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Flashcards in Acute Coronary Syndromes Deck (28)

Causes of Plaque Rupture

Chemical Factors:
T-Lymphocytes – secrete gamma interferon which inhibits collagen synthesis, weakening the cap
Cells within the plaque secrete metalloproteinases which degrade the interstitial matrix

Mechanical Stress:
BP, HR, Contractility – SNS activation


Clinical Symptoms of ACS

Typical Symptoms:
Sudden chest pressure
Radiation down arm (L > R)

Atypical Symptoms:
Upset stomach – gas pains
Confusion in the elderly
Teeth/Jaw pain
Mid-Scapular back pain


Labs, Emergent Care, and H and P of Chest Pain

Pain between nose and naval = ACS needs to be looked into
STEMI needs to be identified within 5-10 minutes
Vessel occlusion with STEMI = open up vessel

Initial Labs: 12 lead EKG, cardiac enzymes, electrolytes, CBC, Lipids, BUN/Cr, glucose, CXR

Emergent Care: IV access, cardiac monitoring, O2, Aspirin, and nitrates

H and P: Dx, EKG, complications, assess for reperfusion


Treatment for ACS

Unstable Angina and NSTEMI: medical therapy and assess risk; if low, stress test or meds only; if high, cath lab

STEMI: medical therapy, urgent lytics or cath lab


Medications for ACS

Thrombolytics, Percutaneous Intervention (PCI)
Thrombin Inhibitors
HMG-CoA Reductase Inhibitors (Statins)
Beta Blockers
ACE Inhibitors
Morphine- last resort


Pathogenesis of a STEMI

Loss of oxygen supply leads to necrosis of viable myocardial tissue beginning within 15 minutes and occurring mainly during 30-90 minutes after acute coronary occlusion

Cath Lab vs. Thrombolytics:
PCI is preferred therapy if possible
Door to balloon time


Types of Stents

1. Balloon angioplasty once placed caused dissection flap then causing a thrombus to form = weeks later a different process occurs and neo-intimal hyperplasia of vessel occurs to narrow vessel thus causing angina = not best result and have to fix again

2. Bare metal stent: stainless steel scaffolding over it to reduce elastic recoil that occurred after procedure, but thrombus still formed and have to be on anti-platelet therapy but the problem causes further promotion of the neo-intimal hyperplasia as the other stent

3. Drug eluting stents: covered with chemical + stainless steel coating to decrease growth (anti-mitotic); higher rates of patency and much more success; standard currently because vessels stay open longer and have less neo-intimal hyperplasia



Thrombolytics are derived from the same substance, t-PA, that is secreted from the endothelium
Activated plasminogen to plasmin to break down fibrin = breaks down clots




Aspirin (ASA); COX inhibitor

Thienopyridines: Ticlodipine, Clopidogrel (Plavix), and Prasugrel (Effient); work at ADP receptors

Direct P2Y12 Inhibitors: Ticangelor (Brilinta); work at ADP receptors

Glycoprotein 2b/3a Inhibitors: (links platelets together) this is the final pathway for inhibition of clot formation
Tirofiban (Aggrastat)
Eptifibatide (Integrelin)
Abciximab (ReoPro)



New drugs must decrease MACE in order to be approved

Major Adverse Cardiovascular Events
Cardiovascular death
Non-fatal myocardial infarction
CABG, repeat PCI


Thienopyridines Mechanism of Action

Thienopyridines: Ticlodipine, Clopidogrel (Plavix), and Prasugrel (Effient); work at ADP receptors

Binds to adenosine diphosphate (ADP) receptor, thus excludes ADP from binding to this platelet receptor

This also inhibits the subsequent ADP mediated activation of the glycoprotein 2b3a complex, which inhibits platelet aggregation.

Approved for UA, NSTEMI, STEMI



Platelets are affected for the remainder of their life span.
Upon stopping, it takes approximately 5 days to see an improvement in bleeding times and platelet activation

Must stop 5 days prior to surgery


CURE Trial

CURE: In those with USA/NSTEMI. Significant risk reduction in CV death, MI, CVA at 12 months with ASA + Plavix compared to ASA plus placebo. RRR of 20%, ARR of 2%

Found that patients that received a stent (PCI) had even better risk reduction



Not used much anymore due to side effects:
Neutropenia (2%)
TTP (1 in 4000)
Aplastic anemia (1 in 8000)



Binds irreversibly to the ADP receptor on platelets for their lifespan.
Prasugrel has a greater antiplatelet effect than clopidogrel because it is metabolized more efficiently.
Results in less MACE compared to Plavix
At expense of increased bleeding rates

Also used in conjunction with aspirin
In those undergoing PCI with unstable syndrome only


Direct P2Y12 Inhibitors

Ticagrelor (Brilinta); similar to prasugrel and clopidogrel

Doesn’t need to be metabolized by liver to become active component
Binds directly, faster, and more reliable
Higher risk of bleeding = always this trade off for these meds


Glycoprotein 2b/3a Inhibitors

Very potent
Assess bleeding risk
Additive when used with other agents
Monitor aPTT closely when using unfractionated heparin
Caution in elderly, females, low body mass
Side Effects: bleeding, Thrombocytopenia

Always use in conjunction with aspirin and anti-thrombins
NSTEMI and unstable angina mostly


TIMI Risk Score

TIMI Risk Score: predicts risk of death, new/recurrent MI, need for urgent revascularization within 14 days

Score of 3-4 = pretty high risk


Thrombin Inhibitors

Heparin: accelerates activity of antithrombin
Thus inactivates factors IIa (thrombin), IXa & Xa

Enoxaparin (Low molecular weight heparin)
Inhibits Factors Xa & IIa (thrombin)

Fondaparinux: inhibits Factors Xa


Heparin vs. Enoxaparin (LMWH)

Weight adjusted dose with variable patient response
Continuous infusion and monitor aPTT
Half life = 90 minutes
Reversal with protamine
Preferred by interventionalist

Weight, adjusted dose with no significant variability
Sq dosing usually bid
No monitoring required
Half life = 270 minutes
No clear reversal agent
Caution with renal disease


Thrombin Inhibitors Side Effects


Heparin induce thrombocytopenia (HIT)
10% of patients after 5 days of therapy (less with enoxaparin)
Monitor CBC daily
Stop heparin with > 50% decrease of PLTs
Measure heparin associated platelet antibody
Start direct thrombin inhibitor
Watch for arterial thrombosis (“white clot”)


Thrombin Inhibitors Use

In conjunction with ASA, thienopyridines and possibly 2b/3a inhibitors.
USA: Usually used until cardiac enzymes are negative or taken to cath lab.
NSTEMI/STEMI: Used until after intervention performed.


Beta Blockers Contraindications

Caution with:
History of asthma
Bradycardia (HR 110



No clear benefit
Probably reasonable if still hypertensive with Beta blocker already on-board

Clear mortality benefit
Started if not hypotensive on B-blocker
Goal is to start before hospital discharge


ACE Inhibitor Side Effects

Anaphylaxis (Angioedema)

Side Effects
Renal dysfunction



Endothelial-independent vasodilator
Decrease Myocardial O2 Demand

If you decrease preload then get reflex tachycardia and that causes increase O2 demand so need to give with a beta blocker


Preventing Recurrent Events: Post-Hospitalization Suggestions

All Patients with ACS:
BP management
Tight control of DM
Smoking cessation
Cardiac Rehab: 36 sessions over 12 weeks
Diet, Exercise, and Psychosocial counseling


Preventing Recurrent Events: Post-Hospitalization Medications

Bulk of effect of beta blockers is the first 2-3 years after infarct, so may see patients taken off these after a few years
ACE inhibitors and statins should remain indefinitely
ASA 81 mg indefinitely
Clopidogrel 75 mg for at least 12 months, or in some cases prasugrel or ticangelor
Lipid therapy to keep LDL