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Coronary Heart Disease

Alternate Names

  • coronary artery disease
  • CHD
  • CAD
  • Atherosclerosis, hardening of the arteries
  • Coronary arteries

Definition

Coronary heart disease, abbreviated as CHD, refers to the narrowing of the coronary arteries that supply blood to the heart. Usually the buildup is the result of abnormal clogging of the arteries with fat deposits and cellular debris, known as atherosclerosis. CHD is a progressive disease that increases the risk of heart attack and sudden death.

What is going on in the body?

In order for the heart to pump as it should, the heart muscle needs a steady supply of oxygen-rich blood. This blood is delivered by the coronary arteries. Two main vessels branch out to supply blood to the entire muscle of the heart. The heart needs more oxygen during exercise and high levels of activity. Less is needed when the person is at rest.
In atherosclerosis, fatty deposits form under the inner lining of the blood vessels. When the coronary arteries become blocked, less blood can get through. The blockage can be small, or it may be large enough to fully obstruct blood flow. When blockage occurs in one or many coronary arteries, the condition is called coronary heart disease.
Small blockages may not always affect the heart's performance. The person may not have symptoms until the heart needs more oxygen-rich blood than the arteries can supply. This commonly occurs during exercise or other activity. The pain that results is called stable angina.
If a blockage is large, angina pain can occur with little or no activity. This is known as unstable angina. In this case, the flow of blood to the heart is so limited that the person cannot do daily tasks without bringing on an angina attack. When the blood flow to an area of the heart is completely blocked, a heart attack occurs.

Risks

What are the causes and risks of the disease?

CHD affects people of all races. It can be caused by a combination of unhealthy lifestyle and genetics. Factors that increase the risk of CHD include:
  • cigarette smoking and secondhand smoke
  • diabetes
  • high blood cholesterol, especially a high level of LDL, that is "bad" cholesterol
  • high blood levels of triglycerides
  • high blood pressure
  • lack of exercise
  • overweight or obesity
Age, gender, and genetic factors that affect heart disease risk are beyond a person's control. These include:
  • increasing age
  • male gender
  • a strong family history of coronary heart disease
  • family history of heart attack
  • family history of high cholesterol

Prevention

What can be done to prevent the disease?

Although family medical history or genetics cannot be changed, a person can lower his or her risk for developing CHD. Here are some steps that a person can take to lower his or her coronary risk factors:
  • Avoid smoking.
  • Control blood cholesterol and LDL.
  • Control diabetes.
  • Exercise regularly.
  • Follow a diet that is designed to lessen the risk factors for heart disease.
  • Keep high blood pressure under control.
Before menopause, women have some protection against heart disease. Experts believe this is due, in part, to the fact that they have adequate levels of the female hormone estrogen in their bodies. This hormone may have a protective effect because it tends to raise HDL ("good") cholesterol, and also lowers total cholesterol.
There is no proof that estrogen replacement therapy has this same protective effect in a woman who has gone through menopause. Estrogen replacement therapy is a form of hormone replacement therapy, or HRT. In fact, the latest recommendation from the American Heart Association, or AHA, does not advise starting HRT for the sole purpose of preventing heart disease because there is not enough data to support it.
This same advisory issued by the AHA in 2001 recommends that women who already have heart disease should not be started on HRT. In fact, a recent study has even shown that if HRT is started after a woman has a heart attack, she may be at a higher risk for worsening of her angina, or having other serious cardiac complications.

Diagnosed

How is the disease diagnosed?

The diagnosis of CHD starts with a medical history and physical exam. An electrocardiogram (ECG) may show abnormalities. However, an ECG may be normal between attacks of angina. A stress ECG is an ECG taken before, during, and after exercise. It is designed to bring on an attack of angina and record the changes that take place in the heart.
Sometimes the person is injected with a substance called thallium during the stress test. Special pictures are then taken of the heart. The thallium scan can show areas of the heart that are damaged.
The most reliable test for diagnosing CHD is a cardiac catheterization. In this procedure, a thin hollow tube or catheter is placed into an artery in the leg or arm. It is then passed through the artery and into the coronary artery. A contrast agent is injected into the tube. This allows the healthcare professional to watch the blood flow through the heart and its arteries. Other techniques that are being used to help in the diagnosis of CHD include stress echocardiograms and new generations of CT scans.

Long Term Effects

What are the long-term effects of the disease?

CHD is a progressive disease that can lead to heart attack and sudden death.

Other Risks

What are the risks to others?

Coronary heart disease is not contagious. However, it does tend to run in families.

Treatments

What are the treatments for the disease?

Several types of medicines are often used together to reduce the symptoms of stable angina caused by CHD.
  • Beta-blockers, such as atenolol (i.e., Tenormin) or metoprolol (i.e., Toprol XL, Lopressor), are used to decrease the work level of the heart.
  • Nitrates, such as nitroglycerin or isosorbide mononitrate (i.e., Imdur, ISMO, Monoket), help to expand the blood vessels that supply the heart.
  • Aspirin may prevent heart attacks and warfarin (i.e., Coumadin, Jantoven) may prevent blood clots. However, the use of warfarin in treating stable angina remains controversial. Statins, such as lovastatin (i.e., Altoprev, Mevacor) to lower the cholesterol and stabilize the plaque.
The American Heart Association recommends that people discuss risks and benefits of the medicine with the healthcare professional. Several surgical procedures can be used to reduce the symptoms of stable angina from coronary artery disease, such as:
  • angioplasty, a procedure in which a tube with a balloon is inserted to reopen the artery
  • atherectomy, which involves removing plaques that cause narrowing of a blood vessel
  • laser surgery, which uses light waves to dissolve plaques
  • placement of a stent, a small flexible metal tube, into the artery at the reopened area to keep it from narrowing again

Side Effects

What are the side effects of the treatments?

Side effects vary depending on the treatment used:
  • Aspirin and warfarin increase the risk of bleeding.
  • Beta-blockers can cause a slow heartbeat, low blood pressure, depression, erectile dysfunction, and unpleasant dreams.
  • Nitrates can cause headaches and low blood pressure.
  • Surgery can result in infection, bleeding, reactions to anesthesia, and even death.

After Treatment

What happens after treatment for the disease?

Most people who have coronary heart disease are advised to start a regular exercise program. A person who has CHD should make every effort to reduce coronary risk factors. This may include smoking cessation, control of other diseases such as diabetes and high blood pressure, and following a healthy diet for heart disease. Medicines may need to be adjusted to get the best response.

Monitor

How is the disease monitored?

The person will have regular examinations and tests by the healthcare professional to check the progress of the coronary heart disease. Any new or worsening symptoms should be reported to the healthcare professional.

Sources

Harrison's Principles of Internal Medicine, 1991

Merck Manual, 1999

Current Medical Diagnosis and Treatment, 1996

Heart Disease: A Textbook of Cardiovascular Medicine, Braunwald, E., 1980

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