Epidemiology of Coronary Heart Disease

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Epidemiology of Coronary Heart Disease
Incidence and prevalence
Mortality rates[1]
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Coronary heart disease (CHD) is the most common cause of death (and premature death) in the UK. 1 in 5 men and 1 in 7 women die from CHD. There are 94,000 deaths from CHD in the UK each year. Death rates from CHD have fallen by 45% for people aged under 65 years in the last 10 years. This fall is fastest in those aged 55 years and over. It is largely due to a reduction in major risk factors (mostly smoking) and improvement in treatment and secondary prevention. The fall is not as high as that in some other countries such as Australia (48%) and Norway (54%). Death rates from CHD are highest in Scotland, and the North of England, and lowest in the South of England. For more than 25 years these rates have been consistently highest in Scotland. Death from CHD is more likely during winter; in 2004/2005, just under 7,000 people died from CHD in England and Wales each month in June and July, compared with around 9,000 in December and January. The average incidence of myocardial infarction is 600 per 100,000 in men aged 30-69 and 200 per 100,000 in women. The incidence increases with age. There are about 52,000 new cases of angina per year in all men living in the UK and about 43,000 new cases in women. About 4% of men and 0.5% of women in the UK have had a heart attack. Prevalence increases with age and is higher in men. 8% of men and 3% of women aged 55 to 64 years and about 14% of men and 8% of women aged 65 to 74 years have, or have had, angina. The prevalence of CHD in Britain according to Quality and Outcomes Framework (QOF) data was 3.7% of all GP registrations. The prevalence of CHD was higher in Scotland (4.6%) than in Wales (4.3%) or England (3.5%). The prevalence is higher in the North of England and Wales than in the South of England. The prevalence is higher in lower socioeconomic groups. Of note, mortality from CHD is falling but morbidity appears to be rising.

Morbidity rates[2]
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Risk factors
The aetiology of CHD is multifactorial. It is the result of interaction between genetic, lifestyle and environmental factors.

Age
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CHD increases with age. This is a non-modifiable risk factor. Traditionally, CHD has been considered a disease of men. However, CHD is the leading cause of death in both men and women.[3] It is responsible for a third of all deaths in women worldwide and half of all deaths in women over the age of 50 years in developing countries.[4] In England and Wales there is a positive correlation between deaths from circulatory diseases and levels of deprivation. There is a marked difference in prevalence of coronary heart disease between and within communities. Men and women living in the West of Scotland are nearly six times more likely to die prematurely from CHD than men and women living in the South West of England. Within London, people living in Tower Hamlets have a three times increased risk of dying prematurely from CHD than those in Kensington and Chelsea. The difference in CHD rates in different socioeconomic groups is related to many factors, including diet, smoking, exercise, and alcohol.

Gender

Social deprivation
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Smoking
In 2001, 27% of adults aged 16 years and over smoked cigarettes in England; 28% of men and 25% of women.
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Mortality from CHD is 60% higher in smokers.[5] Regular exposure to passive smoking increases CHD risk by 25%.[6][7] In 2000, about 1 in 8 deaths from cardiovascular disease (CVD) were attributable to smoking in the UK. World Health Organization (WHO) research estimates that over 20% of CVD is due to smoking.[8]

Poor nutrition
There are national, regional, socioeconomic and ethnic differences in nutrition.

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A WHO report in 2003 stated that a diet high in fat (particularly saturated fat), sodium and sugar and low in complex carbohydrates, fruit and vegetables increases the risk of CVD.[9] It has been recommended that the percentage food energy derived from fat should be 35%, with 11% from saturated fat. The National Diet and Nutrition Survey in 2000/2001 found that the total energy intake from fat was 36% in men and 35% in women with 13% from saturated fat. It also found that the average intake of fruit and vegetables was fewer than 3 portions per day compared with the recommended 5 portions.[10] In the same survey salt intake was 11 g per day for men and 8.1 g for women. However, the Scientific Advisory Committee on Nutrition suggests that salt intake should be no more than 6 g per day. Trans fatty acids reduce high-density lipoprotein (HDL) and increase low-density lipoprotein (LDL) cholesterol and can increase CHD risk. A meta-analysis showed that a 2% increase in the energy intake from trans fatty acids increased CHD incidence by 23%.[11] Eating oily fish rich in omega-3 fatty acids has been shown to reduce CHD mortality.[12] Increased intake in dietary fibre also appears to reduce risk. Physical activity reduces the risk of CHD. The 2002 World Health Report estimated that over 20% of CHD in developed countries was due to physical inactivity.[8] Recommended physical activity levels are 30 minutes of moderate physical activity on 5 or more days per week.[13] Over one third of UK adults are estimated to be inactive (exercised for less than one occasion of 30 minutes per week). 1 to 2 units of alcohol per day reduce the risk of CHD. Alcohol increases HDL cholesterol and reduces thrombotic risk. Higher levels of consumption increase risks from other causes.[14] The World Health Report in 2002 estimated that 2% of CHD in men in developed countries is due to excessive alcohol consumption.[8] Men should drink no more than 3 to 4 units on any one day and women no more than 2 to 3 units. Work stress, lack of social support, depression, anxiety and personality (particularly hostility) can all increase CHD risk.[15] For adults aged 40 to 69 years, each 20 mm Hg rise in usual systolic blood pressure or 10 mm Hg rise in diastolic blood pressure doubles the risk of death from CHD.[16] The INTERHEART study showed that 22% of heart attacks in Western Europe were due to a history of high blood pressure and those with hypertension had almost twice the risk of a heart attack.[17] CHD risk is related to cholesterol levels. The INTERHEART study suggested that 45% of heart attacks in Western Europe are due to abnormal blood lipids.[17] People with low levels of HDL cholesterol have an increased risk of CHD and a worse prognosis after a myocardial infarction. In the UK, it is suggested that the target cholesterol is < 4 mmol/L for people with diabetes or established CVD or for people at high risk of developing CVD. People with HDL cholesterol <1 mmol/L should also be considered for treatment.[18] Obesity is an independent risk factor for CHD. It is also a risk factor for hypertension,hyperlipidaemia, diabetes and impaired glucose tolerance. Central or abdominal obesity is most significant. Those with central obesity have over twice the risk of heart attack.[17] Men with type 2 diabetes have a 2 to 4 times greater annual risk of CHD; women have a 3 to 5 times greater risk.[19] Over 4% of men and 3% of women in England have diagnosed diabetes. The prevalence is increasing. South Asians living in the UK (people from India, Pakistan, Bangladesh and Sri Lanka) have a higher premature death rate from CHD (46% higher for men; 51% higher for women).[1] Hypotheses for this include migration, disadvantaged socioeconomic status, 'proatherogenic diet', lack of exercise, high levels of homocysteine and lipoprotein(a) (Lp(a)), endothelial dysfunction and enhanced plaque and systemic inflammation.[20] The premature death rate from CHD in West Africans and people from the Caribbean is much lower (half the rate compared with the general population for men and two-thirds of the rate for women). First-degree relatives of patients with premature myocardial infarction have double the risk themselves.[21] Premature CHD is that before age 55 years in men and 60 years in women. More than one third of admissions for premature myocardial infarction could be prevented by screening and treating first-degree relatives.[21] Genetic predisposition and shared lifestyle are likely to contribute. Several regions of the human genome have been shown to be associated with either CHD or hypertension.

Infrequent exercise

Alcohol

Psychosocial wellbeing Blood pressure
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Cholesterol
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Overweight and obesity
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Diabetes Ethnicity

Family history
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Serum homocysteine
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It was previously thought that elevated levels of homocysteine is an independent risk factor for IHD, likely due to oxidative damage to the endothelium, platelet activation and thrombus formation. The theory was that dietary supplementation with folic acid could reduce homocysteine levels and therefore CHD incidence. A meta-analysis in 2005 disputed this.[22]
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Economic cost 23



In 2006, CVD cost the healthcare system in the UK around ú14.4 billion. This represents a cost per capita of just under £250. The cost of hospital care for people who have CVD accounts for about 72% of these costs, whereas 20% of the cost is due to drugs. In 2006, production losses due to mortality and morbidity associated with CVD cost the UK over £8.2 billion, with around 55% of this cost due to death and 45% due to illness in those of working age.

Public health targets
Three-year average mortality rates for circulatory diseases (ages under 75 years) for England have fallen by 44.0% since the baseline. The minimum target requirement for a 40% reduction by 2009-2011 has been met, ahead of schedule.[24] The absolute gap in mortality rates for circulatory diseases (ages under 75 years) between the Spearhead Group and England as a whole, has reduced by 35.9% since the baseline, compared with the required target reduction of 40% by 2009-2011. The Spearhead Group consists of the 70 local authority areas that are in the bottom fifth nationally for 3 or more of the following 5 factors: male life expectancy at birth, female life expectancy at birth, cancer mortality rate in the under-75s, CVD mortality rate in the under-75s and the Index of Multiple Deprivation (2004).

Premature Coronary Artery Disease and Familial Hypercholesterolemia
Information last reviewed: February 2012
The heart muscle requires a regular supply of oxygen and food. This is supplied by blood carried by a network of blood vessels known as the coronary arteries. The coronary arteries can become narrowed by ‘furring’ of the artery wall with cholesterol, called atherosclerotic plaques. Blood clots can form on these plaques and block the artery, causing chest pains. The heart muscle supplied by the blocked artery is starved of oxygen and dies soon afterwards, known as a heart attack. This can also cause dangerous arrhythmias. The build-up of plaques in the coronary arteries increases with age and most people who have significant narrowing are usually over 50 years of age. There is a genetic risk for the development of coronary artery disease, but many factors are involved, including smoking, high blood pressure, diabetes and cholesterol levels. Some families, however, carry gene mutations that make them likely to have a very high cholesterol levels. This is known as familial hypercholesterolemia or FH. Families affected usually have members who have suffered from heart attacks, sometimes at very young ages.

What are the symptoms? If you have narrowed arteries you may experience heavy or tight chest pain, called angina, or breathlessness, most commonly during exertion, as a warning. If you have FH you may develop fatty lumps in the skin around the eyes or in the muscle tendons, but, usually, the only way of telling is to have a blood test.

How is it diagnosed? An ECG at rest will often be normal. An exercise ECG may show signs that the heart is being starved of oxygen. Depending on how high your doctor thinks your risk of having narrowed coronary arteries is, a range of different tests may also be offered, such as an ECHO during exercise, a special MRI scan or a CT scan of the coronary arteries. If he or she thinks your risk is high then you may be offered coronary angiography to diagnose the condition.

Treatment and advice If you have coronary artery disease you should receive advice on your life-style, including stopping smoking, a healthy diet and regular exercise. If your cholesterol levels are high they can be treated with tablets, known as statins, to reduce the risk of further artery furring. Tablets can also treat symptoms of chest pain and reduce the chance of a heart attack. If your angiogram suggests a very tight narrowing in one of the coronary arteries then a catheter can be used to open up the narrowing by blowing up a balloon at the narrowing (known as angioplasty) and inserting a metal tube (stent) to keep the artery open. If your angiogram shows more severe furring, especially if both the right and the left coronary arteries are affected, then a bypass operation may be required to improve the blood supply to the heart.

Coronary heart disease
Coronary artery disease; Arteriosclerotic heart disease; CHD; CAD
Last reviewed: June 22, 2012.

Coronary heart disease (CHD) is a narrowing of the small blood vessels that supply blood and oxygen to the heart. CHD is also called coronary artery disease.

Causes, incidence, and risk factors
Coronary heart disease (CHD) is the leading cause of death in the United States for men and women. Coronary heart disease is caused by the buildup of plaque in the arteries to your heart. This may also be calledhardening of the arteries.    Fatty material and other substances form a plaque build-up on the walls of your coronary arteries. The coronary arteries bring blood and oxygen to your heart. This buildup causes the arteries to get narrow. As a result, blood flow to the heart can slow down or stop.

A risk factor for heart disease is something that increases your chance of getting it. You cannot change some risk factors for heart disease, but others you can change. See: Heart disease - risk factors

Symptoms
Symptoms may be very noticeable, but sometimes you can have the disease and not have any symptoms. This is especially true in the early stages of heart disease. Chest pain or discomfort (angina) is the most common symptom. You feel this pain when the heart is not getting enough blood or oxygen. How bad the pain is varies from person to person.    It may feel heavy or like someone is squeezing your heart. You may feel it under your breast bone (sternum), but also in your neck, arms, stomach, or upper back. The pain usually occurs with activity or emotion, and goes away with rest or a medicine callednitroglycerin. Other symptoms include shortness of breath and fatigue with activity (exertion).

Women, elderly people, and people with diabetes are more likely to have symptoms other than chest pain, such as:    Fatigue Shortness of breath General weakness

Signs and tests
Your doctor or nurse will examine you. Your doctor will often order more than one test before making a diagnosis. Tests may include:

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Coronary angiography -- an invasive test that evaluates the heart arteries under x-ray Echocardiogram stress test Electrocardiogram (ECG) Electron-beam computed tomography (EBCT) to look for calcium in the lining of the arteries -- the more calcium, the higher your chance for CHD Exercise stress test Heart CT scan Nuclear stress test

Treatment
You may be asked to take one or more medicines to treat blood pressure, diabetes, or high cholesterol levels. Follow your doctor's directions closely to help prevent coronary artery disease from getting worse. Goals for treating these conditions in people who have coronary artery disease:    Blood pressure less than or equal to 140/90 (even lower for patients with diabetes, kidney disease, or heart failure) HbA1c levels if you have diabetes at a level recommended by your doctor LDL cholesterol level less than or equal to 100 mg/dL (even lower for some patients)

Treatment depends on your symptoms and how severe the disease is. Your doctor may give you one or more medicines to treat heart disease, blood pressure, diabetes, or high cholesterol. Follow your doctor's directions closely to help prevent coronary artery disease from getting worse. Never stop taking your medicines without talking to your doctor first. Stopping heart medicines suddenly can make your angina worse or cause a heart attack. Your doctor may refer you to a cardiac rehabilitation program to help improve your heart's fitness. Procedures and surgeries used to treat CHD include:    Angioplasty and stent placement, called percutaneous coronary interventions (PCIs) Coronary artery bypass surgery Minimally invasive heart surgery

Expectations (prognosis)
Everyone recovers differently. Some people can maintain a healthy life by changing their diet, stopping smoking, and taking medications exactly as the doctor prescribes. Others may need medical procedures such as angioplasty or surgery. Although everyone is different, early detection of CHD generally results in a better outcome.

Calling your health care provider
If you have any risk factors for CHD, contact your doctor to discuss prevention and possible treatment. Immediately contact your health care provider, call the local emergency number (such as 911), or go to the emergency room if you have:    Angina or chest pain Shortness of breath Symptoms of a heart attack

The heart is a muscular organ that pumps blood to the body at an average of 72 times per minute. Oxygen and nutrients serve as a fuel supply to the pump and are carried to heart in the form of

blood that flows through the coronary arteries. Thus, the coronary arteries serve as fuel pipe lines to the heart muscle.

The three major coronary arteries (Left Anterior Descending (LAD), Circumflex (Circ) and Right Coronary Artery (RCA)) and their respective branches each supply a designated portion of the heart, as follows: The LAD supplies blood to the front (anterior) portion of the heart and the septum (muscle partition that separates the Left Ventricle (LV) and Right Ventricle (RV)). TheCirc supplies the back (posterior) portion of the LV. The RCA supplies the bottom (inferior) portion of the ventricle and also the RV in 90% of cases. In the other 10%, the Circ sends a branch to the inferior wall of the LV. Coronary arteries have muscle fibers within their walls. By contracting the muscle, the artery can reduce blood flow; relaxing the muscle increases flow. In this way, the coronary arteries can regulate blood flow to different portions of the heart. Occasionally, the muscle within a coronary artery may go into spasm and markedly reduce blood flow to the heart muscle. This condition is known as coronary spasm. Typically, the chest discomfort of coronary artery spasm occurs at rest, and usually during the early morning hours. When the spasm is relieved (spontaneously or with the use of medications), the blood vessel goes back to its normal appearance and function. A temporary decrease in blood supply can cause chest discomfort while a persistent decrease can result in permanent muscle damage or a heart attack. Atherosclerosis is by far the commonest cause of coronary artery blockage. Unlike coronary spasm which creates a temporary blockage, atherosclerosis results in a fixed blockage. Occasionally, atherosclerosis may be accompanied by coronary spasm. The diagrams below show the various stages of progression of atherosclerosis and development of coronary artery blockages. The round picture on the left of each illustration is a cross-sectional view of the coronary artery, while the picture on the right is a longitudinal section at the same level.

The inner lining of the normal coronary artery is smooth and free of blockages or obstructions.

However, as we get older, lipids or fatty substances (cholesterol and triglycerides) are deposited as fatty streaks. The streaks are only minimally raised and thus do not produce any obstruction or symptoms.

Patients with one or more risk factors for CAD are susceptible to the increased buildup of fatty layers, known as atheroma (pronounced athe-a-roma). This buildup of material begins to encroach upon the inner channel and starts to interfere with the free flow of blood through the coronary artery.

Major risk factors for developing CAD include:
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Hyperlipidemia (high cholesterol level, particularly the "bad" component known as LowDensity Lipoprotein (LDL)) High blood pressure Diabetes Cigarette smoking Strong family history of CAD Male gender, obesity, age above 50 years, lack of exercise, stress and tension can also predispose to the development of atherosclerosis

The deposit of atheroma within the inner lining of arteries is called atherosclerosis (pronounced athrow-sklee-rosis). It is estimated that 1/3 of adult Americans develop some form of CAD. Significant atherosclerosis may be confined to the coronary arteries or may be associated with blockages within the arteries of the neck and those supplying blood to the lower limbs (legs)

As atherosclerosis progresses, fibers begin to grow into and around the fatty layers of atheroma, causing the blockage to harden and turn into a plaque (pronounced plak). The enlarging plaque (above) increases the encroachment into the inner channel of the coronary artery. When the channel is reduced by more than 50% (of the diameter) the artery may become obstructed enough to decrease blood flow to the heart muscle during times of increased need (exercise, emotional stress, etc.). During such times, the blood pressure and heart rate are both elevated and increase the need of oxygen and nutrients by the heart muscle.

The imbalance between the supply and demand of oxygen can cause chest discomfort (tightness, fullness, heaviness or pain) in the center of the chest and/or over the left breast). This is known as angina (pronounced an-ji-na) or angina pectoris. When the coronary artery blockage is severe enough to completely cut off the supply of oxygen and nutrients to the heart muscle, a heart attack can result. However, atherosclerosis may maintain a stable pattern for several years or even decades if the plaques grow slowly or remain relatively stationary. These patients may not notice worsening of angina during the time of stability and are said to have stable angina.

In other cases, plaques within the inner lining of the coronary artery may develop a slight crack or rupture. Note that the rupture involves only the surface and does not go through the wall of the artery. It is similar to a superficial crack on the plaster of a swimming pool lining, and blood does not escape out of the artery. Plaque rupture stimulates the production of blood clots that tries to seal off the superficial crack. The clot also gets into the crack and causes it to rise and further obstruct the channel of the artery. The sudden increase in the obstruction caused by the raised ruptured plaque and associated clot can transform a mild blockage into a critical one within a matter of hours (above). The decrease in blood flow to the heart muscle is severely reduced and the patient begins to have severe and prolonged chest pain that occurs at rest and may even awaken him or her from a sound sleep. This is known as unstable angina. If the clot does not fully close off the channel of the artery (as in the example above) enough blood flow is maintained to the heart muscle, and a heart attack may not develop if appropriate and prompt treatment is employed.

However, the clot may continue to grow in many cases. This can completely fill the open channel of the artery (above) and cut off blood flow to the part of the heart muscle that it supplies. Without oxygen and nutrients, the patient suffers from a heart attack and the involved heart muscle can get permanently damaged. The good news is that there are several forms of treatment that can get rid of the blood clot and restore flow across the artery. However, this can only be employed if the patient is rushed to the emergency room of the nearest hospital. Every minute counts in salvaging heart muscle. Coronary artery blockages and heart attacks may also be seen in patients who use "Crack" cocaine. This is becoming the commonest cause of heart attacks in young adults who are treated in emergency rooms in the USA.

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