http://emedicine.medscape.

com/article/1960472-overview

ACUTE MYOCARDIAL INFARCTION

Overview
Acute myocardial infarction (MI) indicates irreversible myocardial injury resulting in necrosis
of a significant portion of myocardium (generally >1 cm). The term "acute" denotes
infarction less than 5 days old, when the inflammatory infiltrate is primarily neutrophilic.
Acute MI may be either of the nonreperfusion type, in which case the obstruction to blood
flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow is
long enough in duration (generally hours) but is reversed or restored after myocardial cell
death occurs.

Pathophysiology
Acute myocardial infarction (MI) generally refers to segmental (regional) myocardial
necrosis, typically endocardium-based, secondary to occlusion of an epicardial artery. In
contrast, concentric subendocardial necrosis may result from global ischemia and
reperfusion in cases of prolonged cardiac arrest with resuscitation.
The area of infarct occurs in the distribution of the occluded vessel. Left main coronary
artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the
left anterior descending coronary artery causes necrosis limited to the anterior wall. There is
often extension to the anterior portion of the ventricular septum with proximal left coronary
occlusions.
In hearts with a right coronary dominance (with the right artery supplying the posterior
descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct.
With a left coronary dominance (about 15% of the population), a proximal circumflex
occlusion will infarct the posterior wall; in the right dominant pattern, a proximal obtuse
marginal thrombus will cause a lateral wall infarct only, and the distal circumflex is a small
vessel.
The anatomic variation due to microscopic collateral circulation, which is not evident at
autopsy, plays a large factor in the size of necrosis and distribution. Unusual patterns of
supply to the posterior wall, such as wraparound left anterior descending or posterior
descending artery supplied by the obtuse marginal artery, may also result in unexpected
areas of infarct in relation to the occluded proximal segment.
A proximal occlusion at the level of an epicardial artery results in a typical distribution that
starts at the subendocardium and progresses towards the epicardium (the so-called
wavefront phenomenon).[1] Therefore, an area of necrosis or scarring is considered to have
an "ischemic pattern" if it is largest at the endocardium, with a wedge-shaped extension up
to the epicardial surface.
Ischemic injury, however, may be located in the mid myocardium or even the subepicardium
if the level of the coronary occlusion is distal within the myocardium. Therefore, in cases of
thromboemboli from epicardial thrombi (especially plaque erosions), there may be patchy
infarction, often associated with visible thrombi within the myocardial vessels, not centered

in the endocardium but occurring anywhere in the myocardium, including midepicardial and
subepicardial locations.

Etiology
Acute myocardial infarction (MI) results from lack of oxygen supply to the working
myocardium. Regional infarcts are due to lack of blood flow that occurs when an epicardial
artery is blocked by atheroma or thrombus, or other obstructions. Global subendocardial
infarcts occur when there is lack of oxygenation despite circulationfor example, when
there is a respiratory arrest followed by prolonged hypoxemia.
Autopsies of hospital inpatients dying of acute regional MI reveal an acute thrombus
overlying atherosclerotic plaque in more than 95% of cases when the coronary arteries are
carefully inspected.[2] In the remaining hearts, there will be severe coronary diseases without
thrombus.
Rare causes of acute MI include no apparent cause (usually attributed to coronary spasm),
coronary embolism (varied causes, including valve vegetations and tumors), spontaneous
coronary artery dissections, congenital anomalies of the coronary origins, and thrombosis in
nonatherosclerotic normal coronary arteries (hypercoagulable states).
Risk factors
There is a known genetic predisposition to coronary artery disease that leads to acute MI. In
general, about 50-85% of the risk of coronary atherosclerosis is secondary to acquired
conditions. The remainder is secondary to genetic polymorphisms, which involve pathways
of inflammation, lipid metabolism, coagulation, the renin-angiotensin-aldosterone system,
and other components of atherogenesis.[3, 4]

Epidemiology
Acute myocardial infarctions (MIs) are common. In the United States, they result in the
hospitalization of approximately 4 men and 2 women per 1000 population each year.

Clinical Features
The symptoms of acute myocardial infarction (MI) are chest pain, which may radiate to the
arm or jaw, sweating, nausea, and chest tightness or pressure. The diagnosis rests on
laboratory findings of myocardial necrosis, which causes leakage of myocardial enzymes,
such as troponin, into the circulating blood. Acute infarcts are divided by
electrocardiographic findings into ST-elevation myocardial infarction (STEMI) and non STelevation infarction (non-STEMI).
STEMI is usually the result of blockage of a coronary artery with large elevations of cardiac
enzymes in the serum and eventually result in Q waves on the electrocardiogram. In
contrast, non-STEMI, which overlaps with the acute coronary syndrome unstable angina,
causes modest elevations of cardiac enzymes in the serum and pathologically shows small
or patchy areas of necrosis. Q waves do not develop in non-STEMI.

Gross Findings
The earliest change that can be grossly discerned in the evolution of acute myocardial
infarction (MI) is pallor of the myocardium, which is visible 12 hours or later after the onset
of irreversible ischemia. The gross detection of infarction can be enhanced by the use of
tetrazolium salt solutions, which form a colored precipitate on gross section of fresh heart
tissue in the presence of dehydrogenase-mediated activity. Myocardial necrosis can be
detected as early as 2-3 hours in dogs and in humans by this method.
In nonreperfused MI, the infarcted area is well defined at 2-3 days, with a central area of
yellow discoloration surrounded by a thin rim of highly vascularized hyperemia (see the first
image below). In reperfused MI, the infarcted region appears red because of trapping of the
red cells and hemorrhage from ruptured necrotic capillaries (see the second image below).

Acute myocardial infarct. At 3 days, there is a zone of yellow necrosis surrounded by darker
hyperemic borders. The arrow points to a transmural infarct in the posterior wall of the left
ventricle, in this short axis slice through the left and right ventricular chambers.

Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely
hemorrhagic. There is a rupture track through the center of this posterior left ventricular
transmural infarct. The mechanism of death was hemopericardium.
At 5-7 days, the regions are much more distinct, with a central soft area and a depressed
hyperemic border. At 1-2 weeks, the infarct begins to appear depressed, especially at the
margins where organization takes place, and the borders take on a white hue.
Healing may be complete as early as 4-6 weeks for small infarcts or may take as long as 2-3
months for large ones (see the images below). Areas of congestion and vasodilatation within
healed scars may appear hemorrhagic. In these cases, mottled myocardium that gives the
gross appearance of acute MI may, upon histologic examination, demonstrate only old
fibrosis.

Healing myocardial infarction, lateral left ventricle. In this heart, there is a variegated or
mottled appearance to the lateral left ventricle (left). This infarct began 19 days prior to
death.

Early healed myocardial infarction, anterior septum. There is a glistening gelatinous

appearance to this infarction, that occurred 6 weeks prior to death, from embolization during
valve surgery.
Healed infarcts are white from the scarring, and the ventricular wall may be thinned
(aneurysmal), especially in transmural infarction (see the image below). In general, infarcts
that occupy more than 50% of the ventricular wall, from the subendocardial to the epicardial
surface, are considered transmural and are associated with Q-wave changes on
electrocardiography.

Healed myocardial infarction, anterior left ventricle. There is diffuse scarring (white) with
marked thinning of the ventricle (aneurysm).

Microscopic Findings
Microscopically, the diagnosis of acute myocardial infarction (MI) rests on the presence of
necrotic myocardium, with an interface of acute inflammation separating it from viable
myocardium. Areas of inflammation with a scar or areas of mummified dead myocardium
bordered by granulation tissue do not indicate the presence of acute MI.
The earliest morphologic characteristic of MI occurs between 12 and 24 hours after the
onset of chest pain. Hypereosinophilia of the cytoplasm as assessed by hematoxylin-eosin

staining is characteristic of myocardial ischemia (see the first image below). Neutrophil
infiltration is present by 24 hours at the border areas (see the second image below).

Acute myocardial infarct. The earliest change is hypereosinophilia (above) with an intense
pink cytoplasm. There is no inflammation at border between the necrotic myocardium and
the viable myocardium (left and below), indicating that the necrosis is about 12-24 hours in
age.

Acute myocardial infarct. After 24 hours, there is a neutrophilic infiltrate at the border of the
infarct. Viable myocardium is at the left, and neutrophils with apoptosis (karyorrhexis) are
seen infiltrating the necrotic muscle. This patient experienced abdominal pain 35 hours prior
to death.
As the infarct progresses between 24 and 48 hours, coagulation necrosis is established, with
various degrees of nuclear pyknosis, early karyorrhexis, and karyolysis. The myocyte
striations are preserved and the sarcomeres elongate. The border areas show prominent
neutrophil infiltration by 48 hours.
At 3-5 days, the central portion of the infarct shows loss of myocyte nuclei and striations; in
smaller infarcts, neutrophils invade the infarct and fragment, resulting in more severe
karyorrhexis (nuclear dust). By 5-7 days, macrophages and fibroblasts begin to appear in the
border areas. By 1 week, neutrophils decline and granulation tissue is established (see the
image below), with neocapillary invasion and lymphocytic and plasma cell infiltration.

Healing myocardial infarct. This patient died 8 days after experiencing sudden chest pain at
rest. There is a large area of necrosis with hypereosinophilia of myocytes, with a rim of
viable myocardium at the very bottom. At the border, there is chronic inflammation with
early granulation tissue, with ingrowth of endothelial cells.

Although lymphocytes may be seen as early as 2-3 days, they are not prominent in any
stage of infarct evolution. Eosinophils may be seen within the inflammatory infiltrate but are
present in only 24% of infarcts. There is phagocytic removal of the necrotic myocytes by
macrophages, and pigment is seen within macrophages.[6]
By the second week, fibroblasts are prominent, but they may appear as early as 1 week at
the periphery of the infarct (see the image below). There is continued removal of the
necrotic myocytes as the fibroblasts are actively producing collagen, and angiogenesis
occurs in the area of healing.

Healing myocardial infarct. At 10 days to 2 weeks, there is chronic inflammation,

hemosiderin-laden macrophages, and early fibroblasts without significant collagen
deposition.
Healing continues and, depending on the extent of necrosis, may be complete as early as 4
weeks or may require 8 weeks or longer to complete (see the image below). The central area
of large infarction may remain unhealed and show mummified myocytes for extended
periods, even though the infarct borders are completely healed.

Healed myocardial infarct. At 3 months, there is dense scar, which is blue on this Masson
trichrome stain. This infarct was subendocardial, in the posterior left ventricle near the
ventricular septum.
The histologic dating of MI may be important from a medicolegal point of view. There is no
way of determining infarct age exactly, however, both because the histologic features that
define the stages of repair overlap and because infarcts may enlarge, resulting in
heterogeneity from one area to another. The border zone between necrotic myocardium and
viable myocardium is the focus of dating, which depends on the reaction of viable
myocardium to the area of infarct.
At 24 hours of occlusion followed by reperfusion after 6 hours in a canine model, myocytes
are thin, hypereosinophilic, and devoid of nuclei or showing karyorrhexis, with ill-defined
borders and interspersed areas of interstitial hemorrhage. There is a diffuse but mild
neutrophil infiltration. Within 2-3 days, macrophage infiltration is obvious and there is
phagocytosis of necrotic myocytes and early stages of granulation tissue.

Infarct healing is more rapid in dogs than in humans, most likely because of nondiseased
adjoining coronary arteries (collaterals) and a lack of underlying myocardial disease. In
humans with acute MI, there is often chronic ischemia secondary to extensive
atherosclerotic disease.
In humans, if reperfusion occurs within 4-6 hours after the onset of chest pain or
electrocardiographic (ECG) changes, there is myocardial salvage, and the infarct is likely to
be subendocardial without transmural extension. There will be a nearly confluent area of
hemorrhage within the infarcted myocardium, with extensive contraction band necrosis.
Within a few hours of reperfusion, sparse neutrophils are evident within the area of necrosis,
but they are usually sparse.
Macrophages begin to appear by day 2-3; by day 3-5, fibroblasts appear, with an
accelerated rate of healing as compared with that of nonreperfused infarcts. Subendocardial
infarcts may be fully healed as early as 2-3 weeks. Larger infarcts and those reperfused after
6 hours take longer to heal. Infarcts reperfused after 6 hours show larger areas of
hemorrhage than do occlusions with more immediate reperfusion.

Immunohistochemistry
Immunohistochemistry is of limited use in the diagnosis of acute myocardial infarction (MI).
Immunolocalization of complement or fibrin may be helpful in identifying areas of myocyte
necrosis, where there is leakage of extracellular proteins into the myocytes. In addition,
markers of ischemia include hypoxia-inducible factor-1, complement leaking into myocytes,
and cyclooxygenase-2, which can be demonstrated immunohistochemically.

Prognosis and Predictive Factors

The morbidity and mortality of myocardial infarction (MI) result from arrhythmias, cardiac
rupture, heart failure, valve insufficiency, and embolization.
Arrhythmias include ventricular tachyarrhythmias, which are the most common cause of
sudden death, especially early after infarction, and various degrees of heart block.
Cardiac rupture occurs in approximately 5% of patients, has a high mortality, and is
increased in frequency in patients experiencing their first infarct, hypertensive patients, and
women.[7]
The risk of heart failure is proportional to the size of the infarct and the presence of papillary
muscle necrosis. The size of infarct may be significantly decreased with prompt reperfusion
after the first symptoms, either by thrombolytic treatment or by percutaneous intervention.
Stem cell treatment is an investigative approach to minimizing myocardial infarct size.
Infarction or rupture of the posteromedial papillary muscle causes acute mitral insufficiency,
which greatly worsens cardiac output and which may be treated surgically. The improvement
in prognosis that has occurred in the last decade is due to early treatment with thrombolytic
agents and reperfusion.[8]

Mural thrombosis over the area of infarction may result in embolization and concomitant
stroke but is decreased in incidence with anticoagulation therapy. [9]

Diagnostic Considerations
Epigastric or chest symptoms from myocardial ischemia may incorrectly be attributed to a GI source.
Often, this occurs despite the presence of dyspnea or diaphoresis, symptoms that are difficult to attribute
to the GI system. Additionally, patients with myocardial ischemia may report relief or improvement with GI
remedies (eg, antacids). Remember that even myocardial ischemia can worsen with recumbency (eg,
angina decubitus) because of an increase in venous return and a temporary greater workload.
The discomfort of myocardial ischemia may erroneously be attributed to a musculoskeletal etiology.
Tenderness of the chest wall is reported in as many as 5% of patients who prove to have an MI. If no
injury or event is defined that could have led to a soft tissue injury, the clinician should be reluctant to
render a diagnosis of musculoskeletal chest pain.
Younger patients are overly represented in cases of missed MI. Most likely, this is because of the inherent
bias that this is a disease of those who are late middle-aged and older. Approach each patient with chest
symptoms as an individual who could have the disease.
Unfortunately, in a series of missed MI, the failure to recognize ischemic changes is frequent. The inferior
leads, in particular, must be scrutinized carefully for any evidence of ST-segment elevation by using a
straight edge across the T-P segments. Another common error is to recognize ischemic changes and then
discharge the patient without definitively proving that the changes were pre-existent. Nonischemic causes
of ST-segment elevation include LVH, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalemia,
and LV aneurysm. Nonischemic causes may lead to overtreatment.
The diagnosis of an MI may be missed in the setting of a left bundle-branch block, and there may be
delays in, or a failure of, administering thrombolytics or initiating PCI. This is usually because of delays in
ECG performance, interpretation, and decision-making, and it is also affected by the availability of
thrombolytics in the ED. Excluding patients based on age alone will deny some the significant benefit of
thrombolysis.

Differential Diagnoses

Acute Coronary Syndrome

Angina Pectoris
Anxiety
Anxiety Disorders
Aortic Dissection
Aortic Regurgitation
Aortic Stenosis
Asthma
Biliary tract disease
Cholecystitis
Cholecystitis and Biliary Colic
Cholelithiasis
Chronic Obstructive Pulmonary Disease and Emphysema
Compartment Syndrome, Abdominal
Contusions
Depression
Dissection, Aortic
Dyspepsia
Endocarditis

Esophageal reflux
Esophageal Spasm
Esophagitis
Gastritis, Acute
Gastroenteritis
Gastroesophageal Reflux Disease
Heart arrhythmias
Heart rupture
Herpes Zoster
Hypotension
Mitral Regurgitation
Mitral Valve Prolapse
Myocarditis
Myopericarditis
Pancreatitis
Pericarditis and Cardiac Tamponade
Pericarditis, Acute
Pleurodynia
Pneumonia
Pneumothorax
Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum
Pulmonary Embolism
Pulmonary Hypertension, Primary
Radicular pain
Shock, Cardiogenic
Stroke Imaging
Tachycardia myopathy
Unstable Angina
Ventricular Septal Defect

http://www.patient.co.uk/doctor/Acute-Myocardial-Infarction.htm

Acute Myocardial
Infarction
This PatientPlus article is written for healthcare professionals so the
language may be more technical than the condition leaflets. You may find
the abbreviations list helpful.
An acute myocardial infarction is caused by necrosis of myocardial tissue due to
ischaemia, usually due to blockage of a coronary artery by a thrombus. Most myocardial

infarctions are anterior or inferior but may affect the posterior wall of the left ventricle
to cause a posterior myocardial infarction.

Definition
Myocardial infarction is now considered part of a spectrum referred to as acute coronary
syndrome. This refers to a spectrum of acute myocardial ischaemia that also includes
unstable angina and non-ST segment elevation myocardial infarction (NSTEMI). 1 The
new criteria for diagnosing myocardial infarction are detection of rise and/or fall of
cardiac biomarkers (preferably troponin) with at least one value above the 99th
percentile of the upper reference limit, together with evidence of myocardial ischaemia
with at least one of the following:2 3
,

Symptoms of ischaemia.
Electrocardiogram (ECG) changes indicative of new ischaemia (new ST-T changes
or new left bundle branch block (LBBB)).
Development of pathological Q-wave changes in the ECG.
Imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality.

Epidemiology4

Coronary heart disease (CHD) is the most common cause of death in the UK. CHD
is responsible for the deaths of approximately one in five men and one in six
women.
The average incidence of myocardial infarction for those aged between 30 and
69 years is about 600 per 100,000 for men, and 200 per 100,000 for women.
Mortality rates after ST elevation MI are equal at 30 days, if both sexes receive
equivalent care. Mortality rates become significantly higher for women three years
after discharge.5
Premenopausal women appear to be protected from atherosclerosis.
Incidence increases with age and elderly people also tend to have higher rates of
morbidity and mortality from their infarcts.
Incidence rates of myocardial infarction are lower in the South of England
compared with the North of England, Scotland and Northern Ireland.

Risk factors

Non-modifiable risk factors for atherosclerosis include increasing age, male,

family history of premature CHD, premature menopause.
Modifiable risk factors for atherosclerosis include smoking, diabetes mellitus (and
impaired glucose tolerance), metabolic syndrome, hypertension, hyperlipidaemia,
obesity and physical inactivity.6
Certain ethnic groups have higher risk of CHD. In the UK, the highest recorded
rates of coronary artery disease mortality are in people born in India, Pakistan and

Bangladesh.7South Asians are thought to have a 40-60% higher risk of CHD-related

mortality compared to other populations.

Presentation

o
o

Chest pain (central chest pain may not be the main symptom):
Three-quarters of patients present with characteristic central or epigastric
chest pain radiating to the arms, shoulders, neck, or jaw.
The pain is described as substernal pressure, squeezing, aching, burning,
or even sharp pain.
Radiation to the left arm or neck is common.
Chest pain may be associated with sweating, nausea, vomiting, dyspnoea,
fatigue, and/or palpitations.
Shortness of breath: may be the patient's anginal equivalent or a
symptom of heart failure.
Atypical presentations are common and tend to be seen in women, older
men, people with diabetes and people from ethnic minorities. Atypical symptoms
include abdominal discomfort or jaw pain; elderly patients may present with altered
mental state.

Signs
Cardiovascular examination findings can vary enormously:

Low-grade fever, pale and cool, clammy skin.

Hypotension or hypertension can be observed depending on the extent of the
myocardial infarction.
Dyskinetic cardiac impulse (in anterior wall myocardial infarction) can be
palpated occasionally.
Third and fourth heart sound, systolic murmur if mitral regurgitation or
ventricular septal defect develops, pericardial rub.
There may be signs of congestive heart failure, including pulmonary rales,
peripheral oedema, elevated jugular venous pressure.

Assessment for possible acute coronary syndrome2

Consider the history of the pain, any cardiovascular risk factors, history of
ischaemic heart disease and any previous treatment, and previous investigations
for chest pain.
Symptoms that may indicate acute coronary syndrome include:
Pain in the chest and/or other areas (e.g. the arms, back or jaw) lasting for
longer than 15 minutes.
Chest pain with nausea and vomiting, marked sweating and/or
breathlessness, or haemodynamic instability.

New-onset chest pain, or abrupt deterioration in stable angina, with

recurrent pain occurring frequently with little or no exertion and often lasting longer
than 15 minutes.
The response to glyceryl trinitrate (GTN) should not be used to make a
diagnosis and symptoms should not be assessed differently in men and women or
among different ethnic groups.
Patients with pre-existing angina should be advised that when an attack of
angina occurs, they should:8
Stop what they are doing and rest.
Use GTN spray or tablets as instructed.
Take a second dose of GTN after 5 minutes if the pain has not eased.
Take a third dose of GTN after a further 5 minutes if the pain has still not
eased.
Call 999 for an ambulance if the pain has not eased after another 5
minutes (i.e. 15 minutes after onset of pain), or earlier if the pain is intensifying or
the person is unwell.

Differential diagnosis

Cardiovascular: stable angina, another form of acute coronary syndrome

(unstable angina or NSTEMI), acute pericarditis, myocarditis, aortic stenosis, aortic
dissection, pulmonary embolism.
Respiratory: pneumonia, pneumothorax.
Gastrointestinal: oesophageal spasm, oesophagitis, gastro-oesophageal reflux,
acute gastritis, cholecystitis, pancreatitis.
Musculoskeletal chest pain.

Consider nonatherosclerotic causes of myocardial infarction in younger patients or if

there is no evidence of atherosclerosis: coronary emboli from sources such as an
infected cardiac valve, coronary occlusion secondary to vasculitis, coronary artery
spasm, cocaine use, congenital coronary anomalies, coronary trauma, increased oxygen
requirement (e.g. hyperthyroidism) or decreased oxygen delivery (e.g. severe anaemia).

Investigations

If diagnosis is suspected, immediately arrange urgent hospital assessment and

admission. Call 999 ambulance.
ECG:
May be helpful in a pre-hospital setting if the diagnosis is uncertain or in a
remote area in the assessment for pre-hospital thrombolysis, but otherwise should
not delay getting the patient to hospital.
Features may initially be normal but abnormalities include new ST
segment elevation; initially peaked T waves and then T-wave inversion; new Q
waves; new conduction defects.

Do not exclude an acute coronary syndrome when people have a normal

resting 12-lead ECG.

In hospital

o
o
o
o
o

FBC to rule out anaemia; leukocytosis is common; monitor potassium levels

(electrolyte disturbances may cause arrhythmias, especially potassium and
magnesium); renal function - estimated glomerular filtration rate (eGFR) - should be
measured prior to starting an angiotensin-converting enzyme (ACE) inhibitor. Lipid
profile needs to be obtained at presentation because levels can change after 12-24
hours of an acute illness. Measure C-reactive protein (CRP) and other markers of
inflammation.
Cardiac enzymes:
See separate article Cardiac Enzymes and Markers for Myocardial
Infarction.
Cardiac troponins T and I are highly sensitive and specific for cardiac
damage. The risk of death from an acute coronary syndrome is directly related to
troponin level and patients with no detectable troponins have a good short-term
prognosis.9 Serum levels increase within 3-12 hours from the onset of chest pain,
peak at 24-48 hours, and return to baseline over 5-14 days. Troponin levels may
therefore be normal initially and should be repeated.
Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart.
CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values
within 24 hours, and return to baseline after 48-72 hours. Sensitivity and specificity
are not as high as for troponin levels.
Serial ECGs and continuous ECG monitoring in a coronary care unit (CCU).
CXR: to assess the patient's heart size and the presence or absence of
heart failure and pulmonary oedema. This may also assist in differential diagnosis.
Pulse oximetry and blood gases: monitor oxygen saturation.
Cardiac catheterisation and angiography: cardiac angiography defines the
patient's coronary anatomy and the extent of the disease.
Echocardiography can define the extent of the infarction and assess
overall ventricular function and can identify complications, such as acute mitral
regurgitation, left ventricular rupture or pericardial effusion.
Myocardial perfusion scintigraphy using single photon emission computed
tomography (SPECT): the National Institute for Health and Clinical Excellence (NICE)
recommends that myocardial perfusion scintigraphy using SPECT should be the first
test used for:10
People where stress ECG may not give accurate or clear results, e.g.
women, people who have certain unusual patterns in the electrical activity of their
heart, people with diabetes or people for whom exercise is difficult or impossible.
The diagnosis of people who are less likely to have coronary artery disease
and who are at lower risk of having heart problems in the future. The likelihood of a
person having coronary artery disease can be assessed by considering a number of
factors, e.g. age, sex, ethnic background and family history as well as the results of
physical examination and investigations.
As an investigation in people who still have symptoms following a
myocardial infarction or despite having had treatment to improve coronary artery
blood flow.

Management
See separate articles Acute Myocardial Infarction Management, Secondary Prevention of
Cardiovascular Disease and Cardiac Rehabilitation

Complications
See separate article Complications of Acute Myocardial Infarction.

Prognosis

Mortality rates from coronary heart disease (CHD) have been falling in the UK
since the late 1970s, and have fallen 24% in a 10-year period for people under the
age of 75 years.4
The mortality of acute coronary syndrome with clinical myocardial infarction
treated with modern treatments including thrombolysis has been estimated to be
12-15% within six months of the acute coronary syndrome.11
However, up to 50% of people who have an acute myocardial infarction die within
30 days of the event, and over half of these deaths occur before medical assistance
arrives or the patient reaches hospital. About one third of all deaths occur within
the first hour, usually as the result of an acute fatal arrhythmia.
Prognosis correlates with the degree of myocardial necrosis. Greater degrees of
myocardial necrosis are associated with a worse prognosis. The degree of
myocardial necrosis can be estimated by various factors - for example: 4
The rise in serum troponin T.
Degree and extent of ECG changes.
Degree of left ventricular dysfunction on echocardiography.
The prognosis also depends on the timing and nature of intervention; the
prognosis is improved with successful early reperfusion, preserved left ventricular
function and short-term and long-term treatment with beta-blockers, aspirin, statins
and ACE inhibitors.1
Elderly patients with acute myocardial infarction are at increased risk of
developing complications and should be treated aggressively.

Prevention
See separate article Primary Prevention of Cardiovascular Disease.