Myocardial Infarction: Practice Essentials, Background, Definitions 26/12/2019, 10:06 PM

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Myocardial Infarction
Updated: May 07, 2019
Author: A Maziar Zafari, MD, PhD, FACC, FAHA; Chief Editor: Eric H Yang, MD more...

OVERVIEW

Practice Essentials
Myocardial infarction (MI) (ie, heart attack) is the irreversible death (necrosis) of heart muscle
secondary to prolonged lack of oxygen supply (ischemia). Approximately 1.5 million cases of MI
occur annually in the United States. See the images below.

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.

Background
Myocardial infarction (MI) usually results from an imbalance in oxygen supply and demand, which
is most often caused by plaque rupture with thrombus formation in an epicardial coronary artery,
resulting in an acute reduction of blood supply to a portion of the myocardium. (See Etiology for
details.)

The electrocardiographic (ECG) results of an acute MI are seen below.

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Acute inferior myocardial infarction.

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 not clinically recognized by patients,
families, and health care providers. (See Presentation.) The appearance of cardiac biomarkers in
the circulation generally indicates myocardial necrosis and is a useful adjunct to diagnosis. (See
Workup.)

MI is considered part of a spectrum referred to as acute coronary syndrome (ACS). The ACS
continuum representing ongoing myocardial ischemia or injury consists of unstable angina, non–
ST-segment elevation MI (NSTEMI)—collectively referred to as non–ST-segment acute coronary
syndrome (NSTE ACS)—and ST-segment elevation MI (STEMI). Patients with ischemic
discomfort may or may not have ST-segment or T-wave changes denoted on the
electrocardiogram (ECG). ST elevations seen on the ECG reflect active and ongoing transmural
myocardial injury. Without immediate reperfusion therapy, most patients with STEMI develop Q
waves, reflecting a dead zone of myocardium that has undergone irreversible damage and death.

Those without ST elevations are diagnosed either with unstable angina or NSTEMI―differentiated
by the presence of cardiac enzymes. Both these conditions may or may not have changes on the
surface ECG, including ST-segment depressions or T-wave morphological changes.

MI may lead to impairment of systolic or diastolic function and to increased predisposition to

arrhythmias and other long-term complications.

Coronary thrombolysis and mechanical revascularization have revolutionized the primary

treatment of acute MI, largely because they allow salvage of the myocardium when implemented
early after the onset of ischemia. (See Treatment.)

The modest prognostic benefit of an opened infarct-related artery may be realized even when
recanalization is induced only 6 hours or more after the onset of symptoms; that is, when the
salvage of substantial amounts of jeopardized ischemic myocardium is no longer likely. The
opening of an infarct-related artery may improve ventricular function and collateral blood flow;
prevent ventricular remodeling, as well as decrease infarct expansion, ventricular aneurysm
formation, and left ventricular dilatation; and reduce late arrhythmia associated with ventricular
aneurysms, and mortality. [5, 6, 7]

Evidence suggests a benefit from the use of beta-blockers, angiotensin-converting enzyme (ACE)
inhibitors, angiotensin II receptor blockers, and statins.

The American College of Cardiology (ACC)/American Heart Association (AHA)/European Society

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of Cardiology/World Heart Federation released the Observations From the TRITON-TIMI 38 Trial
(Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With
Prasugrel–Thrombolysis in Myocardial Infarction 38), which better outlines a universal definition of
MI, along with a classification system and risk factors for cardiovascular death. [8]

(See Treatment for more details.)

Definitions
The third universal definition of myocardial infarction
Myocardial infarction (MI), commonly known as a heart attack, is defined pathologically as the
irreversible death of myocardial cells caused by ischemia. Clinically, MI is a syndrome that can be
recognized by a set of symptoms, chest pain being the hallmark of these symptoms in most
cases, supported by biochemical laboratory changes, electrocardiographic (ECG) changes, or
findings on imaging modalities able to detect myocardial injury and necrosis.

According to the third universal definition of MI, implemented by a joint task force from the
European Society of Cardiology (ESC), American College of Cardiology (ACC) Foundation,
American Heart Association (AHA), and the World Heart Federation (WHF), MI is diagnosed when
either of the following two criteria are met. [9]

1. Detection of an increase or decrease in cardiac biomarker values (preferably using cardiac

troponin [cTn]) with at least one value above the 99th percentile of the upper reference limit (URL)
and with at least one of the following findings:

Symptoms of ischemia
New or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle
branch block (LBBB)
Development of pathologic Q waves on the ECG
Imaging evidence of new loss of viable myocardium or a new regional wall motion
abnormality
Identification of an intracoronary thrombus by angiography or autopsy

2. Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic
changes or injury or new BBB on ECG, but death occurred before cardiac biomarker levles were
obtained, or before cardiac biomarker values would be increased.

Types of MI

The Joint ESC/ACCF/AHA/WHF Task Force further classified MI into 5 types on the basis of the
underlying cause [7] :

Type 1 (spontaneous MI): Related to atherosclerotic plaque rupture, ulceration, fissuring,

erosion, or dissection with intraluminal thrombus in one or more of the coronary arteries,
leading to decreased myocardial blood flow or distal platelet emboli and thereby resulting in
myocyte necrosis. The patient may or may not have underlying obstructive coronary artery

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disease (CAD).
Type 2 (MI secondary to an ischemic imbalance): MI consequent to increased oxygen
demand or a decreased supply (eg, coronary endothelial dysfunction, coronary artery
spasm, coronary artery embolus, tachyarryhthmias/bradyarrhythmias, anemia, respiratory
failure, hypertension, or hypotension).
Type 3 (MI resulting in death when biomarker values are unavailable): Sudden, unexpected
cardiac death before blood samples for biomarkers could be drawn or before their
appearance in the circulation.
Type 4a (MI related to percutaneous coronary intervention [PCI]): Elevation of biomarker
values (cTn is preferred) to more than 5 times the 99 th percentile of the URL in patients with
normal baseline values (< 99 th percentile URL) or a rise of values over 20% if the baseline
values are elevated but stable or falling. In addition, any of the following are required: (1)
symptoms suggestive of myocardial ischemia; (2) new ischemic ECG changes or new BBB;
(3) angiographic loss of patency of a major coronary artery or a side branch or persistent
slow flow or no flow or embolization; or (4) demonstration of the new loss of viable
myocardium or new regional wall motion abnormality by cardiac imaging.
Type 4b (MI related to stent thrombosis): MI associated with stent thrombosis as detected by
coronary angiography or autopsy in the setting of myocardial ischemia in combination with a
rise and/or fall of cardiac biomarkers with at least one value above the 99 th percentile URL.
Type 5 (MI related to coronary artery bypass grafting [CABG]): Elevation of cardiac
biomarker values more than 10 times the 99 th percentile URL in patients with normal
baseline cTn values. In addition, either (1) new pathologic Q waves or new BBB, (2)
angiographic-documented new graft or native coronary artery occlusion, or (3) evidence of
new loss of viable myocardium or new regional wall motion abnormality by cardiac imaging
is required.

Acute coronary syndrome

The term "acute coronary syndrome" (ACS) refers to a spectrum of conditions that occur due to
acute myocardial ischemia and/or infarction as a result of an abrupt reduction in blood flow
through the coronary artery circulation.

ACS is divided into two main categories, non–ST elevation (NSTE) ACS and ST-elevation MI
(STEMI)

NSTE ACS

NSTE ACS is further divided into unstable angina (UA) and non–ST-elevation myocardial
infraction (NSTEMI). These two conditions resemble each other very closely. UA is distinguished
from NSTEMI by the absence of an elevation of cardiac biomarker levels. [1]

STEMI

The major discriminating feature of STEMI is the presence of symptoms of myocardial

ischemia/injury along with persistent ECG ST-segment elevation in addition to the presence of
cardiac biomarkers. [2]

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Pathophysiology
Cellular effects of myocardial infarction (MI)
Myocardial injury and myocardial cell death

For the normal heart to continue to function and to steadily pump blood efficiently to meet the
demands of the body, it needs to have a constant supply of oxygen and nutrients provided mainly
by the coronary circulation. A condition called myocardial ischemia happens if blood supply to the
myocardium does not meet the demand. If this imbalance persists, it triggers a cascade of cellular,
inflammatory and biochemical events, leading eventually to the irreversible death of heart muscle
cells, resulting in MI.

Evolution of MI and ventricular remodeling

The spectrum of myocardial injury depends not only on the intensity of impaired myocardial
perfusion but also on the duration and the level of metabolic demand at the time of the event.
Severe loss of the ability of the heart muscle cell to contract can be observed as early as within 60
seconds. Persistence of oxygen deprivation to the myocardium through the cessation of blood
supply will lead to irreversible myocardial injury within 20 to 40 minutes and up to several hours,
depending on several factors including the existing metabolic state of the body and presence of
coronary collateral blood flow. [10]

Typical MI initially manifests as coagulation necrosis that is ultimately followed by a healing

process characterized by formation of myocardial scarring, known as myocardial fibrosis. This
mechanism allows significant architectural changes to the composition, shape and contractile
function of the myocardium, especially in the left ventricle, which is the major contributor to the
contractile function of the heart. Eventually the left ventricle dilates and changes to a more
spherical shape, in a process known as ventricular remodeling. Despite being an irreversible
process, ventricular remodeling is a regulated process, therefore, specific treatment strategies
and agents should be used in acute MI management in order to reduce the occurrence and
severity of ventricular remodeling. [11]

Reperfusion injury

In some occasions, restoration of blood flow to the damaged myocardium triggers further ischemic
cellular damage, this paradoxical effect is known as reperfusion injury. This process involves a
complex interaction between oxygen free radicals and intracellular calcium, leading to
acceleration of myocardial damage and death, microvascular dysfunction and fatal arrhythmias.
The role of nitric oxide (an endothelium-derived relaxing factor) as a cardioprotective agent
against reperfusion injury, has been demonstrated, as nitric oxide works to inactivate oxygen free
radicals, therefore, ameliorating the process of reperfusion injury. [12] Despite the improved
understanding of the process of reperfusion injury, there are no specific therapies to prevent it.

Stunned and hibernating myocardium

Stunned myocardium is a condition of transient left ventricular dysfunction following an ischemic

event to the myocardium. It occurs if coronary blood flow was impaired for a brief period of time (5
to 15 minutes). Usually, stunned myocardium persists for hours or days following the re-
establishment of coronary blood flow.

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However, prolonged exposure of the myocardium to an ischemic state, results in an impairment of

its contractile function, which can be partial or complete, this is known as myocardial hibernation,
and is reversible with revascularization.

Both myocardial stunning and hibernation occur because of loss of essential metabolites required
for normal myocardial contractility, such as adenosine, which is needed for adenosine
triphosphate (ATP)-dependent contraction. [13]

Plaque
The atheromatous plaque responsible for acute MI develops in a dynamic process in multiple
stages. Starting with arterial intimal thickening, which consists of vascular smooth muscles with
very minimal or no inflammatory cells, this process can be observed soon after birth.
Subsequently, the formation of fibrous cap atheroma occurs, which has a lipid-rich necrotic core
that is surrounded by fibrous tissue. Eventually, a thin-cap fibroatheroma develops, this is also
known as a vulnerable plaque which is composed mainly of a large necrotic core separated from
the vascular lumen by a thin fibrous cap that is infiltrated by inflammatory cells and is deficient of
smooth muscle cells, making it vulnerable to rupture. [14, 15]

The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of
plaque rupture, and less frequently plaque erosion.

The Brasilia Heart Study Group indicates that changes in high-density lipoprotein (HDL) during an
MI may alter the antiatherogenic function of HDL to transport lipids from arterial walls. [16] The
investigators noted a simultaneous decrease in lipid transfer to HDL and in the capacity of HDL to
efflux cholesterol from cells occurs in the acute period after an MI.

In a nested case-control study that evaluated the associations of plasma metabolic markers with
the risks of incident MI, ischemic stroke, and intracerebral hemorrhage, investigators found
positive associations of lipoproteins and lipids with MI and ischemic stroke but not with
intracerebral hemorrohage, as well as positive associations between triglyceride concentrations
and MI. [17] Except for small HDL, there was also an inverse association of HDL particles with MI,
and an inverse association of cholesterol in large HDL with MI and ischemic stroke. The study
cohort included 912 patients with MI, 1146 with ischemic stroke, 1138 with intracerebral
hemorrhage, and 1466 control subjects. [17]

Etiology
Atherosclerosis is the disease primarily responsible for most acute coronary syndrome (ACS)
cases. Approximately 90% of myocardial infarctions (MIs) result from an acute thrombus that
obstructs an atherosclerotic coronary artery. Plaque rupture and erosion are considered to be the
major triggers for coronary thrombosis. Following plaque erosion or rupture, platelet activation and
aggregation, coagulation pathway activation, and endothelial vasoconstriction occur, leading to
coronary thrombosis and occlusion.

Within the coronary vasculature, flow dynamics and endothelial shear stress are implicated in the

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pathogenesis of vulnerable plaque formation. [18] A large body of evidence indicates that in
numerous cases, culprit lesions are stenoses of less than 70% and are located proximally within
the coronary tree. [19, 20] Coronary atherosclerosis is especially prominent near branching points
of vessels. [21] Culprit lesions that are particularly prone to rupture are atheromas containing
abundant macrophages, a large lipid-rich core surrounded by a thinned fibrous cap.

Nonmodifiable risk factors for atherosclerosis include the following:

Age

Sex

Family history of premature coronary heart disease

Male-pattern baldness

Modifiable risk factors for atherosclerosis include the following [22] :

Smoking or other tobacco use

Hypercholesterolemia and hypertriglyceridemia, including inherited lipoprotein disorders

Dyslipidemia

Diabetes mellitus

Hypertension

Obesity (abdominal obesity)

Psychosocial stress

Sedentary lifestyle and/or lack of exercise

Reduced consumption of fruits and vegetables

Poor oral hygiene

Type A personality

Elevated homocysteine levels

Presence of peripheral vascular disease

MI can also occur for causes other than atherosclerosis. Nonatherosclerotic causes of MI include
the following:

Coronary occlusion secondary to vasculitis

Ventricular hypertrophy (eg, left ventricular hypertrophy, hypertrophic cardiomyopathy)

Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis

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Coronary trauma

Primary coronary vasospasm (variant angina)

Drug use (eg, cocaine, amphetamines, ephedrine)

Arteritis

Coronary anomalies, including aneurysms of coronary arteries

Factors that increase oxygen requirement, such as heavy exertion, fever, or hyperthyroidism

Factors that decrease oxygen delivery, such as hypoxemia of severe anemia

Aortic dissection, with retrograde involvement of the coronary arteries

Respiratory infections, particularly influenza [23, 24]

In addition, MI can result from hypoxia due to carbon monoxide poisoning or acute pulmonary
disorders.

Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki
disease, Takayasu arteritis, progeria, and cystic medial necrosis.

Acute MI is rare in childhood and adolescence. Although adults acquire coronary artery disease
from lifelong deposition of atheroma and plaque, which causes coronary artery spasm and
thrombosis, children with acute MI usually have either an acute inflammatory condition of the
coronary arteries or an anomalous origin of the left coronary artery. Intrauterine MI also does
occur, often in association with coronary artery stenosis. [25]

Epidemiology
United States statistics
Coronary artery disease (CAD) is the leading cause of death in the United States; approximately
500,000-700,000 deaths related to CAD occur each year, making it the cause of death in an
estimated one third of all deaths in the population for those older than 35 years.

Approximately 1.5 million cases of myocardial infarction (MI) occur annually in the United States;
the yearly incidence rate is approximately 600 cases per 100,000 people. The proportion of
patients diagnosed with non–ST-elevation MI (NSTEMI) compared with ST-elevation MI (STEMI)
has progressively increased. Despite an impressive decline in age-adjusted death rates
attributable to acute MI since the mid-1970s, the total number of MI-related deaths in the United
States has not declined. [26]

The death rate related to acute MI is approximately three times higher in men than in women. It is
more frequent in black patients compared to white patientss, an excess that disappears by age 75
years. Among the Hispanic population, coronary mortality is not as high as it is among black

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individuals and white persons. [27]

European statistics
CAD is also the number one cause of death in European countries.

In the European Union, death rates related to CAD dropped by almost 30% between the mid
1960s to the mid and late 1990s; however, within Eastern European countries, there was an
increase in death rates related to acute MI in the early1990s, followed by a subsequent decline. In
the Russian Federation, cardiovascular mortality remained the same. [28]

Cardiovascular disease in other developed countries and in developing

nations
An analysis of death certificates from the World Health Organization (WHO)
database demonstrated that CAD mortality in Japan was significantly lower than in the United
States and Europe, and it was further reduced by about 30% by the mid 1990s. [28]

In China, there has been a significant increase in mortality related to CAD, this is most likely
attributed to the increase in cardiovascular disease risk factors, predominantly smoking and
dyslipidemia. [29]

The incidence of CAD and related mortality is expected to rise dramatically in other developing
countries including India, Latin America, the Middle East and Sub-Saharan Africa, with an
estimated 80% increase, from approximately 9 million in 1990 to a projected 20 million by 2020.
[30, 31]

It is believed that these international trends in the incidence of CAD and subsequent acute MI are
largely related to consequences of social and economic changes in these countries, resulting in
better healthcare access and increases in life expectancy, in addition to adoption of westernized
diets, reduction in physical activity, and higher rates of smoking.

A major Canadian-led global study (INTERHEART trial) in 52 countries across Africa, Asia,
Australia, Europe, the Middle East, and North and South America, has identified 9 easily
measured risk factors (smoking, abnormal blood lipid levels, hypertension, diabetes, obesity, diet,
physical activity, alcohol consumption, and psychosocial factors) that account for over 90% of the
risk for acute MI. [22] The INTERHEART investigators found that these risk factors are the same in
almost every geographic region and every racial/ethnic group worldwide, and they are consistent
in men and women. The INTERHEART trial showed that smoking 1-5 cigarettes daily increased
the risk of an acute MI by 40%, and the risk increased with the amount of tobacco smoked per
day. It also concluded that all forms of tobacco, including filtered and nonfiltered cigarettes, pipes
and cigars, and chewing tobacco, are harmful, and that abdominal obesity is a greater risk factor
than body-mass index (BMI), indicating that measurement of waist-to-hip ratio could replace BMI
as an indicator of obesity. [22, 31, 32]

Prognosis
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Acute myocardial infarction (MI) is associated with a 30% mortality rate; about 50% of the deaths
occur prior to arrival at the hospital. An additional 5-10% of survivors die within the first year after
their myocardial infarction. Approximately half of all patients with an MI are rehospitalized within 1
year of their index event.

Overall, prognosis is highly variable and depends largely on the extent of the infarct, the residual
left ventricular function, and whether the patient underwent revascularization.

Better prognosis is associated with the following factors:

Successful early reperfusion (ST-elevation MI [STEMI] goals: patient arrival to fibrinolysis

infusion within 30 minutes OR patient arrival to percutaneous coronary intervention [PCI]
within 90 minutes)

Preserved left ventricular function

Short-term and long-term treatment with beta-blockers, aspirin, and angiotensin-converting

enzyme (ACE) inhibitors

Poorer prognosis is associated with the following factors:

Advanced age

Diabetes mellitus

Previous vascular disease (eg, cerebrovascular disease or peripheral vascular disease)

Elevated thrombolysis in MI (TIMI) risk score for unstable angina/non–ST elevation acute
coronary syndrome (NSTE-ACS) (TIMI risk score includes 7 factors: age ≥65 y, ≥3 risk
factors for cardiac disease, previous coronary disease, ST-segment deviation ≥0.5 mm, ≥2
episodes of angina in last 24 hours, aspirin use within prior week, and elevated cardiac
enzyme levels) [1, 3, 33]

Delayed or unsuccessful reperfusion

Poorly preserved left ventricular function (the strongest predictor of outcome)

Evidence of congestive heart failure (Killip classification ≥II) [34] or frank pulmonary edema
(Killip classification ≥III) [35]

Elevated B-type natriuretic peptide (BNP) levels [36, 37, 38]

Elevated high sensitive C-reactive protein (hs-CRP), a nonspecific inflammatory marker [39]

Involvement of electrocardiograph (ECG) lead aVR [40, 41]

Depression

It has been shown that five baseline parameters at presentation of patients with acute MI account
for over 90% of the prognostic predictors of 30-day mortality from acute MI. These parameters
include age, systolic blood pressure on presentation, Killip classification, heart rate, and anatomic
location of the MI.

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Killip classification
The Killip classification is widely used in patients presenting with acute MI for the purpose of risk
stratification, as follows [42] :

Killip class I includes individuals with no clinical signs of heart failure

Killip class II includes individuals with rales or crackles in the lungs, an S 3 gallop, and
elevated jugular venous pressure
Killip class III describes individuals with frank acute pulmonary edema
Killip class IV describes individuals in cardiogenic shock or hypotension (measured as
systolic blood pressure < 90 mmHg), and evidence of low cardiac output (oliguria, cyanosis,
or impaired mental status).

Patient Education
Patients with active symptoms of acute coronary syndrome (ACS) should be instructed to call
emergency services (eg, 911 in the United States), and they should be transported by emergency
medical services personnel, not by themselves, family, or friends. Patients should be instructed to
go to the emergency department immediately if the suspected ACS symptoms last longer than 20
minutes at rest or are associated with near syncope/syncope or hemodynamic instability.

If nitroglycerin is prescribed to a patient with suspected ACS, the patient should be instructed to
take a dose if symptoms arise. If no relief is experienced 5 minutes after the first dose, the patient
should contact emergency services. If relief is experienced within 5 minutes of the first
nitroglycerin dose, repeated doses can be given every 5 minutes for a maximum of 3 doses total.
If by then the symptoms have not yet fully resolved, the patient, a family member, or a caregiver
should contact emergency services. [1]

Diet plays an important role in the development of coronary artery disease (CAD). Educate post–
myocardial infarction (MI) patients about the role of a low-cholesterol and low-salt diet. A dietitian
should see and evaluate all patients prior to discharge from the hospital. Additionally, emphasis on
exercise training should be made, because current evidence demonstrates that cardiac
rehabilitation after MI results in lower rates of recurrent cardiovascular events. [43]

All patients should be educated regarding the critical role of smoking in the development of CAD.
Smoking cessation classes should be offered to help patients avoid smoking after their MI.

For patient education resources, see the Heart Health Center and Cholesterol Center, as well as
High Cholesterol, Cholesterol Charts (What the Numbers Mean), Lifestyle Cholesterol
Management, Chest Pain, Coronary Heart Disease, Heart Attack, Angina Pectoris, Cholesterol-
Lowering Medications, and Statins for Cholesterol.

Clinical Presentation

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