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Previously, atherosclerosis seemed as an insipid collection of cholesterol in the artery made worse by the formation of smooth muscles, a view that has changed presently. The concept argued that endothelial denuding injury caused platelet aggregation and release of platelet factors. This, in turn, triggered a proliferation of smooth muscles in the interior walls of the arteries. The affected cells enhanced their matrix to trap lipoproteins resulting in the formation of plaque.
Latest investigations, however, expose the presence of immune cells and other mediators in the arterial matter. This indicates the role of inflammation in the development of atherosclerosis. Gene-targeting technology presented a possibility to test the roles of various factors when carrying out experiments on mice. The results showed a synergistic effect of both hypercholesterolemia and immune mechanisms (Libby et al, 2009).
The body utilizes the inflammatory mechanism to defend itself against infection. It also utilizes the mechanism in repairing damaged tissues. The immune system has two arms; innate immunity and adaptive immunity. Both forms contribute to the development of inflammatory response observed in atherosclerosis. The innate immune system has monocytes as the most prominent cellular component. The initialization stage involves the attachment of mononuclear phagocytes to the activated endothelial cells through leucocyte adhesion molecules. Cell migration into the Intima has facilitated protein mediators known as cytokines. The monocytes mature into macrophages and multiply.
The macrophages produce additional mediators triggering spontaneous reproduction. Upon initialization, monocyte entry does not cease but also proceeds in the established atherosclerotic lesion. Hyperlipidemia, a disease, has also shown a link to the dimorphism of monocytes in humans. The disease causes increased production of proinflammatory monocytes, cytokines and macrophage mediators. Recent evidence also highlights the possibility of mast cell involvement in the development of atherosclerosis (Libby et al, 2009).
In adaptive immunity, the phenomenon recognizes the role of dendritic cells. Upon an encounter with antigens, T lymphocytes initiate an immune reaction. The dendritic cells surround the atherosclerotic plaque to conduct antigens to the T lymphocytes. Renewed exposure of lymphocytes to antigen triggers inflammation. Various T cells exist. T Helper cells fall into two functional categories; Th1 and Th2.
Th1s response promotes inflammation through the secretion of cytokines. Some evidence links Th2 cells with the development of aneurism. Various independent experimental results indicate that humoral immunity diminishes atherosclerosis. Mice with hypercholesterolemia develop strong humoral response towards epitopes of oxidized Low-density Lipoproteins. This discovery has opened research into vaccination of oxidized LDL as a means of mitigating atherosclerosis (Libby et al, 2009).
Atherosclerosis involves the formation of plaques inside the artery walls because of fatty deposits. These significantly reduce blood flow posing a risk to the dependent organ. Consequently, the artery walls lose elasticity and become hard. The condition is responsible for high mortality rate among heart diseases. Usually, diagnosis follows symptoms or detection of complications. Methods of detection include blood tests, angiography, ultrasound, stress testing, electrocardiogram and X-ray CT. Angiography is the most common method. The method involves surgery into the arteries to find evidence and severity of stenosis.
Though commonly used, it is not an accurate technique and prompts using a catheter on the patient. Doppler sonography, which utilizes ultrasonic waves, is the method of choice in diagnosis. It holds the advantage of being nonintrusive. Doppler imaging allows evaluation of temporal and spatial flow characteristics in different areas of the arterial system. Doppler waveform exhibits significant changes in blood flow. The Doppler frequency shifts on the waveform measure the blood flow velocity and shows any form of disturbance. Results are presented on a sonogram where the horizontal axis represents time and the vertical axis, frequency. Research is underway to explore the possibility of using similarity-based weighting method for diagnosis of the disease from the artery Doppler signals (Polat et al, 2008).
Treatment for atherosclerosis involves administration of Statins. Statins is the name given to a group of Hydroxymethylglutaryl coenzyme A reductase inhibitors. These components, when applied, exhibit reduced incidence of cardiovascular happenings. Cardiovascular risk factors can be indicated by monitoring changes in the Carotid intima-media Thickness (CIMT). CIMT was previously applied to identify risk factors but recently as an independent factor for cardiovascular events.
Increase in CIMT points to increased risk of cardiovascular events. Satins not only slow down the progress but also recedes carotid atherosclerosis. The mode of action involves reduction of cholesterol as well as inhibition of atherogenic oxidized LDL. Two Statins, namely, lovastatin and simvastatin exhibited the ability to inhibit smooth muscle cell formation in both in-vivo and in-vitro trials (Bedi et al, 2010).
LDL-C has a direct relationship with risk of developing coronary heart disease. Statins reduce both the LDL-C and the risk of coronary heart disease. The period to experience the benefits of statin administration has remained vague due to inaccurate quantitative techniques such as coronary angiograms. Measurement of CIMT gives better results on atherosclerosis progression. Such a study by the Scandinavian Simvastatin Survival group suggested reduced heart events one to two years upon treatment initiation.
Another study by a group that seeks to justify the use of statins for primary prevention (JUPITER) showed results of reduced CIMT within twelve months. An independent group, Arterial Biology (ARBITER), in their investigation on the treatment effects of reducing Cholesterol, further validated the result. In the study, patients were put on pravastatin or atorvastatin, and their CIMT monitored. Significant difference appeared after 12 months (Bots et al, 2009).
References
Bedi, U., Singh, M., Singh, P., Bhuriya, R., Bahekar, A., Molnar, J., && Arora, R. (2010). Effects of statins on progression of carotid atherosclerosis as measured by carotid intimalmedial thickness: a meta-analysis of randomized controlled trials. Journal Of Cardiovascular Pharmacology & Therapeutics, 15(3), 268-273. Web.
Bots, M., Palmer, M., Dogan, S., Plantinga, Y., Raichlen, J., Evans, G., && Crouse, J. (2009). Intensive lipid lowering may reduce progression of carotid atherosclerosis within 12 months of treatment: the METEOR study. Journal Of Internal Medicine,265(6), 698-707. Web.
Libby, P., Ridker, P., & Hansson, G. (2009). Inflammation in atherosclerosis from pathophysiology to practice. Journal Of The American College Of Cardiology (JACC), 54(23), 2129-2138. Web.
Polat, K., Latifoglu, F., Kara, S., & Günes, S. (2008). Usage of a novel, similarity-based weighting method to diagnose atherosclerosis from carotid artery Doppler signals. Medical & Biological Engineering & Computing, 46(4), 353-362.
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