Unstable Ischemic Cardiac Syndromes

Question 1

How to differentiate between UA and non stemi MI?

Answer 1

non stemi MI has elevated cardiac enzymes

Question 2

How to differentiate between stemi/non stemi MI?

Answer 2

stemi MI has st elevation –> differentiated by size of affected vessel, extent of underlying CAD, and presence of collaterals

Question 3

What accounts for progression from stable angina to ACS?

Answer 3

plaque rupture/erosion, intravascular thrombosis, or vasconstriction/spasm –> exposure of plaque contents to the vessel leading to thrombosis/occlusion in an unpredictable way

Question 4

Are more occluding stenoses more vulnerable to rupture and therefore more likely to cause MI?

Answer 4

cannot predict which vessel occlusion is going to cause an ACS…could be the less occluded vessel or a more occluded vessel –> this is why we don’t just stent any random occluded vessel

Question 5

Whats the difference between UA/NSTEMI vs. STEMI

Answer 5

STEMI involves transmural infarction

Question 6

How long does it take troponins to leach into the bloodstream post infarction?

Answer 6

it takes time for cells to die –> 30-40 minutes before leaching –> 2-3 hours before assay can pick it up!

Question 7

What do physical signs/symptoms in a pt with chest pain suggest about risk?

Answer 7

high risk –> cardiogenic/sympathetic symptoms are bad

Question 8

Acute care of ACS

Answer 8

1. anti-ischemic: nitroglycerin, beta blocker, calcium channel blocker
2. antithrombotics:
   antiplatelets: aspirin, thenopyridines, IIb/IIIa inhibitors
   anticoagulants: heparin, thrombin blockers, Xa inhibitors
3. reperfusion: PCI, CABG

Question 9

Why do we give heparin?

Answer 9

stops progression of thrombus by sucking up factor Xa thereby reducing thrombin activation–> does not break down thrombus!

*heparin, bivalirudin are mainstays of reducing thrombin

Question 10

MOA of clopidogrel

Answer 10

irreversibly inhibits a receptor called P2Y12, an adenosine diphosphate (ADP) chemoreceptor on platelet cell membranes –> reduced platelet activity

Question 11

MOA of aspirin

Answer 11

irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation

Question 12

What is the most important treatment element in STEMI vs NSTEMI?

Answer 12

reperfusion! –> fibrinolytics (tPA), PCI, CABG

Question 13

What is ischemic preconditioning?

Answer 13

tissues that are exposed to ischemic insults become more resistant to ischemia in the future