Myocardial infarction (
MI) or
acute myocardial infarction
(
AMI), commonly known as a
heart
attack, is the interruption of
blood
supply to part of the
heart, causing some
heart cells to die. This is most commonly due to occlusion
(blockage) of a
coronary artery
following the rupture of a
vulnerable
atherosclerotic plaque, which is an unstable collection of
lipids (fatty acids) and
white blood cells (especially
macrophages) in the wall of an
artery. The resulting
ischemia (restriction in blood supply) and
oxygen shortage, if left untreated for a
sufficient period of time, can cause damage or death (
infarction) of heart muscle tissue
(
myocardium).
Classical symptoms of acute myocardial infarction include sudden
chest pain (typically radiating to the
left arm or left side of the neck),
shortness of
breath,
nausea,
vomiting,
palpitations,
sweating, and
anxiety (often described as a sense of impending
doom). Women may experience fewer typical symptoms than men, most
commonly shortness of breath, weakness, a feeling of indigestion,
and
fatigue. Approximately one
quarter of all myocardial infarctions are silent, without chest
pain or other symptoms. A heart attack is a
medical emergency, and people experiencing
chest pain are advised to alert their
emergency medical services
because prompt protection with an external defibrillator can save
one's life from
primary
ventricular fibrillation which occurs unexpectedly in 10% of
all myocardial infarctions especially during the first hours of
symptoms. Contemporary treatment of many myocardial infarctions can
result in survival and even good outcomes. While it is true that
certain less amenable cases are very massive and rapidly fatal
"widowmakers", it is also true that in small attacks with limited
damage and optimal treatment the heart muscle can be
salvaged.
Heart attacks are the leading cause of death for both men and women
all over the world. Important
risk
factors are previous
cardiovascular disease (such as
angina, a previous heart attack or
stroke), older age (especially men over 40
and women over 50),
tobacco smoking,
high blood levels of certain lipids (
triglycerides,
low-density lipoprotein or "bad
cholesterol") and low levels of
high density lipoprotein (HDL,
"good cholesterol"),
diabetes,
high blood pressure,
obesity,
chronic
kidney disease,
heart failure,
excessive alcohol
consumption, the abuse of certain drugs (such as
cocaine and
methamphetamine), and chronic high stress
levels.
Immediate treatment for suspected acute myocardial infarction
includes
oxygen,
aspirin, and sublingual
glyceryl trinitrate (also
known as
nitroglycerin and abbreviated
as NTG or GTN).
Pain relief is also often
given, classically
morphine
sulfate. However, a 2009 review about the use of high flow
oxygen for treating myocardial infarction found its administration
increased mortality and infarct size, calling into question the
recommendation for its routine use.
The patient will receive a number of diagnostic tests, such as an
electrocardiogram (ECG, EKG), a
chest
X-ray and
blood
tests to detect elevations in
cardiac markers (blood tests to detect heart
muscle damage). The most often used markers are the
creatine kinase-MB (CK-MB) fraction and the
troponin I (TnI) or
troponin T (TnT) levels. On the basis of the ECG,
a distinction is made between
ST elevation MI
(STEMI) or
non-ST elevation MI (NSTEMI). Most
cases of STEMI are treated with
thrombolysis or if possible with
percutaneous coronary
intervention (PCI, angioplasty and stent insertion), provided
the hospital has facilities for
coronary angiography. NSTEMI is managed
with medication, although PCI is often performed during hospital
admission. In patients who have multiple blockages and who are
relatively stable, or in a few extraordinary emergency cases,
bypass surgery of the
blocked coronary artery is an option.
The phrase "heart attack" is sometimes used incorrectly to describe
sudden cardiac death, which may
or may not be the result of acute myocardial infarction. A heart
attack is different from, but can be the cause of
cardiac arrest, which is the stopping of the
heartbeat, and
cardiac
arrhythmia, an abnormal heartbeat. It is also distinct from
heart failure, in which the pumping
action of the heart is impaired; severe myocardial infarction may
lead to heart failure, but not necessarily.
Classification
There are two basic types of acute myocardial infarction:
- Transmural: associated with atherosclerosis involving major
coronary artery. It can be subclassified into anterior, posterior,
or inferior. Transmural infarcts extend through the whole thickness
of the heart muscle and is usually a result of complete occlusion
of the area's blood supply.
- Subendocardial: involves small area in the subendocardial wall
of the left ventricle, ventricular septum, or papillary muscles.
Subendocardial infarcts are thought to be a result of locally
decreased blood supply, possibly from a narrowing of the coronary
arteries. The subendocardial area is furthest from the heart's
blood supply, and is more suseptible to this type of
pathology.
Clinically, myocardial infarction is further subclassified into ST
elevation MI versus non ST elevation MI based on ECG changes.
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).
The onset of symptoms in myocardial infarction (MI) is usually
gradual, over several minutes, and rarely instantaneous.
Chest pain is the most common symptom of acute
myocardial infarction and is often described as a sensation of
tightness, pressure, or squeezing. Chest pain due to
ischemia (a lack of blood and hence oxygen supply)
of the heart muscle is termed
angina
pectoris. Pain radiates most often to the left
arm, but may also radiate to the lower
jaw,
neck, right arm,
back, and
epigastrium,
where it may mimic
heartburn.
Levine's sign, in which the patient localizes
the chest pain by clenching their fist over the
sternum, has classically been thought to be
predictive of cardiac chest pain, although a prospective
observational study showed that it had a poor positive predictive
value.
Shortness of breath (
dyspnea) occurs when
the damage to the heart limits the
output of the
left
ventricle, causing
left
ventricular failure and consequent
pulmonary edema. Other symptoms include
diaphoresis (an excessive form of
sweating), weakness,
light-headedness,
nausea,
vomiting, and
palpitations. These symptoms are likely
induced by a massive surge of
catecholamines from the
sympathetic nervous 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) and even
sudden
death (frequently due to the development of ventricular
fibrillation) can occur in myocardial infarctions.
Women and older patients experience atypical symptoms more
frequently than their male and younger counterparts. Women also
have more symptoms compared to men (2.6 on average vs 1.8 symptoms
in men). 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 which
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.
Approximately half of all MI patients have experienced warning
symptoms such as chest pain prior to the infarction.
Approximately one fourth of all myocardial infarctions are silent,
without chest pain or other symptoms. These cases can be discovered
later on electrocardiograms or at autopsy without a prior history
of related complaints. A silent course is more common in the
elderly, in patients with
diabetes mellitus and after
heart transplantation, probably
because the
donor heart is not
connected to nerves of the host. In diabetics, differences in
pain threshold,
autonomic neuropathy, and
psychological factors have been cited as possible
explanations for the lack of symptoms.
Any group of symptoms compatible with a sudden interruption of the
blood flow to the heart are called an
acute coronary syndrome.
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.
Causes and risk factors
Heart attack rates are higher in association with intense exertion,
be it
psychological stress or
physical exertion, especially if the
exertion is more intense than the individual usually performs.
Quantitatively, the period of intense exercise and subsequent
recovery is associated with about a 6-fold higher myocardial
infarction rate (compared with other more relaxed time frames) for
people who are physically very fit. For those in poor physical
condition, the rate differential is over 35-fold higher. One
observed mechanism for this phenomenon is the increased arterial
pulse pressure stretching and relaxation of arteries with each
heart beat which, as has been observed with
intravascular ultrasound, increases
mechanical "shear stress" on
atheromas and
the likelihood of plaque rupture.
Acute severe infection, such as
pneumonia,
can trigger myocardial infarction. A more controversial link is
that between
Chlamydophila
pneumoniae infection and atherosclerosis. While this
intracellular organism has been demonstrated in atherosclerotic
plaques, evidence is inconclusive as to whether it can be
considered a causative factor. Treatment with antibiotics in
patients with proven atherosclerosis has not demonstrated a
decreased risk of heart attacks or other coronary vascular
diseases.
There is an association of an increased incidence of a heart attack
in the morning hours, more specifically around 9 a.m. . Some
investigators have noticed that the ability of platelets to
aggregate varies according to a circadian rhythm, although they
have not proven causation. Some investigators theorize that this
increased incidence may be related to the circadian variation in
cortisol production affecting the concentrations of various
cytokines and other mediators of inflammation.
Risk factors
Risk factors for
atherosclerosis are
generally risk factors for myocardial infarction:
- Age: Men acquire an independent risk
factor at age 45, Women acquire an independent risk factor at age
55; in addition individuals acquire another independent risk factor
if they have a first-degree male relative (brother,father)who
suffered a coronary vascular event at or before age 55. Another
independent risk factor is acquired if one has a first-degree
female relative (mother,sister) who suffered a coronary vascular
event at age 65 or younger.
Males are more at risk than females.
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.
Non-modifiable risk factors include age, sex, and family history of
an early heart attack (before the age of 60), which is thought of
as reflecting a
genetic
predisposition.
Socioeconomic factors such as a
shorter
education and lower
income (particularly in women), and unmarried
cohabitation may also contribute to the risk of MI. To understand
epidemiological study results, it's important to note that many
factors associated with MI mediate their risk via other factors.
For example, the effect of education is partially based on its
effect on income and
marital
status.
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.
Inflammation is known to be an important step in the process of
atherosclerotic plaque formation.
C-reactive protein (CRP) is a sensitive
but non-specific
marker for
inflammation. Elevated CRP blood
levels, especially measured with high sensitivity assays, can
predict the risk of MI, as well as
stroke and
development of diabetes. Moreover, some drugs for MI might also
reduce CRP levels. 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. Whether CRP plays a direct role in
atherosclerosis remains uncertain.
Inflammation in
periodontal disease may
be linked coronary heart disease, and since
periodontitis is very common, this could have
great consequences for
public health.
Serological studies measuring
antibody levels against typical
periodontitis-causing
bacteria found that
such antibodies were more present in subjects with coronary heart
disease. Periodontitis tends to increase blood levels of CRP,
fibrinogen and
cytokines; thus, periodontitis may mediate its
effect on MI risk via other risk factors.
Preclinical research suggests that
periodontal bacteria can promote aggregation of
platelets and promote the formation of
foam cells. A role for specific periodontal
bacteria has been suggested but remains to be established. There is
some evidence that
influenza may trigger a
acute myocardial infarction.
Baldness,
hair
greying, a diagonal
earlobe crease
(
Frank's sign) and possibly other
skin features have been suggested as
independent risk factors for MI.Their role remains controversial; a
common denominator of these signs and the risk of MI is supposed,
possibly genetic.
Calcium deposition is another part of
atherosclerotic plaque formation. Calcium deposits in the coronary
arteries can be detected with
CT scans.
Several studies have shown that coronary calcium can provide
predictive information beyond that of classical risk factors.
The European Society of Cardiology and the European Association for
Cardiovascular Prevention and Rehabilitation have developed an
interactive tool for prediction and managing the risk of heart
attack and stroke in Europe. HeartScore is aimed at supporting
clinicians in optimising individual cardiovascular risk reduction.
The Heartscore Programme is available in 12 languages and offers
web based or PC version (
[737166]).
Pathophysiology
Acute myocardial infarction refers to two subtypes of
acute coronary syndrome, namely
non-ST-elevated myocardial infarction and
ST-elevated myocardial infarction, which are most
frequently (but not always) a manifestation of
coronary artery disease. The most
common triggering event is the disruption of an
atherosclerotic plaque in an epicardial coronary artery, which
leads to a clotting cascade, sometimes resulting in total occlusion
of the artery. Atherosclerosis is the gradual buildup of
cholesterol and fibrous tissue in plaques in the
wall of
arteries (in this case, the
coronary arteries), typically over decades.
Blood stream column irregularities visible on angiography reflect
artery
lumen narrowing as a result
of decades of advancing atherosclerosis. Plaques can become
unstable, rupture, and additionally promote a
thrombus (blood clot) that occludes the artery;
this can occur in minutes. When a severe enough plaque rupture
occurs in the coronary vasculature, it leads to myocardial
infarction (necrosis of downstream myocardium).
If impaired blood flow to the heart lasts long enough, it triggers
a process called the
ischemic
cascade; the heart cells in the territory of the occluded
coronary artery die (chiefly through
necrosis) and do not grow back. A
collagen scar forms in its
place. Recent studies indicate that another form of cell death
called
apoptosis also plays a role in the
process of tissue damage subsequent to myocardial infarction. As a
result, the patient's heart will be permanently damaged. This
Myocardial scarring also puts
the patient at risk for potentially life threatening arrhythmias,
and may result in the formation of a
ventricular aneurysm that can rupture
with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than
normal heart tissue. The difference in conduction velocity between
injured and uninjured tissue can trigger
re-entry or a feedback loop that
is believed to be the cause of many lethal arrhythmias. The most
serious of these arrhythmias is
ventricular fibrillation
(
V-Fib/VF), an extremely fast and chaotic heart rhythm
that is the leading cause of sudden cardiac death. Another life
threatening arrhythmia is
ventricular tachycardia
(
V-Tach/VT), which may or may not cause sudden cardiac
death. However, ventricular tachycardia usually results in rapid
heart rates that prevent the heart from pumping blood effectively.
Cardiac output and
blood pressure may fall to dangerous levels,
which can lead to further coronary ischemia and extension of the
infarct.
The
cardiac defibrillator is a device
that was specifically designed to terminate these potentially fatal
arrhythmias. The device works by delivering an electrical shock to
the patient in order to depolarize a critical mass of the heart
muscle, in effect "
rebooting" the heart. This
therapy is time dependent, and the odds of successful
defibrillation decline rapidly after the onset of cardiopulmonary
arrest.
Diagnosis
The diagnosis of myocardial infarction is made by integrating the
history of the presenting illness and physical examination with
electrocardiogram findings and
cardiac markers (
blood tests for
heart
muscle cell damage).
Myocardial infarction: diagnosis and
investigations -
GPnotebook,
retrieved November 27, 2006. A
coronary angiogram allows
visualization of narrowings or obstructions on the heart vessels,
and therapeutic measures can follow immediately. At
autopsy, a
pathologist
can diagnose a myocardial infarction based on
anatomopathological findings.
A
chest radiograph and routine
blood tests may indicate complications or precipitating causes and
are often performed upon arrival to an
emergency department. New regional wall
motion abnormalities on an
echocardiogram are also suggestive
of a myocardial infarction. Echo may be performed in equivocal
cases by the on-call cardiologist. In stable patients whose
symptoms have resolved by the time of evaluation,
technetium-99m
2-methoxyisobutylisonitrile (Tc99m MIBI) or
thallium-201 chloride can be used in
nuclear medicine to visualize areas
of reduced blood flow in conjunction with physiologic or
pharmocologic stress. Thallium may also be used to determine
viability of tissue, distinguishing whether non-functional
myocardium is actually dead or merely in a state of hibernation or
of being stunned.
Diagnostic criteria
WHO criteria formulated in 1979 have classically been used to
diagnose MI; a patient is diagnosed with myocardial infarction if
two (probable) or three (definite) of the following criteria are
satisfied:
- Clinical history of ischaemic type chest pain lasting for more
than 20 minutes
- Changes in serial ECG tracings
- 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. According to the new guidelines, a cardiac
troponin rise accompanied by either typical
symptoms, pathological Q waves, ST elevation or depression or
coronary intervention are diagnostic of MI.
Physical examination
The general appearance of patients may vary according to the
experienced symptoms; the patient may be comfortable, or restless
and in severe distress with an increased
respiratory rate. A cool and
pale skin is common and points to
vasoconstriction. Some patients have
low-grade fever (38–39 °C).
Blood
pressure may be elevated or decreased, and the
pulse can be become
irregular.Kasper DL, Braunwald E, Fauci
AS, Hauser SL, Longo DL, Jameson JL.
Harrison's Principles of
Internal Medicine. p. 1444. New York: McGraw-Hill, 2005. ISBN
0-07-139140-1.
If heart failure ensues, elevated
jugular venous pressure and
hepatojugular reflux, or swelling of
the legs due to peripheral
edema may be found
on inspection. Rarely, a cardiac bulge with a pace different from
the pulse rhythm can be felt on
precordial examination. Various
abnormalities can be found on
auscultation, such as a third and fourth
heart sound,
systolic murmurs, paradoxical splitting of the
second heart sound, a
pericardial
friction rub and
rales over the lung.Kasper
DL,
et al. Harrison's Principles of Internal
Medicine. p. 1450.
Electrocardiogram
The primary purpose of the
electrocardiogram is to detect
ischemia or acute coronary injury in broad,
symptomatic
emergency
department populations. However, the standard 12 lead
ECG has several limitations. An
ECG represents a brief sample in time.
Because unstable ischemic syndromes have rapidly changing supply
versus demand characteristics, a single ECG may not accurately
represent the entire picture.Cannon CP at al.
Management of
Acute Coronary Syndromes. p. 175. New Jersey: Humana Press,
1999. ISBN 0-89603-552-2. It is therefore desirable to obtain
serial 12 lead ECGs, particularly if the first ECG is
obtained during a pain-free episode. Alternatively, many
emergency departments and
chest pain centers use computers capable
of continuous ST segment monitoring. The standard 12 lead ECG also
does not directly examine the
right
ventricle, and is relatively poor at examining the posterior
basal and lateral walls of the
left
ventricle. In particular, acute myocardial infarction in the
distribution of the circumflex artery is likely to produce a
nondiagnostic ECG. The use of additional ECG leads like right-sided
leads V3R and V4R and posterior leads V7, V8, and V9 may improve
sensitivity for right ventricular and posterior myocardial
infarction. In spite of these limitations, the 12 lead ECG stands
at the center of risk stratification for the patient with suspected
acute myocardial infarction. Mistakes in interpretation are
relatively common, and the failure to identify high risk features
has a negative effect on the quality of patient care.
The 12 lead ECG is used to classify patients into one of three
groups:
- those with ST segment elevation or new bundle branch block
(suspicious for acute injury and a possible candidate for acute
reperfusion therapy with thrombolytics
or primary PCI),
- those with ST segment depression or T wave inversion
(suspicious for ischemia), and
- those with a so-called non-diagnostic or normal ECG.
A normal ECG does not rule out acute myocardial infarction.
Sometimes the earliest presentation of acute myocardial infarction
is the hyperacute T wave, which is treated the same as ST segment
elevation. In practice this is rarely seen, because it only exists
for 2–30 minutes after the onset of infarction. Hyperacute T waves
need to be distinguished from the peaked T waves associated with
hyperkalemia. The current guidelines
for the ECG diagnosis of acute myocardial infarction require at
least 1 mm (0.1 mV) of ST segment elevation in the limb leads,
and at least 2 mm elevation in the precordial leads. These
elevations must be present in anatomically contiguous leads. (I,
aVL, V5, V6 correspond to the lateral wall; V1-V4 correspond to the
anterior wall; II, III, aVF correspond to the inferior wall.) This
criterion is problematic, however, as acute myocardial infarction
is not the most common cause of ST segment elevation in
chest pain patients. Over 90% of healthy men have
at least 1 mm (0.1 mV) of ST segment elevation in at least one
precordial lead. The clinician must therefore be well versed in
recognizing the so-called ECG mimics of acute myocardial
infarction, which include
left ventricular hypertrophy,
left bundle branch block,
paced rhythm,
early repolarization,
pericarditis,
hyperkalemia, and
ventricular aneurysm.
Cardiac markers
Cardiac markers or cardiac enzymes are proteins that leak out of
injured myocardial cells through their damaged cell membranes into
the bloodstream. Until the 1980s, the enzymes
SGOT and
LDH were used to assess cardiac
injury. Now, the markers most widely used in detection of MI are
MB subtype of the enzyme
creatine kinase and cardiac
troponins T and I as they are more specific for
myocardial injury. The cardiac troponins T and I which are released
within 4–6 hours of an attack of MI and remain elevated for up to 2
weeks, have nearly complete tissue specificity and are now the
preferred markers for asssessing myocardial damage. Elevated
troponins in the setting of chest pain may accurately predict a
high likelihood of a myocardial infarction in the near future. New
markers such as
glycogen phosphorylase
isoenzyme BB are under investigation.
The diagnosis of myocardial infarction requires two out of three
components (history, ECG, and enzymes). When damage to the heart
occurs, levels of cardiac markers rise over time, which is why
blood tests for them are taken over a
24-hour period. Because these enzyme levels are not elevated
immediately following a heart attack, patients presenting with
chest pain are generally treated with the assumption that a
myocardial infarction has occurred and then evaluated for a more
precise diagnosis.
Angiography
In difficult cases or in situations where intervention to restore
blood flow is appropriate, coronary
angiography can be performed. A
catheter is inserted into an artery (usually the
femoral artery) and pushed to the
vessels supplying the heart. A radio-opaque dye is administered
through the catheter and a sequence of x-rays (fluoroscopy) is
performed. Obstructed or narrowed arteries can be identified, and
angioplasty applied as a therapeutic
measure (see below). Angioplasty requires extensive skill,
especially in emergency settings. It is performed by a physician
trained in
interventional
cardiology.
Histopathology
Histopathological examination
of the heart may reveal infarction at autopsy. Under the
microscope, myocardial infarction presents as a circumscribed area
of ischemic, coagulative
necrosis (cell
death). On gross examination, the infarct is not identifiable
within the first 12 hours.
Although earlier changes can be discerned using
electron microscopy, one of the earliest
changes under a normal microscope are so-called
wavy
fibers. Subsequently, the myocyte
cytoplasm becomes more
eosinophilic (pink) and the cells lose their
transversal striations, with typical changes and eventually loss of
the
cell nucleus. The interstitium at
the margin of the infarcted area is initially infiltrated with
neutrophils, then with
lymphocytes and
macrophages, who
phagocytose ("eat") the myocyte debris. The
necrotic area is surrounded and progressively invaded by
granulation tissue, which will replace
the infarct with a fibrous (
collagenous)
scar (which are typical steps in
wound healing). The interstitial space (the
space between cells outside of blood vessels) may be infiltrated
with
red blood cells.
These features can be recognized in cases where the perfusion was
not restored; reperfused infarcts can have other hallmarks, such as
contraction band
necrosis.
Prevention
The risk of a recurrent myocardial infarction decreases with strict
blood pressure management and lifestyle changes, chiefly
smoking cessation, regular
exercise, a sensible
diet for patients with heart disease,
and
limitation
of alcohol intake.
Patients are usually commenced on several long-term medications
post-MI, with the aim of preventing secondary cardiovascular events
such as further myocardial infarctions,
congestive heart failure or
cerebrovascular accident
(CVA). Unless contraindicated, such medications may include:
- Antiplatelet drug therapy such
as aspirin and/or clopidogrel should be continued to reduce the
risk of plaque rupture and recurrent myocardial infarction. Aspirin
is first-line, owing to its low cost and comparable efficacy, with
clopidogrel reserved for patients intolerant of aspirin. The
combination of clopidogrel and aspirin may further reduce risk of
cardiovascular events, however the risk of hemorrhage is increased.
- Beta blocker therapy such as
metoprolol or carvedilol should be commenced. These have been
particularly beneficial in high-risk patients such as those with
left ventricular dysfunction and/or
continuing cardiac ischaemia. β-Blockers
decrease mortality and morbidity. They also improve symptoms of
cardiac ischemia in NSTEMI.
- ACE inhibitor therapy should be
commenced 24–48 hours post-MI in hemodynamically-stable patients,
particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior
location of infarct (as assessed by ECG), and/or evidence of left
ventricular dysfunction. ACE inhibitors reduce mortality, the
development of heart failure, and
decrease ventricular remodelling post-MI.
- Statin therapy has been shown to reduce
mortality and morbidity post-MI. 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.
- The aldosterone
antagonist agent eplerenone has been
shown to further reduce risk of cardiovascular death post-MI in
patients with heart failure and left ventricular dysfunction, when
used in conjunction with standard therapies above.
- Omega-3 fatty acids, commonly
found in fish, have been shown to reduce mortality post-MI. While
the mechanism by which these fatty acids decrease mortality is
unknown, it has been postulated that the survival benefit is due to
electrical stabilization and the prevention of ventricular fibrillation. However,
further studies in a high-risk subset have not shown a clear-cut
decrease in potentially fatal arrhythmias due to omega-3 fatty
acids.
Management
A heart attack is a
medical
emergency which demands both immediate attention and activation
of the
emergency medical
services. The ultimate goal of the management in the acute
phase of the disease is to salvage as much myocardium as possible
and prevent further complications. As time passes, the risk of
damage to the heart muscle increases; hence the phrase that in
myocardial infarction, "time is muscle," and "time wasted is muscle
lost".
Oxygen,
aspirin,
glyceryl trinitrate
(nitroglycerin) and
analgesia are usually
administered as soon as possible. In many areas, first responders
are trained to administer these prior to arrival at the hospital.
Morphine is classically used if nitroglycerin is not effective due
to its ability to dilate blood vessels, which may aid in blood flow
to the heart as well as relieve pain. Morphine may also cause
hypotension (usually in the setting of hypovolemia), and should be
avoided in the case of right ventricular infarction. Moreover, the
CRUSADE trial demonstrated an increase in mortality with
administering morphine in the setting of NSTEMI. A 2009 review of
high flow oxygen in myocardial infarction found increased mortality
and infarct size, calling into question the recommendation about
its routine use.
Of the front line agents, aspirin and
streptokinase have been shown to markedly
reduce mortality. Streptokinase activates plasminogen, which is
fibrinolytic (see section on thrombolysis below).
Once the diagnosis of myocardial infarction is confirmed, other
pharmacologic agents are often given. These include
beta blockers, anticoagulation (typically with
heparin), and possibly additional
antiplatelet agents such as
clopidogrel.
While these agents can decrease mortality in the setting of an
acute myocardial infarction, they can lead to complications and
potentially death if used in the wrong setting.
Cocaine associated myocardial infarction
should be managed in a manner similar to other patients with acute
coronary syndrome except
beta blockers
should not be used and
benzodiazepines should be administered
early.
The treatment itself may have complications. If attempts to restore
the blood flow are initiated after a critical period of only a few
hours, the result may be a
reperfusion injury instead of
amelioration.
First aid
As myocardial infarction is a common medical emergency, the signs
are often part of
first aid courses. The
emergency action
principles also apply in the case of myocardial
infarction.
When symptoms of myocardial infarction occur, people wait an
average of three hours, instead of doing what is recommended:
calling for help immediately. Acting
immediately by calling the emergency services can save your life
for two reasons. First and most importantly, the emergency services
can immedialetely save your life from primary
ventricular fibrillation which
occurs unexpectedly in more than 10% of all infarction especially
during the first hour of symptoms and second, immediate treatment
of myocardial infarction can prevent sustained damage to the heart
("time is muscle").
Certain positions allow the patient to rest in a position which
minimizes breathing difficulties. A half-sitting position with
knees bent is often recommended. Access to more oxygen can be given
by opening the window and widening the collar for easier
breathing.
Aspirin can be given quickly (if the patient
is not
allergic to aspirin); but taking
aspirin before calling the
emergency medical services may be
associated with unwanted delay. Aspirin has an
antiplatelet effect which inhibits
formation of further
thrombi (blood clots)
that clog arteries. Chewing is the preferred method of
administration, so that the Aspirin can be
absorbed quickly. Dissolved
soluble preparations or
sublingual
administration can also be used. U.S. guidelines recommend a dose
of 162–325 mg. Australian guidelines recommend a dose of
150–300 mg.
Glyceryl
trinitrate (nitroglycerin)
sublingually (under the tongue) can be given if
available.
If an
automated
external defibrillator (AED) is available the rescuer should
immediately bring the AED to the patient's side and be prepared to
follow its instructions, especially should the victim lose
consciousness.
If possible the rescuer should obtain basic information from the
victim, in case the patient is unable to answer questions once
emergency medical
technicians arrive. The victim's name and any information
regarding the nature of the victim's pain will be useful to health
care providers. The exact time that these symptoms started may be
critical for determining what interventions can be safely attempted
once the victim reaches the medical center. Other useful pieces of
information include what the patient was doing at the onset of
symptoms, and anything else that might give clues to the pathology
of the chest pain. It is also very important to relay any actions
that have been taken, such as the number or dose of aspirin or
nitroglycerin given, to the EMS personnel.
Other general first aid principles include monitoring pulse,
breathing,
level of
consciousness and, if possible, the blood pressure of the
patient. In case of
cardiac arrest,
cardiopulmonary
resuscitation (CPR) can be administered.
Automatic external defibrillation (AED)
Since the publication of data showing that the availability of
automated external
defibrillators (AEDs) in public places may significantly
increase chances of survival, many of these have been installed in
public buildings,
public transport
facilities, and in non-ambulance emergency vehicles (e.g.
police cars and
fire
engine). AEDs analyze the heart's rhythm and determine whether
the rhythm is amenable to
defibrillation ("shockable"), as in
ventricular tachycardia and
ventricular fibrillation.
Emergency services
Emergency Medical
Services (EMS) Systems vary considerably in their ability to
evaluate and treat patients with suspected acute myocardial
infarction. Some provide as little as first aid and early
defibrillation. Others employ highly trained paramedics with
sophisticated technology and advanced protocols. Early access to
EMS is promoted by a
9-1-1 system currently available to 90% of the population in the
United States. Most are capable of providing
oxygen, IV access, sublingual
nitroglycerine,
morphine, and
aspirin. Some
are capable of providing
thrombolytic
therapy in the prehospital setting.
With
primary PCI
emerging as the preferred therapy for ST segment elevation
myocardial infarction,
EMS can play a key role in
reducing
door to balloon intervals
(the time from presentation to a hospital
ER to the restoration of coronary
artery blood flow) by performing a 12 lead
ECG
in the field and using this information to triage the patient to
the most appropriate medical facility. In addition, the 12 lead ECG
can be transmitted to the receiving hospital, which enables time
saving decisions to be made prior to the patient's arrival. This
may include a "cardiac alert" or "STEMI alert" that calls in off
duty personnel in areas where the
cardiac cath lab is not staffed 24
hours a day. Even in the absence of a formal alerting program,
prehospital 12 lead ECGs are independently associated with reduced
door to treatment intervals in the emergency department.
Reperfusion
The concept of reperfusion has become so central to the modern
treatment of acute myocardial infarction, that we are said to be in
the reperfusion era. Patients who present with suspected acute
myocardial infarction and ST segment elevation (STEMI) or new
bundle branch block on the 12 lead
ECG are
presumed to have an occlusive thrombosis in an epicardial coronary
artery. They are therefore candidates for immediate reperfusion,
either with
thrombolytic therapy,
percutaneous coronary
intervention (PCI) or when these therapies are unsuccessful,
bypass surgery.
Individuals without ST segment elevation are presumed to be
experiencing either unstable angina (UA) or non-ST segment
elevation myocardial infarction (NSTEMI). They receive many of the
same initial therapies and are often stabilized with
antiplatelet drugs and
anticoagulated. If their condition remains
(
hemodynamically) stable, they can be
offered either late
coronary
angiography with subsequent restoration of blood flow
(revascularization), or
non-invasive stress testing to determine if there is
significant ischemia that would benefit from revascularization. If
hemodynamic instability develops in individuals with NSTEMIs, they
may undergo urgent coronary angiography and subsequent
revascularization. The use of thrombolytic agents is
contraindicated in this patient subset, however.
The basis for this distinction in treatment regimens is that ST
segment elevations on an ECG are typically due to complete
occlusion of a coronary artery. On the other hand, in NSTEMIs there
is typically a sudden narrowing of a coronary artery with preserved
(but diminished) flow to the distal myocardium. Anticoagulation and
antiplatelet agents are given to prevent the narrowed artery from
occluding.
At least 10% of patients with STEMI don't develop myocardial
necrosis (as evidenced by a rise in cardiac markers) and subsequent
Q waves on EKG after reperfusion therapy. Such a successful
restoration of flow to the infarct-related artery during an acute
myocardial infarction is known as "aborting" the myocardial
infarction. If treated within the hour, about 25% of STEMIs can be
aborted.
Thrombolytic therapy
Thrombolytic therapy is indicated for the treatment of STEMI if the
drug can be administered within 12 hours of the onset of symptoms,
the patient is eligible based on exclusion criteria, and primary
PCI is not immediately available. The effectiveness of
thrombolytic therapy is highest in the first 2
hours. After 12 hours, the risk associated with thrombolytic
therapy outweighs any benefit. Because irreversible injury occurs
within 2–4 hours of the infarction, there is a limited window of
time available for reperfusion to work.
Thrombolytic drugs are contraindicated for the treatment of
unstable angina and NSTEMI and for the treatment of individuals
with evidence of
cardiogenic
shock.
Although no perfect thrombolytic agent exists, an ideal
thrombolytic drug would lead to rapid reperfusion, have a high
sustained patency rate, be specific for recent thrombi, be easily
and rapidly administered, create a low risk for intra-cerebral and
systemic bleeding, have no antigenicity, adverse hemodynamic
effects, or clinically significant drug interactions, and be cost
effective. Currently available thrombolytic agents include
streptokinase,
urokinase, and
alteplase
(recombinant
tissue
plasminogen activator, rtPA). More recently, thrombolytic
agents similar in structure to rtPA such as
reteplase and
tenecteplase have been used. These newer agents
boast efficacy at least as good as rtPA with significantly easier
administration. The thrombolytic agent used in a particular
individual is based on institution preference and the age of the
patient.
Depending on the thrombolytic agent being used,
adjuvant anticoagulation with
heparin or
low molecular weight heparin
may be of benefit. With TPa and related agents (reteplase and
tenecteplase), heparin is needed to maintain coronary artery
patency. Because of the anticoagulant effect of fibrinogen
depletion with streptokinase and urokinase treatment, it is less
necessary there.
Intracranial bleeding (ICB) and subsequent
cerebrovascular accident (CVA) is a
serious side effect of thrombolytic use. The risk of ICB is
dependent on a number of factors, including a previous episode of
intracranial bleed, age of the individual, and the thrombolytic
regimen that is being used. In general, the risk of ICB due to
thrombolytic use for the treatment of an acute myocardial
infarction is between 0.5 and 1 percent.
Thrombolytic therapy to abort a myocardial infarction is not always
effective. The degree of effectiveness of a thrombolytic agent is
dependent on the time since the myocardial infarction began, with
the best results occurring if the thrombolytic agent is used within
two hours of the onset of symptoms. If the individual presents more
than 12 hours after symptoms commenced, the risk of intracranial
bleed are considered higher than the benefits of the thrombolytic
agent. Failure rates of thrombolytics can be as high as 20% or
higher. In cases of failure of the thrombolytic agent to open the
infarct-related coronary artery, the patient is then either treated
conservatively with anticoagulants and allowed to "complete the
infarction" or
percutaneous coronary
intervention (PCI, see below) is then performed. Percutaneous
coronary intervention in this setting is known as "rescue PCI" or
"salvage PCI". Complications, particularly bleeding, are
significantly higher with rescue PCI than with primary PCI due to
the action of the thrombolytic agent.
Percutaneous coronary intervention
The benefit of prompt, expertly performed primary percutaneous
coronary intervention over thrombolytic therapy for acute ST
elevation myocardial infarction is now well established. When
performed rapidly by an experienced team, primary PCI restores flow
in the culprit artery in more than 95% of patients compared with
the spontaneous recanalization rate of about 65%. Logistic and
economic obstacles seem to hinder a more widespread application of
percutaneous coronary intervention (PCI)
via
cardiac catheterization,
although the feasibility of regionalized PCI for STEMI is currently
being explored in the United States.Rokos IC, Larson DM, Henry TD,
et al.; "Rationale for establishing regional ST-elevation
myocardial infarction receiving center (SRC) networks."
Am
Heart J 2006;
152(4):661-7. PMID 16996830 The
use of percutaneous coronary intervention as a therapy to abort a
myocardial infarction is known as primary PCI. The goal of primary
PCI is to open the artery as soon as possible, and preferably
within 90 minutes of the patient presenting to the emergency room.
This time is referred to as the
door-to-balloon time. Few hospitals can
provide PCI within the 90 minute interval, which prompted the
American College of Cardiology (ACC) to launch a national Door to
Balloon (D2B) Initiative in November 2006. Over 800 hospitals have
joined the D2B Alliance as of March 16, 2007.
One
particularly successful implementation of a primary PCI protocol is
in the Calgary Health Region
under the auspices of the Libin
Cardiovascular Institute of Alberta
. Under this model, EMS teams responding to
an emergency electronically transmit the ECG directly to a digital
archiving system that allows emergency room physicians and/or
cardiologists to immediately confirm the diagnosis. This in turn
allows for redirection of the EMS teams to facilities prepped to
conduct time-critical angioplasty, based on the ECG analysis. In an
article published in the
Canadian Medical
Association Journal in June 2007, the Calgary implementation
resulted in a median time to treatment of 62 minutes.
The current guidelines in the United States restrict primary PCI to
hospitals with available emergency bypass surgery as a backup, but
this is not the case in other parts of the world.
Primary PCI involves performing a coronary
angiogram to determine the anatomical location of
the infarcting vessel, followed by balloon
angioplasty (and frequently deployment of an
intracoronary stent) of the thrombosed arterial segment. In some
settings, an extraction catheter may be used to attempt to aspirate
(remove) the thrombus prior to balloon angioplasty. While the use
of intracoronary
stents do not improve the
short term outcomes in primary PCI, the use of stents is widespread
because of the decreased rates of procedures to treat restenosis
compared to balloon angioplasty.
Adjuvant therapy during primary PCI includes intravenous
heparin,
aspirin, and
clopidogrel.
Glycoprotein IIb/IIIa
inhibitors are often used in the setting of primary PCI to
reduce the risk of ischemic complications during the procedure. Due
to the number of antiplatelet agents and anticoagulants used during
primary PCI, the risk of bleeding associated with the procedure is
higher than during an elective PCI.
Coronary artery bypass surgery
Despite the guidelines, emergency bypass surgery for the treatment
of an acute myocardial infarction (MI) is less common than PCI or
medical management. In an analysis of patients in the U.S.
National Registry of
Myocardial Infarction (NRMI) from January 1995 to May 2004, the
percentage of patients with
cardiogenic shock treated with primary PCI
rose from 27.4% to 54.4%, while the increase in CABG treatment was
only from 2.1% to 3.2%.
Emergency coronary artery bypass graft surgery (CABG) is usually
undertaken to simultaneously treat a mechanical complication, such
as a ruptured papillary muscle, or a ventricular septal defect,
with ensueing cardiogenic shock. In uncomplicated MI, the
mortality rate can be high when the surgery
is performed immediately following the infarction. If this option
is entertained, the patient should be stabilized prior to surgery,
with supportive interventions such as the use of an
intra-aortic balloon pump. In
patients developing cardiogenic shock after a myocardial
infarction, both PCI and CABG are satisfactory treatment options,
with similar survival rates.
Coronary artery bypass surgery involves an artery or vein from the
patient being implanted to bypass
narrowings or occlusions on the coronary arteries.
Several arteries and veins can be used, however
internal mammary artery grafts have
demonstrated significantly better long-term patency rates than
great saphenous vein grafts. In
patients with two or more coronary arteries affected, bypass
surgery is associated with higher long-term
survival rates compared to percutaneous
interventions. In patients with single vessel disease, surgery is
comparably safe and effective, and may be a treatment option in
selected cases. Bypass surgery has higher costs initially, but
becomes
cost-effective in the
long term. A surgical bypass graft is more
invasive initially but bears less risk of
recurrent procedures (but these may be again
minimally invasive).
Monitoring for arrhythmias
Additional objectives are to prevent life-threatening arrhythmias
or conduction disturbances. This requires monitoring in a
coronary care unit and protocolised
administration of
antiarrhythmic
agents. Antiarrhythmic agents are typically only given to
individuals with life-threatening arrhythmias after a myocardial
infarction and not to suppress the
ventricular ectopy that is
often seen after a myocardial infarction.
Austere environments
- Wilderness first aid
In
wilderness first aid, a
possible heart attack justifies
evacuation by the fastest available
means, including
MEDEVAC, even in the
earliest or precursor stages. The patient will rapidly be incapable
of further exertion and have to be carried out.
- Air travel
Certified personnel traveling by commercial aircraft may be able to
assist an MI patient by using the on-board
first aid kit, which may contain some cardiac
drugs (such as
glyceryl
trinitrate spray,
aspirin, or
opioid painkillers), an AED, and
oxygen. Pilots may divert the flight to land at a
nearby airport.
Cardiac monitors
are being introduced by some airlines, and they can be used by both
on-board and ground-based physicians.
Rehabilitation
Cardiac
rehabilitation aims to optimize function and
quality of life in those afflicted with a
heart disease. This can be with the help of a physician, or in the
form of a cardiac rehabilitation program.
Physical exercise is an important
part of
rehabilitation after a
myocardial infarction, with beneficial effects on cholesterol
levels, blood pressure, weight,
stress and
mood. Some patients become afraid of
exercising because it might trigger another infarct. Patients are
stimulated to exercise, and should only avoid certain exerting
activities. Local authorities may place limitations on
driving motorised
vehicles. Some people are afraid to have
sex after a heart attack. Most people
can resume sexual activities after 3 to 4 weeks. The amount of
activity needs to be dosed to the patient's possibilities.
New therapies under investigation
Patients who receive
stem cell
treatment by
coronary artery
injections of
stem cells derived
from their own
bone marrow after a
myocardial infarction (MI) show improvements in left ventricular
ejection fraction and
end-diastolic volume not seen with
placebo. The larger the initial infarct
size, the greater the effect of the infusion.
Clinical trials of
progenitor cell infusion as a treatment
approach to ST elevation MI are proceeding.
There are currently 3
biomaterial and
tissue engineering approaches for
the treatment of MI, but these are in an even earlier stage of
medical research, so many questions
and issues need to be addressed before they can be applied to
patients. The first involves
polymeric left
ventricular restraints in the prevention of
heart failure. The second utilizes
in vitro engineered cardiac
tissue, which is subsequently implanted
in
vivo. The final approach entails injecting cells and/or a
scaffold into the myocardium to create
in
situ engineered cardiac tissue.
Complications
Complications may occur immediately following the heart attack (in
the
acute phase), or may need time
to develop (a
chronic problem).
After an infarction, an obvious complication is a second
infarction, which may occur in the domain of another
atherosclerotic coronary artery, or in the same zone if there are
any live cells left in the infarct.
Congestive heart failure
A myocardial infarction may compromise the function of the heart as
a pump for the
circulation, a
state called
heart failure. There are
different types of heart failure; left- or right-sided (or
bilateral) heart failure may occur depending on the affected part
of the heart, and it is a low-output type of failure. If one of the
heart valves is affected, this may cause dysfunction, such as
mitral regurgitation in the
case of left-sided coronary occlusion that disrupts the blood
supply of the papillary muscles. The incidence of heart failure is
particularly high in patients with diabetes and requires special
management strategies.
Myocardial rupture
Myocardial rupture is most common
three to five days after myocardial infarction, commonly of small
degree, but may occur one day to three weeks later. In the modern
era of early revascularization and intensive pharmacotherapy as
treatment for MI, the incidence of myocardial rupture is about 1%
of all MIs. This may occur in the free walls of the
ventricles, the
septum
between them, the
papillary
muscles, or less commonly the
atria.
Rupture occurs because of increased pressure against the weakened
walls of the heart chambers due to heart muscle that cannot pump
blood out effectively. The weakness may also lead to ventricular
aneurysm, a localized dilation or
ballooning of the heart chamber.
Risk factors for myocardial rupture include completion of
infarction (no revascularization performed), female sex, advanced
age, and a lack of a previous history of myocardial infarction. In
addition, the risk of rupture is higher in individuals who are
revascularized with a thrombolytic agent than with PCI. The shear
stress between the infarcted segment and the surrounding normal
myocardium (which may be hypercontractile in the post-infarction
period) makes it a nidus for rupture.
Rupture is usually a catastrophic event that may result a
life-threatening process known as
cardiac tamponade, in which blood
accumulates within the
pericardium or
heart sac, and compresses the heart to the point where it cannot
pump effectively. Rupture of the intraventricular septum (the
muscle separating the left and right ventricles) causes a
ventricular septal defect with
shunting of blood through the defect
from the left side of the heart to the right side of the heart,
which can lead to right ventricular failure as well as pulmonary
overcirculation. Rupture of the papillary muscle may also lead to
acute
mitral regurgitation and
subsequent
pulmonary edema and
possibly even
cardiogenic
shock.
Life-threatening arrhythmia
Since the electrical characteristics of the infarcted tissue change
(see
pathophysiology
section),
arrhythmias are a frequent
complication. The re-entry phenomenon may cause rapid heart rates
(
ventricular tachycardia and
even
ventricular
fibrillation), and ischemia in the
electrical conduction
system of the heart may cause a
complete heart block (when the
impulse from the
sinoatrial node,
the normal cardiac pacemaker, does not reach the heart
chambers).
Pericarditis
As a reaction to the damage of the heart muscle,
inflammatory cells are attracted. The
inflammation may reach out and affect the heart sac. This is called
pericarditis. In
Dressler's syndrome, this occurs several
weeks after the initial event.
Cardiogenic shock
A complication that may occur in the acute setting soon after a
myocardial infarction or in the weeks following it is
cardiogenic shock. Cardiogenic shock is
defined as a hemodynamic state in which the heart cannot produce
enough of a
cardiac output to supply
an adequate amount of oxygenated blood to the tissues of the
body.
While the data on performing interventions on individuals with
cardiogenic shock is sparse, trial data suggests a long-term
mortality benefit in undergoing revascularization if the individual
is less than 75 years old and if the onset of the acute myocardial
infarction is less than 36 hours and the onset of cardiogenic shock
is less than 18 hours. If the patient with cardiogenic shock is not
going to be revascularized, aggressive hemodynamic support is
warranted, with insertion of an
intra-aortic balloon pump if not
contraindicated. If diagnostic coronary angiography does not reveal
a culprit blockage that is the cause of the cardiogenic shock, the
prognosis is poor.
Prognosis
The prognosis for patients with myocardial infarction varies
greatly, depending on the patient, the condition itself and the
given treatment. Using simple variables which are immediately
available in the
emergency room,
patients with a higher risk of adverse outcome can be identified.
For example, one study found that 0.4% of patients with a low risk
profile had died after 90 days, whereas the
mortality rate in high risk patients was
21.1%.
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 which one looks at.
Although studies differ in the identified variables, some of the
more
reproduced risk stratifiers
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
concentration,
peripheral vascular
disease and elevation of cardiac markers.
Assessment of
left ventricular
ejection fraction may increase the
predictive power of some risk stratification models. The prognostic
importance of Q-waves is debated. Prognosis is significantly
worsened if a mechanical complication (
papillary muscle rupture, myocardial free
wall rupture, and so on) were to occur.
There is evidence that case fatality of myocardial infarction has
been improving over the years in all ethnicities.
Epidemiology
Myocardial infarction is a common presentation of
ischemic heart disease. The WHO
estimated that in 2002, 12.6 percent of deaths worldwide were from
ischemic heart disease. Ischemic heart disease is the leading cause
of death in developed countries, but third to
AIDS and
lower
respiratory infections in developing countries.
In the
United
States
, diseases of the heart
are the leading cause of
death, causing a higher mortality than
cancer (malignant
neoplasms). Coronary heart disease is responsible
for 1 in 5 deaths in the U.S.. Some 7,200,000 men and 6,000,000
women are living with some form of coronary heart disease.
1,200,000 people suffer a (new or recurrent) coronary attack every
year, and about 40% of them die as a result of the attack. This
means that roughly every 65 seconds, an American dies of a coronary
event.
In
India
, cardiovascular disease (CVD) is the leading cause
of death. The deaths due to CVD in India were 32% of all
deaths in 2007 and are expected to rise from 1.17 million in 1990
and 1.59 million in 2000 to 2.03 million in 2010. Although a
relatively new epidemic in India, it has quickly become a major
health issue with deaths due to CVD expected to double during
1985-2015. Mortality estimates due to CVD vary widely by state,
ranging from 10% in Meghalaya to 49% in Punjab (percentage of all
deaths). Punjab (49%), Goa (42%), Tamil Nadu (36%) and Andhra
Pradesh (31%) have the highest CVD related mortality estimates.
State-wise differences are correlated with prevalence of specific
dietary risk factors in the states. Moderate physical exercise is
associated with reduced incidence of CVD in India (those who
exercise have less than half the risk of those who don't). CVD also
affects Indians at a younger age (in their 30s and 40s) than is
typical in other countries.
Legal implications
At
common law, a myocardial infarction is
generally a
disease, but may sometimes be an
injury. This has implications for no-fault
insurance schemes such as
workers'
compensation. A heart attack is generally not covered; however,
it may be a
work-related injury if
it results, for example, from unusual emotional stress or unusual
exertion. Additionally, 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 who has suffered from a myocardial infarction may
be prevented from participating in activity that puts other
people's lives at risk, for example driving a car or flying an
airplane.
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