Acute Coronary Syndrome Myocardial Infarction and Unstable Angina Clinical St. Paul University Philippines Lecturio Academy
Acute Coronary Syndrome Myocardial Infarction and Unstable Angina Clinical St. Paul University Philippines Lecturio Academy
Acute Coronary Syndrome Myocardial Infarction and Unstable Angina Clinical St. Paul University Philippines Lecturio Academy
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
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
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
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]
Moderately suspicious 1
Slightly suspicious 0
ECG Significant ST depression (≥ 0.5 mm in 2 2
contiguous leads)
Normal 0
45–65 years 1
< 45 years 0
Normal 0
Factors Points
Age ≥ 65 years 1
≥ 0.5 mm ST deviation 1
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
70– 5
89/min
90– 10
109/min
110– 17
149/min
150– 26
199/min
≥ 44
200/min
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
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
ST-segment deviation 17
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.
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)
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)
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.
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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