Acute Coronary Syndrome

(Myocardial Infarction and Unstable

Angina) (Clinical)
Acute coronary syndrome (ACS) encompasses conditions that include confirmed or
suspected myocardial ischemia or myocardial infarction (MI). ACS, which includes
non-ST-elevation MI (NSTEMI), ST-elevation MI (STEMI), and unstable angina, usually
results from thrombus formation on a ruptured atherosclerotic plaque in the
epicardial arteries. Patients most commonly present with chest pain but also may
have atypical symptoms. Diagnosis is by clinical history, ECG changes, elevated
cardiac enzymes (preferably, high-sensitivity cardiac troponin), and/or evidence of
wall motion abnormalities on imaging. Both STEMI and NSTEMI have loss of
myocardial tissue, but STEMI is due to transmural ischemia (indicating complete
major coronary artery obstruction). NSTEMI occurs because of subendocardial
ischemia (indicating partial major coronary artery obstruction). Unstable angina
occurs when ischemia does not result in infarction (no troponin elevation and
typically with non-ST-elevation changes on ECG). Management of STEMI depends
on the timing of the presentation and local resources with regard to thrombolytic
therapy versus percutaneous intervention. Both unstable angina and NSTEMI are
managed the same way, with both conservative (medical) and invasive strategies
available. Additionally, routine medical therapy includes dual antiplatelet therapy,
nitrates, oxygen, pain control, and beta-blockers.

Last updated: January 16, 2024

CONTENTS

Overview
Pathophysiology
Clinical
Presentation
Diagnosis
Management
Complications
Differential
Diagnosis
References

Overview
Definitions[2,12,18]
Myocardial infarction (MI):
MI, commonly known as a “heart attack,” is defined as acute
myocardial injury and tissue death resulting from ischemia.
Official definition uses clinical and diagnostic findings.
Defined as the rise and/or fall of cardiac biomarkers (cardiac
troponin (cTn) preferred) with ≥ 1 value above the 99th percentile
of the upper reference limit and ≥ 1 of the following:
Ischemic symptoms
ECG changes consistent with ischemia (new ST-segment-T-
wave changes or new left bundle branch block (LBBB))
Pathologic Q waves in the ECG
Imaging showing new findings of myocardial tissue loss or
regional wall motion abnormality
Intracoronary thrombus by angiography (or by autopsy)
Acute coronary syndrome (ACS):
ACS is a broad term defined by a condition in which
myocardial ischemia or infarction is suspected or confirmed; it
includes:
Unstable angina:
Myocardial ischemia without elevated cardiac biomarkers
(no myocardial infarction); may or may not have ECG
changes
With the advent of high-sensitivity troponin,
unstable angina is becoming less common (as cases are
categorized as NSTEMI, which has troponin elevation).
Non-ST-elevation MI (NSTEMI): myocardial ischemia associated
with elevated cardiac biomarkers and ST–T-wave abnormalities
(which include ST depressions and/or T-wave inversions)
ST-elevation MI (STEMI): myocardial ischemia associated with
elevated cardiac biomarkers and ST-segment elevation in at least
2 contiguous leads

Epidemiology[10,12,24]
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:
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[6,7,10]
The risks of MI increase proportionately with increases in risk
factors for coronary atherosclerosis (also known as coronary artery
disease (CAD)).
 Nonmodifiable:
Older age (prevalence increases after age 35 years)
increases risk, with elderly patients 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
Gender: men at higher risk than women
Ethnicity: Blacks, Hispanics, and Southeast Asians at
increased risk
Family history: positive family history of CAD (premature
CAD) → ↑ CAD mortality risk:
A 1st-degree male relative < 45 years of age
A 1st-degree female relative < 55 years of age
Modifiable:
Smoking
Diabetes
Hypertension
Hyperlipidemia
Obesity
Poor diet (e.g., trans fat, sweets, high processed meat
consumption)
Sedentary lifestyle

Classification[1,2,18]
Classification of MI according to the assumed cause:
Type 1: acute thrombus on a ruptured atherosclerotic plaque
Type 2: ↑ oxygen demand in the myocardium 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

[7]
 Characteristics of unstable versus stable plaque:[7]
Unstable plaque:
Thin fibrous cap
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)
Thrombus develops on an atherosclerotic plaque, causing
ischemia (decreased blood flow) but no tissue infarction →
unstable angina[20]
In the atherosclerotic plaque, there are increasing numbers
of lipid-laden macrophages and foam cells.
↑ Plaque growth → ↑ elastases and proteases that cause
thinning of the fibrous cap → plaque fissuring or rupture
Exposed subendothelial components trigger
platelet activation and aggregation, and platelet products
promote vasoconstriction and thrombus formation.
Nonocclusive thrombus → unstable angina (ischemia
occurs even at rest)
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) → resulting in myocardial
cell death → NSTEMI
Complete occlusion → transmural infarction → STEMI
 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
The classic symptom of MI in most patients is acute chest pain.
However, some patients may present with more vague symptoms.
[2,11,12]
Symptoms[2,11,12]
Typical:
Chest pain:
Retrosternal
Dull, squeezing/pressure-like pain
May radiate to the left arm, shoulder, or jaw (radiation rarely
goes below the umbilicus or above the mandible)
Usually constant, lasting ≥ 20–30 minutes
Levine’s sign: clenched hand over chest/sternum when
individual having chest pain is asked to localize the
sensation
Suggestive of ACS: rest angina, new-onset chest pain that
limits physical activity, escalating chest pain with ↑
frequency and duration
Angina equivalents: discomfort in the chest, shoulders, arms,
neck, back, upper abdomen, or jaw; shortness of breath/dyspnea
and fatigue
Diaphoresis
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
Compared to stable angina (chest pain on exertion/stress),
unstable angina:
Occurs at rest or with previously tolerated levels of exertion
Has no predictable pattern
Is not relieved with rest or nitroglycerin

Physical examination[11,15]
 Vitals:
Tachycardia
Bradycardia with right coronary artery (RCA) 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
The approach to diagnosis may vary according to practice
location. The following information is based on management
guidelines from the American Heart Association/American College
of Cardiology, the National Institute for Health and Care
Excellence, and the European Society of Cardiology.
The goals of the initial evaluation are to identify life-threatening
etiologies and ensure stability of the individual. Patients presenting
with acute chest pain are evaluated with ECG (obtained within 10
minutes).

ECG[2,5,11,12,15]
ACS is not ruled out with a normal initial ECG:
Serial ECGs are recommended, especially if symptoms
persist, until ACS is ruled out.
Consider adding leads V7–V9 to rule out posterior MI.
Findings in unstable angina:
May be normal (or show nonspecific changes)
Transient evidence of subendocardial ischemia:
ST-segment depression
T-wave flattening
T-wave inversion
Findings in NSTEMI:
ST depression (not elevation) in 2 contiguous leads
Inverted T waves in 2 contiguous leads
May be normal or have nonspecific changes
Findings in STEMI:
Evolution:
Tall, peaked (hyperacute) T waves may be seen early
in the course.
≥ 1-mm ST elevation in ≥ 2 contiguous leads
Reciprocal ST depression
Pathologic Q waves typically emerge between 6 and
16 hours after symptom onset
T-wave inversion follows, with Q waves getting
deeper
ST-segment normalization, usually still with T-wave
inversion
T-wave normalization over several hours to days
New LBBB and symptoms → STEMI until proven otherwise
If ECG shows ST–T-wave depression in II, III, aVF (inferior wall
ischemia):
Obtain leads V4R, V5R, and V6R (to check for right
ventricular infarct).
Obtain leads V7–V9 (to check for posterior MI).
ECG also assists in identifying nonischemic causes, such as
pericarditis, myocarditis, and new arrhythmia.
Normal → add other tests (labs)
Diffuse ST elevation → pericarditis
New arrhythmia → treat according to guidelines
Table: Localization of STEMI on ECG

Artery occluded Leads with ST elevation Location of

MI

Proximal LAD V1–V2 Septal

LAD V3–V4 Anterior

Distal LAD V5–V6 Apical

LCX or LAD I, aVL Lateral

RCA (more common) II, III, aVF Inferior

or LCX

RCA or LCX V7–V9 (ST depressions Posterolateral

in V1–V3)

LAD: left anterior descending artery

LCX: left circumflex artery
RCA: right coronary artery
Table: ECG diagnosis of acute MI with baseline LBBB (Sgarbossa
criteria)[5]

ST change Amount of change Points

ST elevation ≥ 1 mm concordant with QRS complex 5

≥ 5 mm discordant with QRS complex 2

ST depression ≥ 1 mm in V1, V2, or V3 3

Score ≥ 3 points: consistent with MI

MI: myocardial infarction
Laboratory evaluation[2,11,15,17,18]
Cardiac enzymes:
Structural proteins in the heart that are released as a result of
myocardial injury
High-sensitivity cardiac troponin (hs–cTn), which more
accurately detects myocardial injury, is preferred.
 Detection of hs–cTn takes less time (from onset of chest
pain) than conventional troponin assays.
Hs-cTn is superior to CK-MB in diagnosing myocardial
injury.
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
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
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:
Not typically ordered
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.
Other tests (to assess associated risks or triggering factors, and
prognosis):
B type natriuretic peptide (BNP) or N-terminal pro-BNP (NT-
proBNP)
Lipid panel
Metabolic panel
Hemoglobin A1c
Complete blood count
Toxicology testing (e.g., cocaine, methamphetamine)

ECG and lab 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: ECG and lab comparison within acute coronary syndrome

Diagnosis Clinical features ECG findings Laboratory

findings

Unstable Ischemic chest pain None Normal

angina that occurs at rest or ST- troponin
with previously segment
tolerated levels of depression
exertion TWI

NSTEMI Prolonged ischemic None Elevated

chest pain in any ST- troponin
setting segment
depression
TWI

STEMI Prolonged ischemic ST- Elevated

chest pain in any segment troponin
setting elevation
New LBBB

LBBB: left bundle branch block

TWI: T-wave inversion
Imaging[2,11,15,18,28]
Chest X-ray: often ordered to evaluate for other causes of chest
pain
Potential findings consistent with alternative causes of
chest pain:
Pneumonia
Pneumothorax
Mediastinal widening → aortic dissection
Presence of cardiomegaly and pulmonary congestion (due
to heart failure) can be identified.
 Transthoracic echocardiography (TTE):
Recommended in the initial evaluation of those with
intermediate risk for major CAD events
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
Coronary CT angiography:
May be utilized for high-risk patients in an attempt to avoid
coronary angiography (e.g., bleeding risk, poor vascular
access)
Benefits:
Rapid
Can exclude obstructive CAD
Can identify high-risk plaque and plaque burden
May be combined with functional flow reserve or
perfusion studies to assess the significance of effect
of stenosis on the myocardium

Diagnostic approach
Principles:[11]
If STEMI is detected in the initial evaluation, guidelines for STEMI
should be followed.
In those presenting with unstable angina/NSTEMI:
Routine use of clinical decision pathways based on risk is
recommended.
Assessment of the cardiac risk is first performed and then
followed by testing/procedure, which will likely benefit the
patient.

Diagnosis of STEMI:[12]
 Diagnosed by:
Presenting symptoms can be chest pain, dyspnea,
arrhythmia, cardiac arrest, or other angina equivalents.
ECG findings (as outlined above)
Laboratory tests (hs–cTn)
Additional studies:
Complete blood count, metabolic panel including
renal function, coagulation studies
Additional labs as indicated
Echocardiography if with suspected valvular heart
disease, heart failure
Next steps:
Continuous telemetry
Serial cardiac enzymes
Assess for other life-threatening conditions (e.g.,
heart failure, aortic dissection)
Assess for bleeding risk and coagulation disorders
Stabilize patient and initiate routine medical therapy
Choose reperfusion strategy.
Diagnosis of NSTEMI/unstable angina:[11,13,15,18,25]
Diagnosed by:
Presenting symptoms
ECG findings (e.g., ST-segment depression, T-wave
inversions, or can be normal)
Laboratory test (hs–cTn: normal in unstable angina,
elevated in NSTEMI)
Additional labs including complete blood count, metabolic
panel including renal function, coagulation studies
Additional imaging as indicated
Next steps:
Continuous telemetry
Serial cardiac enzymes
Assess for other life-threatening conditions (e.g.,
heart failure, aortic dissection).
Assess for bleeding risk and coagulation disorders.
Stabilize patient and initiate routine medical therapy.
Risk-stratify:
Determines the short-term adverse effects
Determines further cardiac testing and management
needed
 Different scoring systems developed for risk stratification:
HEART score (https://www.mdcalc.com/calc/1752/heart-
score-major-cardiac-events):
History, ECG, Age, Risk factors, Troponin
One of the most commonly used
Low-risk (a score of ≤ 3): low major adverse
cardiovascular events (MACE) rate (1.7%)
Moderate-risk (score of 4–6): MACE rate of
approximately 12%–17%
High-risk (≥ 7): MACE rate of 50%–65%
TIMI score (https://www.mdcalc.com/calc/111/timi-risk-score-
ua-nstemi#pearls-pitfalls):[14]
Thrombolysis In Myocardial Infarction
Determines probability of ischemic events or mortality
in unstable angina or NSTEMI using 7 factors (which
are assigned 1 point each)
HEART score helps stratify undifferentiated chest
pain better than the TIMI score.
GRACE ACS risk score
(https://www.mdcalc.com/calc/1099/grace-acs-risk-
mortality-calculator#use-cases):
Global Registry of Acute Coronary Events
Estimates in-hospital and 6-month mortality rate in
ACS
Variables: age, heart rate, systolic blood pressure, ST-
segment deviation, renal function, congestive
heart failure, cardiac arrest, and elevated biomarkers
Recommended in UK (National Institute for Health
and Care Excellence)[13,15] and Europe (European
Society of Cardiology)[18]

Table: Heart score

Factors Characteristics Points

History Highly suspicious 2

Moderately suspicious 1

Slightly suspicious 0
 ECG Significant ST depression (≥ 0.5 mm in 2 2
contiguous leads)

Nonspecific repolarization changes 1

Normal 0

Age > 65 years 2

45–65 years 1

< 45 years 0

Risks ≥ 3 risk factors or history of atherosclerotic 2

disease

1–2 risk factors 1

No known risk factors 0

Troponin ≥ 3 times the normal limit 2

1–2 times the normal limit 1

Normal 0

Low risk: a score ≤ 3

Moderate/intermediate risk: score of 4–6
High risk: ≥ 7
Table: Thrombolysis in myocardial infarction (TIMI) score

Factors Points

Age ≥ 65 years 1

≥ 3 Risk factors for coronary artery disease (e.g., diabetes, 1

hypertension, hyperlipidemia, smoking)

Prior history of coronary artery stenosis of ≥ 50% 1

≥ 2 episodes of angina 24 hours prior to presentation 1

Aspirin use in the past 7 days 1

≥ 0.5 mm ST deviation 1

Elevated cardiac biomarkers 1

Low risk: score of 0–2

Intermediate risk: score of 3–5
High risk: score of 6 or 7

Table: Global registry of acute coronary cvents (GRACE) ACS

score

Factors Value Points

Age < 39 0
years

40–49 18
years

50–59 36
years
 60–69 55
years

70–79 73
years

80–89 91
years

≥ 90 100
years

Heart rate < 0

70/min

70– 5
89/min

90– 10
109/min

110– 17
149/min

150– 26
199/min

≥ 44
200/min

Systolic blood pressure < 80 40

mm Hg

80–99 37
mm Hg

100–119 30
 mm Hg

120–139 23
mm Hg

140–159 17
mm Hg

160–199 7
mm Hg

≥ 200 0
mm Hg

Serum creatinine 0–0.39 1

mg/dL

0.4– 4
0.79
mg/dL

0.8–1.19 7
mg/dL

1.2–1.59 10
mg/dL

1.6–1.99 13
mg/dL

2.0– 21
3.99
mg/dL

≥4 28
mg/dL
 Killip class I 0
(https://www.mdcalc.com/calc/3990/killip-
classification-heart-failure) (classifies heart
II 15
failure in confirmed ACS)

III 29

IV 44

Cardiac arrest on admission N/A 30

ST-segment deviation 17

Elevated cardiac enzymes 13

Low risk: ≤ 88
Intermediate risk: 89–118
High risk: ≥ 119
ACS: acute coronary syndrome

Management
Approach to management may vary according to practice location.
The following information is based on the management guidelines
of the American Heart Association/American College of
Cardiology, the National Institute for Health and Care Excellence,
and the European Society of Cardiology.

Routine medical therapy in ACS

Prompt recognition of the diagnosis of acute MI is imperative in
order to realize the benefit from reperfusion therapy.
Prompt recognition of the diagnosis of acute MI is imperative in
order to realize the benefit from reperfusion therapy. All forms of
ACS have similar medical principles, except that in
unstable angina and NSTEMI, fibrinolysis has not shown benefit.
Initiate medical therapy, preferably within 20 minutes after
presentation.
Admission to coronary care unit/chest pain unit
Continuous ECG or telemetry monitoring
Anti-ischemic therapy:[12,15,18,23,25]
Oxygen support in:
O2 saturation < 94% (< 90%, per European guidelines)
Respiratory distress present
Heart failure present
Other high-risk features of hypoxia
Nitrates: vasodilation → ↓ preload → ↓ oxygen demand → ↓
symptoms:
Sublingual nitroglycerin (maximum: 3 tablets)
IV nitroglycerin if with persistent pain, hypertension,
heart failure
May cause hypotension: avoid if with low BP, if individual is
on phosphodiesterase inhibitor, or in right ventricular
infarction (inferior-wall MI)
Morphine:
↓ Anxiety and the adrenergic drive that causes further
vasoconstriction
Give only if with unreasonable amount of pain (relief of
ischemic pain → ↓ preload)
Indiscriminate use can lead to more adverse effects such
as respiratory depression (higher risk of death).
Give at an initial dose of 2–4 mg IV.[24]
 Beta-blockers:
Start within 24 hours
↓ Heart rate and contractility → ↓ oxygen demand→ ↓
symptoms
Cardioselective medications (e.g., metoprolol) are
preferred.
For heart failure/reduced systolic function (not
decompensated): use bisoprolol, sustained-release
metoprolol, or carvedilol.
Avoid in heart failure or cardiogenic shock, bradycardia,
PR interval > 0.24 second, 2nd- or 3rd-degree heart block,
severe reactive airway disease or active asthma, cocaine-
induced MI
Calcium-channel blockers (CCBs):
Nondihydropyridine CCBs if with contraindications to
beta-blockers
Also an option for recurrent ischemia
Statin therapy (high-intensity therapy regardless of LDL):
Benefits:[26]
Suppresses the secretion of inflammatory mediators
Reduces plaque volume
Thickens the fibrous cap
Options:
Atorvastatin 40–80 mg daily
Rosuvastatin 20–40 mg daily
Antithrombotic therapy:[12–14,18,25]
Dual antiplatelet therapy (DAPT) with aspirin and a platelet P2Y12
receptor blocker:
Most STEMI cases and NSTEMI/unstable angina receive
DAPT.
Selection depends on the reperfusion strategy and patient
characteristics.
Aspirin:
Given in all cases, unless with contraindications
Initial aspirin dose given: 100–325 mg (lower dose on
discharge: 75–100 mg daily)
 Platelet P2Y12 receptor blocker options:
Prasugrel:
Loading dose of 60 mg, then 10 mg daily
Not typically recommended if patient is ≥ age 75 or is
< 60 kg
Should not be used if previous ischemic or
hemorrhagic stroke, TIA, moderate-to-severe liver
disease, or on anticoagulation
Ticagrelor:
Loading dose of 180 mg, then 90 mg twice daily
Can cause transient dyspnea → rarely requires
discontinuation of therapy
Should not be used if previous hemorrhagic stroke,
moderate-to-severe liver disease, or on
anticoagulation
Clopidogrel:
Loading dose of 300–600 mg, then 75 mg daily
Option if ticagrelor and prasugrel are not available or
are contraindicated
GPIIb/IIIa inhibitors or GPI (IV eptifibatide or tirofiban):
Not routine, but considered in cases with intermediate- or
high-risk features prior to angiography/
percutaneous coronary intervention
Not given in those being treated conservatively
Bleeding risk should be low.
Use should be guided by a cardiologist
Anticoagulation (options):
Unfractionated heparin (UFH): preferred if invasive
treatment (angiography +/– revascularization) will be
performed within 48 hours
Enoxaparin
Fondaparinux (STEMI: not for primary PCI)
Bivalirudin:
STEMI: only for PCI
NSTEMI: only for early invasive strategy
Additional recommendations regarding antithrombotic therapy:
[18]

Use established bleeding risk scores (e.g., CRUSADE score

(https://www.mdcalc.com/calc/1784/crusade-score-post-mi-
bleeding-risk)) before initiating antithrombotic therapy.
Use of proton pump inhibitor with DAPT is recommended.

Other considerations:[12,18]
 Red blood cell transfusion if hemoglobin < 8 g/dL (or hemoglobin
8–10 g/dL if hemodynamically unstable)
Treat associated arrhythmias.
IV saline to ↑ cardiac output and perfusion with right ventricular
MI
Discontinue any nonsteroidal antiinflammatory drugs (NSAIDs)

Treatment approach for STEMI

Reperfusion options:[12–14,23]
Percutaneous coronary intervention (PCI):
Improves survival
↓ Rate of intracranial hemorrhage and recurrent MI as
compared with fibrinolysis
Access via the radial or femoral artery → diagnostic
angiography → intervention (e.g., stenting, thrombectomy)
to open the acutely obstructed coronary artery
Fibrinolysis:
Tenecteplase and reteplase (fibrin-specific) are preferred.
Streptokinase and alteplase are other options.
PCI indications and considerations:[12–14]
PCI with stenting is indicated in:
Cases where patient is within 120 minutes from a PCI-
capable medical facility (symptom onset ≤ 12 hours)
Cases of STEMI with cardiogenic shock
Symptom onset > 12 hours with evidence of ongoing
ischemia
Contraindications:
Unable to take DAPT
Increased risk of bleeding (thrombocytopenia, peptic ulcer,
severe coagulopathy)
Multiple PCI restenosis
Drug-eluting stents are preferred over bare metal stents.

Fibrinolysis indications and considerations:[12,13]

 Fibrinolysis is indicated in cases where the patient is > 120
minutes from a PCI-capable medical facility (symptom onset ≤ 12
hours).
Absolute contraindications:
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis
Serious closed-head or facial trauma within 3 months
Relative contraindications:
Poorly controlled hypertension (systolic BP > 180 mm Hg)
Recent internal bleeding (within 4 weeks)
Ischemic stroke (> 3 months)
Prolonged cardiopulmonary resuscitation (> 10 minutes)
Major surgery within 3 weeks
Pregnancy
Active peptic ulcer
Current anticoagulant use
Outcomes:
Resolution of ST elevation and improved hemodynamics
and symptoms → successful reperfusion
If reperfusion is not achieved → angiography in PCI-
capable facility
Not a candidate for reperfusion therapy:[13]
Presentation late in the illness
Moribund state
Significant comorbidities/extremely poor health (risks that
outweigh benefits)
Indications for CABG surgery after MI:[12,14]
Failure of thrombolytics or PCI to reperfuse damaged
myocardium
Hemodynamically important mechanical complications (e.g.,
rupture, coronary dissection during PCI)
Anatomy not amenable to PCI
Severe multivessel disease or left main artery disease
Life-threatening arrhythmias (usually from persistent ischemia)

Table: Treatment strategy in STEMI[12,21,23]

Treatment Routine medical Indications
therapy

Primary Beta-blockers, Within 120 minutes

PCI nitrates, statin from a PCI-capable
DAPT: ASA + medical facility
ticagrelor/prasugrel* (symptom onset ≤ 12
(preferred) hours)
Anticoagulation Cardiogenic shock
options: Symptom onset > 12
UFH 70–100 hours with ongoing
units/kg bolus ischemia
(lower if GP inhibitor
is given)
Bivalirudin 0.75
mg/kg IV bolus
(then 1.75 mg/kg/hr)
Consider IV GPI:
Tirofiban 25 µg/kg
just before PCI
Eptifibatide 180
µg/kg IV bolus then
2 µg/kg/min

Fibrinolysis > 120 minutes from a

PCI-capable medical
facility (symptom onset
≤ 12 hours)
 Beta-blockers,
nitrates, statin
DAPT: ASA +
ticagrelor/prasugrel*
(preferred)
Anticoagulation
options:
UFH 60 units/kg
bolus (then 12
units/kg/hr)
Enoxaparin 30 mg
IV bolus (then 1
mg/kg every 12
hours)
Fondaparinux (if
unlikely to be
referred for PCI) 2.5
mg IV bolus then
2.5 mg SC daily

No Beta-blockers, Contraindications to
reperfusion nitrates, statin PCI and fibrinolysis
DAPT: ASA +
ticagrelor/prasugrel*
(preferred)
Anticoagulation
options:
UFH 50–70 units/kg
bolus then 12
units/kg/hr
Enoxaparin 30 mg
IV bolus (then 1
mg/kg every 12
hours)

*Either ticagrelor or prasugrel. Clopidogrel is an alternative option.

ASA: aspirin
DAPT: dual antiplatelet therapy
GPI: GPIIb/IIIa inhibitors
PCI: percutaneous intervention
UFH: unfractionated heparin
Treatment approach for NSTEMI and unstable
angina[13,14,18,25]
There are 2 main management strategies:
Ischemia-guided strategy:
Avoids invasive procedures unless there is hemodynamic
instability or recurrent/refractory ischemia
Some cases stabilize with medical therapy, thus avoiding
costly procedures.
Invasive therapy or coronary angiography (early invasive
therapy means within 24 hours, delayed invasive therapy means
within 25–72 hours):
Rapidly provides stratification by assessing coronary
anatomy
Generally accepted indications include high-risk features:
Angina refractory to pharmacologic therapy
Unstable arrhythmias (e.g., ventricular
tachyarrhythmias)
Depressed ejection fraction
New mitral regurgitation
Cardiogenic shock
Helps determine candidates for revascularization (
coronary artery bypass surgery (CABG) or
percutaneous coronary intervention (PCI) with stenting)
PCI: usually performed for single-vessel disease and
clinical instability
CABG: usually performed for diabetes with multivessel
disease or multivessel disease with left ventricular
dysfunction

Table: Treatment strategies in NSTEMI and unstable angina[25]

Treatment PCI Routine Indications

medical
therapy

Ischemia- N/A
guided
therapy
 Beta-blockers, Low-risk score:
nitrates, statin TIMI: 0 or 1
DAPT GRACE: < 109
Anticoagulation Physician/individual
options: preference (as long
Enoxaparin as there are no
1mg/kg every high-risk features)
12 hours
Fondaparinux
2.5 mg daily
If initial therapy
is ineffective,
proceed with
invasive
therapy.

Invasive Immediate Refractory angina

therapy (within 2 Heart failure signs
hours) and symptoms
New or worsening
mitral regurgitation
Hemodynamic
instability
Sustained VT or VF
Recurrent angina at
rest despite
optimized medical
therapy

Early None of the

(within 24 indications for
hours) immediate invasive
therapy
GRACE: > 140
New ST depression
Change in troponin
(dynamic pattern
indicating ongoing
ischemia)

Delayed
Beta-blockers, (25–72 None of the
nitrates, statin hours) indications for
DAPT immediate or early
Anticoagulation invasive therapy
options: Diabetes
UFH 60 GFR < 60
units/kg (then mL/min/1.73 m2
12 LVEF < 40%
units/kg/hr) Postinfarction
Bivalirudin 0.1 angina
mg/kg IV GRACE risk score
bolus (then 109–140; TIMI
0.25 score ≥ 2
mg/kg/hr) PCI within 6
GPI in months
intermediate- to Prior CABG
high-risk cases
(e.g., elevated
troponin)
considered for
early invasive
strategy
After ICA,
management
leads to ≥ 1 of
the following:
Continued
medical
therapy
PCI with
stenting
CABG
CABG: coronary artery bypass graft
DAPT: dual antiplatelet therapy
GPI: GPIIb/IIIa inhibitors
LVEF: left ventricular ejection fraction
PCI: percutaneous intervention
UFH: unfractionated heparin
VF: ventricular fibrillation
VT: ventricular tachycardia
Post-MI care[12–14]
Improved long-term prognosis is seen with:
Antiplatelet therapy to ↓ the risk of recurrent coronary artery
thrombosis or, with PCI, coronary artery stent thrombosis
Indefinite intake of aspirin
P2Y12 receptor blocker:
Medically managed → up to 12 months
Coronary stenting → for at least 12 months
ACEi or ARB therapy (if indicated) to prevent remodeling of the
left ventricle
Statin therapy
Anticoagulation in the presence of left ventricular thrombus or
chronic atrial fibrillation to prevent embolization
Referral to cardiac rehabilitation

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.[7,10,12]
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:
Caused by left anterior descending artery occlusion
(LAD supplies the anterior part of the
interventricular septum)
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 (post-MI) 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
May have pericardial effusion (abnormal amount of
fluid in the pericardial cavity of the heart)
Can be complicated by cardiac tamponade
/hemopericardium
Ventricular aneurysm presenting with:
Seen in totally occluded LAD
Persistent ST elevations and T-wave inversions > 3
weeks post-MI
Signs of angina (e.g., dyspnea on exertion)
Systolic murmur and/or S3/S4 sounds

Differential Diagnosis
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 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.
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.
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