NOTES

NOTES
ACUTE CORONARY SYNDROMES

GENERALLY, WHAT ARE THEY?

PATHOLOGY & CAUSES TREATMENT
▪ Signs and symptoms caused by decreased MEDICATIONS
blood flow in the coronary arteries to the ▪ Oxygen as needed
extent that the muscle cannot function ▪ Pain control with nitrates and/or morphine
properly, or even dies
▪ Antiplatelets
▪ Acute coronary syndromes are almost
▪ Anticoagulants
always due to atherosclerosis
▪ Nitrates: decreases preload by vasodilation
▪ Beta blockers: reduces cardiac demand by
SIGNS & SYMPTOMS decreasing heart rate, BP and contractility
(first-line choice: metoprolol)
▪ See individual disorders ▪ Statins: HMG-CoA reductase inhibitor
that reduces production of cholesterol to
improve lipid profile
DIAGNOSIS
OTHER INTERVENTIONS
▪ See individual disorders
▪ Hospital admission with continuous
monitoring
▪ Reestablish blood flow via catheterization /
revascularization
▪ Lifestyle changes: improve diet (reduce
intake of saturated fat), smoking cessation,
control blood pressure, strict management
of diabetes mellitus, increase exercise,
weight loss, improve lipid profile

Figure 1.1 Illustration depicting ST depression and ST elevation seen in myocardial infarctions.

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 MYOCARDIAL INFARCTION (MI)
osms.it/myocardial-infarction
COMPLICATIONS
PATHOLOGY & CAUSES ▪ Heart failure: heart muscle fails to
compensate for damage; risk related to
▪ Death of heart muscle cells due to lack of size/territory of infarct and individual’s
oxygen-rich blood flow baseline cardiac function
▪ Plaque buildup (fat, cholesterol, proteins, ▪ Cardiac arrhythmia: may be seen
calcium, white blood cells) takes years to within minutes after MI or years later. If
form in lumen undiagnosed MI, may be cause of death
▪ Blood platelets adhere to plaque and ▪ Left ventricular (LV) failure and pulmonary
enhance clotting process, creating edema: happens after left ventricular
blockage infarction, free wall rupture, ventricular
▪ Necrosis of myocardial cells follows series septal defect, papillary muscle rupture with
of events mitral regurgitation
▫ < 24 hrs: early coagulative necrosis, cell ▪ Postinfarction pericarditis, papillary muscle
debris in blood, edema, wavy fibers and rupture (might lead to acute, severe mitral
hemorrhage regurgitation), interventricular septal
▫ 1–3 days: extensive necrosis, tissue has rupture, ventricular pseudoaneurysm
acute inflammation with neutrophils formation, ventricular free wall rupture
▫ 3–14 days: macrophages and (might lead to ventricular free wall rupture
granulation tissue in margins leading to pericardial tamponade/ventricular
▫ > 14 days: contracted scar forms pseudoaneurysm), true ventricular
aneurysm, Dressler syndrome

TYPES
MNEMONIC: DARTH VADER
ST segment elevation myocardial infarction
(STEMI) Complications of MI
▪ Coronary artery completely blocked; full Death
thickness of myocardial wall involved Arrythmia
▪ ECG shows ST elevation, possible Q waves Rupture (free ventricular wall/
ventricular septum/papillary
Non-ST segment elevation MI (NSTEMI) muscles)
▪ Coronary artery not completely blocked, Tamponade
subendocardium may be especially Heart failure (acute or chronic)
vulnerable to ischemia
Valve disease
▪ ECG shows ST depression
Aneurysm of ventricles
Dressler's syndrome
RISK FACTORS thromboEmbolism (mural
▪ Modifiable risk factors: older age, smoking, thrombus)
high blood pressure, diabetes mellitus, high Recurrence/ mitral
cholesterol, low levels of physical activity, Regurgitation
obesity, excessive alcohol use, illegal drug
use (e.g., cocaine, amphetamines), chronic
stress
▪ Non-modifiable risk factors: family history,
biological male

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 Chapter 1 Acute Coronary Syndromes

SIGNS & SYMPTOMS TREATMENT

▪ Acute chest pain lasting > 20 min, ▪ STEMI first priority: emergent reperfusion
radiating to arm/jaw via percutaneous coronary intervention (e.g.
▪ Uncomfortable chest/back/neck/ catheterization)/thrombolysis
jaw/stomach pain, dyspnea, fatigue, ▫ Very time sensitive
diaphoresis, and/or nausea ▪ NSTEMI: reperfusion via percutaneous
▪ Feeling of fullness/indigestion coronary intervention (not thrombolysis)
▫ Less time sensitive than in STEMI

DIAGNOSIS MEDICATIONS
LAB RESULTS ▪ Heparin, aspirin + clopidogrel, beta
blockers, ACE inhibitors, statins
▪ Usually detected with diagnostic laboratory
work for cardiac enzymes ▪ Control symptoms with morphine and
nitroglycerin
▫ Troponin I, troponin T most specific,
sensitive markers: rise apparent within
2–4 hrs, peaking ~24 hrs
▫ CK-MB can detect reinfarction after
initial MI: levels increased 4 hrs after
infarction, peak at 24 hrs, return to
normal after 48 hrs

OTHER DIAGNOSTICS
ECG
▪ Can confirm diagnosis; time sensitive, not
accurate after 6 hours
▪ < 30 min: ST segment elevation
▫ Only seen in STEMIs Figure 1.3 Gross pathology of a ruptured
▫ ST depression/no ST segment deviation papillary muscle, a serious complication of
would be seen in NSTEMIs myocardial infarction.
▪ < 24 hrs: T wave inversion
▪ > 24 hrs: Q waves appear

Figure 1.4 Histological appearance of the

myocardium following a myocardial infarct.
Figure 1.2 A pathology pot containing a heart
exhibiting an anterior myocardial infarction,
usually the result of left anterior descending
artery disease.

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 PRINZMETAL'S ANGINA
osms.it/prinzmetals-angina

PATHOLOGY & CAUSES TREATMENT

▪ AKA vasospastic angina/variant angina MEDICATIONS
Calcium channel blockers
CAUSES
▪ Coronary artery vasospasms; occur Vasodilators
spontaneously even at rest ▪ Increases coronary blood flow to heart
▪ Vasospasms: constriction of the smooth
muscle surrounding the artery, reducing
blood flow through the vessel
▫ Cause of vasospasms not
well understood; likely due to
vasoconstrictors such as platelet
thromboxane A2
▫ Coronary artery vasospasms cause
ischemia throughout all of the heart
layers

SIGNS & SYMPTOMS

▪ Same as stable angina, except pain may
occur at rest
▪ Pain described as pressure, squeezing,
burning, or tightness; can radiate to the
either/both arms, jaw, shoulders, and back;
lasts less than 20 minutes
▪ Other symptoms: Levine’s sign (a clenched
fist held over the chest), dyspnea,
diaphoresis, fatigue, nausea, and epigastric
pain

DIAGNOSIS
DIAGNOSTIC IMAGING
▪ Transient ST segment elevation
▪ Illustrates transmural ischemia

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 Chapter 1 Acute Coronary Syndromes

UNSTABLE ANGINA
osms.it/unstable-angina

PATHOLOGY & CAUSES DIAGNOSIS

▪ Episodic chest pain that either LAB RESULTS
▫ Is new in onset ▪ Serial troponins measured for individuals
▫ Occurs at rest unpredictably with unstable angina to rule out myocardial
▫ Rapidly worsens over time infarction
▫ Occurs within 48 hrs after acute MI ▪ Troponin released after injury to myocytes
is a marker for myocardial injury
▪ Usually caused by ruptured atherosclerotic
plaque → formation of thrombosis on top
of plaque → almost complete blockage in OTHER DIAGNOSTICS
blood vessel → ischemia → pain
ECG
▪ Medical emergency: high risk of
progression to MI ▪ Can present with ST segment depression
▫ Angina: myocytes still alive ▫ May also present with T wave
inversions
▫ Myocardial infarction: death of
myocytes ▫ Illustrates subendocardial ischemia

SIGNS & SYMPTOMS TREATMENT

▪ Unstable angina, NSTEMIs are
▪ Same as stable angina, except pain may
indistinguishable at initial evaluation
occur at rest
▫ Elevated troponins indicating myocardial
▪ Pain described as pressure, squeezing,
infarction not detectable for hours
burning, or tightness; can radiate to the
either/both arms, jaw, shoulders, and back; ▫ Initial management identical
lasts less than 20 minutes
▪ Other symptoms: Levine’s sign (a clenched MEDICATIONS
fist held over the chest), dyspnea,
diaphoresis, fatigue, nausea, and epigastric Clopidogrel
pain
Low-molecular-weight-heparin (LMWH)
▪ Prevents clot formation

Enoxaparin
▪ Drug of choice based on empirical evidence

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