The Pharmacological treatment of acute coronary syndrome

Question 1

2 ways that coronary disease can present

Answer 1

1) Stable coronary artery disease

2) Unstable coronary artery disease

Question 2

Causes of instability

Answer 2

1) Inflammation
2) Shear stress
3) Oxidative stress
- all lead to development of atherosclerotic plaque that may rupture producing a thrombus (atherothrombosis)

Question 3

Rationale for drugs used in treatment of acute coronary syndrome - categories (targets)

Answer 3

1) Antithrombotic therapy
2) Plaque stabilization
3) Cardioprotection
4) Symptom relief

Question 4

Antithrombotic therapy examples + rationale

Answer 4

• antiplatelet agents
• antithrombins
• improve blood supply

Question 5

Plaque stabilization examples + rationale

Answer 5

• cholesterol lowering drugs (statins)

- reduces recurrent thrombosis

Question 6

Cardioprotection examples + rationale

Answer 6

• beta blockers
• statins
• prevents ischemic related complications

Question 7

Symptom relief example

Answer 7

Nitroglycerin

Analgesics

Question 8

How to improve coronary blood supply mechanically

Answer 8

Percutaneous coronary intervention

Question 9

How to improve coronary blood supply pharmacologically

Answer 9

Dissolve the offending obstruction (antiplatelet and antithrombin therapy)

Question 10

Targets for antithrombotic therapy

Answer 10

1) Platelets

2) Fibrin

Question 11

How to block fibrin

Answer 11

Target components that produce thrombin in the coagulation cascade
Becauses thrombin then converts fibrinogen into fibrin

Question 12

Targets antiplatelet therapy

Answer 12

Things that cause activation of platelets:

Serotonic, epinephrine, thromboxane A2, ADP, Collagen, TF, thrombin

Question 13

Standard antithrombin therapy

Answer 13

Unfractionated heparin (UFH)

Question 14

Standard antiplatelet therapy

Answer 14

Aspirin (ASA)

Question 15

MOA of unfractionated heparin

Answer 15

1. Binds to AT
2. AT/UFH combo binds FXa or thrombin
   Bind in Xa: II -1:1 ratio

Question 16

MOA of ASA

Answer 16

-inhibits throboxane A2 (factor that leads to platelet activation and aggregation)

Question 17

MOA LMWH

Answer 17

• binds to AT

- LMWH AT complex binds to FXa and thrombin in 3-4:1 ratio

Question 18

MOA Clopidogrel/Prasugrel/Ticagretor + negative effect

Answer 18

• blocks ADP mediated platelet activation

- works but some bleeding

Question 19

MOA statins

Answer 19

1) block acetate --> cholesterol
Leads to
-decrease LDL production
-upregulation of LDL receptors
-decrease serum LDL

Question 20

Pharmacological ways to reduce MVO2 (4)

Answer 20

1) Reduced afterload
- via vasodilation
- ca2+ blockers, beta blokers, RAS antagonism
2) Reduction in contractility
- via beta 1 blockade or ca2+ blockage
- B blockers, Ca2+ blockers
3) Reduction in preload
- via venodilation
- diuretic, nitroglycerin
4) Increase in fibrillatory threshold
- via B-1 blockade
- beta blocker

Question 21

Contraindications for beta blocker use as treatment of acute MI

Answer 21

-HR < 60
SBP 0.24 seconds
2nd or 3rd AV block
Severe bronchoplastic lung disease

Question 22

How can blocks RAS

Answer 22

1) Block renin - aliskerin
2) Block ACE - ace-inhibitor
3) block aldosterone - spironolactone, eplerenone
4) block angiotensin receptor (AT1) - ARB