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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 6-8 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.
What causes a heart attack?
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 1 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
While heart attacks can occur at any time, most 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
Approximately 50% of patients who develop heart attacks have warning symptoms such as
exertional angina or rest angina prior to their heart attacks.
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
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?
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
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
*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.
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.
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
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:
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.
Silent heart attacks (heart attacks with little or no symptoms) are more common among
women than among men.
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.
Women are less likely than men to have the typical findings on the ECG that are necessary to
diagnose a heart attack quickly.
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.
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.
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 3-5 years, but the increase in heart disease
and pulmonary emboli occurred early on, in the first year.
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