Heart Attack

(Myocardial Infarction)

Medical Authors and Editors: Dennis Lee, MD and Daniel Kulick, MD, FACC, FSCAI
Revising Medical Editor: Jay Marks, MD

← What is a heart attack?

← What causes a heart attack?
← What are the symptoms of a heart attack?
← What are the complications of a heart attack?
← What are the risk factors for atherosclerosis and heart attack?
← How is a heart attack diagnosed?
← How is a heart attack treated?
← What can a patient expect during recovery from a heart attack?
← How can a second heart attack be prevented?
← What about heart attacks in women?
← What is new in heart attack?
← Heart Attack At A Glance
← Related heart attack articles:
Heart attack - on WebMD
Heart attack - on eMedicineHealth
← Read what your doctor is reading:
Heart attack - on Medscape

What is a heart attack?

A heart attack (also known as a myocardial infarction) is the death of heart muscle from
the sudden blockage of a coronary artery by a blood clot. Coronary arteries are blood
vessels that supply the heart muscle with blood and oxygen. Blockage of a coronary
artery deprives the heart muscle of blood and oxygen, causing injury to the heart
muscle. Injury to the heart muscle causes chest pain and pressure. If blood flow is not
restored within 20 to 40 minutes, irreversible death of the heart muscle will begin to
occur. Muscle continues to die for six to eight hours at which time the heart attack
usually is "complete." The dead heart muscle is replaced by scar tissue.

Approximately one million Americans suffer a heart attack each year. Four hundred
thousand of them die as a result of their heart attack.

Click here to view interactive photos of hearts that have suffered a heart attack.

What causes a heart attack?

Atherosclerosis

Atherosclerosis is a gradual process in which plaques (collections) of cholesterol are

deposited in the walls of arteries. Cholesterol plaques cause hardening of the arterial
walls and narrowing of the inner channel (lumen) of the artery. Arteries that are narrowed
by atherosclerosis cannot deliver enough blood to maintain normal function of the parts
of the body they supply. For example, atherosclerosis of the arteries in the legs causes
reduced blood flow to the legs. Reduced blood flow to the legs can lead to pain in the
legs while walking or exercising, leg ulcers, or a delay in the healing of wounds to the
legs. Atherosclerosis of the arteries that furnish blood to the brain can lead to vascular
dementia (mental deterioration due to gradual death of brain tissue over many years) or
stroke (sudden death of brain tissue).

In many people, atherosclerosis can remain silent (causing no symptoms or health

problems) for years or decades. Atherosclerosis can begin as early as the teenage
years, but symptoms or health problems usually do not arise until later in adulthood
when the arterial narrowing becomes severe. Smoking cigarettes, high blood pressure,
elevated cholesterol, and diabetes mellitus can accelerate atherosclerosis and lead to
the earlier onset of symptoms and complications, particularly in those people who have a
family history of early atherosclerosis.

Coronary atherosclerosis (or coronary artery disease) refers to the atherosclerosis that
causes hardening and narrowing of the coronary arteries. Diseases caused by the
reduced blood supply to the heart muscle from coronary atherosclerosis are called
coronary heart diseases (CHD). Coronary heart diseases include heart attacks, sudden
unexpected death, chest pain (angina), abnormal heart rhythms, and heart failure due to
weakening of the heart muscle.

Atherosclerosis and angina pectoris

Angina pectoris (also referred to as angina) is chest pain or pressure that occurs when
the blood and oxygen supply to the heart muscle cannot keep up with the needs of the
muscle. When coronary arteries are narrowed by more than 50 to 70 percent, the
arteries cannot increase the supply of blood to the heart muscle during exercise or other
periods of high demand for oxygen. An insufficient supply of oxygen to the heart muscle
causes angina. Angina that occurs with exercise or exertion is called exertional angina.
In some patients, especially diabetics, the progressive decrease in blood flow to the
heart may occur without any pain or with just shortness of breath or unusually early
fatigue.

Exertional angina usually feels like a pressure, heaviness, squeezing, or aching across
the chest. This pain may travel to the neck, jaw, arms, back, or even the teeth, and may
be accompanied by shortness of breath, nausea, or a cold sweat. Exertional angina
typically lasts from one to 15 minutes and is relieved by rest or by placing a nitroglycerin
tablet under the tongue. Both resting and nitroglycerin decrease the heart muscle's
demand for oxygen, thus relieving angina. Exertional angina may be the first warning
sign of advanced coronary artery disease. Chest pains that just last a few seconds rarely
are due to coronary artery disease.

Angina also can occur at rest. Angina at rest more commonly indicates that a coronary
artery has narrowed to such a critical degree that the heart is not receiving enough
oxygen even at rest. Angina at rest infrequently may be due to spasm of a coronary
artery (a condition called Prinzmetal's or variant angina). Unlike a heart attack, there is
no permanent muscle damage with either exertional or rest angina.

Atherosclerosis and heart attack

Occasionally the surface of a cholesterol plaque in a coronary artery may rupture, and a
blood clot forms on the surface of the plaque. The clot blocks the flow of blood through
the artery and results in a heart attack (see diagram below). The cause of rupture that
leads to the formation of a clot is largely unknown, but contributing factors may include
cigarette smoking or other nicotine exposure, elevated LDL cholesterol, elevated levels
of blood catecholamines (adrenaline), high blood pressure, and other mechanical and
biochemical forces.

Unlike exertional or rest angina, heart muscle dies during a heart attack, and loss of the
muscle is permanent.

While heart attacks can occur at any time, more heart attacks occur between 4:00 A.M.
and 10:00 A.M. because of the higher blood levels of adrenaline released from the
adrenal glands during the morning hours. Increased adrenaline, as previously discussed,
may contribute to rupture of cholesterol plaques.

Approximately 50% of patients who develop heart attacks have warning symptoms such
as exertional angina or rest angina prior to their heart attacks, but these symptoms may
be mild and discounted.

What are the symptoms of a heart attack?

Although chest pain or pressure is the most common symptom of a heart attack, heart
attack victims may experience a diversity of symptoms that include:

← Pain, fullness, and/or squeezing sensation of the chest

← Jaw pain, toothache, headache

← Shortness of breath

← Nausea, vomiting, and/or general epigastric (upper middle abdomen) discomfort

← Sweating

← Heartburn and/or indigestion

← Arm pain (more commonly the left arm, but may be either arm)

← Upper back pain

← General malaise (vague feeling of illness)

← No symptoms (Approximately one quarter of all heart attacks are silent, without
chest pain or new symptoms. Silent heart attacks are especially common among
patients with diabetes mellitus.)

Even though the symptoms of a heart attack at times can be vague and mild, it is
important to remember that heart attacks producing no symptoms or only mild symptoms
can be just as serious and life-threatening as heart attacks that cause severe chest pain.
Too often patients attribute heart attack symptoms to "indigestion," "fatigue," or "stress,"
and consequently delay seeking prompt medical attention. One cannot overemphasize
the importance of seeking prompt medical attention in the presence of symptoms
that suggest a heart attack. Early diagnosis and treatment saves lives, and delays
in reaching medical assistance can be fatal. A delay in treatment can lead to
permanently reduced function of the heart due to more extensive damage to the heart
muscle. Death also may occur as a result of the sudden onset of arrhythmias such as
ventricular fibrillation.

What are the complications of a heart attack?

Heart failure

If a large amount of heart muscle dies, the ability of the heart to pump blood to the rest
of the body is diminished, and this can result in heart failure. The body retains fluid, and
organs, for example, the kidneys, begin to fail

Ventricular fibrillation

Injury to heart muscle also can lead to ventricular fibrillation. Ventricular fibrillation occurs
when the normal, regular, electrical activation of heart muscle contraction is replaced by
chaotic electrical activity that causes the heart to stop beating and pumping blood to the
brain and other parts of the body. Permanent brain damage and death can occur unless
the flow of blood to the brain is restored within five minutes.

Most of the deaths from heart attacks are caused by ventricular fibrillation of the heart
that occurs before the victim of the heart attack can reach an emergency room. Those
who reach the emergency room have an excellent prognosis; survival from a heart
attack with modern treatment should exceed 90%. The 1% to 10% of heart attack victims
who die later include those victims who suffer major damage to the heart muscle initially
or who suffer additional damage at a later time.

Deaths from ventricular fibrillation can be avoided by cardiopulmonary resuscitation

(CPR) started within five minutes of the onset of ventricular fibrillation. CPR requires
breathing for the victim and applying external compression to the chest to squeeze the
heart and force it to pump blood. When paramedics arrive, medications and/or an
electrical shock (cardioversion) can be administered to convert ventricular fibrillation
back to a normal heart rhythm and allow the heart to pump blood normally. Therefore,
prompt CPR and a rapid response by paramedics can improve the chances of survival
from a heart attack. In addition, many public venues now have defibrillators that provide
the electrical shock needed to restore a normal heart rhythm even before the
paramedics arrive. This greatly improves the chances of survival.

What are the risk factors for atherosclerosis and heart attack?

Factors that increase the risk of developing atherosclerosis and heart attacks include
increased blood cholesterol, high blood pressure, use of tobacco, diabetes mellitus,
male gender, and a family history of coronary heart disease. While family history and
male gender are genetically determined, the other risk factors can be modified through
changes in lifestyle and medications.

← High Blood Cholesterol (Hyperlipidemia). A high level of cholesterol in the

blood is associated with an increased risk of heart attack because cholesterol is
the major component of the plaques deposited in arterial walls. Cholesterol, like
oil, cannot dissolve in the blood unless it is combined with special proteins called
lipoproteins. (Without combining with lipoproteins, cholesterol in the blood would
turn into a solid substance.) The cholesterol in blood is either combined with
lipoproteins as very low-density lipoproteins (VLDL), low-density lipoproteins
(LDL) or high-density lipoproteins (HDL).

The cholesterol that is combined with low-density lipoproteins (LDL cholesterol) is

the "bad" cholesterol that deposits cholesterol in arterial plaques. Thus, elevated
levels of LDL cholesterol are associated with an increased risk of heart attack.

The cholesterol that is combined with HDL (HDL cholesterol) is the "good"
cholesterol that removes cholesterol from arterial plaques. Thus, low levels of
HDL cholesterol are associated with an increased risk of heart attacks.

Measures that lower LDL cholesterol and/or increase HDL cholesterol (losing
excess weight, diets low in saturated fats, regular exercise, and medications)
have been shown to lower the risk of heart attack. One important class of
 medications for treating elevated cholesterol levels (the statins) have actions in
addition to lowering LDL cholesterol which also protect against heart attack. Most
patients at "high risk" for a heart attack should be on a statin no matter what the
levels of their cholesterol. For more, please see the Cholesterol and Your Heart
article.

← High Blood Pressure (Hypertension). High blood pressure is a risk factor for
developing atherosclerosis and heart attack. Both high systolic pressure (when
the heart beats) and high diastolic pressure (when the heart is at rest) increase
the risk of heart attack. It has been shown that controlling hypertension with
medications can reduce the risk of heart attack. For more, please see the High
Blood Pressure article.

← Tobacco Use (Smoking). Tobacco and tobacco smoke contain chemicals that
cause damage to blood vessel walls, accelerate the development of
atherosclerosis, and increase the risk of heart attack. For more, please see the
Smoking and Quitting Smoking article.

← Diabetes (Diabetes Mellitus). Both insulin dependent and non-insulin

dependent diabetes mellitus (type 1 and 2, respectively) are associated with
accelerated atherosclerosis throughout the body. Therefore, patients with
diabetes mellitus are at risk for reduced blood flow to the legs, coronary heart
disease, erectile dysfunction, and strokes at an earlier age than non-diabetic
subjects. Patients with diabetes can lower their risk through rigorous control of
their blood sugar levels, regular exercise, weight control, and proper diets. For
more, please see the Diabetes article.

← Male Gender. At all ages, men are more likely than women to develop
atherosclerosis and coronary heart disease. Some scientists believe that this
difference is partly due to the higher blood levels of HDL cholesterol in women
than in men. However, this gender difference narrows as men and women grow
older.

← Family History of Heart Disease. Individuals with a family history of coronary

heart diseases have an increased risk of heart attack. Specifically, the risk is
higher if there is a family history of early coronary heart disease, including a heart
attack or sudden death before age 55 in the father or other first-degree male
relative, or before age 65 in the mother or other female first-degree female
relative.

How is a heart attack diagnosed?

When there is severe chest pain, suspicion that a heart attack is occurring usually is
high, and tests can be performed quickly that will confirm the heart attack. A problem
arises, however, when the symptoms of a heart attack do not include chest pain. A heart
attack may not be suspected, and the appropriate tests may not be performed.
Therefore, the initial step in diagnosing a heart attack is to be suspicious that one has
occurred.
Electrocardiogram. An electrocardiogram (ECG) is a recording of the electrical activity
of the heart. Abnormalities in the electrical activity usually occur with heart attacks and
can identify the areas of heart muscle that are deprived of oxygen and/or areas of
muscle that have died. In a patient with typical symptoms of heart attack (such as
crushing chest pain) and characteristic changes of heart attack on the ECG, a secure
diagnosis of heart attack can be made quickly in the emergency room and treatment can
be started immediately. If a patient's symptoms are vague or atypical and if there are
pre-existing ECG abnormalities, for example, from old heart attacks or abnormal
electrical patterns that make interpretation of the ECG difficult, the diagnosis of a heart
attack may be less secure. In these patients, the diagnosis can be made only hours later
through detection of elevated cardiac enzymes in the blood.

Blood tests. Cardiac enzymes are proteins that are released into the blood by dying
heart muscles. These cardiac enzymes are creatine phosphokinase (CPK), special sub-
fractions of CPK (specifically, the MB fraction of CPK), and troponin, and their levels can
be measured in blood. These cardiac enzymes typically are elevated in the blood
several hours after the onset of a heart attack. A series of blood tests for the enzymes
performed over a 24 hour period are useful not only in confirming the diagnosis of heart
attack, but the changes in their levels over time also correlates with the amount of heart
muscle that has died.

The most important factor in diagnosing and treating a heart attack is prompt
medical attention. Rapid evaluation allows early treatment of potentially life-threatening
abnormal rhythms such as ventricular fibrillation and allows early reperfusion (return of
blood flow to the heart muscle) by procedures that unclog the blocked coronary arteries.
The more rapidly blood flow is reestablished, the more heart muscle that is saved.

Large and active medical centers often have a "chest pain unit" where patients
suspected of having heart attacks are rapidly evaluated. If a heart attack is diagnosed,
prompt therapy is initiated. If the diagnosis of heart attack is initially unclear, the patient
is placed under continuous monitoring until the results of further testing are available.

Click here to read the Heart Attack Treatment article.

What about heart attacks in women?

Risk of heart attacks in women

Coronary artery disease (CAD) and heart attacks are erroneously believed to occur
primarily in men. Although it is true that the prevalence of CAD among women is lower
before menopause, the risk of CAD rises in women after menopause. At age 75, a
woman's risk for CAD is equal to that of a man's. CAD is the leading cause of death and
disability in women after menopause. In fact, a 50-year-old woman faces a 46% risk of
developing CAD and a 31% risk of dying from coronary artery disease. In contrast, her
probability of contracting and dying from breast cancer is 10% and 3%, respectively.

The risk factors for developing CAD in women are the same as in men; they are
increased blood cholesterol, high blood pressure, smoking cigarettes, diabetes mellitus,
and a family history of coronary heart disease at a young age.
Smoking cigarettes

Even "light" smoking raises the risk of CAD. In one study, middle-aged women who
smoked 1 to 14 cigarettes per day had a twofold increase in strokes (caused by
atherosclerosis of the arteries to the brain) whereas those who smoked more than 25
cigarettes per day had a risk of stroke 3.7 fold higher than that of nonsmoking women.
Furthermore, the combination of smoking and the use of birth control pills increase the
risk of heart attacks even further, especially in women over 35.
Quitting smoking immediately begins to reduce the risk of heart attacks. The risk
gradually decreases back down to the same risk of nonsmoking women after several
years of not smoking.

Cholesterol treatment guidelines in women

Current NCEP (National Cholesterol Education Program) treatment guidelines for

undesirable cholesterol levels are the same for women as for men. For more information
about the NCEP guidelines, please read The Guidelines on Cholesterol for Adults article.

Diagnosis of heart attacks in women

Women are more likely to encounter delays in establishing the diagnosis of heart attack
than men. This is in part because women tend to seek medical care later than men, and
in part because diagnosing heart attacks in women can sometimes be more difficult than
diagnosing heart attacks in men. The reasons are:

1. Women are more likely than men to have atypical heart attack symptoms such as
neck and shoulder pain, abdominal pain, nausea, vomiting, fatigue, and
shortness of breath.
2. Silent heart attacks (heart attacks with little or no symptoms) are more common
among women than among men.
3. Women have a higher occurrence than men of chest pain that is not caused by
heart disease, for example chest pain from spasm of the esophagus.
4. Women are less likely than men to have the typical findings on the ECG that are
necessary to diagnose a heart attack quickly.
5. Women are more likely than men to have angina (chest pain due to lack of blood
supply to the heart muscle) that is caused by spasm of the coronary arteries or
caused by disease of the smallest blood vessels (microvasculature disease).
Cardiac catheterization with coronary angiograms (x-ray studies of the coronary
arteries that are considered most reliable tests for CAD) will reveal normal
coronary arteries and therefore cannot be used to diagnose either of these two
conditions.
6. Women are more likely to have misleading, or "false positive" noninvasive tests
for CAD then men.

Because of the atypical nature of symptoms and the occasional difficulties in diagnosing
heart attacks in women, women are less likely to receive aggressive thrombolytic
therapy or coronary angioplasty, and are more likely to receive it later than men. Women
also are less likely to be admitted to a coronary care unit.

For more, please read the Heart Attack Symptoms - Different In Women! article.
Treatment of heart attacks in women

Thrombolytic (fibrinolytic or clot dissolving) therapy has been shown to reduce death
from heart attacks similarly in men and women; however, the complication of strokes
from the thrombolytic therapy may be slightly higher in women than in men.

Emergency percutaneous transluminal coronary angioplasty (PTCA) or coronary

stenting for acute heart attack is as effective in women as in men; however women may
have a slightly higher rate of procedure-related complications in their blood vessels
(such as bleeding or clotting at the point of insertion of the PTCA catheter in the groin)
and death. This higher rate of complications has been attributed to women's older age,
smaller artery size, and greater severity of angina. The long-term outcome of angioplasty
or stenting however, is similar in men and women, and should not be withheld due to
gender.

The immediate mortality from coronary artery bypass graft surgery (CABG) in women is
higher than that for men. The higher immediate mortality rate has been attributed to
women's older age, smaller artery size, and greater severity of angina (the same as for
PTCA). Long term survival, rate of recurrent heart attack and/or need for reoperation,
however, are similar in men and women after CABG.

Estrogen and coronary heart disease in women

After menopause, the production of estrogen by the ovaries gradually diminishes over
several years. Along with this reduction, there is an increase in LDL ("bad" cholesterol)
and a small decrease in HDL ("good" cholesterol). These changes in lipid levels are
believed to be one of the reasons for the increased risks of developing CAD after
menopause. Women who have had their ovaries surgically removed (oophorectomy) or
experience an early menopause also have an accelerated risk of CAD.

Since treatment with estrogen hormone results in higher HDL and lower LDL cholesterol
levels, doctors thought for many years that estrogen would protect women against CAD
(as well protect against dementia and stroke). Many studies have found that
postmenopausal women who take estrogen have lower CAD rates than women who do
not. Unfortunately many of the studies were observational studies (studies in which
women are followed over time but decide on their own whether or not they wish to take
estrogen). Observational studies have serious shortcomings because they are subject to
selection bias; for example, women who choose to take estrogen hormones may be
healthier and have a lower risk of heart attacks than those who do not. In other words,
something else in the daily habits of women who take estrogen (such as exercise or
healthier diet) may make them less likely to develop heart attacks. Therefore, only a
randomized trial (a study in which women agree to be assigned to estrogen or a placebo
or sugar pill at random but are not told which pills they took until the end of the study)
can establish the whether hormone therapy after menopause can prevent CAD.

HERS trial results

The Heart and Estrogen/progestin Replacement Study (HERS), was a randomized

placebo-controlled trial of the effect of the daily use of estrogens plus
medroxyprogesterone (progestin) on the rate of heart attacks in postmenopausal women
who already had CAD. The HERS trial did not find a reduction in heart attacks in women
who took hormone therapy. This lack of benefit in preventing heart attacks occurred
despite an 11% lower LDL and a 10% higher HDL cholesterol level in the women treated
with hormones. The study also found that more women in the hormone-treated group
experienced blood clots in the veins and gallbladder disease than women in the placebo-
treated group. (Blood clots in the veins are dangerous because these clots can travel to
the lungs and cause pulmonary embolism, a condition with chest pain, shortness of
breath, and even shock and death.) However, the increase in gallbladder disease and
blood clots among healthy users of estrogen who do not have heart disease is very
small.

Based on the results of this study, researchers concluded that estrogen is not effective in
preventing coronary artery disease and heart attacks in postmenopausal women who
already have CAD. It should be noted, however, that the results of the HERS trial only
apply to women who have known CAD prior to starting hormone therapy and not to
women without known coronary artery disease.

WHI trial results

The Women's Health Initiative (WHI) was the first randomized controlled trial designed to
determine the long-term benefits and risks of treatment with estrogens plus
medroxyprogesterone (progestin) in healthy menopausal women (women without CAD).
The results were reported in a series of articles in 2002, 2003, and 2004. The estrogen +
progestin portion of the WHI study had to be stopped earlier than planned, after just 5.2
years, because the increase in coronary heart disease, stroke, and pulmonary embolism
among women who use estrogen + progesterone outweighed the benefits of reduced
bone fractures and colon cancer. The estrogen-alone portion of the WHI was stopped
because women who took estrogen alone had no reduction in heart attack risk, yet there
was a significant increase in stroke risk.

The increase in breast cancer became apparent after three to five years, but the
increase in heart disease and pulmonary emboli occurred early on, in the first year.

For additional information on the WHI results, please read the article, The Women's
Health Initiative in Perspective: The Last Straw for Estrogen Therapy?

Recommendations for the use of estrogens plus medroxyprogesterone

(progestin) in women

Medicinenet Medical Editors believe that:

← Decision regarding use of hormone therapy has to be individualized, and all

women should discuss with their physicians what is best for her.

← Estrogens plus medroxyprogesterone (progestin) is still the best therapy for hot
flashes. Despite the WHI study, many women remain good candidates for
estrogens plus medroxyprogesterone (progestin) therapy (or estrogen alone if
they have had hysterectomy). This is especially true if hormone therapy is limited
to the shortest duration, optimally less than five years.
 ← Estrogens with or without medroxyprogesterone (progestin) should not be used
to prevent or treat either Alzheimer's disease, heart disease, or stroke.

← While estrogens plus medroxyprogesterone (progestin) are effective in

preventing osteoporosis and related bone fractures, women concerned about the
risk of hormone therapy should discuss with their doctors, the use of other non-
hormonal alternatives to prevent and treat osteoporosis.

What is new in heart attack?

Greater public awareness about heart attacks and changes in lifestyle have contributed
to a dramatic reduction in the incidence of heart attacks during the last four decades.
Improved anticoagulant drugs such as hirudin and hirulog, are being tested and may
complement current therapies. The role of the "super aspirins" (Reopro and Integrilin) is
currently being investigated as well. More effective versions of TPA are being developed.
Increasingly, paramedics can do ECGs in the field, diagnose a heart attack, and take
patients directly to hospitals that have the ability to do PTCA and stenting. This can save
time and reduce damage to the heart. Recent data has shown that lowering blood LDL
levels even further than previously suggested may further decrease the risk of heart
attacks. Research also has shown that inflammation may play a role in the development
of atherosclerosis, and this is an active area of current investigation. There also is early
evidence that with genetic engineering it may be possible to develop a drug that can be
administered to clear plaques from arteries (a "scavenger molecule").

Heart Attack At A Glance

← A heart attack results when a blood clot completely obstructs a coronary artery
supplying blood to the heart muscle and heart muscle dies.

← The blood clot that causes the heart attack usually forms at the site of rupture of
an atherosclerotic, cholesterol plaque on the inner wall of a coronary artery.

← The most common symptom of heart attack is chest pain.

← The most common complications of a heart attack are heart failure, and
ventricular fibrillation.

← The risk factors for atherosclerosis and heart attack include elevated cholesterol
levels, increased blood pressure, tobacco use, diabetes, male gender and a
family history of heart attacks at an early age.

← Heart attacks are diagnosed with electrocardiograms and measurement of

cardiac enzymes in blood

← Early reopening of blocked coronary arteries reduces the amount of damage to

the heart and improves the prognosis for a heart attack.
← Medical treatment for heart attacks may include anti-platelet, anti-coagulant, and
clot dissolving drugs as well as angiotensin converting enzyme (ACE) inhibitors,
beta blockers and oxygen.

← Interventional treatment for heart attacks may include coronary angiography with
percutaneous transluminal coronary angioplasty (PTCA), coronary artery stents,
and coronary artery bypass grafting (CABG).

← Patients suffering a heart attack are hospitalized for several days to detect heart
rhythm disturbances, shortness of breath, and chest pain.

← Further heart attacks can be prevented by aspirin, beta blockers, ACE inhibitors,
discontinuing smoking, weight reduction, exercise, good control of blood
pressure and diabetes, following a low cholesterol and low saturated fat diet that
is high in omega-3-fatty acids, taking multivitamins with an increased amount of
folic acid, decreasing LDL cholesterol, and increasing HDL cholesterol.
←