Heart Disease: a Gradual Accumulation of Fatty Deposits in Coronary Arteries Or Atherosclerosis

Our modern society is facing a worldwide phenomenon in terms of the levels of inactivity and the effects this phenomenon can cause in terms of the overall health level. There is an indisputable need for the levels of awareness on this matter to increase as it is directly correlated to the increased level of people suffering from associated non-communicable diseases such as heart disease, diabetes, chronic respiratory disease, obesity, and stroke, and cancer, attributed to physical inactivity.

One of the most common diseases plaguing our world at the moment is that of heart disease. The root cause of coronary heart disease (also known as coronary artery disease) occurs where a gradual accumulation of fatty deposits, called 'plaque' or 'atheroma' narrows the coronary arteries. The coronary arteries are the blood vessels which provide blood for the heart. This is where atherosclerosis comes to exist as it refers to this accumulation of fats, cholesterol, and other substances in and on the walls of the artery thus limiting blood flow. The plaque can burst, which causes a blood clot. While atherosclerosis is mostly considered an issue of the heart, it can damage arteries in the body anywhere.

Given that this is a worldwide and widespread phenomenon thorough research is constantly being conducted in order to identify some of the aspects that aid in the development of atherosclerosis in order to further our knowledge in what precautionary measures to take to avoid it and even how to combat patients with preexisting atherosclerosis. To do so we have to examine this disease down to every contributing factor to its development and try to analyze and evaluate how each one contributes to the worsening of this disease. By doing so we can make our approach in combatting the disease more specified to different contributing factors

Given that research on atherosclerosis and its contributing factors and underlying causes is constantly being conducted, studies report that one of the contributing factors of the development and progression of atherosclerosis is the role of oxidized LDL or low-density lipoprotein which is a molecule that is comprised of lipid (fat) and protein. The reason that lipoproteins seem to be a contributing factor to the development and progression of atherosclerosis is due to the fact they are the transportation system of lipids (fat) in the blood. Furthermore and reinforcing this notion is the fact that Low-density lipoprotein is also the transportation system of cholesterol taken from the liver to blood tissue. LDL is often called the 'bad' cholesterol because a high LDL level leads to a buildup of cholesterol in your arteries. Studies have identified that oxidized low-density lipoprotein can act as a harmful type of cholesterol. Oxidized low-density lipoprotein in the body can be produced when normal LDL cholesterol is damaged by chemical interactions with free radicals. Free radicals are oxygen-containing molecules with an uneven number of electrons making them very susceptible to reacting with other molecules. The combination of some inflammatory responses and these free radicals can cause stiffening of the arteries meaning atherosclerosis.

Research is constantly being conducted on the role of oxidized low-density lipoproteins on atherosclerosis and thus we can gain a great insight of how the whole procedure takes place. Oxidized LDL moves rapidly into arterial walls and engorges them with cholesterol which at a later stage converts into plaque thus blocking the arteries.

In order to understand how oxidized LDL can be attributed as one of the major factors of atherosclerosis, we have to take a look of how exactly it is conducted. Studies dove into this and found that LDLs modification is undertaken by endothelial cells thus the transformation entailing an oxidation process seems to be interiorized and slowly built up avidly by macrophages, leading to the formation of foam cells, and even though it is important to be said that these cells could also be produced from macrophages internalizing native LDLs from the medium through micro pinocytosis, or even by the accumulation of aggregated LDLs or LDL immune complexes. Furthermore, it would appear that studies conducted reported Oxidized LDLs possessing a wide variety of biological properties considered to promote atherosclerosis. One of which is the fact that Oxidized LDLs promote the development of collagen by smooth muscle cells thus leading to the lining of the atherosclerotic plaque in the fibrous cap and the expansion of the lesion scale. Having said that it is important to note that oxidized LDLs could also have an impact in the promotion of fibrous cap thinning, and thus smooth muscle cell apoptosis. In doing so these facts promote the occurrence of vulnerable plaques more susceptible to atherosclerosis.

Furthermore, apoptosis of vascular cells is promoted by the cytotoxicity of oxidized LDL towards vascular cells with the subsequent release in the subendothelial space of lipids and lysosomal enzymes thus speeding up the development of the atherosclerotic plaque. Moreover, it would appear that Oxidized LDLs are essential for the production of macrophages while at the same time hindering their regress from the arterial wall thus making oxidized LDL is key for the activation and development of monocytes as well as macrophages within the arterial wall. Finally, another study reported that it would appear that oxidized LDL may have an integral role in vasoconstriction by inhibiting nitric oxide and increasing endothelin production.

It would appear through the conduction of several types of research on this topic that antioxidants have been identified as having an integral role of the prevention of oxidation of LDL. It would appear that in doing so antioxidants seem to hinder the progress and development of atherosclerosis. A study reported that antioxidants tend to decrease atherosclerotic lesion formation and even decrease LDL oxidation. Antioxidants decrease Oxidative stress which is a result of the imbalance between the heavy accumulation of reactive oxygen species and limited antioxidant defenses. Two of the key regulators of vascular health are endothelium and nitric oxide. In order to examine the effects of antioxidants in this regard, we have to look at where antioxidants are taken from on day to day basis. Antioxidants are found both within our diet as well is in the form of supplements and individual ones can have different effects. It would appear that a high intake of Vitamin E which seems to lower the frequency of clinical events as well as mortality when it comes to heart disease. 

While probucol which is a supplement antioxidant though debatable has shown positive results when it comes to atherosclerosis as it would appear that some studies have claimed that it can inhibit the blockage of arteries and furthermore though not as well supported in research can reverse the effect of hardening of the arteries. It would appear that there is a high debate when it comes to the effect of carotenoids to atherosclerosis with one study reporting that a large amount of carotenoids may be protective against early atherosclerosis while others stating there is no effect in terms of atherosclerosis. Finally, we have flavonoids which have been shown to decrease oxidative stress and thus prevention of cardiovascular disease. They are able to modulate metabolism-related genes, protect of stress, drug-metabolizing enzymes, and detoxify and transport proteins. Having said that it would appear that its overall role is beneficial in overcoming adverse effects of cardiovascular risk factors and in preventing atherosclerosis. Overall it would appear that antioxidants can have an effect on the oxidization of LDL and thus potentially the progress and development of atherosclerosis while it is important to note that more research is to be conducted in order to reach a thorough conclusive verdict when it comes to their overall effect on atherosclerosis.

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