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 alonei. Worldwide it claims over 17.1 million lives a yearii.

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 CVDiii. 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.

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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.

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 the road to producing cholesterol. (See fig.2) Because HMG-COA is required to make further LDL molecules a lack of HMG-COA means less LDL molecules are produced. As most cholesterol is internally produced rather than coming from one’s diet, the blockage of the HMG-COA pathway results in a drop in blood cholesterol as the liver can no longer produce it. The liver cells respond to the lack of cholesterol within the liver and try to uses homeostatic methods to restore balance. With statins this results in LDL receptors (fig.1) which draw LDL molecules out the of the bloodstream and into cells

Therefore the LDL receptors on cells worker harder to compensate for the lack of available cholesterol. This reduces the blood cholesterol levels.

Statins have been shown in meta-analysis of observation studies to be highly effective in reducing initial LDL levels in the bloodiv. Some patients have shown a reduction in LDL levels of over 50% from their baselinev, but the average seems to be a 34% reduction in the first 3 months of taking statins with dietary controlvi. There is a clear statical link between taking statins and reducing the incidence of CHD. ‘10% reduction in plasma cholesterol resulted in a 25% drop in incidence of CHD of 5 years.vii’

However the link between statins and reducing the incidence of strokes is less clearviii. As most strokes actually take place because of anryusms and then hemmorging rather than for ischaemic (oxygen depravation) reasons, statins seem to have a less directly measurable effect. Statins have been shown to have a positive effect on ischaemic strokes- ‘a 19% proportional reduction.ix’

The most comphrensive meta-analysis of the efficacy of statins by the cholesterol trialist collaboration showed 34% reduction with dietary controlx.

The source does not make it clear how much of the average 34% was down to statins alone. Studies have shown that dietary control can have a large effect on LDL levels in the bloodxi even though the majority of Cholesterol is synthesised in the liver, rather than ingested. This is down to lipoprotein structure and the triggers for HMG-COA reductase- Triglycerides. HMG-COA reductase is triggered by high blood triglyceride levels and through the mevalante pathway (fig.2) it creates cholesterol. The cholesterol then binds with the triglycerides to form LDL. If one is on a low-fat diet, HMG-COA reductase isn’t triggered as often by high triglyceride levels, leading to a reduction in LDL cholesterol. This also explains why diabetics are up to 60% more at risk of CVD than non-diabeticsxii. I doubt the relablity and generalisability of these figures, as there was no way to corroborate them. To truly judge the efficacy of statins we need a clinical trial without dietary control factors which have been shown to be as effective in reducing cholesterol ‘as a low dose, first generation statinxiii’.

Cardio-vascular disease is an umbrella term covering many different but interrelated symptoms and causes. Taking Statins does reduce the risk of cardiovascular disease, but by how much depends on the form that an indivuals cardiovascular event takes. It would be more helpful, instead of prescribing statins for everyone to examine their risk factors and make an indivual treatment plan to reduce there personal risk of cardiovascular disease. If a patient has extremely high blood pressure, a family history of strokes and smokes 60 a day, they will have a high risk of CVD. But that doesn’t mean they have to have high cholesterol. They can still have a total cholesterol level of 160 mmol/l. This is perfectly possible and quite likely. An American study of patients who had died of CHD’s lipid levels revealed that 35% of their cholesterol levels were below 200 mmol/l, with the American national average being 220 mmol/l and 250 mmol/l being considered borderline risk for cardiovascular problemsxiv. (See figure 4.)

These figures suggest that 35% of people with CHD, would not have got the full benefit from statins as cholesterol problems was not their most predominate risk factor. They would have benefitted more from anti-cogulants, blood thinners and ACE inhibitors to lower blood pressure and vasoconstriction rather than statins as their blood cholesterol level is normal and well below the national average. This just goes to show that blanket treatment for an individual palliative disease will not be as successful as targeted treatment. And for a disease that affects 1 in 3 Britiansxv, I believe we need targeted treatment. The money that would be spent on promoting statins to patients and on the drugs themselves would be better spent speeding up the implementation of the governments CVD screening program which is rolling out over the next ten yearsxvi. The program is designed to catch sighs of CVD early and help people make lifestyle changes to reduce their risk and therefore cut the incidence rate.

But some disagree with this plan, believing there are more cost effective ways to tackle CVD. Wald and Law professors of preventative medicine at St. Barts proposed to tackle the high incidence rate of CVD by broad spectrum prophylaxis. They created the polypill- a pill designed to cover many of the preventable of CVD causes and they aim to target the pill to as much of the at risk population as possiblexvii. The polypill contains a Statin, Ace inhibitor, diuretic, beta blocker, aspirin and folic acid neatly covering the main preventable causes of CVD.

Wald and Law are confident that the Polypill would sigfinacly reduces rates of CVD. ‘The Polypill strategy, based on a single daily pill containing six components as specified, would prevent 88% of heart attacks and 80% of strokes.xviii’ If everyone should be taking a pill to reduce cardiovascular disease without employing any lifestyle change factors, it should be the Polypill. Unfortunately, the polypill has not been shown to cut mortality rates from CVDxix, which lifestyle changes such as daily aerobic exercise have been shown to reduce the mortality rate for myocardial infarction by 25%xx. However, the polypill is still in clinical trails.

If the government did decide to reduce the incidence rate of CVD by give everyone statins on the NHS they would have to be free. There is a clear correlation between socio-economic class and incidence levels of CVDxxi, and those in poor economic standing are not going to pay the prescription charge of 7.20 each month for a drug which might reduce their risk of CVD. So the project would be missing those to really need it. With the screening program, they would be given personalised advice on how to reduce their own risk- some of which is for free like aerobic exercise and cutting down on alcohol and smoking.

Making statins free on the NHS would be very expensive and cost the tax payer a lot of money. Realiscally, the money would be better spent on a public health education program or advertisement scheme to inform the public about the danger of CVD, its preventable risk factors and about the new screening scheme. It is estimated that 60% of the reduction in CVD mortality since 1980 is due to improved access to carexxii. This figure is in the Britsh journal of cardiac nursing, I believe it is accurate as the source is reliable. Spending the money on the screening program and public health education would improve access and understanding about health issues and save more lives.

It is clear however, that lifestyle change should always be the first port of call in the prophylaxis of CVD. Cessation of smoking, a lifestyle change which can easily be tackled in primary care can reduce one’s risk of CVD by up to 70%xxiii, far more than 25% taking statins offersxxiv and has other health and financial benefits as well. Doing daily aerobic exercise can reduce your risk of CVD by up to 54%xxv , will naturally lower your blood cholesterol levelsxxvi and help prevent other health problems like obesity and diabetes. Changing your diet can affect your blood cholesterol level as much as ‘a low dosage statinxxvii’ and can influence other risk factors for CVD like insulin dependency and salt levels.

In conclusion, lifestyle changes are highly effective at controlling cholesterol levels and reducing your risk of cardiovascular disease. Statins are highly effective on CHD, but haven’t been successfully linked to reducing stroke ratesxxviii. Satins only control cholesterol levels, but lifestyle changes can influence many of the changeable risk factor for CVD and make you on the whole healthier. If we were all on statins as Mike Rich says ‘There is a danger that lifestyle factors could be overlooked in favour of popping a pillxxix’ and with a disease that affects 1 in 3 peoplexxx that is a danger we cannot afford.

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