Unstable Ischemic Coronary Syndromes

Question 1

What’s the difference between ischemia and infarction?

Answer 1

In infarction, cells are dead or dying.

Question 2

What distinguishes unstable angina from non-ST elevation MI (NSTEMI)?

Answer 2

In NSTEMI, cardiac enzymes will be elevated, as cells are dying.
Otherwise (by ECG, etc.) these look pretty similar.

Question 3

3 outcomes of plaque rupture in a coronary artery?

Answer 3

Thrombus formation -> spontaneous lysis -> return to stable angina (or… asymptomatic CAD).
Thrombus formation -> healing / incorporation -> progression of stenosis.
Thrombus formation -> occlusion of coronary artery -> MI.

Question 4

What pathophysiology underlies most acute coronary syndrome? What are 2 other causes?

Answer 4

Most common: plaque rupture.

Less common: intravascular thrombosis (i.e. emboli) and vasospasm.

Question 5

Review: What’s the most important variable for the risk of an individual plaque rupturing?
Can we actually assess this risk?

Answer 5

Fibrous cap thickness. Thinner is riskier.

No, we can’t asses the risk of individual plaques rupturing at this point.

Question 6

Does stenosis predict plaque rupture?

Answer 6

Nope. Extent of stenosis of coronary arteries can give you some sense of overall atherosclerotic burden, but it’s often not the most stenotic lesion that’s going to rupture.

Question 7

What’s important in a history suggesting high-risk unstable angina or NSTEMI?

Answer 7

Change in angina pattern, or new onset of angina type chest pain. (more frequently, with less exertion, more severe, etc.)

Question 8

What does physical exam of a patient with high-risk unstable angina or NSTEMI reveal?

Answer 8

May be normal or show hemodynamic compromise (cardiogenic “pre-shock” or shock)

Question 9

What does an ECG of a patient with high-risk unstable angina or NSTEMI show?

Answer 9

ST segment depression or T wave inversion

Question 10

How are biomarkers changed in high-risk unstable angina or NSTEMI?

Answer 10

High-risk unstable angina: biomarkers are normal.

NSTEM: biomarkers elevated, indicating cellular death.

Question 11

How does epicardial (i.e. transmural) ischemia appear in ECG?

Answer 11

ST segment elevation.

If you see ST elevation, it’s likely a STEMI.

Question 12

What’s a key cardiac biomarker to remember?

Answer 12

Troponin.

Others, like creatine kinase and myoglobin are used… but he really emphasizes troponin

Question 13

How long after MI is troponin released?

When do levels peak, and how long afterward are the detectable?

Answer 13

Released at 20-30mins of ischemia.
Peak at 12 hours.
Detectable for 7 days.
(Says Wikipedia. Not important to know the exact numbers)

Question 14

Are troponin levels correlated with increased mortality?

Answer 14

Yes, higher troponin means more cell death, and this is bad.

Question 15

3 aspects of acute care of acute coronary syndromes (ACS)? (excluding STEMI, I guess)

Answer 15

Anti-ischemic therapy (Nitroglycerin, beta-blockers, CCBs).
Anti-thrombotics (antiplatelets, anticoagulents).
Reperfusion (PCI or CABG)

Question 16

Does adding clopidogrel to aspirin improve outcomes?

Answer 16

Yep.

Question 17

Review: What’s the MoA of clopidogrel, plasugrel, and ticagrelor?

Answer 17

Inhibition of P2Y(12) - a receptor on platelets.

Question 18

Does combining platelet inhibitors (eg. GP IIb/IIIa inhibitors) with PCI improve outcomes?

Answer 18

Yes.

Question 19

Is invasive therapy recommended for NSTEMI?

Answer 19

Yes. PCI definitely improves outcomes.

Question 20

Does NSTEMI or STEMI carry a greater risk of recurrent ischemia?

Answer 20

NSTEMI has a greater risk of recurrent ischemia.

Question 21

Does NSTEMI or STEMI carry a greater risk of reduced LV function and CHF?

Answer 21

STEMI is more likely to cause LV dysfunction and CHF.

Question 22

Classic symptoms of MI (not all will necessarily be present)?

Answer 22

Chest pain (pretty much always happens… except in neuropathy, transplanted hearts).
Diaphoresis, nausea, arm pain.
SOB (due to pulm. edema, acute MR, arrhythmia).
Hypotension.

Question 23

Physical exam finding during MI?

Answer 23

(may all be negative, but...)
Cool and clammy skin.
Evelated or decreased BP and/or HR.
Increased JVP.
"Late systolic bulge." (asynchronous contraction)
Increased S3
Mitral regurg..
Pulm. edema.
Pericardial friction rub.

Question 24

3 things ECG can tell you about acute MI?

Answer 24

Diagnosing it.
Localizing it.
Determining eventual size.

Question 25

What will you see in ECG of early STEMI?

Answer 25

ST elevation

Question 26

What appears in ECG of later STEMI, once irreversible damage has occurred?

Answer 26

Q waves.

Question 27

What’s perhaps the most important part of STEMI treatment?

Answer 27

Reperfusion via fibrinolytics, PCI, or CABG.

PCI is preferred, if possible

Question 28

What are some factors that can prevent against myocardial necrosis in MI?

Answer 28

Ischemic preconditioning.

Presence of collateral bloodflow from chronic ischemia.