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‫‪Myocardial Infarction‬‬
‫‪By :‬‬
‫عبد هللا حسن النجار‬
‫إيمان علوى عبد الفتاح‬
‫أميرة سعيد أبوحجازى‬
‫آالء عمر السيد حافظ‬
‫أمانى محمود شريف‬
‫‪1‬‬
Myocardial infarction
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 theleft coronary artery (LCA).
In the diagram, RCA is the right coronary
artery.
Myocardial
infarction (from Latin: Infarctus
myocardii, 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 receiving enough oxygen.
Usually this is because one of the coronary arteries that supplies
blood to the heart develops a blockage due to an unstable
2
buildup ofwhite blood cells, cholesterol and fat. The event is called
"acute" if it is sudden and serious.
A person having an acute MI usually has sudden chest pain that is
felt behind the breast bone and sometimes travels to the left arm
or the left side of the neck. Additionally, the person may
have shortness of breath, sweating, nausea, vomiting, abnormal
heartbeats, and anxiety. Women experience fewer of these
symptoms than men, but usually have shortness of breath,
weakness, a feeling of indigestion, and fatigue.[1] In many cases, in
some estimates as high as 64%, the person does not have chest
pain or other symptoms.[2] These are called "silent" myocardial
infarctions.
Important risk factors are previous cardiovascular disease, old
age, tobacco smoking, high blood levels of certain lipids (lowdensity lipoprotein cholesterol, triglycerides) and low levels of high
density
lipoprotein (HDL)
cholesterol, diabetes, high
blood
pressure, lack of physical activity, obesity, chronic kidney
disease, excessive
alcohol
consumption,
the
use
of cocaine and amphetamines,
and
chronic
high
stress
[3][4][5]
levels.
The main way to determine if a person has had a
myocardial infarction are electrocardiograms (ECGs) that trace the
electrical signals in the heart and testing the blood for substances
associated with damage to the heart muscle. Common blood tests
are creatine kinase (CK-MB) andtroponin. ECG testing is used to
differentiate between two types of myocardial infarctions based on
the shape of the tracing. An ST section of the tracing higher than
the baseline is called an ST elevation MI (STEMI) which usually
requires more aggressive treatment.
Immediate treatments for a suspected MI include aspirin, which
prevents further blood from clotting, and sometimes nitroglycerin to
treat chest pain and oxygen.[6] STEMI is treated by restoring
circulation to the heart, called reperfusion therapy, and typical
methods areangioplasty, where the arteries are pushed open,
and thrombolysis, where the blockage is removed using
medications.[7] 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.[8] People
3
who have multiple blockages of their coronary arteries, particularly
if they also have diabetes, may also be treated with bypass
surgery(CABG).[9][10] Ischemic heart disease, which includes
MI, angina, and heart failure when it happens after MI, was the
leading cause of death for both men and women worldwide in
2011.[11][12]
Classification
The two basic types of acute myocardial infarction, based on
pathology, are:


Transmural AMI is 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.[13] In
addition, on ECG, ST elevation and Q waves are seen.
Subendocardial AMI involves a small area in the
subendocardial wall of the left ventricle, ventricular septum, or
papillary muscles. The subendocardial area is particularly
susceptible to ischemia.[13] In addition, ST depression is seen
on ECG.
In the clinical context, an MI can be further subclassified into a ST
elevation MI (STEMI) versus a non-ST elevation MI (NSTEMI)
based on ECG changes.[14] The phrase "heart attack" is sometimes
used incorrectly to describe sudden cardiac death, which may or
may not be the result of AMI. A heart attack is different from, but
can be the cause of, cardiac arrest, which is the stopping of the
heartbeat, andcardiac arrhythmia, an abnormal heartbeat. It is also
distinct from heart failure, in which the pumping action of the heart
is impaired; however, severe MI may lead to heart failure.[9] A 2007
consensus document classifies MI into five main types:[15]

Type 1 – spontaneous MI related to ischemia due to a primary
coronary event such as plaque erosion and/or rupture,
fissuring, or dissection
4
Type 2 – MI 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:
 Type 4a – MI associated with PCI
 Type 4b – MI associated with stent thrombosis as
documented by angiography or at autopsy
 Type 5 – MI 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
5
Back view
The onset of symptoms in myocardial infarction (MI) is usually
gradual, over several minutes, and rarely instantaneous.[16] Chest
pain is the most common symptom of acute MI and is often
described as a sensation of tightness, pressure, or squeezing.
Chest pain due toischemia (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,[9][17] where it
may mimic heartburn. Levine's sign, in which patients localize the
chest pain by clenching their fists over their sternums, has
classically been thought to be predictive of cardiac chest pain,
although a prospective observational study showed it had a poor
positive predictive value.[18]
Shortness of breath (dyspnea) occurs when the damage to the
heart limits the output of theleft ventricle, causing left ventricular
failure and consequent pulmonary edema. Other symptoms
include diaphoresis (an
excessive
form
[19]
of sweating), weakness, light-headedness, nausea, vomiting,
and palpitations. These symptoms are likely induced by a massive
surge
of catecholamines from
the sympathetic
nervous
[20]
system 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) andsudden death (frequently due to the
development of ventricular fibrillation) can occur in MIs.[9]
6
Female, elderly, and diabetic patients report atypical symptoms
more
frequently
than
their
male
and
younger
[21][22]
counterparts.
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, 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] Women may also
experience back or jaw pain during an episode.[24]
At least one-fourth of all MIs are silent, without chest pain or other
symptoms.[2][25] 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 MIs vary between 22 and 64%.[2] A silent
course is more common in the elderly,[2] in patients with diabetes
mellitus[26] and after heart transplantation, probably because
thedonor heart is not fully innervated by the nervous system of the
recipient.[27] In people with diabetes, differences in pain
threshold, autonomic neuropathy, and psychological factors have
been cited as possible explanations for the lack of symptoms.[26]
Any group of symptoms compatible with a sudden interruption of
the blood flow to the heart are called an acute coronary
syndrome.[28]
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
noncatastrophic
differentials
includegastroesophageal
[29]
reflux and Tietze's syndrome.
7
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 stressor 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 six-fold higher MI 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 andatherosclerosis.[30] While this intracellular
organism has been demonstrated in atherosclerotic plaques,
evidence is inconclusive as to whether it can be considered a
causative factor.[30] Treatment with antibiotics in patients with
8
proven atherosclerosis has not demonstrated a decreased risk of
heart attacks or other coronary vascular diseases.[31]
An increased incidence of a heart attack is associated with time of
day especially in the morning hours, more specifically around 9
am.[32][33][34] Some investigators have noticed the ability of platelets
to aggregate varies according to a circadian rhythm, although they
have not proven causation.[35]
Risk factors
Myocardial infarction results from atherosclerosis.[9] Smoking
appears to be the cause of about 36% of coronary artery
disease and obesity 20%.[36] Lack of exercise has been linked to 712% of cases.[36][37] Job stress appear to play a minor role
accounting for about 3% of cases.[36]
Risk factors for MI include:







Sex: At any given age, men are more at risk than women,
particularly before menopause,[38] but because in general
women live longer than men, ischemic heart disease causes
slightly more total deaths in women.[3]
Diabetes mellitus (type 1 or 2)[39]
High blood pressure[40]
Dyslipidemia/hypercholesterolemia (abnormal
levels
of lipoproteins in the blood), particularly high low-density
lipoprotein, low high-density lipoprotein and high triglycerides[40]
Tobacco smoking, including secondhand smoke[40]
Short-term exposure to air pollution, including carbon
monoxide, nitrogen
dioxide,
and sulfur
dioxide,
but
[41]
not ozone.
Family history of ischaemic heart disease or MI, 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).[3]
9






Obesity[42] (defined by a body mass index of more than
30 kg/m², or alternatively by waist circumference or waist-hip
ratio).
Lack of physical activity[3]
Psychosocial factors including, low socioeconomic status,
social isolation, negative emotions and stress increase the risk
of and are associated with worse outcomes after
MI. 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.[43]
Alcohol — 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.[44]
Hyperhomocysteinemia (high homocysteine)
in homocysteinuria is
associated
with
premature
[45]
atherosclerosis, whether elevated homocysteine in the
normal range is causal is contentious.[46]
Inflammation is known to be an important step in the process
of atherosclerotic plaque formation.[47] C-reactive protein (CRP) is
a sensitive but nonspecific 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.[47] Moreover, some drugs for MI might also reduce CRP
levels.[47]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.[48]Whether CRP plays a direct role in atherosclerosis
remains uncertain.[47] 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.[49] Serologicalstudies measuring antibody levels against
typical periodontitis-causing bacteria found that such antibodies
were more present in subjects with coronary heart
disease.[50] Periodontitis tends to increase blood levels of
10
CRP, fibrinogen, and cytokines;[51] thus, periodontitis may mediate
its effect on MI risk via other risk factors.[52] Preclinical
research suggests that periodontal bacteria can promote
aggregation of platelets and promote the formation of foam
cells.[53][54] A role for specific periodontal bacteria has been
suggested but remains to be established.[55] There is some
evidence that influenza may trigger an acute myocardial
infarction.[56]
Baldness, hair greying, a diagonal earlobe crease (Frank's sign[57])
and possibly other skin features have been suggested as
independent risk factors for MI.[58] Their role remains controversial;
a common denominator of these signs and the risk of MI is
supposed, possibly genetic.[59]
Calcium deposition is another part of atherosclerotic plaque
formation. Calcium deposits in the coronary arteries can be
detected withCT scans. Several studies have shown that coronary
calcium can provide predictive information beyond that of classical
risk factors.[60][61][62]
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.[63] Nonmodifiable 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, many factors associated with MI mediate their risk by
other factors. For example, the effect of education is partially
based on its effect on income and marital status.[43]
Pathophysiology
11
A myocardial infarction occurs when
anatherosclerotic plaque slowly builds up in the inner lining of
a coronary artery and then suddenly ruptures, causing
catastrophicthrombus 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-ST-elevated and ST-elevated
MIs, which are most frequently (but not always) a manifestation
of coronary artery disease.[14] The most common triggering event is
the disruption of anatherosclerotic plaque in an epicardial coronary
artery, which leads to a clotting cascade, sometimes resulting in
total occlusion of the artery.[64][65] Atherosclerosis is the gradual
12
buildup of cholesterol and fibrous tissue in plaques in the wall
of arteries (in this case, thecoronary arteries), typically over
decades.[66] Blood stream column irregularities visible on
angiography reflect artery lumen narrowing as a result of decades
of advancing atherosclerosis.[67] Plaques can become unstable,
rupture, and additionally promote athrombus (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 MI (necrosis of downstream myocardium).[64][65]
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 throughnecrosis) and
do not grow back. A collagen scar forms in their place. Recent
studies indicate that another form of cell death, apoptosis, also
plays a role in the process of tissue damage subsequent to
MI.[68] 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 (VFib/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, VT 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 device was specifically designed to
terminate these potentially fatal arrhythmias. The device works by
delivering an electrical shock to the patient to depolarize a critical
mass of the heart muscle, in effect "rebooting" the heart. This
13
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 a patient
is at high risk for myocardial infarction before conducting imaging
tests to make a diagnosis.[69] Patients who have a normal ECG and
who are able to exercise, for example, do not merit routine
imaging.[69] 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.[69]
The diagnosis of MI 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
whilecoronary
angiogram allows
visualization of narrowing or obstructions in the heart
vessels.[70] At autopsy, a pathologist can diagnose an MI 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
an MI. Echo may be performed in equivocal cases by the on-call
cardiologist.[71] 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 physiological or pharmacological stress.[71] Thallium may also
be used to determine viability of tissue, distinguishing whether
nonfunctional 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 MI if two (probable) or
three (definite) of the following criteria are satisfied:
14
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
cardiactroponin 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 MI decreases with strict blood pressure
management and lifestyle changes, chiefly smoking cessation,
regularexercise, a sensible diet for those with heart disease,
and limitation of alcohol intake. People are usually commenced on
several long-term medications post-MI, with the aim of preventing
secondary cardiovascular events such as further MIs, congestive
heart failure, orcerebrovascular accident. 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 MI. 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, but 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 highrisk patients such as those with left ventricular dysfunction
and/or continuing cardiac ischaemia.[79] β-Blockers decrease
mortality and morbidity. They also improve symptoms of cardiac
ischemia in NSTEMI.
ACE inhibitor therapy should be commenced 24–48 hours after
MI in hemodynamically stable patients, particularly in patients
with a history of MI, diabetes mellitus, hypertension, anterior
15
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.[80]
 Statin therapy has been shown to reduce mortality and
morbidity.[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 after MI in patients
with heart failure and left ventricular dysfunction, when used in
conjunction with standard therapies above.[84] Spironolactone,
another option, 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, no clear-cut
decrease in potentially fatal arrhythmias occurs 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.[8] Early treatment of heart attack patients with an
16
inexpensive beta-blocker drug called metoprolol, while in transit to
the hospital, can significantly reduce damage to the heart during
an MI.[92]
STEMI
Percutaneous coronary intervention (PCI) is the treatment of
choice for STEMI if it can be performed in a timely manner. [93] If
PCI cannot be performed within 90 to 120 minutes
then fibrinolysis,
preferably
within
30
minutes,
is
[94][95]
recommended.
If after fibrinolysis, significant cardiogenic
shock, continued severe chest pain, or less than a 50%
improvement in ST elevation after 90 minutes occurs, then rescue
PCI is indicated emergently.[95][96] After PCI, people are generally
placed on dual antiplatelet therapy for at least a year (which is
generally aspirin and clopidogrel).[97]
Prognosis
The prognosis after MI varies greatly, depending on a person's
health, the extent of the heart damage, and the treatment given.
For the period 2005–2008 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.[98] Using variables available in
the emergency room, people with a higher risk of adverse outcome
can be identified. One study found 0.4% of patients with a low-risk
profile died after 90 days, whereas in high-risk people it was
21.1%.[99]
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.[99][100][101] Assessment
of left
ventricular ejection
[102]
fraction may increase the predictive power.
The prognostic
importance of Q-waves is debated.[103] Prognosis is significantly
worsened if a mechanical complication such as papillary muscle or
myocardial free wall rupture occurs.[104] Morbidity and mortality
from myocardial infarction has improved over the years due to
better treatment.[105]
17
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 pump blood adequately 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 MI.
Epidemiology
Myocardial infarction is a common presentation of ischemic heart
disease/coronary
artery
disease.
The World
Health
Organizationestimated in 2004, that 12.2% of worldwide deaths
were from ischemic heart disease;[12] with it being the leading
cause of death in high- or middle-income countries and second
only
to lower
respiratory
infections in lower-income
[12]
countries. Worldwide, more than 3 million people have STEMIs
and 4 million have NSTEMIs a year.[106]
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 USA in
2008.[107] 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.[108] 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.[12]
18
Economics
In 2011, AMI was one of the top five most expensive conditions
seen during inpatient hospitalizations in the U.S., with an
aggregate cost of about $11.5 billion for 612,000 hospital stays.[109]
Legal implications[edit]
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
[110]
covered;
however, it may be a work-related injury if it results,
for example, from unusual emotional stress or unusual
exertion.[111] 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.[112]
Research
Patients
who
receive stem
cell
treatment by coronary
artery injections of stem cells derived from their own bone
marrow after an 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 STEMI are proceeding.[113]
Currently, three biomaterial and tissue engineering approaches are
used for the treatment of post-MI 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 uses 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.[114]
19
References
1. Jump up^ Kosuge, M; Kimura K, Ishikawa T et al. (March
2006). "Differences between men and women in terms of
clinical features of ST-segment elevation acute myocardial
infarction".Circulation
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