Most Common Cause Of Premature Death Biology Essay


Heart Disease, by itself, is the UK's biggest killer and the most common cause of premature death in the UK (death before the age of 75) ( 2008). One in five men and one in seven women die from heart disease which accounts for around 94,000 deaths in the UK each year ( 2.5 million people are living with heart disease in the UK.

In 1999 the government produced a "White Paper" known as "Saving Lives, Our Healthier Nation" (1999) which set out a Government action plan for tackling poor health by improving the health of everyone in the UK. It discusses individuals and health, tackling the wider causes of ill-health within communities. 'Saving lives' deals with the specific issues of Coronary Heart Disease (CHD). It put in place targets for government initiatives set to improve knowledge about healthy living and improvements in diagnosis and treatment of CHD. It sets tough but attainable targets in priority areas. It is now however over 10 years since this document was produced and there has been no comparison of statistics of death due to CHD Between 1990- 1999 and 2000-2009. From this government report it set a target to reduce the death rate from coronary heart disease and stroke and related diseases in people less than 75 years by at least two fifths by 2010, saving up to 200,000 lives in total.

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Reduction in CHD can be brought about by individuals reducing the risk factors at which they expose themselves too. Although People can hold a genetic predisposition for CHD, Can changing environmental and physical factors vastly reduce the chances of a person experiencing a myocardial infarction (MI)?

Coronary arteries supply the heart with an oxygen rich blood supply straight from the heart. Within the aorta, Superior to the aortic valve is two vessels known as the Right and left coronary arteries. The right coronary artery branches into off into the Right marginal artery and the Posterior descending artery which provides blood supply to the right atrium, right ventricle and the bottom portion of both ventricles and back of the septum. The main portion of the right coronary artery provides blood to the right side of the heart, which pumps blood to the lungs. The rest of the right coronary artery and its main branch, the posterior descending artery, together with the branches of the circumflex artery, run across the surface of the heart's underside, supplying the bottom portion of the left ventricle and back of the septum ( (See figure 1). The Left main stem of the left coronary arteries branches off into the Left Anterior Descending Artery (LAD) and the Circumflex artery. The Circumflex artery supplies

Figure 1: Shows the blood supply of the left and right coronary arteries. Accessed on 20/02/2010blood to the left atrium, side and back of the left ventricle which is the main pumping chamber of the heart creating the highest pressures. The Left Anterior Descending artery (LAD), supplies the front and bottom of the left ventricle and the front of the septum. Deoxygenated blood is then carried through a series of veins within the myocardium and deposited via the coronary sinus into the right atrium.

Over time these arteries can become blocked reducing the flow of oxygen and nutrient rich blood to the muscle cells. This happens through a complex process which causes a disease is known as Atherosclerosis. Damage can occur at any point within an artery due to a number of reasons. At these lesion sites. This causes Functional Impairment of the arterial endothelium resulting in either increased lipid influx or initiation of an inflammatory vessel wall response (Braunwald. 2001). The damage to the endothelium initiates white blood cell propagation to the cell wall. The white blood cells roll along the wall of the artery following a chemical signal, once they have entered the lesion site they then change their properties and become Macrophages.

Cholesterol which travels within the blood stream, comes in two forms, Low density Lipoprotein, (LDL) which is known as bad cholesterol and High density Lipoprotein (HDL) which is known as the good cholesterol as it is believed to help remove the LDL from the system. LDL is more likely to enter the lesion site of an artery when damage occurs (Braunwald 2005). Within the lesion site the macrophage start to engulf the LDL within the endothelium, the macrophages can absorb vast numbers of LDL molecules but due to this they start to modify into foam cells which are much larger and denser than the original Macrophage. Due to the nature of the foam cell they become trapped within the endothelium which causes the inflammation of the lumen to become permanent. This puts the area of the artery at higher risk of further damage occurring due to the endothelial wall no longer being smooth, thus further reduction in blood flow to the heart will occur (see figure 2)

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(Figure 2) shows the foam cells causing reduction of Lumen size. ( accessed on 23/02/2010)

Over time the reduction of blood flow will become greater. As the lesion site grows the wall of the artery will also start to become thinner. This then leaves the wall of the artery of the wall at high risk of rupture. If this happens then platelet aggregation can form around the lesion site which further reduces size of the lumen and if severe enough can cause complete occlusion of the artery, causing the patient to experience a Myocardial Infarction (heart attack) or if the clot breaks off and goes to the brain, a stroke.

Cholesterol is a vital ingredient with in the body to maintain complete homeostasis. Cholesterol is a combination of Alcohol, steroid and Lipid which is found in the cell membrane of all Animals ( The lipoprotein transport system has two major roles, to transport triglycerides from the intestine and the liver to the sites where it is needed and the transport of cholesterol to peripheral tissue for membrane synthesis and for steroid hormone production, or it is taken to the liver for bile acid synthesis (Braunwald. 2005). It is important that a certain amount of cholesterol is maintained, although maintaining the correct levels of the two different types of cholesterol is even more important. LDL (Low Density Lipoprotein) is known as the bad cholesterol. This form of Lipoprotein is transported from the liver to other parts of the body to aid production of hormones whilst HDL (High density Lipoprotein) known as the good cholesterol, transport cholesterol from the rest of the body to the liver so that it can be excreted.

In a healthy person high levels of HDL will be present along with low levels of LDL so that hormone production still takes place and high numbers of HDL are present to carry the unused LDL to be expelled from the body. If these levels are reversed and there is a high level of LDL and low level of HDL then high numbers of LDL travel around the blood system and can bond to the walls of the coronary arteries. This forms a fatty streak along the artery which in turn can build up causing the artery to occlude. This occlusion site will also be at high risk of rupture as this area of artery will no longer be smooth. This can cause rupture which in turn causes further occlusion of the artery eventually ending in complete occlusion.

Several main risk factors have been identified as putting a person at higher risk of acquiring CHD. These risk factors can be put into two groups, these are Modifiable and fixed (Braunwald. 2001) fixed risk factors are, Age, Gender and Family history (Genetic predisposition) and Modifiable are, Raised Blood pressure, Smoking, Obesity, Raised cholesterol levels, Physical inactivity and Diabetes mellitus.

As a person gets older they become much higher risk of developing CHD. Although it is said that women experience their first event of heart disease around 10 years later than men (Anand et al. 2008). The Interheart study (2008) found that the median age for women experiencing first MI was 65 Vs 56 in men. It was also found in a review of the Framingham Population (1986) that a 10 year gap existed between the sexes in incidence of MI. This tie's in with another fixed risk factors for CHD which is Sex. Up until women reach the age of menopause, women are thought to hold a certain level of immunity against CHD, Heller (1979) stated that "Many have thought that young women are protected from CHD by ovarian hormones and that they lose this protection after the menopause, when concentrations of these hormones are Reduced".

Over the last decade more research has been performed which looks at genetic make up as a predisposition to acquired heart disease. Hubacek (1999) states that "risk factors for atherosclerosis, would suppose that the genetic makeup of Individuals would influence the sensitivity to this stimulus" It is thought that due to modifications within the gene CD-14 which effects Monocyte Maturation and sensitivity, thus some individuals could have a greater Inflammatory response than others. This gene is passed through the generation's which puts genetically hereditant family at higher risk of acquired heart disease.

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For the people whom hold these fixed contributors to CHD the only way to lower the risk is by changing their modifiable risk factors. High blood pressure puts the arteries within the heart under greater strain and pressure. Due to this higher pressure the lumen within the arteries are at higher risk of sustained injury. Once this injury occurs the cycle of inflammatory response then starts to narrow the arteries until the point at which rupture and total occlusion occurs causing a Myocardial Infarction (Braunwald. 2005). Obesity, Physical inactivity and raised cholesterol levels can all be linked together when concerned with CHD. Patients whom are Obese tend to be physically inactive along with a daily intake of unbalanced diet. This unbalanced diet provides the imbalance in healthy cholesterol levels which puts the patient at higher risk of CHD. Obesity and high blood pressure can also go together as a higher pressure is needed to force all the oxygen and nutrient rich blood around the body. Inactivity can lead to obesity if diet intake is not modified to suit the inactivity. Activity of a person improves stroke volume within the heart which means that the heart does not need to work as hard as an inactive person.

Smoking is thought to put a person at twenty percent higher risk of obtaining CHD (Braunwald, 2005). It is not understood entirely the effects that smoking has on the increasing risk of CHD. It has been found that smokers tend to have significantly higher serum cholesterol, triglyceride, and low-density lipoprotein (LDL) levels, but high-density lipoprotein is lower in smokers than in non-smokers (Ambrose. 2003) along with higher levels of free radicals in the blood. It has been recognised that smokers also have higher levels of inflammatory markers, thus exacerbating inflammatory response once damage to the lumen occurs.

The final Risk factor is that of Diabetes Mellitus. Diabetes is thought to play a role in the development of Atherosclerosis, it can cause damage to the tissues that line blood the vessels, it increases platelet adhesiveness and aggregation, increased lipoprotein levels, and alterations in the function of macrophages (colwell. 1991). There for damage to the lumen again can be exacerbated by increased platelet adhesiveness and lipoprotein levels.

There have been a few studies which have followed the progression of MI over a number of years. Mainly these studies look at reduction or increase in numbers of MI over time. The Study which looks at the greatest period of time compares data between 1966/67 to 1993/94 (Vollmink et al, 1998). It looked at the incidence rates of MI of people from the Oxfordshire region. The average age incidence of MI It found "was substantially lower in Oxfordshire than rates reported from MONICA centers in Scotland and Northern Ireland" although reduction in overall MI according to the MONICA study (2003) reported a decrease of 2% per 100,000 and only 1.3% over the Oxfordshire region. It also concluded that"The reduction in CHD mortality in Oxfordshire has resulted from falls in both MI incidence and case fatality". It there for shows that there has been a reduction in numbers of cases of MI over this period which in turn has also helped reduce the numbers of fatalities due to MI although there is a significant improvement in fatality due to CHD.

The MONICA study was a Multi center study which used 21 centers across Europe, Australia and North America over the period of ten years. It found that across the whole board there was reduction in heart disease. It failed to find a link between the major risk factors affecting CHD. They concluded again that case fatality reduction of MI had decreased in number due to a reduction in incidence of MI across the whole board.

The next longest study (Lampe et al. 2000) looked at men aged 50-64years in Great Britain from 1978 - 1996. It found that there was a -2.5% incidence rate change and a 4.2% reduction in deaths from MI. Again it concluded that a vast reduction in deaths due to MI was due to the fact that incidence of MI had reduced. It also stated that middle aged British men are less likely to experience symptoms of angina than in previous decades but are just as likely to have a history of diagnosed CHD. Despite falling rates of new major events and falling symptom prevalence, the need for secondary prevention among middle aged men with established CHD is as great as ever. This could be due to improvement in diagnostic testing and public education about CHD. Improvements in diagnostic testing and understanding of the disease may make for earlier diagnosis. Ongoing research into effects of medication to reduce risk states that all men in USA over the age of 50 should take low dose aspirin and that it could prevent at least 1/3 of first incidence MI (Kauffman. 2000). This could also be a reason why there has been reduced risk of incidence of MI from 1967.

As part of the MONICA study, individual MONICA centres data was released in individual studies (Tunstall-Pedoe et al, 1999). There is a significant difference in the presented data between Glasgow and Belfast. Glasgow saw a reduction in incidence of MI by -1.4% in men and 0.2% in women whereas Belfast saw a difference of -4.6% in men and -2.4% in women. This shows that there is a significant regional difference in the rate of reduction. A reduction in case fatality change saw -2.6% in men and 2.0% in women in Glasgow and -6.0% and -3.9% in Belfast. It shows that although there was an increase in incidence of MI in Glasgow amongst females, that fatality levels in females had still seen a reduction in numbers which contradicts the statement "vast reduction in deaths due to MI was due to the fact that incidence of MI had reduced" (Lampe et al. 2000).


You could go on to discussing the background literature here with regard to your project,. For example, you will need some background physiology (normal) to incl coronary arteries etc, then move on to the pathophys, discussing risk factors/aetiology atherosclerosis (you had a few papers in BM2043 which may help with this), then go on to papers related to your project, try and sub categorise your references and discuss them as subject areas rather than each individual paper (i.e. don';t just go through each paper individually).