Cardiovascular Disease

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See Also:

• Arrhythmias

• Bleeding

• Embolism

• Heart Defects

• Hypertension

• Oedema

Questions Received:

1. What are the diseases and disorders of the heart?

2. What is VT - right CVA, and VF arrest? And what are the secondary complications associated with each? What care should be given to a patient with these problems and who also has a past history of pacemaker and angina on exertion?

3. What is sholine purpra?

4. Why do saturated fats raise blood cholesterol levels by increasing LDLs but polyunsaturated fats do not? What happens in the liver to cause this difference? I know it's something to do with the presence/absence of double bonds but can't find out what! Do we lack enzymes to degrade saturated fats, hence they are converted to cholesterol and so cause elevated LDLs? Can you put me out of my fat misery please?!

5. By what mechanism does aspirin work to prevent MI and CVA? Why do some patients take only 75mg daily and others take 300mg?

6. How many people are suffering from cardiovascular diseases in the UK and the world? What is the cause of it? How much money is spent for hospitalisation and research? Can cardiovascular disease be prevented and how?

Responses:

What are the diseases and disorders of the heart?

20th April 1999

This is a large topic and therefore it is only possible to give a brief account of the common cardiac diseases. For descriptive purposes these can be grouped under several broad headings: diseases affecting the coronary arteries (coronary heart disease - CHD), diseases which affect cardiac rhythm (the arrhythmias or dysrhythmias), valvular disease, and congenital abnormalities.
bullet diseases affecting the coronary arteries

Narrowing of the coronary arteries or one of their branches by atheromatous plaques leads to inadequate perfusion of the myocardium.When oxygen supply to the myocardium is reduced ischaemia occurs and these changes are often expressed in such a way as to produce the retrosternal constricting pain known as angina. Whenever physical activity or stressful events are experienced angina can occur and it is due to an imbalance between oxygen supply to, and demand by, the myocardium. Progressive occlusion of the coronary arteries can lead to the development of a thrombosis. Damage to the tunica intima, the innermost linining of the coronary arteries, leads to the build up of platelets which adhere to the damaged area, local thrombosis with fibrin deposition occurs. Ultimately calcified atheroma occurs which narrows the lumen of the diseased vessel/s. Blood supply to the heart is via the left and right coronary arteries which arise from the aorta. Occlusion in either of these arteries, or their major branches, will give rise to a myocardial infarction. Acute interruption to the blood supply to part of the heart can provoke: acute chest pain, the onset of rhythm disturbances such as ventricular tachycardia or ventricular fibrillation, heart block or asystole. Such disturbances occur as a result of damage to cell membranes. The cells leak sodium, potassium and calcium ions and this makes the cell membrane more excitable, also the membrane fails to conduct in the normal way. The pattern of normal conduction from the SA node across the atria down the AV node and Bundle of His and through the ventricles becomes disrupted. The impulse takes an abnormal pathway and this can result in serious dysrhythmias developing.

Diseases which affect cardiac rhythm

The normal rhythmical pattern of systole followed by diastole - the cardiac cycle - is referred to as sinus rhythm. The intrinsic rate of the sinu-atrial node is 70-80 b.p.m. During the normal range of activities, this rate changes as a result of either sympathetic activity - when the rate increases, or, parasympathetic activity - when the rate slows down. If the heart rhythm changes abnormally, the condition is referred to as either arrhythmia or dysrhythmia:

• Arrhythmia - any deviation from the normal rhythm, usually referring to the heart beat e.g. sinus a., extrasystole, fibrillation, Stokes Adams syndrome, tachycardia.

• Dysrhythmia - disordered rhythm, usually of heart e.g. atrial fibrillation.

(Definitions from: Mosby's Medical, Nursing, and Allied Health Dictionary (4th edition) 1994. Edited by K.N. Anderson, L.E. Anderson, and W.D. Glanze. St Louis: Mosby-Year Book, Inc. Pp.121 & 517. )

• Sinus Bradycardia - the pulse rate is slow - under 60 b.p.m., the rhythm is normal. Sinus bradycardia occurs during sleep when the vagus nerve actively over-rides sympathetic activity upon the S.A. node. Sinus bradycardia is normal in fit people and is common in athletes. The condition also occurs as a result of a vaso-vagal attack e.g. when witnessing or participating in a particularly unpleasent experience. A disease within the S.A. node, hypoxia, raised intracranial pressure, and as a side effect to Beta Blockers, are other instances when sinus bradycardia occurs.

• Sinus Tachycardia - the pulse rate is in excess of 100-140 b.p.m. Sinus tachycardia is a normal response to stress imposed on the body e.g. exercise, when fear and anxiety is experienced, as a result of pain (intense pain though may induce a bradycardia), as a result of shock - in particular hypovolaemic shock. Thyrotoxicosis and some of the drugs used to treat conditions such as asthma are other situations when sinus tachycardia can occur.

• Sinus Arrest - the S.A. node fails to produce a stimulus, as a result contraction of the atria and the ventricles fails to take place, a missed beat occurs. Sinus arrest can be due to ischaemic heart disease and can also occur as a result of drug toxicity.

• Atrial Ectopics - ectopic in this context means that the impulse originates in the walls of the atria and not in the S.A. node. Common causes of atrial ectopics are: smoking, cosuming excess caffeine, digoxin toxicity. Atrial ectopics may herald the development of atrial fibrillation. They can occur as a result of the process of aging.

• Atrial Fibrillation - ectopic atrial activity is very fast e.g. in excess of 360 b.p.m. and irregular. The atrio-ventricular node blocks some of this activity and as result the ventricular rate is often between 70-200 b.p.m. Atrial fibrillation usually occurs as a result of underlying heart disease e.g. coronary heart disease, rheumatic heart disease, hypertension and cardiomyopathy. The condition also occurs in association with thyrotoxicosis and alcoholism.

• Ventricular Tachycardia - this serious rhythm disturbance is due to an irritable focus within the ventricles; it is often preceded by ventricular ectopic beats. This irritable focus replaces the normal impulse that is being conducted down through the S.A. node, as a result the ventricular rate is very high - 120-200 b.p.m. This serious condition can lead to the onset of ventricular fibrillation. The causes of ventricular tachycardia include: myocardial infarction, coronary heart disease, cardiomyopathy and disease of the mytral valve.

• Ventricular Fibrillation - in this most serious arrhythmia the cardiac output virtually ceases. The ventricles do not contract effectively, instead ventricular systole is replaced by "quivering" which occurs throughout the walls of each ventricle. As a result in ventricular fibrillation the pulse is absent and the blood pressure falls. Some of the common causes of ventricular fibrillation are: acute myocardial infarction, myocardial ischaemia, cardiomyopathy, electrocution and hyperkalaemia (elevated potassium levels).

• Asystole - absence of ventricular activity and therefore an emergency situation requiring immediate treatment. Cardio Pulmonary Resuscitation is administered immediately. Asystole can arise as a result of other diseases which give rise to conduction disorders and as a result of advanced cardiac disease.

Disease of the heart valves

The heart valves are important structures which cause the blood to flow in one direction through the heart and into the great vessels - the aorta and pulmonary trunk. Between the atria and the ventricles are the atrioventricular valves. The mitral valve is situated between the left atrium and the left ventricle and the tricuspid valve is between the right atrium and the right ventricle. Each ventricle has an outlet valve containing three cusps. These are known as the semilunar valves. On the left the valve which opens to allow blood to flow into the aorta is the aortic valve. On the right the valve which opens to allow blood to flow into the pulmonary trunkand on to the pulmonary arteries is the pulmonary valve.

Damage to the valves of the heart results in either narrowing (stenosis) or incompetence (regurgitation) where the valve fails to close completely. When a doctor listens to a person's heart with a stethoscope (s)he will listen to heart sounds. As the mitral and tricuspid valves close a sound like the word 'lub' can be heard and this is called the first heart sound. As the semilunar valves close a sound like the word 'dup' can be heard and this is called the second heart sound. Valvular disease impedes the smooth flow of blood from one chamber of the heart to the next, or if one of the semilunar valves becomes damaged from the ventricle into either the aorta or pulmonary artery. Turbulence occurs as the blood is forced either through a tightly stenosed valve or regurgitates back into a chamber of the heart as a result of a weak and incompetent valve. Such turbulance can be picked up as a murmur by the doctor when listening to the heart. Murmurs can occur during systole - systolic murmur or during diastole - diastolic murmur. An echocardiogram provides detailed information on the valve/s and whether these are fuctioning correctly.

• Mitral Stenosis - rheumatic fever can result in mitral stenosis. The cause of rheumatic fever is infection by group A Beta - haemolytic streptococci. An initial infection of the throat with this organism can lead to the development of rheumatic fever. Rheumatic fever can result in all three layers of the heart becoming inflammed and lead to scarred tissue changes occuring on the mitral valve. These changes are responsible for the narrowing in mitral stenosis. Mitral stenosis can also have a congenital origin.

• Mitral Regurgitation - damage to the structure of the mitral valve e.g. chordae tendineae, papillary muscles, produces mitral regurgitation. Again the inflammatory changes resulting from rheumatic heart disease or infectious conditions producing endocarditis and congenital abnormalities are a few common causes.

• Aortic Stenosis - in young people the cause of aortic stenosis is usually congenital whist in older people the cause is due to calcified degenerative changes.

• Aortic Regurgitation - rheumatic fever, endocarditis, degenerative changes, rheumatoid disease, syphilitic aortitis and aortic dissection are amongst the common causes of aortic regurgitation.

• Tricuspid Stenosis - this is a very rare disease which can arises as a result of rheumatic mitral stenosis, right ventricular dysfunction, or as a result of pulmonary hypertension

• Pulmonary Valve Diseases - conditions which affect the pulmonary valve are very rare and when seen the cause is normally congenital.

Congenital Abnormalities

In some babies, the heart may develop abnormally before birth. Many types of defect are possible, either singly or in combination, and they can be a major cause of death during the first year of life. Older children can be seriously disabled by circulatory defects which were not obvious at an earlier age. The main defects are: atrial and ventricular septal defects, coarctation of the aorta, patent ductus arteriosus, transposition of the great vessels, and the tetralogy of Fallot (diagrams). Not all of these defects are apparent at birth, and many affected children remain asymptomatic for several years. In the newborn, congenital heart abnormalities may be suspected because of signs of the following kinds: cyanosis, respiratory distress, hepatic enlargement, abnormal pulse, cardiac enlargement, murmurs, or heart failure.

Some structural defects of the heart and major vessels can be detected by ultrasound scanning before birth. Operations are available for the majority of circulatory defects, but many are hazardous and without a high success rate. The relative importance of genetic and environmental factors in congenital heart disease is difficult to assess given the many variants that are possible, but it appears that the genetic component is not particularly strong in most cases. The recurrence risk for congenital heart disease appears to be in the range 1-4%, but the figure will depend on which type of congenital heart disease appeared in the first baby.

Bibliography

• Cox Collier, I., and Lewis, S.M. (1987) Medical Surgical Nursing, Assessment and Management of Clinical Problems (3rd edition) Chapter 31: Nursing Role in Management - Inflammatory and Valvular Heart Disease. St Louis: Mosby-Year Book, Inc. Pp. 906-910.

• Larsen,W.J. (1993) Human embryology. Edinburgh: Churchill Livingstone. Pp. 155-163.

What is VT - right CVA, and VF arrest? And what are the secondary complications associated with each? What care should be given to a patient with these problems and who also has a past history of pacemaker and angina on exertion?

1st June 1999

There is always a risk with abbreviations like this in that they can be misinterpreted, unless they are accompanied by a full explanation. VT I take to mean ventricular tachycardia, right CVA to mean cerebral vascular accident (now more commonly referred to as CVE: cerebral vascular event) and VF to mean ventricular fibrillation.

First of all ventricular tachycardia - tachycardia is a term used to describe a heart rate above 100 beats per minute. In ventricular tachycardia the ventricular rate is 120-200 per minute and is normally due to the presence of an irritable focus within the ventricles. Impulses arising from this stimulus override those which originate in the sinoatrial node, the pacemaker. The normal intrinsic regulatory mechanism which controls the emptying of the ventricles is lost with the result that the ventricles contract at a much higher rate and incompletely. This produces a fall in cardiac output resulting in hypotension (shock) and unconsciousness. Patients may also complain of dizziness and breathlessness (dyspnoea). Treatment is aimed at restoring normal rhythm and preventing the onset of ventricular fibrillation - a secondary complication.

Ventricular fibrillation - in ventricular fibrillation the ventricular rate is both rapid and irregular - 300-350 per minute. In this serious form of arrhythmia the ventricular pumping action is lost, there is no cardiac output and the blood pressure falls. The condition constitutes a cardiac arrest and Basic Life Support (BSL) and/or Advanced Life Support (ALS) have to employed. This includes DC shock initially with 200 joules. If this fails to restore normal rhythm a further shock of 200 joules is given. If this also fails a third shock using 360 joules is employed. Some of the main secondary complications associated with ventricular fibrillation are: cardiac failure, hypotension and acute renal failure. If untreated ventricular fibrillation will lead to death.

Cerebral vascular event (stroke) - this is a neurological disturbance involving part of the brain and can be caused either by ischaemia (interruption of blood supply due to thrombosis or embolism) or haemorrhage (intracerebral or subarachnoid). Such events deprive neurons of an adequate supply of oxygen and nutrients. The effects depend upon the area of the brain involved and whether the cause is ischaemic or haemorrhagic. A person who develops a CVE is at least initially likely to require skilled nursing care as well as physiotherapy. Such an event frequently produces a degree of sensory and/or motor loss (hemiplegia) and victims commonly feel bewildered and anxious, particularly so if the speech area of the brain (Broca's area) is involved resulting in either aphasia or dysphasia. Also early intervention by the nursing and physiotherapy teams enables a rehabilitation programme to be instigated and potential complications to be reduced.

The most appropriate care for someone who has sustained a CVE is the "team" approach which involves the medical and nursing staff, physiotherapist, pharmacist and speech and language therapist. The aims of care are to preserve those areas where the person is independent and to provide support towards those Activities of Daily Living (ADLs) which the person is unable to fulfil. At the same time the prevention of potential complications has to be taken into account.

Angina, another aspect of the question, is commonly managed by restoring the imbalance between the oxygen supply and demand of the myocardium. Either the demand on the myocardium is reduced by reducing physical effort or the oxygen supply to the myocardium is improved by administering drugs such as nitrates. "Nitrates are vasodilators which best affect veins, though they also affect arteries to some extent. In most instances they work by bringing about a sudden dilatation of veins which reduces pre-load and thus cardiac output and the work load of the heart." (Smith 1987)

Compliance with medication, avoiding obesity and not smoking would be sound advice to give to someone who has angina.

References

• Haslett, C., Chilvers, E.R., Hunter, J.A.A., and Boon, N. (editors) (1999) Davidson’s principles and practice of medicine (18th edition). (Table 14.25, p. 982).

• Smith, S. (1987) How drugs act - drugs in angina and myocardial infarction. Nursing Times, 83(22), (Jun 3).

What is sholine purpra?

13th June 1999

We think you may be referring to Henoch-Schonlein purpura. This is an autoimmune disease affecting blood vessels in children. Autoimmune means that the immune system of the child is turning against normal cells in the vessel walls and triggering inflammation. The process is mediated by the type of antibodies known as immunoglobulin A (IgA). The three main symptoms are a purpuric (purplish) rash occurring on the lower extremities, abdominal pain from renal involvement, and arthritis, although not all of these may be present in particular cases (Kraft, Mckee, and Scott, 1998). The cause is unknown but this condition may be associated with infections, food reactions, exposure to cold, insect bites and drug allergies. Treatment is supportive and it is important to monitor kidney function in affected children.

Reference

• Kraft, D.M., Mckee, D., and Scott, C. (1998) Henoch-Schonlein purpura: a review. American Family Physician, 58(2), 405-408, 411 (Aug).

Why do saturated fats raise blood cholesterol levels by increasing LDLs but polyunsaturated fats do not? What happens in the liver to cause this difference? I know it's something to do with the presence/absence of double bonds but can't find out what! Do we lack enzymes to degrade saturated fats, hence they are converted to cholesterol and so cause elevated LDLs? Can you put me out of my fat misery please?!

18th August 1999

There are several potential mechanisms by which an intake of saturated fat could lead to increased blood cholesterol:

• Unsaturated fatty acids tend to favour the formation of HDLs. Presumably this is linked to the reaction involving the enzyme lecithin cholesterol acyl transferase (LCAT) in which unsaturated fatty acids are transferred from plasma lecithin (a phospholipid) onto the cholesterol molecule to form an ester. HDL then transports this cholesterol to the liver where it is broken down. Hence unsaturated fatty acids would tend to reduce plasma cholesterol. Conversely saturated fatty acid or low levels of unsaturated fatty acid would elevate cholesterol levels in plasma because HDL levels relative to LDL have decreased.

• Low-density lipoprotein (LDL) particles tend to contain cholesterol esters rich in saturated fatty acids, whereas high-density lipoprotein (HDL) contains unsaturated fatty acids. Thus a high proportion of saturated fatty acids in the diet could (in theory at least) increase LDLs

• Saturated fatty acids and cholesterol tend to be present together in foods such as animal fat. Hence consumption of food rich in saturated fatty acids would raise cholesterol levels concurrently. (However, a recent study by Kromhaut (1999) indicates that this does not apply in the case of stearate which does not raise LDL)

• Saturated fatty acids may have some regulatory effects on cholesterol synthesis which tends to raise plasma cholesterol levels (via LDL), an effect which is not produced by unsaturated fatty acid.

There is clear epidemiological evidence that diets rich in cholesterol and saturated fats lead to an increased risk of coronary heart disease as a consequence of high plasma cholesterol levels promoting the development of atherosclerotic plaques in blood vessel walls. Polyunsaturated fatty acids are regarded as being protective because they reduce the risk of atheroma development.

Saturated fats taken in with the diet are incorporated into cholesterol esters (and triglycerides) which form part of the LDL complexes in the blood, whereas polyunsaturated fatty acids are taken up mainly into cholesterol esters in HDL. The chemical composition of these two particles is quite different: LDL contains 80% fat, of which 50% is made up of cholesterol, and 20% protein. HDL contains 55% fat, of which 25% is cholesterol, and 45% protein. Increased levels of LDL have been linked to an increased risk of coronary heart disease and led to its description as "bad cholesterol". Conversely increased HDL levels reduce the risk of coronary heart disease and HDL is referred to as "good cholesterol". Since cholesterol is an essential component of cells and has numerous other roles throughout the body, for example providing a raw material for the synthesis of steroid hormones, we must be careful in the way we attach such labels and keep in mind the need for an appropriate balance.

A large proportion of LDL cholesterol is in the form of esters containing saturated fatty acids, whereas HDL contains unsaturated fatty acids. HDL lipoproteins tend to transport excess cholesterol from peripheral tissues back to the liver where it is broken down. HDL is assembled from apolipoprotein-AI, phospholipid, and free cholesterol discs secreted by the liver and intestines. The free cholesterol is esterified in the mature HDL and can then be transferred to LDL or taken up by the liver or steroid-metabolising tissues.

< Diagram showing biosynthesis of HDL

In contrast, LDL particles are involved in the uptake of cholesterol into tissue cells via a receptor-mediated process. A decrease in the number of LDL receptors on tissue cells has been linked to high circulating levels of plasma cholesterol. Decreased receptors means decreased cholesterol uptake and the raised LDL levels that ensue increase the risk of atheroma. About 20 years ago it was discovered that mutations in the gene that encodes the LDL receptor protein causes familial hypercholesterolaemia. In this condition there are high levels of LDL but tissue cells are unable to take up cholesterol from the blood. People affected by this mutation are at a much higher risk of coronary heart disease and stroke than other people (Brown 1984).

Several factors can influence the levels of circulating HDL (Scott, 1999). For example, there is a difference in levels between women and men: women have higher levels of HDL than men up until the menopause, and this offers them some protection against heart disease. Levels of HDL can also be increased by exercise, weight loss, moderate alcohol intake, and chemicals such as fibric acide derivatives, nicotinic acid, and tamoxifen.

References

• Bowman, W.C., and Rand, M.J. (1984) Textbook of Pharmacology (2nd edition). Blackwells.

• Brown, M.S. (1984) How LDL receptors influence cholesterol and atherosclerosis. Scientific American, 251, 52-60.

• Kromhaut, D. (1999) Fatty acids and CHD from an epidemiological perspective' Lipids, 34, 27-31.

• Lawn, R.M. (1992) Lipoprotein in heart disease. Scientific American, 266, 26-32.

• Ottaway, J.H., and Apps, D.K. (1988) Biochemistry (5th edition). Bailliere-Tyndall.

• Scott, J. (1999) Good cholesterol news. Nature, 400, 816-819.

By what mechanism does aspirin work to prevent MI and CVA? Why do some patients take only 75mg daily and others take 300mg?

29th January 2000

Aspirin (acetylsalicylic acid) has been in use for many years for the management of pain, fever and inflammation. More recently it has been shown to have an effect on platelets and the endothelial lining of blood vessels and is now used in the treatment and prevention of thrombosis. Aspirin inhibits the first step in the coagulation of blood - aggregation of platelets (Bhagat, 1994). Through this anti-clotting action aspirin reduces the risk of myocardial infarction (MI) in patients with unstable angina and increases survival in patients who have had acute myocardial infarction. It also reduces the risk of stroke (cerebrovascular accident, CVA) in patients with transient ischaemic attacks.

The beneficial effects of aspirin in thromboembolic disease are thought to be due to the inhibition of platelet thromboxane A2 synthesis:

< Thromboxane A2

This is a powerful inducer of platelet aggregation and is formed via the action of the enzyme cyclo-oxygenase. It acts on surface receptors carried by platelets and activates phospholipase C causing the formation of inositol triphosphate. This causes a rise in intracellular calcium ions (Ca++) which triggers aggregation of platelets.

However the endothelial cells of the vascular wall produce a prostaglandin known as prostacyclin which acts as the physiological antagonist of thromboxane A2. Indeed normal platelet function may result from a balance between these two prostaglandins.

< Prostacyclin

This stimulates different receptors on the platelet and activates the enzyme adenyl cyclase. The resulting increase in cyclic AMP is associated with a decrease in intracellular Ca2+ and inhibition of platelet aggregation.

Aspirin prevents thromboxane A2 formation by irreversibly inhibiting the enzyme, cyclo-oxygenase. Aspirin doses as low as 75 mg per day can have this effect, even 40 mg according to Goodman and Gilman (1995). A single dose of aspirin will inhibit the platelet cyclo-oxygenase for the lifetime of the platelet (8-11 days). However the action of aspirin is selective in that doses of 75-150 mg daily will impair synthesis of thromboxane without unduly affecting prostacyclin synthesis. (Prostacyclin is also synthesised by a different ‘type’ of cyclo-oxygenase in the vascular epithelium). These amounts are substantially below the 2400 mg per day required to control pain and inflammation. Clinicians often administer aspirin 300 mg per day on alternate days in order to produce this selective inhibition thus allowing the vascular cyclo-oxygenase time to recover (Neal, 1997). Thus the balance of the anti-aggregatory effect of prostacyclin and the pro-aggregatory effect of thromboxane A2 is shifted in a beneficial direction. Doses above 300 mg are less efficacious since prostacyclin is adversely affected to a large degree and side-effects begin to appear, notably gastric bleeding and tinnitus.

Aspirin (160-320 mg daily) has been shown to improve the survival rates of patients with acute myocardial infarction. In patients with unstable angina, aspirin has been shown to reduce total mortality by 50% (Lewis, 1983). An American study in 1989 involving 22,000 volunteers taking aspirin 320 mg daily for 5 years showed a 45% decrease in the incidence of myocardial infarction and a 72% fall in fatal cases of myocardial infarction (Steering Committee, 1989). Some physicians have advocated the prophylactic use of aspirin in healthy populations in order to prevent myocardial infarction and stroke but current medical opinion suggests that this approach should only be used in patients with risk factors for cardiovascular disease.

References

• Bhagat, K. (1994) Aspirin. Nursing Standard, 8 (49), 52-54 (Aug 31).

• Goodman and Gilman's Pharmacological Basis of Therapeutics , 9th edition, Mc Graw-Hill.

• Laurence, D.R., and Bennett, P.N. (1992) Clinical pharmacology (7th edition). Edinburgh: Churchill Livingstone.

• Lewis, H.D. (1983) Protective effects of aspirin against myocardial infarction. New England Journal of Medicine, 309, 396-403.

• Neal, M.J. (1997) Medical pharmacology at a glance (3rd edition). Blackwell.

• Steering Committee (1989) US Physicians' Health Study Research Group: Report on the aspirin component of the Physicians' Health Study. New England Journal of Medicine, 321, 129-135 (1989).

How many people are suffering from cardiovascular diseases in the UK and the world? What is the cause of it? How much money is spent for hospitalisation and research? Can cardiovascular disease be prevented and how?

1st February 2001

Cardiovascular disease refers to a variety of diseases and conditions affecting the heart and blood vessels in the human body. It is by far the largest single killer in the UK, Europe and the US, and is responsible for 4 out of 10 deaths each year. The immediate cause of most of these deaths is heart attack or stroke, but those events are the end result of a disease called atherosclerosis that begins many years before symptoms are detected.

In atherosclerosis, fatty deposits known as plaque and containing cholesterol begin to form in the walls of arteries. Fibrous connective tissue invades the plaque and calcification may occur. These changes make the artery wall less elastic - "hardening of the arteries". The growing plaque narrows the artery and the normally smooth endothelium becomes damaged, with the result that blood flow through the narrowed vessel becomes turbulent. Blood platelets stick to the plaque and initiate the formation of a blood clot (thrombus) that further blocks the artery.

The coronary arteries supplying the heart are highly susceptible to atherosclerosis, and as they narrow the blood flow to the heart muscle decreases. Chest pains and shortness of breath during mild exertion are symptoms of this condition. A person with atherosclerosis is at high risk of forming a thrombus in a coronary artery - coronary thrombosis. Complete blockage of a coronary artery results in a heart attack. Sometimes a piece of thrombus breaks loose as an embolus and travels through the blood stream, becoming lodged in a vessel of smaller diameter and blocking its flow. Arteries already narrowed by plaque formation are likely places for an embolus to lodge. An embolism in an artery in the brain causes the cells fed by that artery to die - a form of stroke. The outcome will depend on which part of the brain is affected, but may include memory loss, speech impairment, or paralysis.

In the US the rate of deaths from cardiovascular disease is 260.2 per 100,000 population (1996 figures). About 960,000 Americans die of cardiovascular disease each year accounting for 40% of all deaths. It is the leading cause of death in middle age, killing more than 160,000 people between the ages of 35 and 64 each year. About 58 million Americans ( almost one quarter of the population) live with some form of the disease. Stroke accounts for some level of disability amongst 1 million people nationwide. Almost 6 million hospitalisations each year are due to cardiovascular disease. The estimated cost of cardiovascular disease in the US was $287 billion - this figure includes health expenditure and lost productivity resulting from illness and death.

The major risk factors for cardiovascular disease are:

• Diet rich in fat

• Sedentary lifestyle

• Cigarette smoking

• High blood pressure

• Obesity

• Certain medical conditions, eg: diabetes

• Genetic disposition

Cigarette smoking is probably the major cause of heart disease - smokers have twice the rate of cardiovascular disease compared with non-smokers. Nearly one-fifth of all deaths from heart disease are linked to smoking. Sedentary people have twice the risk compared to those who are physically active. It is thought that one half of all Americans do not achieve the recommended level of physical activity.

UK figures for cardiovascular disease show similarities to those of the US in that cardiovascular disease is responsible for 43% of all deaths (1995 figures) – values refer to the rates of deaths per 100,000 of the population:

The most important solution to cardiovascular disease lies with prevention and not treatment. Prevention of cardiovascular disease relies on public awareness and education. Changes in diet can prevent atherosclerosis. Diets rich in fruit and vegetables and low in red meat and low in saturated fatty acids are cardioprotective. Measures to prevent weight gain and obesity can lower the risk of cardiovascular disease. Smokers who quit their habit in time can lessen their chances of dying from a heart attack or stroke.

Reference

• National Centre for Chronic Disease Prevention, USA: www.cdc.gov/nccdphp/bb_heartdisease/index.htm (This will open a new browser window.)

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