Myocardial infarction | Wikipedia audio article
04
October

By Adem Lewis / in , , , , , , , , , , , , , , , /


Myocardial infarction (MI), also known as
a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage
to the heart muscle. The most common symptom is chest pain or discomfort
which may travel into the shoulder, arm, back, neck or jaw. Often it occurs in the center or left side
of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like
heartburn. Other symptoms may include shortness of breath,
nausea, feeling faint, a cold sweat or feeling tired. 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, among others. 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 and extreme cold, among others. A number of tests are useful 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 an STEMI is about 10%. Rates of MI for a given age have decreased
globally between 1990 and 2010. In 2011, a 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). 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 other causes of acute coronary syndromes,
such as unstable angina, a myocardial infarction occurs when there is cell death, as measured
by a blood test for biomarkers (the cardiac protein troponin or the cardiac enzyme CK-MB). 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 a myocardial infarction and to sudden cardiac death. 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 causing 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=====
Pain===Chest pain is the most common symptom 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. 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. Pain that responds to nitroglycerin does not
indicate the presence or absence of a myocardial infarction.===Other symptoms===
Chest pain may be accompanied by sweating, nausea or vomiting, and fainting, and these
symptoms may also occur without any pain at all. In women, the most common symptoms of myocardial
infarction include shortness of breath, weakness, and fatigue. 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 due to inadequate blood
flow to the brain and cardiogenic shock, and sudden death, frequently due to the development
of ventricular fibrillation, can occur in myocardial infarctions. Cardiac arrest, and atypical symptoms such
as palpitations, occur more frequently in women, the elderly, those with diabetes, in
people who have just had surgery, and in critically ill patients.”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.===Women===In women, myocardial infarctions can present
with different symptoms. The classic presentation of chest pain occurs
in about 50% of women. Women can also commonly experience back or
neck pain, indigestion, heartburn, lightheadedness, shortness of breath, fatigue, nausea, or pain
in the back of the jaw. These symptoms are often overlooked or mistaken
for another condition.==Causes==
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 is 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, 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. And 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) have 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. As of 2013, there is no evidence of benefit
from antibiotics or vaccination, however, calling the association into question. 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
is 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 dissection.==Mechanism=====
Atherosclerosis===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, and 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 or coronary artery bypass grafts 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 puts 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.==Diagnosis=====
Criteria===An acute 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 Q waves Changes in the motion of the heart wall on
imaging Demonstration of a thrombus on angiogram or
at autopsy.===Types===Myocardial infarctions are generally clinically
classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to 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 a number of 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, are 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 is able
to 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 heart muscle. The taking of an ECG is an important part
in 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 product
a waveform with different labelled 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.===Imaging===
Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial
infarction. Tests such as chest X-rays can be used to
explore and exclude alternate causes of a person’s symptoms. Tests such as stress echocardiography and
myocardial perfusion imaging can confirm a diagnosis when a person’s history, physical
examination (including cardiac examination) ECG, and cardiac biomarkers suggest the likelihood
of a problem.Echocardiography, an ultrasound scan of the heart, is able to visualize the
heart, its size, shape, and any abnormal motion of the heart walls as they beat that may indicate
a myocardial infarction. The flow of blood can be imaged, and contrast
dyes may be given to improve image. Other scans using radioactive contrast include
SPECT CT-scans using thallium, sestamibi (MIBI scans) or tetrofosmin; or a PET scan using
Fludeoxyglucose or rubidium-82. These nuclear medicine scans can visualize
the perfusion of heart muscle. SPECT may also be used to determine viability
of tissue, and whether areas of ischemia are inducible.Medical societies and professional
guidelines recommend that the physician confirm a person is at high risk for myocardial infarction
before conducting imaging tests to make a diagnosis, as such tests are unlikely to change
management and result in increased costs. Patients who have a normal ECG and who are
able to exercise, for example, do not merit routine imaging.===Differential diagnosis===
There are many causes of chest pain, which can originate from the heart, lungs, gastrointestinal
tract, aorta, and other muscles, bones and nerves surrounding the chest. In addition to myocardial infarction, other
causes include angina, insufficient blood supply (ischemia) to the heart muscles without
evidence of cell death, gastroesophageal reflux disease; pulmonary embolism, tumors of the
lungs, pneumonia, rib fracture, costochondritis, heart failure and other musculoskeletal injuries. Rarer severe differential diagnoses include
aortic dissection, esophageal rupture, tension pneumothorax, and pericardial effusion causing
cardiac tamponade. The chest pain in an MI may mimic heartburn. Causes of sudden-onset breathlessness generally
involve the lungs or heart – including pulmonary edema, pneumonia, allergic reactions and asthma,
and pulmonary embolus, acute respiratory distress syndrome and metabolic acidosis. There are many different causes of fatigue,
and myocardial infarction is not a common cause.==Management==A myocardial infarction requires immediate
medical attention. Treatment aims to preserve as much heart muscle
as possible, and to prevent further complications. Treatment depends on whether the myocardial
infarction is a STEMI or NSTEMI. Treatment in general aims to unblock blood
vessels, reduce blot clot enlargement, reduce ischemia, and modify risk factors with the
aim of preventing future MIs. In addition, the main treatment for myocardial
infarctions with ECG evidence of ST elevation (STEMI) include thrombolysis or percutaneous
coronary intervention, although PCI is also ideally conducted within 1–3 days for NSTEMI. In addition to clinical judgement, risk stratification
may be used to guide treatment, such as with the TIMI and GRACE scoring systems.===Pain===
The pain associated with myocardial infarction may be treated with nitroglycerin or morphine. Nitroglycerin (given under the tongue or intravenously)
may improve the blood supply to the heart, and decrease the work the heart must do. It is an important part of therapy for its
pain relief, despite there being no benefit to overall mortality. Morphine may also be used, and is effective
for the pain associated with STEMI. The evidence for benefit from morphine on
overall outcomes, however, is poor and there is some evidence of potential harm.===Anticoagulation===
Aspirin, an antiplatelet anticoagulant, is given as a loading dose with the goal of reducing
the clot size and reduce further clotting in the affected artery. It is known to decrease mortality associated
with acute myocardial infarction by at least 50%. P2Y12 inhibitors such as clopidogrel, prasugrel
and ticagrelor are given concurrently, also as a loading dose, with the dose depending
on whether further surgical management or fibrinolysis is planned. Prasugrel and ticagrelor are recommended in
European and American guidelines, as they are active more quickly and consistently than
clopidogrel. P2Y12 inhibitors are recommended in both NSTEMI
and STEMI, including in PCI, with evidence also to suggest improved mortality. Heparins, particularly in the unfractionated
form, act at several points in the clotting cascade, help to prevent the enlargement of
a clot, and are also given in myocardial infarction, owing to evidence suggesting improved mortality
rates. In very high-risk scenarios, inhibitors of
the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.There
is varying evidence on the mortality benefits in NSTEMI. A 2014 review of P2Y12 inhibitors such as
clopidogrel found they do not change the risk of death when given to people with a suspected
NSTEMI prior to PCI, nor do heparins change the risk of death. They do decrease the risk of having a further
myocardial infarction.===Angiogram===
Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI
if it can be performed in a timely manner, ideally within 90–120 minutes of contact
with a medical provider. Some recommend it is also done in NSTEMI within
1–3 days, particularly when considered high-risk. A 2017 review, however, did not find a difference
between early versus later PCI in NSTEMI.PCI involves small probes, inserted through peripheral
blood vessels such as the femoral artery or radial artery into the blood vessels of the
heart. The probes are then used to identify and clear
blockages using small balloons, which are dragged through the blocked segment, dragging
away the clot, or the insertion of stents. Coronary artery bypass grafting is only considered
when the affected area of heart muscle large, and PCI is unsuitable, for example with difficult
cardiac anatomy. After PCI, people are generally placed on
aspirin indefinitely and on dual antiplatelet therapy (generally aspirin and clopidogrel)
for at least a year.===Fibrinolysis===
If PCI cannot be performed within 90 to 120 minutes in STEMI then fibrinolysis, preferably
within 30 minutes of arrival to hospital, is recommended. If a person has had symptoms for 12 to 24
hours evidence for effectiveness of thrombolysis is less and if they have had symptoms for
more than 24 hours it is not recommended. Thrombolysis involves the administration of
medication that activates the enzymes that normally dissolve blood clots. These medications include tissue plasminogen
activator, reteplase, streptokinase, and tenecteplase. Thrombolysis is not recommended in a number
of situations, particularly when associated with a high risk of bleeding or the potential
for problematic bleeding, such as active bleeding, past strokes or bleeds into the brain, or
severe hypertension. Situations in which thrombolysis may be considered,
but with caution, include recent surgery, use of anticoagulants, pregnancy, and proclivity
to bleeding. Major risks of thrombolysis are major bleeding
and intracranial bleeding. Pre-hospital thrombolysis reduces time to
thrombolytic treatment, based on studies conducted in higher income countries, however it is
unclear whether this has an impact on mortality rates.===Other===
In the past, high flow oxygen was recommended for everyone with a possible myocardial infarction. More recently, no evidence was found for routine
use in those with normal oxygen levels and there is potential harm from the intervention. Therefore, oxygen is currently only recommended
if oxygen levels are found to be low or if someone is in respiratory distress.If despite
thrombolysis there is significant cardiogenic shock, continued severe chest pain, or less
than a 50% improvement in ST elevation on the ECG recording after 90 minutes, then rescue
PCI is indicated emergently.Those who have had cardiac arrest may benefit from targeted
temperature management with evaluation for implementation of hypothermia protocols. Furthermore, those with cardiac arrest, and
ST elevation at any time, should usually have angiography. Aldosterone antagonists appear to be useful
in people who have had an STEMI and do not have heart failure.===Rehabilitation===
Cardiac rehabilitation benefits many who have experienced myocardial infarction, even if
there has been substantial heart damage and resultant left ventricular failure. It should start soon after discharge from
the hospital. The program may include lifestyle advice,
exercise, social support, as well as recommendations about driving, flying, sport participation,
stress management, and sexual intercourse.==Prevention==
There is a large crossover between the lifestyle and activity recommendations to prevent a
myocardial infarction, and those that may be adopted as secondary prevention after an
initial myocardial infarction, because of shared risk factors and an aim to reduce atherosclerosis
affecting heart vessels.===Primary prevention=======
Lifestyle====Physical activity can reduce the risk of cardiovascular
disease, and people at risk are advised to engage in 150 minutes of moderate or 75 minutes
of vigorous intensity aerobic exercise a week. Keeping a healthy weight, drinking alcohol
within the recommended limits, and quitting smoking reduce the risk of cardiovascular
disease.Substituting polyunsaturated fats such as olive oil and rapeseed oil instead
of saturated fats may reduce the risk of myocardial infarction, although there is not universal
agreement. Dietary modifications are recommended by some
national authorities, with recommendations including increasing the intake of wholegrain
starch, reducing sugar intake (particularly of refined sugar), consuming five portions
of fruit and vegetables daily, consuming two or more portions of fish per week, and consuming
4–5 portions of unsalted nuts, seeds, or legumes per week. The dietary pattern with the greatest support
is the Mediterranean diet. Vitamins and mineral supplements are of no
proven benefit, and neither are plant stanols or sterols.Public health measures may also
act at a population level to reduce the risk of myocardial infarction, for example by reduce
unhealthy diets (excessive salt, saturated fat and trans fat) including food labeling
and marketing requirements as well as requirements for catering and restaurants, and stimulating
physical activity. This may be part of regional cardiovascular
disease prevention programs, or through the health impact assessment of regional and local
plans and policies.Most guidelines recommend combining different preventive strategies. A 2015 Cochrane Review found some evidence
that such an approach might help with blood pressure, body mass index and waist circumference. However, there was insufficient evidence to
show an effect on mortality or actual cardio-vascular events.====Medication====
Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates
of myocardial infarctions. They are often recommended in those at an
elevated risk of cardiovascular diseases.Aspirin has been studied extensively in people considered
at increased risk of myocardial infarction. Based on numerous studies in different groups
(e.g. people with or without diabetes), there does not appear to be a benefit strong enough
to outweigh the risk of excessive bleeding. Nevertheless, many clinical practice guidelines
continue to recommend aspirin for primary prevention, and some researchers feel that
those with very high cardiovascular risk but low risk of bleeding should continue to receive
aspirin.===Secondary prevention===
There is a large crossover between the lifestyle and activity recommendations to prevent a
myocardial infarction, and those that may be adopted as secondary prevention after an
initial myocardial infarct. Recommendations include stopping smoking,
a gradual return to exercise, eating a healthy diet, low in saturated fat and low in cholesterol,
and drinking alcohol within recommended limits, exercising, and trying to achieve a healthy
weight. Exercise is both safe and effective even if
people have had stents or heart failure, and is recommended to start gradually after 1–2
weeks. Counselling should be provided relating to
medications used, and for warning signs of depression. Previous studies suggested a benefit from
omega-3 fatty acid supplementation but this has not been confirmed.====Medications====
Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease
the risk of death. Other medications include:
Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel
or ticagrelor (“dual antiplatelet therapy” or DAPT) for up to twelve months. If someone has another medical condition that
requires anticoagulation (e.g. with warfarin) this may need to be adjusted based on risk
of further cardiac events as well as bleeding risk. In those who have had a stent, more than 12
months of clopidogrel plus aspirin does not affect the risk of death.Beta blocker therapy
such as metoprolol or carvedilol is recommended to be started within 24 hours, provided there
is no acute heart failure or heart block. The dose should be increased to the highest
tolerated. Contrary to what was long believed, the use
of beta blockers does not appear to affect the risk of death, possibly because other
treatments for MI have improved. When beta blocker medication is given within
the first 24–72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from
a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the medication causes
a temporary decrease in the heart’s ability to pump blood.ACE inhibitor therapy should
be started within 24 hours, and continued indefinitely at the highest tolerated dose. This is provided there is no evidence of worsening
kidney failure, high potassium, low blood pressure, or known narrowing of the renal
arteries. Those who cannot tolerate ACE inhibitors may
be treated with an angiotensin II receptor antagonist.Statin therapy has been shown to
reduce mortality and subsequent cardiac events, and should be commenced with the aim of lowering
LDL cholesterol. Other medications, such as ezetimibe, may
also be added with this goal in mind.Aldosterone antagonists (spironolactone or eplerenone)
may be used if there is evidence of left ventricular dysfunction after an MI, ideally after beginning
treatment with an ACE inhibitor.====Other====
A defibrillator, an electric device connected to the heart and surgically inserted under
the skin, may be recommended. This is particularly if there are any ongoing
signs of heart failure, with a low left ventricular ejection fraction and a New York Heart Association
grade II or III after 40 days of the infarction. Defibrillators detect potentially fatal arrhythmia
and deliver an electrical shock to the person to depolarize a critical mass of the heart
muscle.==Prognosis==
The prognosis after myocardial infarction varies greatly depending on the extent and
location of the affected heart muscle, and the development and management of complications. Prognosis is worse with older age, and social
isolation. Anterior infarcts, persistent ventricular
tachycardia or fibrillation, development of heart blocks, and left ventricular impairment
are all associated with poorer prognosis. Without treatment, about a quarter of those
affected by MI die within minutes, and about forty percent within the first month. Morbidity and mortality from myocardial infarction
has however improved over the years due to earlier and better treatment: in those who
have an STEMI in the United States, between 5 and 6 percent die before leaving the hospital
and 7 to 18 percent die within a year.It is unusual for babies to experience a myocardial
infarction, but when they do, about half die. In the short-term, neonatal survivors seem
to have a normal quality of life.===Complications===Complications may occur immediately following
the myocardial infarction or may take time to develop. Disturbances of heart rhythms, including atrial
fibrillation, ventricular tachycardia and fibrillation and heart block can arise as
a result of ischemia, cardiac scarring, and infarct location. Stroke is also a risk, either as a result
of clots transmitted from the heart during PCI, as a result of bleeding following anticoagulation,
or as a result of disturbances in the heart’s ability to pump effectively as a result of
the infarction. Regurgitation of blood through the mitral
valve is possible, particularly if the infarction causes dysfunction of the papillary muscle. Cardiogenic shock as a result of the heart
being unable to adequately pump blood may develop, dependent on infarct size, and is
most likely to occur within the days following an acute myocardial infarction. Cardiogenic shock is the largest cause of
in-hospital mortality. Rupture of the ventricular dividing wall or
left ventricular wall may occur within the initial weeks. Dressler’s syndrome, a reaction following
larger infarcts and a cause of pericarditis is also possible.Heart failure may develop
as a long-term consequence, with an impaired ability of heart muscle to pump, scarring,
and increase in size of the existing muscle. Aneurysm of the left ventricle myocardium
develops in about 10% of MI and is itself a risk factor for heart failure, ventricular
arrhythmia and the development of clots.Risk factors for complications and death 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.==Epidemiology==
Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in
2004, that 12.2% of worldwide deaths were from ischemic heart disease; 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. Worldwide, more than 3 million people have
STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as
women.Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income
countries, although cardiovascular disease still accounted for one in three of all deaths
in the US in 2008. For example, rates of death from cardiovascular
disease have decreased almost a third between 2001 and 2011 in the United States.In contrast,
IHD is becoming a more common cause of death in the developing world. For example, in India, IHD had become the
leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths)
and deaths due to IHD were expected to double during 1985–2015. Globally, disability adjusted life years (DALYs)
lost to ischemic heart disease are predicted to 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.==Society and culture==
Depictions of heart attacks in popular media often include collapsing or loss of consciousness
which are not common symptoms; these depictions contribute to widespread misunderstanding
about the symptoms of myocardial infarctions, which in turn contributes to people not getting
care when they should.===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 the administration
of no-fault insurance schemes such as workers’ compensation. In general, a heart attack is not covered;
however, it may be a work-related injury if it results, for example, from unusual emotional
stress or unusual exertion. 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 an MI may be prevented from participating in activity that puts other
people’s lives at risk, for example driving a car or flying an airplane


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