Free Essay On Atherosclerosis

Introduction

Atherosclerosis is a continuum of lesions caused by the deposits of cholesterol in the arterial wall, which is favored by the circulating oxidized low density lipoprotein (LDL) cholesterol (Adelmann, 2011). The genetic predisposition to atherosclerosis is associated with specific genes or certain gene variants. The platelet glycoprotein IIIa is viewed to be a prothrombotic predisposing factor among those with a family history of premature myocardial infarction. This genetic predisposition to atherosclerosis appears to interact with a cholesterol level (Shoenfeld, Harats and Wick, 2001). Genetic disorders involving a low, high density lipoprotein (HDL) cholesterol are also associated with an increased risk for atherosclerosis. The risk is also identified among first degree relatives with low HDL cholesterol and low Apolipoprotein A-1. This genetic abnormality is viewed as a result of DNA inversion (Indolfi, 2002).

Pathophysiology on the cellular level

The tissue involvement in atherosclerosis consists of plaque formation that occludes the lumen of the muscular artery. Ischemic necrosis occurs as a result of the infarction of the tissue being supplied by the atherosclerotic artery. As the plaques continue to grow, the impingement of the lumen occurs, with a resulting decrease in the supply of blood to the tissue. Organ atrophy subsequently occurs as a result of chronic ischemia to the affected tissue (Rubin and Strayer, 2008). The thrombotic response is also known as influenced by varying conditions, one of which it the thrombogenicity of the arterial wall, including blood components and the lipid pool interaction. The tissue factor (TF) is viewed as the primary cofactor of cellular etiology that influences the coagulation pathway and is believed to have a role in the determination of plaque thombogenicity (Tremoli, Camera, Toschi and Colli, 1999).

Pathophysiology on the molecular level

The molecular markers of atherosclerosis risks involve the accumulation of lipid-containing lipoproteins that begin to accumulate to the intima of the arterial walls. Sequential events occur involving the activation of the inflammatory response, a process that also initiates the recruitment of the leukocytes, including the release of the growth factors that produce cellular migration and proliferation (Mannarino and Pirro, 2008). Among the increasing molecular risks for atherosclerosis is the presence of the lipid markers involving hyperlipidemia and hypercholesteremia. The inflammatory response is indicated by the presence of inflammatory markers, such as the soluble CD40 ligand, C-reactive protein and interleukin 18 as among many others.

Pathophysiology of biochemicals

The cellular biomarkers in atherosclerosis involve the activities of the myeloperoxidase (MPO) that can help predict the risks of coronary artery disease. The MPO is the protein produced by the polymorphonuclear neutrophils and macrophages that is released during the inflammatory process. The MPO is usually produced by the inflammatory cells that are found in the ruptured plaques, thus is considered to be a marker of the cellular plaques (Nicholls, 2014). The plasma MPO level usually increases in coronary heart disease and is usually associated with the risk of increased atherosclerotic events. The circulating blood cellular markers like the MPO are usually measured by MRI for diagnostic purpose and identifying risks to atherosclerosis.
Lindner (1985) provides that the biochemical findings in atherosclerosis consisting of the metabolic disturbances together with the smooth muscle cell functions and proteoglycans are indicative of the early development and progression of atherosclerotic changes. Thus, the metabolic disturbances occurring during the early formation of the atherosclerotic lesions can indicate whether the condition progresses or relapses. The decrease or increase in the catabolic and anabolic process can indicate regressive atherosclerotic lesions. It has been hypothesized that the metabolic insufficiency of the arterial wall can perpetuate the formation of early atherosclerotic lesions and may help indicate the progression of atherosclerosis.

Diagnosis and Treatment

Diagnosis of atherosclerosis begins with a complete health history of the patient, primarily focusing on risk factors and symptoms of ischemia (McCance & Huether). Furthermore, the health care provider will complete a physical examination to inspect blood flow to the tissues. The provider will also request blood work to be drawn to measure lipids, blood glucose, and high sensitivity CRP. If the provider feels that vessels and tissues have been occluded and affected by plaque build up, x-ray films, electrocardiography, ultrasonography, CT, MRI, and angiography tests will be ordered to further examine the affected vessels (McCance & Huether).
Treatment begins at the presymptomatic stages, if possible (McCance & Huether). It is better to catch an illness in its beginning stage, before it poses a large threat to the body’s tissues. In this beginning stage, atherosclerosis is treated with drugs that aim to stabilize and reverse the plaques before they rupture. if the atherosclerosis cannot be halted at this stage, the occlusion will continue to grow and obstruct blood flow to tissues. At this stage, a patient will require interventions, such as removing the plaque or opening the vessel with stents. The patient should also be advised to continue to change his or her lifestyle to prevent further complications. If a myocardial infarction ensues because the previous interventions were not helpful or the disease had gone unsuspected, patients may undergo surgical treatments such as bypass grafts (McCance & Huether).

References

Adelmann, G.A. 2011. Cardiology Essentials In Clinical Practice. London:Springer-Verlag.
Indolfi, G. 2002. Genetic factors in atherosclerosis: Status and perspectives. European Heart
Lindner J. 1985. New Morphological and Biochemical Aspects of Atherosclerosis. Pathology,
Research and Practice. 180(4): 329-35.
Mannarino, E. and Pirro, M. 2008. Molecular Biology of Atherosclerosis. Clinical Cases in
Mineral and Bone Metabolism. 5(1): 57–62.
McCance, K.L., Huether, S.E. (2014) Pathophysiology: The Biologic Basis for Disease in
Adults and Children, 7th edn., St. Louis, Missouri: Elsevier.
Nicholls, S.J. 2014. Imaging Coronary Atherosclerosis. London: Springer Science.
Rubin, R. and Strayer, D.S. 2008. Rubin’s Pathology.Clinicopathologic Foundations of
Medicine. Philadelphia: Lippincott Williams & Wilkins.
Shoenfeld, Y., Harats, D. and Wick, G. 2001. Atherosclerosis and Autoimmunity. Amsterdam,
Netherlands: Elsevier.
Tremoli, E., Camera, M., Toschi, V. and Colli, S. 1999. Tissue Factor in Atherosclerosis.
Atherosclerosis. 144(2):273-83.