HEART ATTACK
(MYOCARDIAL INFARCTION)
POWER POINTS about HEART ATTACK:
A heart attack is caused by a blood clot obstructing a coronary artery that supplies
blood to the heart muscle, causing death of muscle.
Cholesterol plaque accumulated on the inner wall of a coronary artery is usually the
site of blood clot formation.
A heart attack can cause chest pain and electrical instability of the heart.
Electrical instability of the heart can cause life threatening abnormal heart rhythm.
Treatment of heart attack include prompt administration of medications to dissolve
and prevent blood clots, balloon angioplasty (PTCA) to open obstructed artery, and
medications that open (dilate) blood vessels. Early reopening of a blocked coronary
artery reduces amount of heart muscle damage, 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.
What is a heart attack?
A heart attack (myocardial infarction) is the death of heart muscle due to the loss of blood
supply. Usually, 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 to the heart
muscle. Death of the heart muscle 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 can not 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 be treated
with medications once the patient reaches the hospital. Therefore, 90% to 95% of heart
attack victims who make it to the hospital survive. The 5% to 10% who later die are those
who have suffered major heart muscle damage.
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 on the artery walls which is caused by deposits of cholesterol on
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.
Heart muscle which is starved of blood oxygen, a condition called ischemia causes chest
pain (angina). Chest pain that occurs with exercise is called exertional angina. Exertional
angina is reversible, and subsides with rest. Occasionally, for unknown reasons, the
surface of the cholesterol plaque can become sticky, causing blood clotting. When a blood
clot forms on top of this plaque, the artery becomes completely blocked, causing death of
the heart muscle (heart attack).
Unlike exertional angina, death of the heart muscle from a heart attack is permanent.
Chest pain or pressure is a common symptom of heart attack. Heart attacks most
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. Interestingly, heart attacks do not
usually happen during exercise, although exercise is commonly associated with exertional
angina. One quarter of all heart attacks are silent, without chest pain.
Heart attack victims may complain of:
chest pressure
sweating
jaw pain
heartburn
arm pain
indigestion
back pain
general malaise
nausea
shortness of breath
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 muscle ischemia (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 creatinine phosphokinase (CPK) in the
blood. CPK is a muscle protein enzyme which is released into the blood circulation by
dying heart muscles when their surrounding membranes dissolve.
Treatment
The immediate goal of treatment is to quickly open blocked arteries and restore blood
flow to the heart muscles; 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 the patient after a heart attack.
The fastest method of opening a blocked artery, provided the hospital has a cardiac
catheterization facility, is to perform an immediate 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.
Medications, if given early, are also effective in opening arteries. Clot- dissolving
medications (thrombolytic agents) such as tissue plasminogen- activator (t-PA) and
streptokinase given intravenously can open 80% of the blocked arteries within 90 minutes.
The earlier they are administered, the better the chance of an early artery opening. If
thrombolytic agents are given too late (greater than 6 hours after the onset of chest pain),
most of the muscle damage has already occurred.
Anti-platelet agents, like aspirin, reduce the tendency of platelets in the blood to clump
and clot. This decreases the possibility of recurrent closure of the artery and improves the
chances of survival.
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 hours.
Nitroglycerin, a blood vessel dilator or vasodilator (which opens the blood vessel by
relaxing the muscular wall of the blood vessel) is given either under the tongue or
intravenously to prevent blood vessel spasm and to minimize the area of the heart attack.
ACE (angiotensin converting enzyme) inhibitors, another class of vasodilators, are given
orally after a 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 allowing the
damaged muscles to recover.
In some patients, PTCA can be technically difficult to perform. In others, PTCA and
medications fail to achieve reperfusion or maintain open arteries. These patients may be
considered for coronary artery bypass graft (CABG) surgery.
Heart attack patients are monitored in the hospital for 3 to 6 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, medications, or bypass surgery.
Patients gradually increase their activity under observation. Before discharge, low level
stress tests are useful for detecting significant residual narrowing in the coronary arteries,
rhythm changes, and heart muscle failure. They also guide the physicians in prescribing
activity regimens after discharge.
Recovery
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 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 four weeks, while a large heart attack results in a
six week recovery period. 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 activity which causes
shortness of breath or sweating.
Prevention
Aspirin and beta blockers (propranolol, metoprolol, atenolol, timolol) 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. ACE inhibitor medication
(mentioned above) aids in the healing process and improves long-term survival.
A full stress test, often with nuclear isotope imaging or soundwave testing
(echocardiography), is usually done at 4 to 8 weeks after the original heart attack to
determine whether further treatment is needed, such as a coronary artery bypass graft
surgery. Favorable stress testing results permit initiation of a program of cardiac
rehabilitation.
Future Outlook for Heart Attack Survivors:
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, derived from leech proteins, are being tested to complement
current therapies. Newer versions of t-PA are being developed to achieve a higher
percentage of open arteries. Work is being done with direct laser energy and ultrasound
waves to attack both the blood clot and the underlying plaque. 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.
