in heart failure, as atherosclerosis is a common cause in some areas of heart failure. Atrial fibrillation and ventricular tachycardia are also important manifestations that can occur. Acute myocardial infarction and ventricular fibrillation can also lead to sudden death. The history of angina, physical examination and some tests such as electrocardiogram, chest x-ray and blood tests are very important for the diagnosis. The morphology of a myocardial infarction develops over time and shows arterial damage and healing, as ischemia causes coagulation necrosis accompanied by acute inflammation. The inflammatory infiltrate is subsequently replaced by granulation tissue and fibrosis occurs. During the First 12 Hours very simple histological changes are noted in the myocardium. Four hours after the block, myocardial edema occurs due to damaged endothelial cells, ruined capillaries and wavy-shaped fibers appear due to separation of cardiac myocytes from the edema fluid. Contraction bands also appear due to the influx of calcium and contraction of the fibers of these separated myocytes. During the period from 12 to 72 hours, pallor and a frame of red rings appear in the infarcted tissue. Coagulative necrosis also becomes more evident. Within about eighteen hours neutrophils begin to infiltrate the edges of the lesion. Very acute inflammation begins by the 2nd day and reaches its peak by the 3rd day. During the period of 4 to 10 days, the lesion becomes increasingly soft and yellow, macrophages replace neutrophils, phagocytosis and degradation of necrotic tissue stars which negatively affect the integrity of the myocardial structure and can cause myocardial rupture Furthermore, fibroblasts and new capillaries begin to form. reach the lesion from the edges to create an area of ​​granulation tissue. During the period of 10 days to 8 weeks, all dead tissue is removed by phagocytes and the granulation tissue is rearranged into a scar. Myocardial infarction can lead to some complications; as sudden death often due to arrhythmia and ventricular fibrillation. Arrhythmias are the most common complication, even if they are very dangerous for the patient's life, in most cases only self-limiting arrhythmias occur with minimal hemodynamic consequences. Arrhythmias that appear late, i.e. after 48 hours, reflect the extent of ventricular damage. They indicate an unfavorable prognosis and can recur, while early ones (24-48 hours), due to ischemia, rarely recur and do not indicate the extent of the infarction. Cardiogenic shock also occurs in fifteen% of patients due to severe damage to the myocardium which.