Heart Attack
(Myocardial Infarction)
What is
a heart attack?
A heart attack (also called a myocardial infarction) is the death of part of the
heart muscle due to its sudden loss of blood supply. Typically, the loss of blood
supply is caused by a complete blockage of a coronary artery by a blood clot.
A coronary artery is an artery that supplies blood (along with essential nutrients)
to the heart muscle. Death of the heart muscle often causes chest pain and electrical
instability of the heart muscle tissue. Electrical instability of the heart causes
ventricular fibrillation (chaotic electrical disturbance). Orderly transmission
of electrical signals in the heart is important for the regular beating (pumping)
of the heart. A heart undergoing ventricular fibrillation simply quivers, and
cannot pump or deliver oxygenated blood to the brain. Permanent brain damage and
death can occur unless oxygenated blood flow is restored within five minutes.
Approximately one million Americans suffer a heart attack annually. Four hundred
thousand of these victims die as a result. Many of the heart attack deaths are
due to ventricular fibrillation of the heart that occurs before the victim can
reach any medical assistance or the emergency room. These electrical disturbances
of the heart can often be successfully treated with medications or other means
by paramedics in the “field,” or upon arrival to the hospital. Approximately 90%
to 95% of heart attack victims who reach the hospital survive. The 5% to 10% who
later die are those who have suffered major heart muscle damage, or who suffer
an “extension” or enlargement of their heart attack.
Early heart attack deaths can be avoided if a bystander starts CPR (cardiopulmonary
resuscitation) within five minutes of the onset of ventricular fibrillation. CPR
involves breathing for the victim and applying external chest compression to make
the heart pump. When paramedics arrive, medications and/or electrical shock (cardioversion)
to the heart can be administered to convert ventricular fibrillation to a normal
heart rhythm. Therefore, prompt CPR and rapid paramedic response can improve the
survival chances from a heart attack.
What causes a heart attack?
A heart attack is caused by the formation of a blood clot on a cholesterol plaque
located on the inner wall of an artery to the heart (coronary artery). Cholesterol
is a fatty chemical which is part of the outer lining of cells in the body. Cholesterol
plaque is the formation of a hard, thick substance within the artery walls which
is caused by deposits of cholesterol in the artery walls; a process that begins
in the late teens. Over time, the accumulation of cholesterol plaque causes thickening
of the artery walls and narrowing of the arteries; a process called atherosclerosis.
Plaque accumulation can be accelerated by smoking, high blood pressure, elevated
cholesterol, and diabetes. Ultimately, atherosclerosis causes significant narrowing
of the coronary arteries. During exercise or excitement, the narrowed coronary
arteries cannot increase the blood supply to meet the increased oxygen demand
of the heart muscle. When the heart muscle is thus deprived of blood oxygen, a
condition called ischemia results; ischemia may be associated with chest pain
(angina pectoris). Typically, angina occurs with exertion, and subsides with rest.
When the narrowing in the artery becomes critical, angina at rest or “unstable”
angina may result. Unstable angina can be the harbinger of a heart attack in the
near future.
Occasionally the surface of the cholesterol plaque in the artery may rupture,
which leads to the formation of blood clot on the surface of the plaque, which
then completely occludes blood flow in the vessel and results in a heart attack
(see diagram). The cause of this “plaque rupture” is largely unknown, but contributing
factors may include cigarette smoking, elevated LDL cholesterol, elevated levels
of blood catecholamines (adrenaline), high blood pressure, and other mechanical
and biochemical forces.
Unlike exertional angina, death of the heart muscle from a heart attack is permanent.
For more information, please see the Cholesterol article of MedicineNet.com.
What are the symptoms of a heart attack?
Chest pain or pressure is a common symptom of heart attack. Cardiac chest pain
is often vague, or dull, and may be described as a pressure or band-like sensation,
squeezing, heaviness, or other discomfort. Heart attacks frequently occur from
4:00 A.M. to 10:00 A.M. due to higher adrenaline amounts released from the adrenal
glands during the morning hours. Increased adrenaline in the bloodstream can contribute
to the above mentioned plaque rupture. Interestingly, heart attacks do not usually
happen during exercise, although exercise is commonly associated with exertional
angina. Approximately one quarter of all heart attacks are silent, without chest
pain. In diabetics, the incidence of “silent” heart attacks may be much higher.
Heart attack victims may complain of:
- chest pressure
- sweating
- jaw pain
- heartburn and/or indigestion
- arm pain (more commonly
the left arm, but may be either)
- upper back pain
- general malaise (vague
feeling of illness)
- nausea
- shortness of breath
How is a
heart attack diagnosed?
The initial diagnosis of a heart attack is made by a combination of clinical symptoms
and characteristic electrocardiogram (EKG) changes. An EKG
is a recording of the electrical activity of the heart, and can detect areas of
ischemic heart muscle (muscle which is deprived of oxygen) and/or dead tissue
in the heart. However, confirmation of a heart attack can only be made hours later
through detection of elevated cardiac enzymes in the blood. Cardiac enzymes are
muscle proteins which are released into the blood circulation by dying heart muscles
when their surrounding membranes dissolve. Such enzymes include creatine kinase
(CK), special subforms of CK, and troponin. Achieving PROMPT MEDICAL ATTENTION
is the THE MOST IMPORTANT FACTOR for an improved prognosis with a heart attack.
Rapid evaluation allows early treatment of potentially life-threatening arrhythmias,
and permits early “reperfusion” (return of blood flow) of the heart muscle, as
described below. The sooner that reperfusion is established, the smaller the resultant
heart attack will be. Large and active cardiac centers often have a “chest pain
unit”, where patients are rapidly screened for the presence of a heart attack,
and prompt therapy is initiated. If the diagnosis of heart attack is initially
unclear, the patient is observed in a monitored setting, until the results of
further testing are available.
What are the treatment options for a heart attack?
The immediate goal of treatment is to quickly open the blocked artery and restore
blood flow to the heart muscle; a process called "reperfusion." Once the artery
is open, the heart attack is generally halted and the patient becomes pain free.
Early reperfusion minimizes the extent of heart muscle damage and preserves the
pumping function of the heart. Delay in establishing reperfusion can result in
irreversible death to the heart muscle cells and reduced pumping force of the
remaining heart muscle. The amount and health of the remaining heart muscle is
the major determinant of the future quality of life and longevity for a patient
after a heart attack. Optimal benefit is obtained if reperfusion can be established
in the first 4- 6 hours of a heart attack.
The most direct method of opening a blocked artery, provided the hospital has
a cardiac catheterization facility, is to perform an immediate coronary angiogram and PTCA (percutaneous
transluminal coronary angioplasty). Under X-ray guidance, a tiny plastic catheter
with a balloon at the end is advanced over a fine guide wire to the blockage site
and inflated, thus pushing the clot and plaque out of the way. PTCA can be effective
in opening up to 95% of arteries, usually within 60 minutes. In addition, the
angiogram allows evaluation of the status of the other coronary arteries, so that
long- term treatment plans may be formulated. Recently, it has been demonstrated
that the placement of a coronary stent (a tiny hollow cylinder) at the time of
PTCA results in even better long term outcomes, with a lower recurrence rate and
lower risk of repeat heart attack. These results may be further enhanced by the
addition of newer “super aspirins” (potent blood thinners that work to antagonize
the blood-clotting effects of platelets in the blood and in the cholesterol plaque),
which are given at the time of PTCA or coronary stenting. For further information,
please see the Angioplasty article of MedicineNet.com.
As an alternative to PTCA or stenting for an acute heart attack, certain clot
dissolving medicines (thrombolytic agents) such as tissue plasminogen activator
(TPA) or streptokinase given intravenously can successfully open up to 80% of
acutely occluded coronary arteries. The earlier these agents are administered,
the better the success at opening the artery, and the more effective the preservation
of heart muscle. If thrombolytic administration is given too late (more than 6
hours after the onset of the heart attack), most of the muscle damage may have
already occurred. When there will be a potential delay in the ability to perform
PTCA, either if the hospital does not have a catheterization laboratory with the
ability to perform PTCA, or if there are logistic reasons why PTCA will be delayed,
thrombolytic therapy is then be promptly administered to allow prompt reperfusion.
PTCA may then be performed in patients who fail to respond to thrombolytic therapy.
Thrombolytic therapy carries a significant bleeding risk, such that some patients
are not candidates for this therapy (patients with recent surgery or major trauma,
recent stroke, bleeding ulcer, or other related
conditions. Anti-platelet agents, like aspirin, reduce the tendency of platelets
in the blood to clump and clot. These agents work in conjunction with the above-mentioned
reprefusion therapies to decrease the possibility of recurrent closure of the
artery and improves the chances of survival. Aspirin is given to ALL patients
with a heart attack, unless there is a history of significant intolerance to aspirin.
An anti-coagulant, heparin, is given intravenously in the hospital as a blood-thinning
agent to prevent blood clots and to maintain an open artery during the initial
24-72 hours. Nitroglycerin, a vasodilator (blood vessel
dilator), which opens the blood vessel by relaxing the muscular wall of the blood
vessel, is given intravenously to prevent blood vessel spasm and to minimize the
size of the heart attack. ACE (angiotensin converting enzyme) inhibitors, another
class of vasodilators, are often given orally after a large heart attack to improve
the heart muscle healing process. Examples of ACE inhibitors include captopril (Capoten), enalapril (Vasotec), lisinopril (Zestril and Prinvil). These
medications reduce the stress load to the heart, thereby helping the damaged heart
muscle to recover. Beta blocking agents, such as propanalol, metoprolol, and atenelol, are also often
given during the acute heart attack to decrease the amount of muscle damage. Long-term
administration of these agents following a heart attack has been shown to improve
survival and reduce the risk of future heart attacks.
In some patients, PTCA can be technically difficult or dangerous to perform. In
others, PTCA and thrombolytic medications may fail to achieve reperfusion or maintain
open arteries. These patients may be considered for coronary artery bypass graft
(CABG) surgery. For more information, please see the Coronary Artery Bypass Graft article
of MedicineNet.com.
How does a patient recover from a heart attack?
Heart attack patients are monitored in the hospital for 3 or more days prior to
discharge home. Rhythm disturbances, shortness of breath due to heart failure,
or recurrent pain are indications for further therapy such as balloon angioplasty
or coronary stenting, additional medications, or bypass surgery. Patients gradually
increase their activity under observation. Before discharge, low level stress
testing may be performed to detect significant residual narrowing in the coronary
arteries, exercise-induced rhythm changes, heart muscle failure, and to help guide
the physicians in prescribing activity regimens after discharge. An abnormal stress
test prior to hospital discharge following a heart attack predicts a high risk
for subsequent cardiac events; if the patient has not yet had a coronary angiogram,
an abnormal pre-discharge stress test is a strong indication that angiography
should be performed. Before resuming full activity or work, several weeks are
needed for the area of the heart attack to heal. After a small heart attack, which
is measured by the size of heart muscle damage, patients can usually resume normal
activities after two weeks. These activities include returning to work as well
as normal sexual activity. A moderate heart attack requires limited, gradually
increasing activity for up to four weeks, while a large heart attack may result
in a recovery period of six weeks or longer. These time frames are necessary for
the dead heart muscle to substantially complete the scarring process. During this
healing period, patients should avoid vigorous exertion and heavy lifting (over
20 pounds) or any strenuous activity which causes shortness of breath or undue
fatigue. Cardiac rehabilitation programs provide a helpful transition to a safe
and full return to a normal lifestyle. In addition, cardiac rehabilitation allows
the prescription of a long-term exercise program individually tailored to each
patient.
How can I prevent a second heart attack?
Aspirin and beta blockers (propranolol, metoprolol,
atenolol) have been shown to reduce chances of a second heart attack and improve
future survival. Beta blockers antagonize the action of adrenaline and relieve
stress to the heart muscles. Stopping smoking, reducing weight and dietary fat,
controlling blood pressure and diabetes, and a reduction of serum cholesterol,
along with regular, carefully prescribed exercise can all improve the quality
of life and longevity after a heart attack. Reduction of LDL cholesterol to a
value below 100 mg/dl has been particularly demonstrated to have a beneficial
effect on long-term prognosis. ACE inhibitor medication (mentioned above) aids
in the healing process and improves long-term survival in selected patients.
In the months following a heart attack, further cardiac stress testing, with or
without adjunctive nuclear or echocardiographic imaging, may be prescribed to
determine if additional therapy will be necessary to prevent future heart attacks.
In addition, special testing may be required to evaluate for the risk of developing
cardiac arrhythmias. All such testing should be discussed with the patient’s health
care team.
What is in the future for heart attack sufferers?
Greater public awareness and lifestyle changes have contributed to a dramatic
reduction in the incidence of heart attacks over the last 4 decades. Improved
blood-thinning agents, such as Hirudin and Hirulog, are being tested to complement
current therapies. The role of the “super aspirins” (Reopro, Integrellin, and
Aggrastat) is currently being investigated as well. Newer versions of t-PA are
being developed to achieve a higher percentage of open arteries to the heart.
Emergency medical teams which rapidly respond, and are able to diagnose heart
attacks and administer emergency drugs in non- hospital settings, as well as performing
electrical defibrillation, have been shown in test cities, such as Seattle, to
improve outcome and save heart muscle. With the widespread application of modern
in-hospital and out of hospital programs for heart attack patients, the long-term
prognosis following a heart attack will only improve.
Heart Attack At A Glance
- A heart attack results
when a blood clot completely obstructs a coronary artery supplying blood to the
heart muscle.
- A heart attack causes death
of part of the heart muscle.
- The site of blood clot
formation during a heart attack is usually a cholesterol plaque on the inner wall
of a coronary artery.
- A heart attack can cause
chest pain, heart failure, and electrical instability of the heart.
- Electrical instability
of the heart can cause life threatening abnormal heart rhythm.
- Treatment of a heart attack
includes:
- Prompt administration of
drugs to dissolve and prevent blood clots
- Performance of angioplasty
or intracoronary stenting to open an obstructed artery
- Medications that open (dilate)
blood vessels.
- Early reopening of a blocked
coronary artery reduces the amount of heart muscle damage, lessens the size of
the heart attack, and improves prognosis.
- Patients suffering a heart
attack are hospitalized for several days to detect heart rhythm disturbance, and
observe for shortness of breath, and chest pain.
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