From Ishmi to Nrsis - Essay Example

yосаrdiаl Infаrсtiоn Name Institution Course Tutor Date Мyосаrdiаl Infаrсtiоn: From Isсhаеmiа to Nесrоsis Abstract Myocardial infarction refers to a heart attack and occurs because of poor blood flow, which leads to insufficient oxygen in the heart tissue. Severe damage to the heart is termed cardiac ischaemia. Prolonged cardiac ischaemia leads to cell necrosis. This paper seeks to explore myocardial infarction from the process of ischaemia to necrosis. The essay defines cardiac ischaemia and the events leading to the condition. The paper looks at the mechanism of ischaemia, which leads to cellular injury. It then discusses the sequential progression in myocardial infarction from reversible cell injury to cell death. The paper also identifies the pattern of tissue necrosis characteristic of myocardial infarction and the associated histological findings at autopsy. The essay explores the major biomarkers measured in laboratory investigations of suspected myocardial infarction. The information in the essay was primarily culled from articles published about myocardial infarction. Introduction Myocardial infarction (MI), ‘acute myocardial infarction’ (AMI), ‘heart attack’ or ‘acute coronary syndrome’. This condition occurs when the flow of blood stops in a certain part of the heart, leading to damage in the heart muscle. It is clear that the heart requires a sufficient supply of oxygenated blood for normal functioning. A heart attack lasts for several hours and the victim might die if not taken care of immediately. It is apparent that one feels chest pain and being tired. It begins with cardiac ischaemia, and this leads to necrosis of the myocardial tissue. At the middle of the infarct, some necrotic tissues is affected once the myocardial cell dies due to inadequate blood flow for several hours. There should be tests carried out once a person feels chest pains for the detection of a possible heart attack. Ischaemia This refers to a condition where a part of the heart is starved of the required oxygen because of one of the heart branches or arteries becomes blocked from supplying oxygenated blood to the heart muscle (Martindale & Metzger, 2014, 31). This is also known as reperfusion injury. Ischaemia in the heart muscle occurs once the oxygenated blood stops flowing as a result of high blood cholesterol, diabetes, obesity, smoking, inadequate exercise, poor diet, increased alcohol or high blood pressure. Ultimately, long-lasting cardiac ischaemia leads to death of the heart tissue, where the myocardial cells dies (Thygesen et al., 2012, 1590). Amongst the risk factors for ischaemia are ‘related left ventricular hypertrophy’, insulin resistance, aging, atherosclerosis, hyperlipidaemia, heart failure, diabetes and ‘systemic arterial hypertension’. When a person is aging, a number of biochemical effects are produced in the heart, which can result in the development of the ischaemic injury and interruption of the responses related to cardio-protective interventions. It is necessary to use the cardio-protection as a therapeutic approach. Coronary thrombosis, also termed acute occlusion, is associated with the arterial lumen and causes macrofocal or transmural necrosis, which occurs in the cardiac walls. There is also experience of acute narrowing of the artery opening, or coronary stenosis, resulting from thrombus and atherosclerotic plague; this causes macrofocal MI (Wahab et al., 2014, 56). The acute narrowing of a number of coronary arteries, or ‘constrictive coronary stenosis’, causes microinfarctions; this condition is known as ‘subendocardial MI’. The ischaemic mechanism leading to cellular injury Cellular injury occurs once the blood pressure becomes very high, representing restriction in the blood supply to all parts of the heart. The heart tissue is damaged through a process known as the ischaemic cascade, resulting to the release of the free radicals from the cell, as the blood vessels are associated with the damage of the heart tissue. In addition, once cardiac ischaemia occurs for a prolonged period, this leads to cell damage (Hung et al., 2013, 172). The reduction of the supply of coronary blood in the myocardium to a very low rate of flow leads to damage of the heart tissue, and thus a lack of sufficient support for the oxidative phosphorylation. The metabolic substrates or readmission of the oxygen is known as reperfusion, and this occurs due to heart failure related to the ischemic metabolites. Cell death or survival is determined by functional, structural and biochemical changes in the myocardium. Ultimately, reperfusion depends on the ischaemia, and local anaemia leads to congestion of a blood sample, which leads to chest pain, or angina pectoris. Atherosclerosis, or prolonged accumulation of plaques with a sufficient amount of cholesterol located in the coronary arteries, leads to inadequate blood flow. There are physiological and biochemical variations in the circulation of the blood in the heart’s arteries, which can be interrupted because of the heart capillaries being compressed. Oxidative stress leads to microvascular injury, as the capillaries become very permeable and there is increased diffusion of the arterioles in the tissues where fluid filtration occurs. Reduction of nitric oxide is followed by reperfusion, where the reperfusion injury is mitigated by the inflammatory response (Dutta et al., 2012, 327). The cellular protein is damaged by the oxygen introduced into the cells from the returned blood flow. Once brain failure occurs because of trauma or stroke, cardiac arrest is experienced. Ischaemia leads to heart failure and sometimes the formation of chronic wounds such as pressure sores. During the reperfusion process, inflammation is experienced, and a serious wound might be caused by the continuation of the process for more than one hour. Increased availability of oxygen, or oxygenation, leads to the conversion of molecular oxygen to hydroxyl or superoxide radicals, which are reactive. The uric acid which is produced by xanthine oxidase acts as a scavenger or a pro-oxidant like peroxynitrite. During reperfusion, production of nitric acid occurs, which interacts with the superoxide and works towards the production of peroxynitrite or the influential direct species. Cellular injury leads to hyperkalaemia because of the abnormal heart beat which occurs (Ranasinghe et al., 2015, 7). The sequential progression from reversible cell injury to cell death in myocardial infarction High exposure to reperfusion may lead to some complications, which can be dealt with therapeutically. Lack of treatment of damaged heart tissue leads to its death resulting from extended trauma, thrombosis and embolism of the atherosclerotic artery. The relative cycle of the ischaemic injury leads to some adaptive responses, which alter the heart’s ability to withstand cardio-protection or ischaemic post-conditioning. The cell injury might be irreversible, and this is likely to lead to apoptosis and necrosis, precipitated by the reperfusion (Wong et al., 2012, 740). The immediate oxygen species lead to cell damage and leakage of the cytochrome, causing the death of the cells, since the triggers of cell death such as calcium are not adequate. The victim experiences uncontrolled autophagy, resulting the death of the cells. The ischemic cascade is the process through which cells are damaged because lack of adequate oxygen leads to the accumulation of metabolic waste materials, leakage of the surrounding tissues, and lack of ability to keep the cell membranes in good condition. The pattern of tissue necrosis characteristic of myocardial infarction and the associated histological findings at autopsy Reperfusion injury is associated with development of arrhythmias, contractile dysfunction and tissue necrosis. The death of the heart muscle occurs due to damage to this muscle and the impaired circulation of the blood, where the heart muscle receives insufficient oxygen. Once there is renewal of the blood supply in the ischemic tissues, more damage, known as reperfusion injury, occurs; this is more critical than the initial ischaemia, which does not result in necrosis. The developed toxins inhibit some enzymes associated with the death of the cells at autopsy (Steg et al., 2012, 2578). The major biomarkers of myocardial infarction measured in laboratory investigations of suspected myocardial infarction MI is measured in the laboratory, where tests are conducted; these include the testing of cardiac enzymes, or biomarkers, which are measured during the presentation. The unstable angina guidelines are followed when measuring the enzymes (Oerlemans et al., 2012, 8). The level of troponins or contractile protein located in the serum is measured, and this is tested during the occurrence of the myocardial necrosis. In addition, the levels of creatine kinase (CK) are determined to identify the duration taken by the onset of the infarction. The relative blood count, lipid profile, chemistry profile and C-reactive protein (CRP), amongst other markers of inflammation, can also be tested. Troponin T and I and cardiac muscle components enter the bloodstream when there is myocardial injury. The troponins remain elevated for more than 2 weeks; thus, they are a recommended marker in the diagnosis of MI compared to lactase dehydrogenase, which is not specific to MI, but elevated during renal failure. There is also the total and MB fraction CK (Nabel & Braunwald, 2012, 57). The total CK is found in the skeletal muscle, and due to some non-cordial conditions, elevations occur. The fraction CK is categorised into creative kinase-MM, creative kinase-BB, and creative kinase-MB isoenzymes, which are unique to the cardiac muscle. Myoglobin is a form of protein that works towards binding oxygen during the muscle injury. BNP are other biomarkers in the heart failure. There is also the LD isoenzymes, which are applied in the diagnosis of the pulmonary system. Conclusion Myocardial infarction, also known as heart attack, occurs as a result of inadequate oxygen in the blood flow. The heart tissue restricts the supply of blood, leading to shortage of oxygen, which is required in the cellular membrane. The dysfunction of the heart tissue leads to ischaemia, which in turn results in damage to the cells, eventually leading to necrosis. People present with cardiac ischaemia because of the experience of chest pain, which occurs because of inadequate blood flow to the heart muscle. Prolonged cardiac ischaemia leads damage to the ischaemic tissue, or the cellular damage, and finally cell death. The reversible cell injury becomes severe and causes death of cells in MI. The identification of tissue necrosis requires laboratory testing of major biomarkers, such as troponins and CK. References Dutta, P., Courties, G., Wei, Y., Leuschner, F., Gorbatov, R., Robbins, C. S., ... & Nahrendorf, M. 2012. Myocardial infarction accelerates atherosclerosis. Nature, 487(7407), 325-329. Hung, J., Teng, T. H. K., Finn, J., Knuiman, M., Briffa, T., Stewart, S., ... & Hobbs, M. 2013. 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