Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Myocardial Infarction
Myocardial infarction is ischemia and death of an area of myocardial tissue due
to insufficient blood flow and oxygenation, usually from thrombus formation on a
ruptured atherosclerotic plaque in the epicardial arteries. Clinical presentation is
most commonly with chest pain, but women and patients with diabetes may
have atypical symptoms. Diagnosis is by clinical history, ECG changes, an
increase in cardiac enzymes, and evidence of wall motion abnormalities on
imaging. Management depends on the timing of the presentation and local
resources with regard to thrombolytic therapy versus percutaneous intervention.
All patients receive nitrates, pain control, aspirin, anticoagulation, and beta-
blockers (unless contraindicated).

Last updated: July 7, 2022

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 1 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

CONTENTS

Overview
Pathophysiology
Clinical
Presentation
Diagnosis
Management
Complications
Differential
Diagnosis
References

Overview
Definition
Myocardial infarction (MI), commonly known as a “heart attack,”
is defined as acute myocardial injury and tissue death resulting
from ischemia.

Epidemiology
One of the leading causes of death in the United
States
Prevalence: 3% in Americans > 20 years of age
Incidence in the United States:
600 cases per 100,000 people
1.5 million cases annually
More common in older patients:

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 2 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Approximately 60%–65% of MIs occur in

patients > 65 years of age.
Approximately 33% of MIs occur in patients >
75 years of age.
80% of all MI-related deaths occur in patients >
65 years of age.
Men > women

Risk factors
The risks of MI increase proportionately with increases in risk
factors for coronary atherosclerosis (also known as
coronary artery disease (CAD)).
Hypertension
Hyperlipidemia
Smoking
Age: elderly individuals are more likely to:
Have STEMI than NSTEMI
Have a silent or unrecognized MI
Present with atypical symptoms (e.g.,
weakness, confusion, syncope)
Have higher in-hospital mortality
Have heart failure associated with an MI
Family history of premature coronary heart disease
(CHD), defined as:
A 1st-degree male relative < 45 years of age
A 1st-degree female relative < 55 years of age

Classification
Classification of MI according to the assumed cause:
Type 1: acute thrombus on a ruptured atherosclerotic
plaque
Type 2: ↑ oxygen demand in the myocardium

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 3 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

without adequate oxygen supply (whether or not

there is underlying atherosclerotic CAD)
Type 3: clinical symptoms of MI with ECG changes,
but with death of the patient occurring before lab
tests are performed
Type 4a: MI associated with
percutaneous coronary intervention (PCI) or from
procedure-related complications associated with ↓
coronary blood flow.
Type 4b: intervention-related MI with stent/scaffold
thrombosis
Type 5: MI related to coronary artery bypass graft (
CABG) surgery
Classification of MI based on ECG findings and pathology:
STEMI:
Due to a major occlusion of a coronary artery,
causing transmural infarction (through the
heart muscle wall)
Produces ECG changes with ST elevation and
Q waves
NSTEMI:
Due to less severe occlusion of a
coronary artery, causing a subendocardial MI
(not through the entire heart muscle wall)
ECG does not show ST elevation

Pathophysiology
Characteristics of unstable versus stable plaque:
Unstable plaque:
Thin fibrous cap

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 4 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Massive inflammatory cell infiltrate

↑ Activity of metalloproteinase enzymes
(weakens the fibrous cap)
↑ Lipid content
Angiogenesis
Rupture of unstable plaque in a
coronary artery → thrombosis
Stable plaque:
Thick fibrous cap
Narrowing of an artery → inability to meet
oxygen demand with ↑ exertion
May lead to stable angina (symptoms only
with exertion)
Coronary artery occlusion → ischemia → death of
the tissue (infarction) in the area of the heart
supplied by that artery:
Partial occlusion of the coronary artery →
affects the inner myocardium (subendocardium
) → may cause:
NSTEMI
Unstable angina (if the ischemia does not
result in cell death)
Complete occlusion → transmural infarction →
STEMI

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 5 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Natural history of vulnerable/unstable plaque:

Unstable atherosclerotic plaques are thought to account for the majority of
myocardial infarctions. Characterization includes macrophage inflammation,
a thin fibrous cap, remodeling, microcalcification, and angiogenesis.

Image by Lecturio.

Clinical Presentation

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 6 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

The classic symptom of MI in most patients is acute chest pain.

However, some patients may present with more vague
symptoms.

Symptoms
Typical:
Chest pain:
Retrosternal
Dull, squeezing/pressure-like pain
May radiate to the left arm, shoulder, or
jaw
Usually constant, lasting ≥ 20–30
minutes
Diaphoresis
Dyspnea
Nausea
Associated symptoms:
Dizziness
“Indigestion” and/or vomiting
Syncope
Epigastric pain (with inferior-wall MI)
Palpitations
Atypical presentation more common in women, the
elderly, or patients with diabetes:
Absence of chest pain or atypical locations/
quality
May present with only the usual associated
symptoms

Physical examination
Vitals:
Tachycardia
Bradycardia with right coronary artery (RCA)

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 7 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

occlusion (supplies the sinoatrial (SA) and

atrioventricular (AV) nodes)
Hypotension
Cardiovascular:
S3 heart sound (early diastolic sound heard at
the end of rapid ventricular filling)
S4 heart sound (late diastolic sound heard at
the onset of atrial contraction)
Jugular venous distention: RCA occlusion →
right-sided heart failure (HF)
Hepatic congestion: RCA occlusion → right-
sided HF
Pulmonary edema: left coronary artery occlusion →
left-sided HF:
Crackles/rales
Wheezing
Skin:
Cool
Pale or cyanotic
Diaphoretic

Diagnosis
Patients presenting with a history of acute chest pain or
suspicious atypical symptoms are evaluated with ECG. Cardiac
troponin levels should be obtained within 10 minutes of the
patient's arrival in the ED. Abnormalities in both confirm the
diagnosis of MI.

ECG
Findings in STEMI and their evolution:

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 8 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Tall, peaked (hyperacute) T waves may be

seen early in the course.
≥ 1-mm ST elevation in ≥ 2 contiguous leads
Reciprocal ST depression
New left bundle branch block (LBBB) and
symptoms → STEMI until proven otherwise
Pathologic Q waves typically emerge between
6 and 16 hours after symptom onset
T-wave inversion follows
ST-segment normalization
T-wave normalization over several hours to
days
Findings in NSTEMI:
ST depression (not elevations)
Nonspecific changes
Inverted T waves

Table: Localization of STEMI on ECG

Artery occluded Leads with ST Location of

elevation MI

Proximal LAD V1–V2 Septal

LAD V3–V4 Anterior

Distal LAD V5–V6 Apical

LCX or LAD I, aVL Lateral

RCA (more II, III, aVF Inferior

common) or LCX

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 9 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

RCA or LCX V7–V9 (ST depressions Posterolateral

in V1–V3)

LAD: left anterior descending artery

LCX: left circumflex artery
RCA: right coronary artery

Laboratory evaluation

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 10 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Cardiac enzymes:
Structural proteins in the heart that are released as a
result of myocardial injury
Troponin I:
Serum levels:
Start to ↑ within 2–3 hours after the onset
of chest pain
Peak levels at 12–48 hours
Return to baseline over 4–10 days
Highest sensitivity and specificity (compared to
other cardiac enzymes)
Serial lab draws are used to assess for a rise
and fall in levels (recheck in 1–3 hours).
The degree of ↑ correlates with the size of the
infarct.
Can be ↑ as the result of causes of coronary
ischemia other than acute MI:
Arrhythmia
Cocaine
PCI
Coronary embolism
Aortic dissection
Can be ↑ with noncoronary ischemia or
myocardial injury:
Electrical shock
Hypoxia
Myocarditis
Takotsubo cardiomyopathy: sudden,
temporary weakening of the heart muscle
(usually related to a stressor)
Patients with CKD:
May have stably ↑ levels in the absence
of myocardial damage

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 11 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

A rise or fall in troponin I value > 20%

over 6–9 hours is indicative of acute MI in
patients with end-stage CKD.
CK-MB isoenzyme:
Less sensitive and specific than troponin
↑ within 3–6 hours after chest pain
Peaks within 12–24 hours
Normalizes 48–72 hours after MI
Continued ↑ after 72 hours is diagnostic of
reinfarction.
The degree of ↑ in CK-MB correlates with the
size of the infarct.
Supporting labs:
LDH and AST → may be ↑, but no longer used in the
diagnosis of MI.
BNP → ↑ in heart failure
Potassium and magnesium levels should be
optimized during management.
Drug screen to evaluate for cocaine or
methamphetamine use.

Comparison within acute coronary syndrome

The following table compares unstable angina, NSTEMI, and
STEMI on the basis of clinical features, ECG, and laboratory
findings.

Table: Comparison within acute coronary syndrome

Diagnosis Clinical features ECG findings Laboratory

findings

Unstable Ischemic chest None Normal

angina pain that occurs troponin

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 12 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

at rest or with ST-

previously segment
tolerated levels of depression
exertion TWI

NSTEMI Prolonged None Elevated

ischemic chest ST- troponin
pain in any segment
setting depression
TWI

STEMI Prolonged ST- Elevated

ischemic chest segment troponin
pain in any elevation
setting New LBBB

LBBB: left bundle branch block

TWI: T-wave inversion

Imaging
Chest X-ray:
Should be done to evaluate for other causes of
chest pain, such as:
Pneumonia
Pneumothorax
Mediastinal widening → aortic dissection
May show pulmonary edema → heart failure
Coronary angiography:
Gold standard test
Findings:
Localizes narrowed or occluded coronary
arteries
New regional wall motion abnormalities
consistent with an ischemic infarct

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 13 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Left ventriculography can assess left

ventricular function.
Determines the need for intervention with stenting
or surgery
Transthoracic echocardiography:
Left ventricular ejection fraction (LVEF) is the
best predictor of survival in STEMI.
New regional wall motion abnormalities can be
visualized
Can evaluate for complications of MI:
Free-wall rupture
Ventricular septal rupture
Mitral regurgitation
Aneurysm formation
Presence of a thrombus

Management
Initial therapy
Prompt recognition of the diagnosis of acute MI is imperative in
order to realize the benefit from reperfusion therapy.
Oxygen: previously used with every patient,
currently used only if:
O2 saturation < 90%
Respiratory distress present
Heart failure present
Other high-risk features of hypoxia
Treat ventricular arrhythmias (if present).
Aspirin:
Prevents thrombus formation/expansion

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 14 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

↓ Mortality
Nitroglycerin (sublingual):
Start if the patient still has chest pain,
hypertension, or heart failure
Vasodilation → ↓ preload → ↓ oxygen
demand → ↓ symptoms
Add IV nitrates if symptoms persist after 3
sublingual doses
Avoid in patients with:
Hypotension
Right ventricular infarction (inferior-wall
MI) → ↓ preload to the right ventricle can
↓ cardiac output even further
Beta-blockers:
↓ Heart rate and contractility → ↓ oxygen
demand→ ↓ symptoms
↓ Mortality
Contraindicated if the patient has:
Heart failure
Bradycardia
Severe reactive airway disease
Cocaine-induced MI
Morphine:
Provides relief of ischemic pain (↓ preload)
↓ Anxiety and the adrenergic drive that causes
further vasoconstriction
Can ↑ mortality
Can cause respiratory depression
Treat heart failure with diuretics (if present).
Start high-dose statin therapy (e.g., atorvastatin) as
early as possible and before PCI.
IV saline to ↑ cardiac output and perfusion with right
ventricular MI
Anticoagulation recommendations vary with the

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 15 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

clinical situation and plan for PCI or thrombolytic

therapy:
Heparin
Low-molecular-weight heparin (LMWH)

Risk stratification
Important for prognosis:
Patients at the highest risk for further cardiac
events may benefit from a more aggressive
therapeutic approach:
Risk scores such as TIMI (Thrombolysis in
Myocardial Infarction), Global Registry of
Acute Coronary Events (GRACE), or
Platelet Glycoprotein IIb/IIIa in
Unstable Angina: Receptor Suppression
Using Integrilin Therapy (PURSUIT) have
good predictive ability.
These scoring systems take into account
markers of predictive outcome for
prognosis.
End points for predictive outcome:
Death
Future MI
Need for urgent revascularization
TIMI risk scores help in decision-making for urgent
revascularization:
Based on:
ECG features
Elevated cardiac enzymes
Evidence of hemodynamic instability
Persistent chest pain despite appropriate
medical therapy
Age

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 16 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Comorbidities (other CHD risk factors)

Recent aspirin use
For TIMI score > 3 with NSTEMI or
unstable angina, revascularization with PCI is
recommended:
Low risk: score of 0–2
Intermediate risk: score of 3–4
High risk: score of 5–7

Reperfusion
PCI:
Indications:
STEMI
NSTEMI with TIMI score > 3
↓ Amount of myocardial damage
↓ Mortality
For patients who present ≤ 2 hours after the
onset of symptoms → PCI with drug-eluting
stent to prevent restenosis, if available:
Improves survival
↓ Rate of intracranial hemorrhage and
recurrent MI as compared with fibrinolysis
If PCI is not readily available, then thrombolytic
agents are recommended for reperfusion:
Tenecteplase and reteplase (fibrin-specific) are
preferred.
Streptokinase and alteplase are other options.
Consider fibrinolytic therapy in patients with ≤
12 hours of symptoms.
All are contraindicated with active bleeding,
recent stroke, or suspected aortic dissection.
For patients with symptoms > 2–3 hours:
Transfer for primary PCI if available within 120

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 17 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

minutes (including transfer time).

Start dual antiplatelet therapy: aspirin plus
P2Y12 inhibitors (clopidogrel, prasugrel,
ticagrelor).
Glycoprotein IIb/IIIa inhibitors (e.g., abciximab)
Indications for CABG surgery after MI:
Failure of thrombolytics or PCI to reperfuse
damaged myocardium
Hemodynamically important mechanical
complications (e.g., rupture)
Anatomy not amenable to PCI

Post-MI care
Improved long-term prognosis is seen with:
Antiplatelet therapy to ↓ the risk of recurrent
coronary artery thrombosis or, with PCI,
coronary artery stent thrombosis
ACEi therapy to prevent remodeling of the left
ventricle
Statin therapy
Anticoagulation in the presence of left ventricular
thrombus or chronic atrial fibrillation to prevent
embolization

Complications
After MI, different risks develop as time passes after the acute
event. Patients with type 2 MI have a higher prevalence of
heart failure, kidney disease as a complication of MI, and
atrial fibrillation.

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 18 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Death: 1 of 3 patients do not survive their initial MI.

Potential complications in the first 1–3 days post-MI:
Ventricular arrhythmia (most common cause of
death)
Acute heart failure
Cardiogenic shock
Pericarditis:
Pleuritic chest pain that increases with
lying supine
Pericardial rub on auscultation
Fever
Dry cough
ECG showing diffuse ST elevations
Pericardial effusion seen on
echocardiogram
3–14 days post-MI:
Free-wall rupture:
Can result in cardiac tamponade or
pseudoaneurysm formation
Incidence is highest during macrophage-
mediated removal of necrotic
myocardium.
Papillary muscle rupture:
Posteromedial papillary muscle rupture
due to posterior descending artery
occlusion
Posteromedial-wall rupture → acute
mitral regurgitation
Holosystolic murmur over the 5th
intercostal space at the midclavicular line
May present with signs of left-sided
heart failure (pulmonary edema, crackles,
dyspnea)
Ventricular septal rupture:

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 19 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Caused by left anterior descending artery

occlusion
Coincides with macrophage infiltration of
the wall
May present as a holosystolic murmur
over the left sternal border
May present with signs of
right-sided heart failure (e.g., jugular
venous distention, peripheral edema) or
biventricular failure
May progress to cardiogenic shock due
to a ↓ in cardiac output
Mural thrombus formation with potential
embolization of the clot can lead to:
Limb ischemia
Stroke
Mesenteric ischemia
Renal infarction
> 14 days post-MI:
Dressler syndrome:
Autoimmune sensitization to antigens
released during cardiomyocyte death
Presents with signs of pericarditis (e.g.,
pleuritic pain, friction rub, fever)
May result in elevation of troponins and
leukocytosis
ECG shows diffuse ST elevations
Pericardial effusion: abnormal amount of
fluid in the pericardial cavity of the heart
Can be complicated by cardiac
tamponade/hemopericardium
Ventricular aneurysm presenting with:
Persistent ST elevations and T-wave
inversions > 3 weeks post-MI

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 20 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Signs of angina (e.g., dyspnea on

exertion)
Systolic murmur and/or S3/S4 sounds

Differential Diagnosis
Unstable angina: presents with chest pain due to
transient myocardial ischemia and may be a warning
sign for the risk of heart attack (MI) in the future.
Diagnosis is by history and examination, ECG, and
stress testing, with possible additional nuclear
medicine imaging, echocardiography, or coronary
angiography. Troponin will be normal. Treatment
includes antiplatelet medications, nitrates, statins,
beta-blockers, and PCI.
Vasospastic angina: uncommon cause of chest pain
due to transient coronary artery spasms. The clinical
presentation of vasospastic angina is characterized
by spontaneous episodes of chest pain due to a
transient decrease in blood flow to the epicardial
arteries. Diagnosis is made by clinical history, normal
exam, and ECG. Cardiac enzymes and PCI are
usually normal. Management includes the
prevention of vasospasm with calcium channel
blockers and the relief of angina with nitrates.
Aortic dissection: due to shearing stress from
pulsatile pressure causing a tear in the tunica intima
of the aortic wall, often associated with hypertension
. Patients with aortic dissection often present with
acute, tearing chest or back pain. Diagnosis is made
by CT imaging. Type A dissections (in the ascending

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 21 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

aorta) are a surgical emergency because of the risk

of imminent rupture. Type B dissections (in the
descending aorta) can often be managed medically
with beta-blockers and calcium channel blockers.
Pulmonary embolism: presents with pleuritic pain,
dyspnea, tachycardia, and occasionally chest pain.
Risk factors for pulmonary embolism are prolonged
immobilization, oral contraceptives or estrogen
therapy, smoking, and obesity. Diagnosis of
venous thromboembolism is made by CT. ECG may
be normal or may show ST-segment changes.
Management is urgent, with anticoagulation to
prevent further propagation of the clot.
Pericarditis: inflammatory disorder of the
pericardium resulting in chest pain that is usually
constant and may manifest with diffuse ST-segment
elevation on ECG. Etiologies can be infectious
(usually viral), post-MI, due to medications, or due to
malignancy. Treatment is supportive if viral or with
management of the underlying cause.
Costochondritis: due to inflammation of the
cartilage in the rib cage. Costochondritis presents
with chest pain that is reproducible on palpation. It
may be due to trauma, strain, or viral infection.
Diagnosis is made clinically and by the exclusion of
coronary disease with appropriate testing.
Treatment is with local measures and NSAIDs.
Esophageal spasm: painful contraction of the
esophagus that can present with severe, intermittent
chest pain. Diagnosis is by ruling out cardiac causes
of chest pain, esophageal manometry, and a
barium swallow study. Management may include
antispasmodic medications and, in some cases,
surgery.

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 22 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

Takotsubo cardiomyopathy: type of nonischemic

cardiomyopathy in which there is transient regional
systolic dysfunction of the left ventricle. Patients
present with symptoms of acute coronary syndrome,
including chest pressure and shortness of breath.
ECG may show ST-segment elevations. Coronary
angiography will not show obstructed arteries.
Echocardiography will demonstrate characteristic
apical wall motion abnormalities. Treatment includes
beta-blockers and the removal of inciting stressors.
Myocarditis: inflammatory disease of the
myocardium that can mimic an acute MI, especially
in younger patients (< 45 years). It may occur alone
or in association with a systemic process. There are
numerous etiologies, but all lead to inflammation
and myocyte injury. The diagnosis is supported by
clinical findings, laboratory evaluation, and cardiac
imaging. Management is supportive and aimed at
addressing complications.

References

1. Reeder, G.S., Kennedy, H.L. (2021). Diagnosis of acute myocardial

infarction. UpToDate. Retrieved May 24, 2021, from
https://www.uptodate.com/contents/diagnosis-of-acute-myocardial-
infarction (https://www.uptodate.com/contents/diagnosis-of-acute-
myocardial-infarction?
search=myocardial%20infarction&source=search_result&selectedTitl
e=2~150&usage_type=default&display_rank=2)
2. Thygesen, K., et al. (2018). Fourth universal definition of myocardial
infarction (2018). Journal of the American College of Cardiology
72:2231–2264. https://doi.org/10.1016/j.jacc.2018.08.1038
(https://doi.org/10.1016/j.jacc.2018.08.1038)
3. Simons, M., Breall, J.A. (2021). Overview of the acute management of
non-ST-elevation acute coronary syndromes. UpToDate. Retrieved

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 23 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

May 24, 2021, from https://www.uptodate.com/contents/overview-of-

the-acute-management-of-non-st-elevation-acute-coronary-
syndromes (https://www.uptodate.com/contents/overview-of-the-
acute-management-of-non-st-elevation-acute-coronary-syndromes?
search=epidemiology%20of%20myocardial%20infarction&topicRef=5
0&source=see_link)

4. Reeder, G.S., Kennedy, H.L. (2021). Overview of the acute

management of ST-elevation myocardial infarction. UpToDate.
Retrieved May 24, 2021, from
https://www.uptodate.com/contents/overview-of-the-acute-
management-of-st-elevation-myocardial-infarction
(https://www.uptodate.com/contents/overview-of-the-acute-
management-of-st-elevation-myocardial-infarction?
search=epidemiology%20of%20myocardial%20infarction&topicRef=5
0&source=see_link)
5. Rafla, S., Kamal, A. (2020). Localization of the occluded vessel in
acute myocardial infarction. Journal of Cardiology and Cardiovascular
Medicine 5:29–33. https://doi.org/10.29328/journal.jccm.1001082
(https://doi.org/10.29328/journal.jccm.1001082)
6. Sweis, R.N., Jivan, A. (2020). Acute myocardial infarction (MI). MSD
Manual Professional Version. Retrieved June 12, 2021, from
https://www.msdmanuals.com/professional/cardiovascular-
disorders/coronary-artery-disease/acute-myocardial-infarction-mi
(https://www.msdmanuals.com/professional/cardiovascular-
disorders/coronary-artery-disease/acute-myocardial-infarction-mi)
7. Ojha, N., Dhamoon, A.S. (2020). Myocardial infarction. StatPearls.
Retrieved June 12, 2021, from
https://www.ncbi.nlm.nih.gov/books/NBK537076/
(https://www.ncbi.nlm.nih.gov/books/NBK537076/)
8. Patibandla, S., Gupta, K., Alsayouri, K. (2020). Cardiac enzymes.
StatPearls. Retrieved June 12, 2021, from
https://www.ncbi.nlm.nih.gov/books/NBK545216/
(https://www.ncbi.nlm.nih.gov/books/NBK545216/)

9. Stark, M., Kerndt, C.C., Sharma, S. (2021). Troponin. StatPearls.

Retrieved June 12, 2021, from
https://www.ncbi.nlm.nih.gov/books/NBK507805/
(https://www.ncbi.nlm.nih.gov/books/NBK507805/)
10. Zafari, A.M., Abdou, M.H. (2019). Myocardial infarction. In Yang, E.H.
(Ed.), Medscape. Retrieved June 12, 2021, from
https://emedicine.medscape.com/article/155919-overview

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 24 of 25
Myocardial Infarction - Lecturio 12/9/22, 11:46 AM

(https://emedicine.medscape.com/article/155919-overview)

https://app.lecturio.com/#/article/3213?return=__app__%2Fcourse%2Fs%2F8382%2Farticles Page 25 of 25