A myocardial infarction (MI), commonly known as a heart attack occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing infarction (tissue death) to the heart muscle. The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. The pain may occasionally feel like heartburn. This is the dangerous type of acute coronary syndrome.
Other symptoms may include shortness of breath, nausea,
feeling faint, a cold sweat; feeling tired, and decreased level of
consciousness. About 30% of people have atypical symptoms. Women more often
present without chest pain and instead have neck pain, arm pain or feel tired.
Among those over 75 years old, about 5% have had an MI with little or no
history of symptoms. An MI may cause heart failure, an irregular heartbeat,
cardiogenic shock or cardiac arrest.
Most MIs occur due to coronary artery disease. Risk factors
include high blood pressure, smoking, diabetes, lack of exercise, obesity, high
blood cholesterol, poor diet, and excessive alcohol intake. The complete
blockage of a coronary artery caused by a rupture of an atherosclerotic plaque
is usually the underlying mechanism of an MI. MIs are less commonly caused by
coronary artery spasms, which may be due to cocaine, significant emotional
stress (often known as Takotsubo syndrome or broken heart syndrome) and extreme
cold, among others. Many tests are helpful to help with diagnosis, including
electrocardiograms (ECGs), blood tests and coronary angiography. An ECG, which
is a recording of the heart's electrical activity, may confirm an ST elevation
MI (STEMI), if ST elevation is present. Commonly used blood tests include
troponin and less often creatine kinase MB.
Treatment of an MI is time-critical. Aspirin is an
appropriate immediate treatment for a suspected MI. Nitroglycerin or opioids
may be used to help with chest pain; however, they do not improve overall
outcomes. Supplemental oxygen is recommended in those with low oxygen levels or
shortness of breath. In a STEMI, treatments attempt to restore blood flow to
the heart and include percutaneous coronary intervention (PCI), where the
arteries are pushed open and may be stented, or thrombolysis, where the
blockage is removed using medications. People who have a non-ST elevation
myocardial infarction (NSTEMI) are often managed with the blood thinner
heparin, with the additional use of PCI in those at high risk. In people with
blockages of multiple coronary arteries and diabetes, coronary artery bypass
surgery (CABG) may be recommended rather than angioplasty. After an MI,
lifestyle modifications, along with long-term treatment with aspirin, beta
blockers and statins, are typically recommended.
Worldwide, about 15.9 million myocardial infarctions
occurred in 2015. More than 3 million people had an ST elevation MI, and more than
4 million had an NSTEMI. STEMIs occur about twice as often in men as women.
About one million people have an MI each year in the United States. In the
developed world, the risk of death in those who have had a STEMI is about 10%.
Rates of MI for a given age have decreased globally between 1990 and 2010. In
2011, an MI was one of the top five most expensive conditions during inpatient
hospitalizations in the US, with a cost of about $11.5 billion for 612,000
hospital stays.
Terminology
Myocardial infarction (MI) refers to tissue death
(infarction) of the heart muscle (myocardium) caused by ischemia, the lack of
oxygen delivery to myocardial tissue. It is a type of acute coronary syndrome,
which describes a sudden or short-term change in symptoms related to blood flow
to the heart. Unlike the other type of acute coronary syndrome, unstable
angina, a myocardial infarction occurs when there is cell death, which can be
estimated by measuring by a blood test for biomarkers (the cardiac protein
troponin). When there is evidence of an MI, it may be classified as an ST
elevation myocardial infarction (STEMI) or Non-ST elevation myocardial
infarction (NSTEMI) based on the results of an ECG.
The phrase "heart
attack" is often used non-specifically to refer to myocardial
infarction. An MI is different from—but can cause—cardiac arrest, where the
heart is not contracting at all or so poorly that all vital organs cease to
function, thus leading to death. It is also distinct from heart failure, in
which the pumping action of the heart is impaired. However, an MI may lead to
heart failure.
Signs and symptoms
Chest pain that may or may not radiate to other parts of the
body is the most typical and significant symptom of myocardial infarction. It
might be accompanied by other symptoms such as sweating.
Pain
Chest pain is one of the most common symptoms of acute
myocardial infarction and is often described as a sensation of tightness,
pressure, or squeezing. Pain radiates most often to the left arm, but may also
radiate to the lower jaw, neck, right arm, back, and upper abdomen. The pain
most suggestive of an acute MI, with the highest likelihood ratio, is pain
radiating to the right arm and shoulder. Similarly, chest pain similar to a
previous heart attack is also suggestive. The pain associated with MI is
usually diffuse, does not change with position, and lasts for more than 20
minutes. It might be described as pressure, tightness, knifelike, tearing,
burning sensation (all these are also manifested during other diseases). It
could be felt as an unexplained anxiety, and pain might be absent altogether.
Levine's sign, in which a person localizes the chest pain by clenching one or
both fists over their sternum, has classically been thought to be predictive of
cardiac chest pain, although a prospective observational study showed it had a
poor positive predictive value.
Typically, chest pain because of ischemia, be it unstable
angina or myocardial infarction, lessens with the use of nitroglycerin, but
nitroglycerin may also relieve chest pain arising from non-cardiac causes.
Other
Chest pain may be accompanied by sweating, nausea or
vomiting, and fainting, and these symptoms may also occur without any pain at all.
Dizziness or lightheadedness is common and occurs due to reduction in oxygen
and blood to the brain. In females, the most common symptoms of myocardial
infarction include shortness of breath, weakness, and fatigue. Females are more
likely to have unusual or unexplained tiredness and nausea or vomiting as
symptoms. Females having heart attacks are more likely to have palpitations,
back pain, labored breath, vomiting, and left arm pain than males, although the
studies showing these differences had high variability. Females are less likely
to report chest pain during a heart attack and more likely to report nausea,
jaw pain, neck pain, cough, and fatigue, although these findings are inconsistent
across studies. Females with heart attacks also had more indigestion,
dizziness, loss of appetite, and loss of consciousness. Shortness of breath is
a common, and sometimes the only symptom, occurring when damage to the heart
limits the output of the left ventricle, with breathlessness arising either
from low oxygen in the blood or pulmonary edema.
Other less common symptoms include weakness,
light-headedness, palpitations, and abnormalities in heart rate or blood
pressure. These symptoms are likely induced by a massive surge of
catecholamines from the sympathetic nervous system, which occurs in response to
pain and, where present, low blood pressure. Loss of consciousness can occur in
myocardial infarctions due to inadequate blood flow to the brain and
cardiogenic shock, and sudden death, frequently due to the development of
ventricular fibrillation. When the brain was without oxygen for too long due to
a myocardial infarction, coma and persistent vegetative state can occur.
Cardiac arrest, and atypical symptoms such as palpitations, occurs more
frequently in females, the elderly, those with diabetes, in people who have
just had surgery, and in critically ill patients.
Absence
"Silent"
myocardial infarctions can happen without any symptoms at all. These cases can
be discovered later on electrocardiograms, using blood enzyme tests, or at
autopsy after a person has died. Such silent myocardial infarctions represent
between 22 and 64% of all infarctions, and are more common in the elderly, in those
with diabetes mellitus and after heart transplantation. In people with diabetes,
differences in pain threshold, autonomic neuropathy, and psychological factors
have been cited as possible explanations for the lack of symptoms. In heart
transplantation, the donor heart is not fully innervated by the nervous system
of the recipient.
Risk factors
The most prominent risk factors for myocardial infarction
are older age, actively smoking, high blood pressure, diabetes mellitus, and
total cholesterol and high-density lipoprotein levels. Many risk factors of
myocardial infarction are shared with coronary artery disease, the primary cause
of myocardial infarction, with other risk factors including male sex, low
levels of physical activity, a past family history, obesity, and alcohol use.
Risk factors for myocardial disease are often included in risk factor
stratification scores, such as the Framingham Risk Score. At any given age, men
are more at risk than women for the development of cardiovascular disease. High
levels of blood cholesterol are a known risk factor, particularly high
low-density lipoprotein, low high-density lipoprotein, and high triglycerides.
Many risk factors for myocardial infarction are potentially
modifiable, with the most important being tobacco smoking (including secondhand
smoke). Smoking appears to be the cause of about 36% and obesity the cause of
20% of coronary artery disease. Lack of physical activity has been linked to
7–12% of cases. Less common causes include stress-related causes such as job
stress, which accounts for about 3% of cases, and chronic high stress levels.
Diet
There is varying evidence about the importance of saturated
fat in the development of myocardial infarctions. Eating polyunsaturated fat
instead of saturated fats has been shown in studies to be associated with a
decreased risk of myocardial infarction, while other studies find little
evidence that reducing dietary saturated fat or increasing polyunsaturated fat
intake affects heart attack risk. Dietary cholesterol does not appear to have a
significant effect on blood cholesterol and thus recommendations about its consumption
may not be needed. Trans fats do appear to increase risk. Acute and prolonged
intake of high quantities of alcoholic drinks (3–4 or more daily) increases the
risk of a heart attack.
Genetics
Family history of ischemic heart disease or MI, particularly
if one has a male first-degree relative (father, brother) who had a myocardial
infarction before age 55 years, or a female first-degree relative (mother,
sister) less than age 65 increases a person's risk of MI.
Genome-wide association studies have found 27 genetic
variants that are associated with an increased risk of myocardial infarction.
The strongest association of MI has been found with chromosome 9 on the short
arm p at locus 21, which contains genes CDKN2A and 2B, although the single
nucleotide polymorphisms that are implicated are within a non-coding region.
The majority of these variants are in regions that have not been previously
implicated in coronary artery disease. The following genes have an association
with MI: PCSK9, SORT1, MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1,
CDKN2A, 2B, ABO, PDGF0, APOA5, MNF1ASM283, COL4A1, HHIPC1, SMAD3, ADAMTS7,
RAS1, SMG6, SNF8, LDLR, SLC5A3, MRPS6, and KCNE2.
Other
The risk of having a myocardial infarction increases with
older age, low physical activity, and low socioeconomic status. Heart attacks
appear to occur more commonly in the morning hours, especially between 6AM and
noon. Evidence suggests that heart attacks are at least three times more likely
to occur in the morning than in the late evening. Shift work is also associated
with a higher risk of MI. One analysis has found an increase in heart attacks
immediately following the start of daylight saving time.
Women who use combined oral contraceptive pills have a
modestly increased risk of myocardial infarction, especially in the presence of
other risk factors. The use of non-steroidal anti-inflammatory drugs (NSAIDs),
even for as short as a week, increases risk.]
Endometriosis in women under the age of 40 is an identified
risk factor.
Air pollution is also an important modifiable risk.
Short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide,
and sulfur dioxide (but not ozone) has been associated with MI and other acute
cardiovascular events. For sudden cardiac deaths, every increment of 30 units
in Pollutant Standards Index correlated with an 8% increased risk of
out-of-hospital cardiac arrest on the day of exposure. Extremes of temperature
are also associated.
A number of acute and chronic infections including
Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas
gingivalis among others have been linked to atherosclerosis and myocardial
infarction. Myocardial infarction can also occur as a late consequence of
Kawasaki disease.
Calcium deposits in the coronary arteries can be detected
with CT scans. Calcium seen in coronary arteries can provide predictive
information beyond that of classical risk factors. High blood levels of the
amino acid homocysteine are associated with premature atherosclerosis; whether
elevated homocysteine in the normal range is causal is controversial.
In people without evident coronary artery disease, possible
causes for the myocardial infarction are coronary spasm or coronary artery
dissection.
Mechanism
Atherosclerosis
The animation shows 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.
The most common cause of a myocardial infarction is the
rupture of an atherosclerotic plaque on an artery supplying heart muscle.
Plaques can become unstable, rupture, and additionally promote the formation of
a blood clot that blocks the artery; this can occur in minutes. Blockage of an
artery can lead to tissue death in tissue being supplied by that artery.
Atherosclerotic plaques are often present for decades before they result in
symptoms.
The gradual buildup of cholesterol and fibrous tissue in
plaques in the wall of the coronary arteries or other arteries, typically over
decades, is termed atherosclerosis. Atherosclerosis is characterized by
progressive inflammation of the walls of the arteries. Inflammatory cells,
particularly macrophages, move into affected arterial walls. Over time, they
become laden with cholesterol products, particularly LDL, and become foam
cells. A cholesterol core forms as foam cells die. In response to growth
factors secreted by macrophages, smooth muscle and other cells move into the
plaque and act to stabilize it. A stable plaque may have a thick fibrous cap
with calcification. If there is ongoing inflammation, the cap may be thin or
ulcerate. Exposed to the pressure associated with blood flow, plaques,
especially those with a thin lining, may rupture and trigger the formation of a
blood clot (thrombus). The cholesterol crystals have been associated with
plaque rupture through mechanical injury and inflammation.
Other causes
Atherosclerotic disease is not the only cause of myocardial
infarction, but it may exacerbate or contribute to other causes. A myocardial
infarction may result from a heart with a limited blood supply subject to
increased oxygen demands, such as in fever, a fast heart rate, hyperthyroidism,
too few red blood cells in the bloodstream, or low blood pressure. Damage or
failure of procedures such as percutaneous coronary intervention (PCI) or
coronary artery bypass grafts (CABG) may cause a myocardial infarction. Spasm
of coronary arteries, such as Prinzmetal's angina may cause blockage.
Tissue death
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 blocked coronary artery die (infarction), chiefly through necrosis, and
do not grow back. A collagen scar forms in their place. When an artery is
blocked, cells lack oxygen, needed to produce ATP in mitochondria. ATP is
required for the maintenance of electrolyte balance, particularly through the
Na/K ATPase. This leads to an ischemic cascade of intracellular changes,
necrosis and apoptosis of affected cells.
Cells in the area with the worst blood supply, just below
the inner surface of the heart (endocardium), are most susceptible to damage.
Ischemia first affects this region, the subendocardial region, and tissue
begins to die within 15–30 minutes of loss of blood supply. The dead tissue is
surrounded by a zone of potentially reversible ischemia that progresses to
become a full-thickness transmural infarct. The initial "wave" of infarction can take place over 3–4 hours. These
changes are seen on gross pathology and cannot be predicted by the presence or
absence of Q waves on an ECG. The position, size and extent of an infarct
depends on the affected artery, totality of the blockage, duration of the
blockage, the presence of collateral blood vessels, oxygen demand, and success
of interventional procedures.
Tissue death and myocardial scarring alter the normal
conduction pathways of the heart and weaken affected areas. The size and
location put a person at risk of abnormal heart rhythms (arrhythmias) or heart
block, aneurysm of the heart ventricles, inflammation of the heart wall
following infarction, and rupture of the heart wall that can have catastrophic
consequences.
Injury to the myocardium also occurs during re-perfusion.
This might manifest as ventricular arrhythmia. The re-perfusion injury is a
consequence of the calcium and sodium uptake from the cardiac cells and the
release of oxygen radicals during reperfusion. No-reflow phenomenon—when blood
is still unable to be distributed to the affected myocardium despite clearing
the occlusion—also contributes to myocardial injury. Topical endothelial
swelling is one of many factors contributing to this phenomenon.
Diagnosis
Criteria
A myocardial infarction, according to current consensus, is
defined by elevated cardiac biomarkers with a rising or falling trend and at
least one of the following:
Symptoms relating to
ischemia
Changes on an electrocardiogram (ECG), such as ST segment
changes, new left bundle branch block, or pathologic Q waves
Changes in the motion of the heart wall on imaging
Types
A myocardial infarction is usually clinically classified as
an ST-elevation MI (STEMI) or a non-ST elevation MI (NSTEMI). These are based
on ST elevation, a portion of a heartbeat graphically recorded on an ECG.
STEMIs make up about 25–40% of myocardial infarctions. A more explicit
classification system, based on international consensus in 2012, also exists.
This classifies myocardial infarctions into five types:
Spontaneous MI related
to plaque erosion and/or rupture fissuring, or dissection
MI related to
ischemia, such as from increased oxygen demand or decreased supply, e.g.,
coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood
pressure, or low blood pressure
Sudden unexpected
cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG
may be taken with suggestive changes, or a blood clot is found in a coronary
artery by angiography and/or at autopsy, but where blood samples could not be
obtained, or at a time before the appearance of cardiac biomarkers in the blood
Associated with
coronary angioplasty or stents
Associated with
percutaneous coronary intervention (PCI)
Associated with stent
thrombosis as documented by angiography or at autopsy
Associated with CABG
Associated with
spontaneous coronary artery dissection in young, fit women
Cardiac biomarkers
There are many different biomarkers used to determine the
presence of cardiac muscle damage. Troponins, measured through a blood test, are
considered to be the best, and are preferred because they have greater
sensitivity and specificity for measuring injury to the heart muscle than other
tests. A rise in troponin occurs within 2–3 hours of injury to the heart
muscle, and peaks within 1–2 days. The level of the troponin, as well as a
change over time, is useful in measuring and diagnosing or excluding myocardial
infarctions, and the diagnostic accuracy of troponin testing is improving over
time. One high-sensitivity cardiac troponin can rule out a heart attack as long
as the ECG is normal.
Other tests, such as CK-MB or myoglobin, are discouraged.
CK-MB is not as specific as troponins for acute myocardial injury, and may be
elevated with past cardiac surgery, inflammation or electrical cardioversion;
it rises within 4–8 hours and returns to normal within 2–3 days. Copeptin may
be useful to rule out MI rapidly when used along with troponin.
Electrocardiogram
Electrocardiograms (ECGs) are a series of leads placed on a
person's chest that measure electrical activity associated with contraction of
the heart muscle. The taking of an ECG is an important part of the workup of an
AMI, and ECGs are often not just taken once but may be repeated over minutes to
hours, or in response to changes in signs or symptoms.
ECG readouts produce a waveform with different labeled
features. In addition to a rise in biomarkers, a rise in the ST segment,
changes in the shape or flipping of T waves, new Q waves, or a new left bundle
branch block can be used to diagnose an AMI. In addition, ST elevation can be
used to diagnose an ST segment myocardial infarction (STEMI). A rise must be
new in V2 and V3 ≥2 mm (0, 2 mV) for males or ≥1.5 mm (0.15 mV) for females or
≥1 mm (0.1 mV) in two other adjacent chest or limb leads. ST elevation is
associated with infarction, and may be preceded by changes indicating ischemia,
such as ST depression or inversion of the T waves. Abnormalities can help
differentiate the location of an infarct, based on the leads that are affected
by changes. Early STEMIs may be preceded by peaked T waves. Other ECG
abnormalities relating to complications of acute myocardial infarctions may
also be evident, such as atrial or ventricular fibrillation.
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