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Mechanisms Involved in the Development of Atherosclerosis - Essay Example

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The author of the "Mechanisms Involved in the Development of Atherosclerosis" paper discusses the laboratory development of cardiac markers used for investigating patients with suspected AMI. The study further extrapolates the development of atherosclerosis. …
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Mechanisms Involved in the Development of Atherosclerosis
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?Discuss the Laboratory Development of Cardiac Markers Used In the Investigations of Patients with Suspected Acute Myocardial Infarction Table of Contents Table of Contents 2 Introduction 3 Mechanisms Involved In the Development of Atherosclerosis 3 Effectiveness of Protein & Enzyme Markers In Terms Of Sensitivity and Specificity in Identifying Myocardial Infarction 5 Identification of New Cardiac Markers for Heart Disease 7 Conclusion 8 References 9 Introduction In the modern day scenario, chest pain and other related symptoms might signify ‘Acute Myocardial Infraction’ (AMI). This syndrome is highly associated with heart attack and atherosclerosis, a disease which has a negative impact on blood cell. Any delays in terms of diagnosis of AMI as well as inaccurate threat identification might result in mortality. Towards diagnosing AMI, cardiac markers are considered as a vital facet (Berliner & et. al., 2013). Focusing on the above aspects, the essay discusses the laboratory development of cardiac markers used for investigating patients with suspected AMI. The study further extrapolates the development of atherosclerosis. Apart from this, the essay also explains the effectiveness of protein as well as enzyme markers with respect to sensitivity along with specificity which is used to identify myocardial infarction. Mechanisms Involved In the Development of Atherosclerosis Clinical event that emerges from the atherosclerosis is directly related with the oxidation of the lipids in ‘Low-density Lipoprotein’ (LDL). LDLs are considered as a key part of progression of atherosclerosis. On the basis of the study of Rovere & et. al. (2013), it can be observed that LDLs are confined in the extracellular matrix of the sub-endothelial space which generates ‘fatty streak’, the first tissue that triggers the development of atherosclerosis. Traditionally, atherosclerosis was thought to be a degenerative disease, resulting from aging. However, with the advancement in medical science, it has been discovered that atherosclerosis is a chronic inflammatory condition which is further converted into acute clinical occurrence by induction of plaque rupture, a collection of lipids. Plague rapture leads to thrombosis, which plays a critical role in the creation of fatty streak, hence atherosclerosis (Berliner & et. al., 2013). The basic mechanism that induces the sequence of events followed in atherosclerosis is represented through the following pictorial presentation: Fig 1: Model Showing the Sequence of Events in Atherosclerosis Source: (Berliner & et. al., 2013) The first stage of atherosclerosis is atherogenesis process. At first, the lipoprotein is moved into the blood vessels. In the second phase, oxidation of lipoprotein starts. During this phase, secrete oxidative product seeds the LDL that is trapped within the sub-endothelial space (Singh & et. al., 2002). Moreover, the trapped LDL goes through oxidative alteration that arises from two phases. The first phase arises before the requirement of monocytes, which results in the oxidation of lipids in LDL with a very little change in Apolipoprotein B (apoB), a primary component of lipoprotein, whereas, the second phase starts with the recruitment of monocytes to the lesion, which has an impact on the creation of blood cell. Lesion contributes to the enormous oxidative volume. Ultimately, this increased oxidative pressure helps to generate atherosclerosis (Razzouk & et. al., 2012). Effectiveness of Protein & Enzyme Markers In Terms Of Sensitivity and Specificity in Identifying Myocardial Infarction Myocardial infraction represents the terminal event within a spectrum of disease named, ‘Acute Coronary Syndromes’ (ACS) and it is also caused by the myocardial ischemia. The expansion of myocardial infraction depends on the presence of collateral blood flow within human body (Rosenfeld, 1996). Diagnosis of myocardial ischemia requires unequivocal Electrocardiography (ECG) changes that remain stable with critical myocardial ischemia. Myocardial infraction further requires the elevated serum of the cardiac enzymes (Kimmenade & Januzzi, 2012). The graphical representation of pathophysiology of acute coronary syndromes has been represented below: Fig: 2: Pathophysiology of Acute Coronary Syndromes & Biomarker Release into the Circulation Source: (Govender, n.d.) CK-MB enzyme is considered as a vital biochemical indicator for identifying the AMI. It has been further revealed that troponins are useful in risk identification of patients suffering from AMI. Troponins represent the regulatory proteins found within skeletal as well as the cardiac muscles. It is sensitive to the myocardial damage which triggers AMI (Subbarao & et. al., 2013). Increased concentrations of proteins within acute phase play a vital role in the identification of patients having unstable coronary plaques. The increased proteins also further represent the plaque disruption that causes the release of cytokines, which is considered as a crucial indicator of AMI (Christenson & Azzay, 2013). Identification of New Cardiac Markers for Heart Disease Biomarkers represent an important part for the evaluation and the identification of patients with heart disease (Apple & et. al., 2012). Medical viewpoint related to biochemical markers has progressed throughout the period of 1980s to 1990s. In the past, non-specific markers were used for identifying heart disease. Subsequently, with the improvement in medical science, new cardiac markers have become available for recognising heart disease (Lewandrowski & et. al., 2002). According to Collinson & et. al., (2013), the foremost purpose of heart is to circulate the extracellular fluid. This further facilitates the transfer of oxygen and other substances from the tissues. Any disturbances within the cardiac functions result in cellular hypoxia in the heart cells. In this context, it is worth mentioning that the conventional and the most commonly used marker represents intracellular proteins; which are considered as one of the key indicators of cardiomyocyte necrosis, a key contributor towards heart disease. Furthermore, natriuretic peptides also are considered as one of the new cardiac markers and they can yield considerable information regarding ongoing functional deterioration of pump activity related to the heart (Bradorff & et. al., 2013; Hildebrandt & et. al., 2010). Conclusion Atherosclerosis has been determined to be a complex disease that signifies the principal constituent of heart attack. Furthermore, it represents an inflammatory process that continues through a sequence of pathological events, involving the cardiovascular system as well as the immune system. From the essay, it can be observed that there are several biomarkers which are used in order to indicate AMI. These markers have evolved over time with the improvement of medical science and can provide considerable information regarding heart functions. Furthermore, it has also been observed that biomarkers are highly associated with the diagnosis of atherosclerosis. Biomarkers help to recognise the biological condition of patients with respect to heart diseases. As a result, they act as an indicator for any kind of abnormal changes in human body with regard to the condition of heart. References Apple, F. S. & et. al., 2012. Analytical Characteristics of High-Sensitivity Cardiac Troponin Assays. IFCC Task Force on Clinical Applications of Cardiac Biomarkers, Vol. 58, Iss. 1, pp. 54-61. Berliner, J. A. & et. al., 2013. Atherosclerosis: Basic Mechanisms Oxidation, Inflammation, and Genetics. Articles. [Online] Available at: http://circ.ahajournals.org/content/91/9/2488.full#sec-2 [Accessed June 27, 2013]. Bradorff, M.M. & et. al., 2013. Improved Troponin T ELISA Specific For Cardiac Troponin T Isoform: Assay Development And Analytical And Clinical Validation. Clinical Chemistry. [Online] Available at: http://www.clinchem.org/content/43/3/458.full. [Accessed June 27, 2013]. Christenson, R. H. & Azzay, M. E., 2013. Biochemical Markers of the Acute Coronary Syndromes. Clinical Chemistry. [Online] Available at: http://www.clinchem.org/content/44/8/1855.full. [Accessed June 27, 2013]. Collinson, P. O. & et. al., 2013. Randomised Assessment of Treatment using Panel Assay of Cardiac markers--Contemporary Biomarker Evaluation (RATPAC CBE). Health Technology Assess, Vol. 7, No. 15. Govender, L. A., No Date. Biochemical Cardiac Markers in Acute Coronary Syndrome. Medicine. [Online] Available at: http://www.kznhealth.gov.za/medicine/coronary1.pdf [Accessed June 27, 2013]. Hildebrandt & et. al., 2010. Age-dependent Values Of N-Terminal Pro-B-Type Natriuretic Peptide Are Superior To A Single Cut-Point For Ruling Out Suspected Systolic Dysfunction In Primary Care. European Heart Journal, Vol. 31, No. 15, pp. 1881-1889. Kimmenade, R. R. & Januzzi, J. L., 2012. Emerging Biomarkers in Heart Failure. Clin Chem, Vol. 58, No. 1, pp. 127-138. Lewandrowski, K. & et. al., 2002. Cardiac Markers for Myocardial Infarction: A Brief Review. American Journal of Clinical Pathology, pp. 93-99. Razzouk, L. & et. al., 2012. Novel Biomarkers for Risk Stratification and Identification of Life-Threatening Cardiovascular Disease: Troponin and Beyond. Abstract. [Online] Available at: http://www.ncbi.nlm.nih.gov/pubmed/22708908. [Accessed June 27, 2013]. Rosenfeld, M. E., 1996. Cellular Mechanisms in the Development of Atherosclerosis. Abstract. [Online] Available at: http://www.ncbi.nlm.nih.gov/pubmed/8964183. [Accessed June 27, 2013] Rovere, M. T. L. & et. al., 2013. Baroreflex Sensitivity and Heart Rate Variability in the Identification of Patients at Risk for Life-Threatening Arrhythmias. Clinical Investigation and Reports. [Online] Available at: http://circ.ahajournals.org/content/103/16/2072.long. [Accessed June 27, 2013]. Singh, R. B. & et. al., 2002. Pathogenesis of Atherosclerosis: A Multifactorial Process. Experimental & Clinical Cardiology, Vol. 7, Iss. 1, pp. 40-53. Subbarao, K. & et. al., 2013. Atherosclerosis and Lipoproteins. Atherosclerosis, Thrombosis and Vascular Biology. [Online] Available at: http://atvb.ahajournals.org/content/24/2/369.long. [Accessed June 27, 2013]. Read More
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