Myocardial infarction

Heart attack
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A heart attack occurs when blood flow to a part of your heart is blocked for a long enough time
that part of the heart muscle is damaged or dies. The medical term for this is myocardial
infarction.

Causes
Most heart attacks are caused by a blood clot that blocks one of the coronary arteries. The
coronary arteries bring blood and oxygen to the heart. If the blood flow is blocked, the heart is
starved of oxygen and heart cells die.
A hard substance called plaque can build up in the walls of your coronary arteries. This plaque is
made up of cholesterol and other cells.
A heart attack may occur when:

Blood platelets stick to tears in the plaque and form a blood clot that blocks blood from
flowing to the heart. This is the most common cause of heart attacks.

A slow buildup of this plaque may almost block one of your coronary arteries.

The cause of heart attacks is not always known. Heart attacks may occur:

When you are resting or asleep

After a sudden increase in physical activity

When you are active outside in cold weather

After sudden, severe emotional or physical stress, including an illness

Many risk factors may lead to a heart attack.

Symptoms

A heart attack is a medical emergency. If you have symptoms of a heart attack, call 911 or your
local emergency number right away.

DO NOT try to drive yourself to the hospital.

DO NOT WAIT. You are at greatest risk of sudden death in the early hours of a heart
attack.

Chest pain is the most common symptom of a heart attack. You may feel the pain in only one
part of your body, or it may move from your chest to your arms, shoulder, neck, teeth, jaw, belly
area, or back.
The pain can be severe or mild. It can feel like:

A tight band around the chest

Bad indigestion

Something heavy sitting on your chest

Squeezing or heavy pressure

The pain usually lasts longer than 20 minutes. Rest and a medicine called nitroglycerin may not
completely relieve the pain of a heart attack. Symptoms may also go away and come back.
Other symptoms of a heart attack can include:

Anxiety

Cough

Fainting

Light-headedness, dizziness

Nausea or vomiting

Palpitations (feeling like your heart is beating too fast or irregularly)

Shortness of breath

Sweating, which may be very heavy

Some people (the elderly, people with diabetes, and women) may have little or no chest pain. Or,
they may have unusual symptoms (shortness of breath, fatigue, and weakness). A "silent heart
attack" is a heart attack with no symptoms.

Exams and Tests

A doctor or nurse will perform a physical exam and listen to your chest using a stethoscope.

The doctor may hear abnormal sounds in your lungs (called crackles), a heart murmur, or
other abnormal sounds.

You may have a fast or uneven pulse.

Your blood pressure may be normal, high, or low.

You will have an electrocardiogram (ECG) to look for heart damage. A troponin blood test can
show if you have heart tissue damage. This test can confirm that you are having a heart attack.
Coronary angiography may be done right away or when you are more stable.

This test uses a special dye and x-rays to see how blood flows through your heart.

It can help your doctor decide which treatments you need next.

Other tests to look at your heart that may be done while you are in the hospital:

Echocardiography

Exercise stress test

Nuclear stress test

Treatment
In the emergency room:

You will be hooked up to a heart monitor, so the health care team can look at how your
heart is beating.

You will receive oxygen so that your heart doesn't have to work as hard.

An intravenous line (IV) will be placed into one of your veins. Medicines and fluids pass
through this IV.

You may get nitroglycerin and morphine to help reduce chest pain.

You may receive aspirin, unless it would not be safe for you. In that case, you will be
given another medicine that prevents blood clots.

Dangerous abnormal heartbeats (arrhythmias) may be treated with medicine or electric

shocks.

EMERGENCY TREATMENTS
Angioplasty is a procedure to open narrowed or blocked blood vessels that supply blood to the
heart.

Angioplasty is often the first choice of treatment. It should be done within 90 minutes
after you get to the hospital, and no later than 12 hours after a heart attack.

A stent is a small, metal mesh tube that opens up (expands) inside a coronary artery. A
stent is often placed after angioplasty. It helps prevent the artery from closing up again.

You may be given drugs to break up the clot. It is best if these drugs are given within 3 hours of
when you first felt the chest pain. This is called thrombolytic therapy.
Some patients may also have heart bypass surgery to open narrowed or blocked blood vessels
that supply blood to the heart. This procedure is also called open heart surgery.
AFTER YOUR HEART ATTACK
After several days, you will be discharged from the hospital.
You will likely need to take medicines, possibly for the rest of your life. Always talk to your
health care provider before stopping or changing how you take any medicines.
While under the care of your health care team, you will learn:

How to take medicines to treat your heart problem and prevent more heart attacks

How to eat a heart-healthy diet

How to be active and exercise safely

What to do when you have chest pain

How to stop smoking

After a heart attack, you may feel sad. You may feel anxious and worry about being careful about
everything you do. All of these feelings are normal. They go away for most people after 2 or 3
weeks. You may also feel tired when you leave the hospital to go home.
Most people who have had a heart attack take part in a cardiac rehab program.

Support Groups
See: Heart disease - resources

Outlook (Prognosis)
After a heart attack, your chance of having another one is higher than if you never had a heart
attack.
How well you do after a heart attack depends on the damage to your heart muscle and heart
valves, and where that damage is located.
If your heart can no longer pump blood out to your body as well as it used to, you may develop
heart failure. Abnormal heart rhythms can occur, and they can be life threatening.
Usually a person who has had a heart attack can slowly go back to normal activities, including
sexual activity. Discuss your activity level with your health care provider.

Alternative Names
Myocardial infarction; MI; Acute MI; ST-elevation myocardial infarction; Non-ST-elevation
myocardial infarction

References
From Wikipedia, the free encyclopedia
Jump to: navigation, search
"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).
Not to be confused with Cardiac arrest.

Myocardial infarction
Classification and external resources

Diagram of a myocardial infarction (2) of the tip of

the anterior wall of the heart (an apical infarct) after
occlusion (1) of a branch of the left coronary artery
(LCA). In the diagram, RCA is the right coronary
artery.
ICD-10
I21-I22
ICD-9
410
DiseasesDB
8664
MedlinePlus
000195
eMedicine
med/1567 emerg/327 ped/2520
MeSH
D009203
Myocardial infarction (MI) or acute myocardial infarction (AMI), is the medical term for an
event commonly known as a heart attack. It happens when blood stops flowing properly to part
of the heart and the heart muscle is injured due to not getting enough oxygen. Usually this is
because one of the coronary arteries that supplies blood to the heart develops a blockage due to
an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is
sudden and serious.
A person having an acute myocardial infarction usually has sudden chest pain that sometimes
travels to the left arm and the left side of the neck. The chest pain is referred to as "retrosternal"
because it is felt behind the breastbone, also called the sternum. Additionally, the person often
suffers from shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety.
The anxiety is often described as a "sense of impending doom."[1] Women experience fewer of
these symptoms than men, but usually have shortness of breath, weakness, a feeling of
indigestion, and fatigue.[2] In many cases, in some estimates as high as 64 percent, the person
does not have chest pain or other symptoms.[3] These are called "silent" myocardial infarctions.

Immediate treatments for a suspected acute myocardial infarction include oxygen to help with
breathing, aspirin, which prevents the blood from clotting and forming further blockages, and
nitroglycerin to treat chest pain.[4]
There are many ways a doctor can test a person to determine if they have had a myocardial
infarction, such as electrocardiograms (ECGs) that trace the electrical signals in the heart,
echocardiography that maps the heart by the sounds that it makes, internal images taken by
magnetic resonance imaging (MRI), and testing the blood for substances associated with damage
to the heart muscle. Common blood tests are for creatine kinase (CK-MB) and troponin, both of
which are released by damaged muscles such as the heart.
ECG testing is used to differentiate between two types of myocardial infarctions based on the
shape of the tracing. When the ST section of the tracing is higher than the baseline it is called an
ST-elevation myocardial infarction (STEMI) which usually requires more aggressive treatment.
STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical
methods are angioplasty where the arteries are pushed opened and thrombolysis where the
blockage is removed using medications.[5] Non-ST elevation myocardial infarction (NSTEMI)
may be managed with medication, although angioplasty may be required if the person is
considered to be at high risk.[6] People who have multiple blockages of their coronary arteries,
particularly if they also have diabetes, may also be treated with bypass surgery (CABG).[7][8]
Ischemic heart disease, which includes myocardial infarction, angina and heart failure when it
happens after myocardial infarction, was the leading cause of death for both men and women
worldwide in 2011.[9][10] Important risk factors are previous cardiovascular disease, older age,
tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol,
triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood
pressure, lack of physical activity and obesity, chronic kidney disease, excessive alcohol
consumption, the use of illicit drugs (such as cocaine and amphetamines), and chronic high stress
levels.[11][12][13]

Contents

1 Classification

2 Signs and symptoms

3 Causes
o 3.1 Risk factors

4 Pathophysiology

5 Diagnosis

6 Prevention

7 Management
o 7.1 STEMI

8 Prognosis
o 8.1 Complications

9 Epidemiology

10 Legal implications

11 Research

12 References

13 External links

Classification
There are two basic types of acute myocardial infarction based on pathology:

Transmural: associated with atherosclerosis involving a major coronary artery. It can be

subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend
through the whole thickness of the heart muscle and are usually a result of complete
occlusion of the area's blood supply.[14] In addition, on ECG, ST elevation and Q waves
are seen.

Subendocardial: involving a small area in the subendocardial wall of the left ventricle,
ventricular septum, or papillary muscles. The subendocardial area is particularly
susceptible to ischemia.[14] In addition, ST depression is seen on ECG.

In the clinical context, a myocardial infarction can be further subclassified into a ST elevation
MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes.[15] The phrase
heart attack is sometimes used incorrectly to describe sudden cardiac death, which may or may
not be the result of acute myocardial infarction. A heart attack is different from, but can be the
cause of cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia, an
abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart
is impaired; however severe myocardial infarction may lead to heart failure.[7] A 2007 consensus
document classifies myocardial infarction into five main types:[16]

Type 1 Spontaneous myocardial infarction related to ischemia due to a primary

coronary event such as plaque erosion and/or rupture, fissuring, or dissection

Type 2 Myocardial infarction secondary to ischemia due to either increased oxygen

demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia,
arrhythmias, hypertension, or hypotension

Type 3 Sudden unexpected cardiac death, including cardiac arrest, often with symptoms
suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or
evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but
death occurring before blood samples could be obtained, or at a time before the
appearance of cardiac biomarkers in the blood

Type 4 Associated with coronary angioplasty or stents:

o Type 4a Myocardial infarction associated with PCI
o Type 4b Myocardial infarction associated with stent thrombosis as documented
by angiography or at autopsy

Type 5 Myocardial infarction associated with CABG

Signs and symptoms

Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red:
other possible areas; view of the chest

Back view
The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes,
and rarely instantaneous.[17] Chest pain is the most common symptom of acute myocardial
infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain
due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina
pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck,
right arm, back, and epigastrium,[7][18] where it may mimic heartburn. Levine's sign, in which the
patient localizes the chest pain by clenching their fist over the sternum, has classically been
thought to be predictive of cardiac chest pain, although a prospective observational study showed
that it had a poor positive predictive value.[19]
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left
ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms
include diaphoresis (an excessive form of sweating),[1] weakness, light-headedness, nausea,
vomiting, and palpitations. These symptoms are likely induced by a massive surge of
catecholamines from the sympathetic nervous system[20] which occurs in response to pain and the
hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to
inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the
development of ventricular fibrillation) can occur in myocardial infarctions.[7]
Female, elderly, and diabetic patients report atypical symptoms more frequently than their male
and younger counterparts.[21][22] Women also report more numerous symptoms compared with
men (2.6 on average vs 1.8 symptoms in men).[21] The most common symptoms of MI in women
include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and
dyspnea have been reported as frequently occurring symptoms that may manifest as long as one
month before the actual clinically manifested ischemic event. In women, chest pain may be less
predictive of coronary ischemia than in men.[23]
At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms.
[3][24]
These cases can be discovered later on electrocardiograms, using blood enzyme tests or at
autopsy without a prior history of related complaints. Estimates of the prevalence of silent
myocardial infarctions vary between 22 and 64%.[3] A silent course is more common in the
elderly,[3] in patients with diabetes mellitus[25] and after heart transplantation, probably because

the donor heart is not fully innervated by the nervous system of the recipient.[26] In people with
diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have
been cited as possible explanations for the lack of symptoms.[25]
Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are
called an acute coronary syndrome.[27]
The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary
embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension
pneumothorax, and esophageal rupture. Other non-catastrophic differentials include
gastroesophageal reflux and Tietze's syndrome.[28]

Causes

The animation shows how plaque buildup or a coronary artery spasm can lead to a heart attack
and how blocked blood flow in a coronary artery can lead to a heart attack.
Heart attack rates are higher in association with intense exertion, be it psychological stress or
physical exertion, especially if the exertion is more intense than the individual usually performs.
[citation needed]
The period of intense exercise and subsequent recovery is associated with about a 6fold higher myocardial infarction rate (compared with other more relaxed time frames) for
people who are very physically fit.[citation needed] For those in poor physical condition, the rate
differential is over 35-fold higher.[citation needed] One observed mechanism for this phenomenon is
increased pulse pressure, which increases stretching of the arterial walls.[citation needed] This
stretching results in significant shear stress on atheromas, which results in debris breaking loose
from these deposits.[citation needed] This debris floats through the blood vessels, eventually clogging
the major coronary arteries.[citation needed]
Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more
controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[29]
While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is

inconclusive as to whether it can be considered a causative factor.[29] Treatment with antibiotics

in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or
other coronary vascular diseases.[30]
There is an association of an increased incidence of a heart attack in the morning hours, more
specifically around 9 a.m.[31][32][33] Some investigators have noticed that the ability of platelets to
aggregate varies according to a circadian rhythm, although they have not proven causation.[34]

Risk factors
Myocardial infarction results from atherosclerosis.[7] Smoking appears to be the cause of about
36% of coronary artery disease and obesity 20%.[35] Lack of exercise has been linked to 7-12% of
cases.[35][36] Job stress appear to play a minor role accounting for about 3% of cases.[35]
Risk factors for myocardial infarction include:

Age[11]

Sex: At any given age men are more at risk than women, particularly before menopause,
[37]
but because in general women live longer than men ischemic heart disease causes
slightly more total deaths in women.[11]

Diabetes mellitus (type 1 or 2)[38]

High blood pressure[39]

Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood),

particularly high low-density lipoprotein, low high-density lipoprotein and high
triglycerides[39]

Tobacco smoking, including secondhand smoke[39]

Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and
sulfur dioxide but not the ozone.[40]

Family history of ischaemic heart disease or myocardial infarction particularly if one has
a first-degree relative (father, brother, mother, sister) who suffered a 'premature'
myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65
(women).[11]

Obesity[41] (defined by a body mass index of more than 30 kg/m, or alternatively by waist
circumference or waist-hip ratio).

Lack of physical activity.[11]

Psychosocial factors including, low socio-economic status, social isolation, negative

emotions and stress increase the risk of myocardial infarction and are associated with
worse outcomes after myocardial infarction. Socioeconomic factors such as a shorter
education and lower income (particularly in women), and unmarried cohabitation are also
correlated with a higher risk of MI.[42]

Alcohol Studies show that prolonged exposure to high quantities of alcohol can
increase the risk of heart attack.

Oral contraceptive pill women who use combined oral contraceptive pills have a
modestly increased risk of myocardial infarction, especially in the presence of other risk
factors, such as smoking.[43]

Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with

premature atherosclerosis,[44] whether elevated homocysteine in the normal range is
causal is contentious.[45]

Inflammation is known to be an important step in the process of atherosclerotic plaque

formation.[46] C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation.
Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk
of MI, as well as stroke and development of diabetes.[46] Moreover, some drugs for MI might also
reduce CRP levels.[46] The use of high-sensitivity CRP assays as a means of screening the general
population is advised against, but it may be used optionally at the physician's discretion in
patients who already present with other risk factors or known coronary artery disease.[47] Whether
CRP plays a direct role in atherosclerosis remains uncertain.[46] Inflammation in periodontal
disease may be linked to coronary heart disease, and, since periodontitis is very common, this
could have great consequences for public health.[48] Serological studies measuring antibody
levels against typical periodontitis-causing bacteria found that such antibodies were more present
in subjects with coronary heart disease.[49] Periodontitis tends to increase blood levels of CRP,
fibrinogen and cytokines;[50] thus, periodontitis may mediate its effect on MI risk via other risk
factors.[51] Preclinical research suggests that periodontal bacteria can promote aggregation of
platelets and promote the formation of foam cells.[52][53] A role for specific periodontal bacteria
has been suggested but remains to be established.[54] There is some evidence that influenza may
trigger an acute myocardial infarction.[55]
Baldness, hair greying, a diagonal earlobe crease (Frank's sign[56]) and possibly other skin
features have been suggested as independent risk factors for MI.[57] Their role remains
controversial; a common denominator of these signs and the risk of MI is supposed, possibly
genetic.[58]
Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the
coronary arteries can be detected with CT scans. Several studies have shown that coronary
calcium can provide predictive information beyond that of classical risk factors.[59][60][61]
Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining
a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. [62]

Non-modifiable risk factors include age, sex, and family history of an early heart attack, which is
thought of as reflecting a genetic predisposition.[citation needed] To understand epidemiological study
results, it is important to note that many factors associated with MI mediate their risk via other
factors. For example, the effect of education is partially based on its effect on income and marital
status.[42]

Pathophysiology
See also: Acute coronary syndrome

A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner
lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation,
totally occluding the artery and preventing blood flow downstream.

Drawing of the heart showing anterior left ventricle wall infarction

Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-STelevated myocardial infarction and ST-elevated myocardial infarction, which are most frequently
(but not always) a manifestation of coronary artery disease.[15] The most common triggering
event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads

to a clotting cascade, sometimes resulting in total occlusion of the artery.[63][64] Atherosclerosis is

the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this
case, the coronary arteries), typically over decades.[65] Blood stream column irregularities visible
on angiography reflect artery lumen narrowing as a result of decades of advancing
atherosclerosis.[66] Plaques can become unstable, rupture, and additionally promote a thrombus
(blood clot) that occludes the artery; this can occur in minutes. When a severe enough plaque
rupture occurs in the coronary vasculature, it leads to myocardial infarction (necrosis of
downstream myocardium).[63][64]
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic
cascade; the heart cells in the territory of the occluded coronary artery die (chiefly through
necrosis) and do not grow back. A collagen scar forms in its place. Recent studies indicate that
another form of cell death called apoptosis also plays a role in the process of tissue damage
subsequent to myocardial infarction.[67] As a result, the patient's heart will be permanently
damaged. This myocardial scarring also puts the patient at risk for potentially life threatening
arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with
catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The
difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a
feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of
these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart
rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is
ventricular tachycardia (V-Tach/VT), which may or may not cause sudden cardiac death.
However, ventricular tachycardia usually results in rapid heart rates that prevent the heart from
pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels,
which can lead to further coronary ischemia and extension of the infarct.
The cardiac defibrillator is a device that was specifically designed to terminate these potentially
fatal arrhythmias. The device works by delivering an electrical shock to the patient in order to
depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time
dependent, and the odds of successful defibrillation decline rapidly after the onset of
cardiopulmonary arrest.

Diagnosis
Main article: Myocardial infarction diagnosis
Medical societies recommend that the physician confirm that a patient is at high risk for
myocardial infarction before conducting imaging tests to make a diagnosis.[68] Patients who have
a normal ECG and who are able to exercise, for example, do not merit routine imaging.[68]
Imaging tests such as stress radionuclide myocardial perfusion imaging or stress
echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG and
cardiac biomarkers suggest the likelihood of a problem.[68]

The diagnosis of myocardial infarction can be made after assessing patient's complaints and
physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm
the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while
coronary angiogram allows visualization of narrowing or obstructions in the heart vessels.[69] At
autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological
findings.
A chest radiograph and routine blood tests may indicate complications or precipitating causes
and are often performed upon arrival to an emergency department. New regional wall motion
abnormalities on an echocardiogram are also suggestive of a myocardial infarction. Echo may be
performed in equivocal cases by the on-call cardiologist.[70] In stable patients whose symptoms
have resolved by the time of evaluation, Technetium (99mTc) sestamibi (i.e. a "MIBI scan") or
thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow
in conjunction with physiologic or pharmacologic stress.[70][71] Thallium may also be used to
determine viability of tissue, distinguishing whether non-functional myocardium is actually dead
or merely in a state of hibernation or of being stunned.[72]
WHO criteria[73] formulated in 1979 have classically been used to diagnose MI; a patient is
diagnosed with myocardial infarction if two (probable) or three (definite) of the following
criteria are satisfied:
1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
2. Changes in serial ECG tracings
3. Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and
troponin
The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.[74]
According to the new guidelines, a cardiac troponin rise accompanied by either typical
symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is
diagnostic of MI.

Prevention
The risk of a recurrent myocardial infarction decreases with strict blood pressure management
and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with
heart disease, and limitation of alcohol intake. People are usually commenced on several longterm medications post-MI, with the aim of preventing secondary cardiovascular events such as
further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA).
Unless contraindicated, such medications may include:[75][76]

Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to

reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line,
owing to its low cost and comparable efficacy, with clopidogrel reserved for patients

intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk
of cardiovascular events, however the risk of hemorrhage is increased.[77]

Beta blocker therapy such as metoprolol or carvedilol should be commenced.[78] These

have been particularly beneficial in high-risk patients such as those with left ventricular
dysfunction and/or continuing cardiac ischaemia.[79] -Blockers decrease mortality and
morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.

ACE inhibitor therapy should be commenced 2448 hours post-MI in hemodynamically

stable patients, particularly in patients with a history of MI, diabetes mellitus,
hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left
ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart
failure, and decrease ventricular remodelling post-MI.[80]

Statin therapy has been shown to reduce mortality and morbidity post-MI.[81][82] The
effects of statins may be more than their LDL lowering effects. The general consensus is
that statins have plaque stabilization and multiple other ("pleiotropic") effects that may
prevent myocardial infarction in addition to their effects on blood lipids.[83]

The aldosterone antagonist agent eplerenone has been shown to further reduce risk of
cardiovascular death post-MI in patients with heart failure and left ventricular
dysfunction, when used in conjunction with standard therapies above.[84] Spironolactone
is another option that is sometimes preferable to eplerenone due to cost.

Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a

measure of decreasing coronary heart disease.[85] In high-risk people there is no clear-cut
decrease in potentially fatal arrhythmias due to omega-3 fatty acids.[86] And they may
increase risk in some groups.[86]

Giving heparin to people with heart conditions like unstable angina and some forms of
heart attacks reduces the risk of having another heart attack. However, heparin also
increases the chance of minor bleeding.[87]

Management
Main article: Myocardial infarction management
An MI requires immediate medical attention. Treatment attempts to salvage as much
myocardium as possible and to prevent further complications, hence the phrase "time is muscle".
[88]
Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if
nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI.[89]
Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size,
calling into question the recommendation about its routine use.[90][91] Other analgesics such as
nitrous oxide are of unknown benefit.[6]

STEMI
Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be
performed in a timely manner.[92] If PCI cannot be performed within 90 to 120 minutes then
fibrinolysis, preferably within 30 minutes, is recommended.[93][94] If after fibrinolysis there is
significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in
ST elevation after 90 minutes then rescue PCI is indicated emergently.[95][94] After PCI people are
generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and
clopidogrel).[96]

Prognosis
The prognosis post myocardial infarction varies greatly, depending on a person's health, the
extent of the heart damage and the treatment given. For the period 20052008 in the United
States, the median mortality at 30 days was 16.6% with a range from 10.9% to 24.9% depending
on the hospital.[97] Using variables available in the emergency room, people with a higher risk of
adverse outcome can be identified. One study found that 0.4% of patients with a low-risk profile
died after 90 days, whereas in high-risk people it was 21.1%.[98]
Some of the more reproduced risk-stratifying factors include: age, hemodynamic parameters
(such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two
or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease and
elevation of cardiac markers.[98][99][100] Assessment of left ventricular ejection fraction may
increase the predictive power.[101] The prognostic importance of Q-waves is debated.[102]
Prognosis is significantly worsened if a mechanical complication such as papillary muscle or
myocardial free wall rupture occurs.[103] Morbidity and mortality from myocardial infarction has
improved over the years due to better treatment.[104]

Complications
Main article: Myocardial infarction complications
Complications may occur immediately following the heart attack (in the acute phase), or may
need time to develop (a chronic problem). Acute complications may include heart failure if the
damaged heart is no longer able to adequately pump blood around the body; aneurysm or rupture
of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the
papillary muscle; Dressler's syndrome; and arrhythmias, such as ventricular fibrillation,
ventricular tachycardia, atrial fibrillation and heart block. Longer-term complications include
heart failure, atrial fibrillation, and the increased risk of a second myocardial infarction.

Epidemiology
Myocardial infarction is a common presentation of ischemic heart disease/coronary artery
disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were
from ischemic heart disease;[10] with it being the leading cause of death in high or middle income

countries and second only to lower respiratory infections in lower income countries.[10]
Worldwide more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[105]
Rates of death from ischemic heart disease have slowed or declined in most high income
countries, although cardiovascular disease still accounted for 1 in 3 of all deaths in the USA in
2008.[106] In contrast, ischemic heart disease is becoming a more common cause of death in the
developing world. For example in India, ischemic heart disease had become the leading cause of
death by 2004 accounting for 1.46 million deaths (14% of total deaths) and deaths due to
ischemic heart disease were expected to double during 19852015.[107] Globally it is predicted
that disability adjusted life years (DALYs) lost to ischemic heart disease will account for 5.5% of
total DALYs in 2030, making it the second most important cause of disability (after unipolar
depressive disorder), as well as the leading cause of death by this date.[10]

Legal implications
At common law, in general a myocardial infarction is a disease, but may sometimes be an injury.
This can create coverage issues in administration of no-fault insurance schemes such as workers'
compensation. In general, a heart attack is not covered;[108] however, it may be a work-related
injury if it results, for example, from unusual emotional stress or unusual exertion.[109] In
addition, in some jurisdictions, heart attacks suffered by persons in particular occupations such as
police officers may be classified as line-of-duty injuries by statute or policy. In some countries or
states, a person having suffered from a myocardial infarction may be prevented from
participating in activity that puts other people's lives at risk, for example driving a car or flying
an airplane.[110]

Research
Patients who receive stem cell treatment by coronary artery injections of stem cells derived from
their own bone marrow after a myocardial infarction (MI) show improvements in left ventricular
ejection fraction and end-diastolic volume not seen with placebo. The larger the initial infarct
size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment
approach to ST elevation MI are proceeding.[111]
There are currently three biomaterial and tissue engineering approaches for the treatment of postMI conditions, but these are in an even earlier stage of medical research. Many questions and
issues must be addressed before they can be applied to patients. The first involves polymeric left
ventricular restraints in the prevention of heart failure. The second utilizes in vitro engineered
cardiac tissue, which is subsequently implanted in vivo. The final approach entails injecting cells
and/or a scaffold into the myocardium to create in situ engineered cardiac tissue.[112]

References
yocardial infarction (MI; ie, heart attack) is the irreversible necrosis of heart muscle secondary to
prolonged ischemia. Approximately 1.5 million cases of MI occur annually in the United States.

Essential update: Influenza vaccination reduces risk of ischemic events

In a case-control study of 559 Australian patients, 275 with acute MI (AMI) and 284 without,
vaccination against the influenza virus reduced the risk of ischemic events, even though the
influenza virus itself was not a significant predictor of AMI.[1, 2]
In all, 12.4% of the vaccinated subjects and 6.7% of the control subjects had influenza (odds
ratio, 1.97; 95% confidence interval [CI], 1.093.54).[2] After adjustment for confounding
variables (eg, age, male sex, high cholesterol levels, current smoker status, and influenza
vaccination in the study year), influenza exposure was not associated with a risk of AMI despite
the association observed in univariate analysis. In the multivariate analysis, flu vaccination was
associated with a 45% reduction in AMI risk.

Signs and symptoms

Patients with typical myocardial infarction may have the following prodromal symptoms in the
days preceding the event (although typical STEMI may occur suddenly, without warning):

Fatigue

Chest discomfort

Malaise

Typical chest pain in acute myocardial infarction has the following characteristics:

Intense and unremitting for 30-60 minutes

Retrosternal and often radiates up to the neck, shoulder, and jaw and down to the ulnar
aspect of the left arm

Usually described as a substernal pressure sensation that also may be characterized as

squeezing, aching, burning, or even sharp

In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness

and gas

The patients vital signs may demonstrate the following in myocardial infarction:

The patients heart rate is often increased secondary to sympathoadrenal discharge

The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular

rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular
arrhythmias; bradyarrhythmias may be present

In general, the patient's blood pressure is initially elevated because of peripheral arterial
vasoconstriction resulting from an adrenergic response to pain and ventricular
dysfunction

However, with right ventricular myocardial infarction or severe left ventricular

dysfunction, hypotension is seen

The respiratory rate may be increased in response to pulmonary congestion or anxiety

Coughing, wheezing, and the production of frothy sputum may occur

Fever is usually present within 24-48 hours, with the temperature curve generally parallel
to the time course of elevations of creatine kinase (CK) levels in the blood. Body
temperature may occasionally exceed 102F

See Clinical Presentation for more detail.

Diagnosis
Laboratory studies
Laboratory tests used in the diagnosis of myocardial infarction include the following:

Cardiac biomarkers/enzymes: The American College of Cardiology/American Heart

Association (ACC/AHA) guidelines on unstable angina/NSTEMI (nonST-segment
elevation myocardial infarction) recommend that in patients with suspected myocardial
infarction, cardiac biomarkers should be measured at presentation

Troponin levels: Troponin is a contractile protein that normally is not found in serum; it is
released only when myocardial necrosis occurs

Creatine kinase (CK) levels: CK-MB levels increase within 3-12 hours of the onset of
chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours

Myoglobin levels: Myoglobin is released more rapidly from infarcted myocardium than
is troponin; urine myoglobin levels rise within 1-4 hours from the onset of chest pain

Complete blood count

Chemistry profile

Lipid profile

C-reactive protein and other inflammation markers

Electrocardiography
The ECG is the most important tool in the initial evaluation and triage of patients in whom an
acute coronary syndrome (ACS), such as myocardial infarction, is suspected. It is confirmatory
of the diagnosis in approximately 80% of cases.
Cardiac imaging
For individuals with highly probable or confirmed ACS, a coronary angiogram can be used to
definitively diagnose or rule out coronary artery disease.
See Workup for more detail.

Management
Prehospital care
For patients with chest pain, prehospital care includes the following:

Intravenous access, supplemental oxygen, pulse oximetry

Immediate administration of aspirin en route

Nitroglycerin for active chest pain, given sublingually or by spray

Telemetry and prehospital ECG, if available

Emergency department and inpatient care

Initial stabilization of patients with suspected myocardial infarction and ongoing acute chest pain
should include administration of sublingual nitroglycerin if patients have no contraindications to
it.
The American Heart Association (AHA) recommends the initiation of beta blockers to all
patients with STEMI (unless beta blockers are contraindicated).
If STEMI is present, the decision must be made quickly as to whether the patient should be
treated with thrombolysis or with primary percutaneous coronary intervention (PCI).[3, 4]
Although patients presenting with no ST-segment elevation are not candidates for immediate
thrombolytics, they should receive anti-ischemic therapy and may be candidates for PCI urgently
or during admission.
Critical care units have reduced early mortality rates from acute myocardial infarction by
approximately 50% by providing immediate defibrillation and by facilitating the implementation

of beneficial interventions. These interventions include the administration of IV medications and

therapy designed to do the following:

Limit the extent of myocardial infarction

Salvage jeopardized ischemic myocardium

Recanalize infarct-related arteries