Should everyone be to taking statins to reduce the risk of cardiovascular disease

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 Should everyone be to taking statins to reduce the risk of cardiovascular disease?

Cardiovascular disease is one of the biggest killers of the modern world.  Approximately 70,000 people die from cardiovascular disease or its complications every year in the UK alone.  Worldwide it claims over 17.1 million lives a year.

Although CVD is a multi-factorial disease with many preventable and non-preventable causes, studies have shown that there is a high correlation between high LDL levels and the incidence of CVD. Statins are a group of drugs designed by the pharmatsuitical industry to reduce levels of LDL in one’s blood.

Low density lipoproteins are protein molecules made up of both triglycerides and cholesterol. Cholesterol is a sterol which means in it insoluble in water. In order for it to pass through the blood stream and diffuse through cell membranes it needs to be attached to a soluble chain molecule such as a triglyceride.

Most cardio-vascular events start with the formation of an atheroma, which is an acculmation of fatty deposits in the artery walls between the inside of the artery (lumen) and the elastic muscle layer. An atheroma can lead to the narrow of the lumen in a process called stenosis which increases the patient’s blood pressure. The blood constantly hitting the atheroma as it juts out into the lumen can cause it to harden.

Often this leads to a disease called atherosclerosis where a calcium plaque has formed on the atheroma making in larger and hard. Sometimes the plaque can grow large enough to completely block the artery, preventing blood flow. This prevents the organ from receiving any oxygen, and it become unable to respire. The lack of oxygen to the heart muscle (apoxcia) can lead to myocardial infarction- muscle death commonly known as a heart attack or if takes place in the brain, a stroke. Atherosclerosis can also cause subtler symptoms such as angina and increased hypertension.

An atheroma begins to form when the endothelium or the inner lining of the artery is ruptured. This usually happens as a result of hypertension. This leaves the elastic muscle layer of the artery wall free to contact with the blood which causes it to become inflamed. Macrophages, specialist white blood cells concerned with protecting your body immune system invade the ruptured wall looking for the bacteria which have caused the inflammation. (see fig.3)

 Cholesterol is essential in the process of forming an atheroma. LDL molecules which contain cholesterol are absorbed by the macrophages in the artery wall causing them to swell and form buffer or foam cells.  The macrophages have indiscriminate ‘scavenger’ receptor sites, which they use to collect large amounts of LDLs, which they then use to form a large amount of cytoplasmic membranes.

Naturally, the more LDL cholesterol there is in one’s blood, the easier it is for Macrophages to form foam cells. These foam cells become embedded in the arterial wall, greatly weakening the elasticity of the artery. This vasoconstriction results in higher blood pressure and increases the risk of another atheroma forming.

Once an atheroma has formed calcium, fibres and muscle from the blood stream begins to build up on the endothelium causing it to protrude further into the lumen. This then forms a plaque which hardens the outer edge of the atheroma. Because of the increased blood pressure around the site of atheroscleorisis, the fibrous cap on the atheroma can rupture ripping the endothelium in the process. As a result platelets in the blood gather at the site of the tear, forming a blood clot or a thrombosis. A thrombus can often block the entire artery causing muscle death or they can break free of the artery walls and travel through the blood stream.

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Therefore by reducing one’s cholesterol levels, one can reduce the size and incidence of atheromas, and therefore atheroslcerosis. Without high levels of atheroslcerosis, the fatal endgames of cardiovascular disease can be reduced. Satins were developed with this goal in mind.

Statins work by competitively inhibiting production of the HMG-COA reductase enzyme in the liver. The statins and the HMG-COA rediutase molecule are very similar at a molecular level. This allows the statin to take the place HMG-COA reductase in the reaction and significantly reduce the rate in which it produces Mevalonic acid which is the next molecule on ...

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