AMI

Myocardial Infarction
Author: Drew Evan Fenton, MD, Hospitalist, Our Health Care Consultants
Contributor Information and Disclosures
Updated: Jun 24, 2010

Introduction

Background
Myocardial infarction (MI) is the rapid development of myocardial necrosis caused by a critical imbalance
between oxygen supply and demand of the myocardium. This usually results from plaque rupture with
thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the
myocardium.

The ECG shows lateral ST-segment elevation that is consistent with a lateral wall AMI.

Although the clinical presentation of a patient is a key component in the overall evaluation of the patient with
MI, many events are either "silent" or are clinically unrecognized, evidencing that patients, families, and health
care providers often do not recognize symptoms of a MI. The appearance of cardiac markers in the circulation
generally indicates myocardial necrosis and is a useful adjunct to diagnosis.

Cardiac markers help to categorize MI, which is considered part of a spectrum referred to as acute coronary
syndrome that includes ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina. This
categorization is valuable because patients with ischemic discomfort may or may not have ST-segment
elevations on their electrocardiogram. Those without ST elevations may ultimately be diagnosed with NSTEMI
or with unstable angina based on the presence or absence of cardiac enzymes. Additionally, therapeutic
decisions, such as administering an intravenous thrombolytic or performing percutaneous coronary intervention
(PCI), are often made based on this categorization.

Pathophysiology
The most common cause of MI is narrowing of the epicardial blood vessels due to atheromatous plaques.
Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus
formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result
in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the
vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can
salvage the myocardium and reduce morbidity and mortality.

Nonatherosclerotic causes of MI include coronary vasospasm as seen in variant (Prinzmetal) angina and in
patients using cocaine and amphetamines; coronary emboli from sources such as an infected heart valve;
occlusion of the coronaries due to vasculitis; or other causes leading to mismatch of oxygen supply and
demand, such as acute anemia from GI bleeding. MI induced by chest trauma has also been reported, usually
following severe chest trauma such as motor vehicle accidents and sports injuries.

Frequency
United States

MI is a leading cause of morbidity and mortality in the United States. Approximately 1.3 million cases of
nonfatal MI are reported each year, for an annual incidence rate of approximately 600 cases per 100,000
people. The proportion of patients diagnosed with NSTEMI compared with STEMI has progressively increased.

International

Cardiovascular diseases account for 12 million deaths annually worldwide. MI continues to be a significant
problem in industrialized countries and is becoming an increasingly significant problem in developing countries.

Mortality/Morbidity
Approximately 500,000-700,000 deaths are caused by ischemic heart disease annually in the United States.

One third of patients who experience STEMI die within 24 hours of the onset of ischemia, and many of the
survivors experience significant morbidity. For many patients, the first manifestation of coronary artery disease
is sudden death likely from malignant ventricular dysrhythmia.

 More than one half of deaths occur in the prehospital setting.

 In-hospital fatalities account for 10% of all deaths. An additional 10% of deaths occur in the first year
postinfarction.
 A steady decline has occurred in the mortality rate from STEMI over the last several decades. This
appears to be due to a combination of a fall in the incidence of MI (replaced in part by an increase in
the incidence of unstable angina) and a reduction in the case-fatality rate once an MI has occurred.

Sex
A male predilection exists in persons aged 40-70 years. Evidence exists that women more often have MIs
without atypical symptoms. The atypical presentation in women might explain the sometimes delayed diagnosis
of MIs in women.

In persons older than 70 years, no sex predilection exists.

Age
MI most frequently occurs in persons older than 45 years.
Certain subpopulations younger than 45 years are at risk, particularly cocaine users, persons with type 1
diabetes mellitus, patients with hypercholesterolemia, and those with a positive family history for early coronary
disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-
degree female relative aged 55 years or younger who experienced a myocardial infarction. In younger patients,
the diagnosis may be hampered if a high index of suspicion is not maintained.

Clinical

History
The history is critical in making the diagnosis of MI and sometimes may provide the only clues that lead to the
diagnosis in the initial phases of the patient presentation.

 Chest pain, usually across the anterior precordium is typically described as tightness, pressure, or
squeezing.
 Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is more frequently
affected; however, a patient may experience pain in both arms.
 Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor
ventricular compliance in the setting of acute ischemia. Dyspnea may be the patient's anginal
equivalent, and, in an elderly person or a patient with diabetes, it may be the only complaint.
 Nausea, abdominal pain, or both often are present in infarcts involving the inferior or posterior wall.
 Anxiety
 Lightheadedness with or without syncope
 Cough
 Nausea with or without vomiting
 Diaphoresis
 Wheezing
 Elderly patients and those with diabetes may have particularly subtle presentations and may complain
of fatigue, syncope, or weakness. The elderly may also present with only altered mental status. Those
with preexisting altered mental status or dementia may have no recollection of recent symptoms and
may have no complaints whatsoever.
 As many as half of MIs are clinically silent in that they do not cause the classic symptoms described
above and consequently go unrecognized by the patient. A high index of suspicion should be
maintained for MI especially when evaluating women, patients with diabetes, older patients, patients
with dementia, and those with a history of heart failure. Patients with a permanent pacemaker in place
may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular
contractions.

Physical
The physical examination can often be unremarkable.

 Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.
 Hypertension may precipitate MI, or it may reflect elevated catecholamine levels due to anxiety, pain,
or exogenous sympathomimetics.
 Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of MI
usually indicates a large infarct secondary to either decreased global cardiac contractility or a right
ventricular infarct.
  Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that
involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be
present.
 Rales may represent congestive heart failure.
 Neck vein distention may represent pump failure. With right ventricular failure, cannon jugular venous
a waves may be noted.
 Third heart sound (S3) may be present.
 A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to
preexisting heart disease or hypertension.
 Dysrhythmias may present as an irregular heartbeat or pulse.
 Low-grade fever is not uncommon.

Causes
The most frequent cause of myocardial infarction (MI) is rupture of an atherosclerotic plaque within a coronary
artery with subsequent arterial spasm and thrombus formation.

Other causes include the following:

 Coronary artery vasospasm

 Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic
stenosis [IHSS], underlying valve disease)
 Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts due to pulmonary
disease usually occur when demand on the myocardium dramatically increases relative to the
available blood supply.)
 Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis
 Cocaine, amphetamines, and ephedrine
 Arteritis
 Coronary anomalies, including aneurysms of the coronary arteries
 Increased afterload or inotropic effects, which increase the demand on the myocardium
 Aortic dissection, with retrograde involvement of the coronary arteries
 Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki
disease, Takayasu arteritis, progeria, and cystic medial necrosis (see Myocardial Infarction in
Childhood).

Risk factors for atherosclerotic plaque formation include the following:

 Age
 Male gender
 Smoking
 Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders
 Diabetes mellitus
 Poorly controlled hypertension
 Type A personality
 Family history
 Sedentary lifestyle
Acute Myocardial Infarction
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, which refers to a range of acute

myocardial ischaemia that also includes unstable angina and non-ST segment elevation myocardial infarction (NSTEMI). 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:1

 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

Epidemiology 2

 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 from CHD are higher for men than women, people living in deprived areas and
in people of South Asian origin. There is evidence of earlier deaths for men than women after
an acute myocardial infarction.3
 Pre-menopausal 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.
 Ethnic group: in the UK, the highest recorded rates of coronary artery disease mortality are in
people born in India, Pakistan and Bangladesh.4
Presentation

 Chest pain (central chest pain may not be the main symptom):
o Three-quarters of patients present with characteristic central or epigastric chest pain
radiating to the arms, shoulders, neck, or jaw.
o The pain is described as substernal pressure, squeezing, aching, burning, or even sharp
pain.
o Radiation to the left arm or neck is common.
o 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 (especially in women, older men, people with diabetes,
and people from ethnic minorities), e.g. 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 develop, pericardial rub.
 There may be signs of congestive heart failure, including pulmonary rales, peripheral
oedema, elevated jugular venous pressure.

Assessment for possible acute coronary syndrome 1

 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:
o Pain in the chest and/or other areas (e.g. the arms, back or jaw) lasting longer than 15
minutes.
o Chest pain with nausea and vomiting, marked sweating and/or breathlessness, or
haemodynamic instability.
o 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:5
o Stop what they are doing and rest.
o Use GTN spray or tablets as instructed.
o Take a second dose of GTN after 5 minutes if the pain has not eased.
o Take a third dose of GTN after a further 5 minutes if the pain has still not eased.
o 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 (999
Ambulance).
 ECG:
o May be helpful 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.
o 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.
o Do not exclude an acute coronary syndrome when people have a normal resting 12-lead
ECG.

In hospital

 Full blood count 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:
o See separate article Cardiac Enzymes and Markers for Myocardial Infarction.
o 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. 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.
o 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 coronary care unit (CCU).
  Chest X-ray: to assess the patient's heart size and the presence or absence of heart failure and
pulmonary oedema. 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: 6
o 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.
o 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.
o 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 Ischaemic
Heart Disease and Cardiac Rehabilitation

Complications
See separate article Complications of Acute Myocardial Infarction.

Prognosis

 Mortality rates from coronary heart disease have been falling in the UK since the late 1970s,
and have fallen 24% in the last 10 years for people under the age of 75 years. 2
 The mortality of acute coronary syndrome with clinical myocardial infarction treated with
modern treatments including thrombolysis has been estimated to be 12-15% within 6 months of
the acute coronary syndrome.2
 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.7
 About one third of all deaths occur within the first hour, usually as the result of an acute fatal
arrhythmia.7
 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:2
o The rise in serum troponin T
o Degree and extent of ECG changes
o 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 betablockers, aspirin, statins and ACE inhibitors.8
 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.

Document references

1. Chest pain of recent onset, NICE Clinical Guideline (March 2010); Assessment and diagnosis of
recent onset chest pain or discomfort of suspected cardiac origin
2. Myocardial infarction - secondary prevention, Clinical Knowledge Summaries (January 2008)
3. Rieves D, Wright G, Gupta G, et al; Clinical trial (GUSTO-1 and INJECT) evidence of earlier
death for men than women Am J Cardiol. 2000 Jan 15;85(2):147-53. [abstract]
4. Bhopal R, Unwin N, White M, et al; Heterogeneity of coronary heart disease risk factors in
Indian, Pakistani, Bangladeshi, and European origin populations: cross sectional study. BMJ.
1999 Jul 24;319(7204):215 [abstract]
5. Angina-stable, Clinical Knowledge Summaries (September 2009)
6. Angina and myocardial infarction - myocardial perfusion scintigraphy, NICE Technology
Appraisal (2003); Coronary imaging: Myocardial perfusion scintigraphy for the diagnosis and
management of angina and myocardial infarction
7. Myocardial infarction - thrombolysis, NICE Technology Appraisal (2002); The clinical
effectiveness and cost effectiveness of drugs for early thrombolysis in the treatment of acute
myocardial infarction
8. Garas S, Zafari AM; Myocardial Infarction, eMedicine, Jan 2010.

Internet and further reading

 National Service Framework for Coronary Heart Disease, Department of Health (March 2000).
 ECG Library; © Stephen Gerred (Medical Registrar Auckland, New Zealand) Dean Jenkins
(Specialist Registrar, Llandough Hospital, Cardiff, Wales)