Pharmacology of Angina and ACS Management

Question 1

How to reduce myocardial oxygen demand

Answer 1

• reduce afterload
• reduce preload
• reduce contractility
• reduce heart rate

Question 2

How restore supply to ischemic tissue?

Answer 2

Prevent further thombosis:
- anti-thrombin (unfractionated heparin) + anti-platelet (ASA)

Reopen the occlusion

• percutaneous catheter intervention (angioplasty, stent)
• surgical (Coronary Artery Bypass Graft)
• pharmacological (fibrinolytics- activate the body’s clot- busting system)

Question 3

Things that aggravate platelets

Answer 3

serotonin, epi, thromboxane A2, ADP, collagen, thrombin, tissue factor

Question 4

What does UFH block?

How does it do this?

Answer 4

• Factor Xa and thrombin

- UFH binds endogenous antithrombin

Question 5

What does ASA block?

Answer 5

ASA blocks thromboxane A2 production

Question 6

What percentage of people do just fine on UFH+ASA therapy and how to guess who won’t?

Answer 6

~80%,
~20% need better intervention
Guess using risk stratification worksheet

Question 7

What is a better alternative to UFH?

Answer 7

low molecular weight heparin (LMWH). It has had it’s sticky bits cleaved so it works better

Question 8

What is the most important side-effect with anti-coagulants?

Answer 8

• you can bleed out

Question 9

3 most important anti-platelets (besides ASA) and what they inhibit

Answer 9

clopidogrel
prasugrel
ticagrelor

**all block ADP mediated activation of platelets

Question 10

What is the effect of bleeding during MI?

Who is most at risk to bleed?

Answer 10

• increases risk of mortality

- female, low BMI, increased age are all independent predictors of bleeding

Question 11

How to stabilize plaques

Answer 11

• use cholesterol lowering drugs to prevent recurrent thrombosis

Question 12

Which anti-cholesterols are known to reduce mortality?

Answer 12

-only statins

Question 13

Effects of statins

Answer 13

• lower serum [LDL]
• increase LDL receptor –> uptake
• anti-inflammatory
• anti-oxidative

Question 14

Vasodilatory drugs used in ACS

Answer 14

• CCB
• B-blocker (via decreased renin release)
• ACEi and ARBs

Question 15

Drugs that reduce contractility in ACS

Answer 15

• CCB

- B-blocker

Question 16

Drugs that reduce heart rate in ACS

Answer 16

• CCB

- B-blocker

Question 17

Drugs that reduce preload in ACS

Answer 17

• diurectics

- nitroglycerin

Question 18

Drugs that increase the fibrillatory threshold

Answer 18

-B-blockers

Question 19

When to avoid the use of B-blockers/CCB?

Answer 19

• if in acute heart failure
• if bradycardic already

-could precipitate cardiogenic shock

Question 20

Differences in AT1 and AT2 receptor actions

-which does ARB block?

Answer 20

AT1: vasoconstriction, cell growth, Na retention, SNS activation, oxidative stress

AT2: vasodilation, antiporliferative, anti-inflammatory, antithrombotic

**ARBs block AT1

Question 21

The general treatment principles of ACS

Answer 21

1) relieve the obstruction
2) reduce inflammation to reduce recurrent events
3) reduce myocardial oxygen demand to limit the damage from ischemia

Question 22

Symptom relief in ACS

Answer 22

• nitroglycerin

- analgesics (e.g. morphine)

Question 23

Examples of fibrinolytics

Answer 23

• tissue plasminogen activator (t-Pa)

- tenecteplase (recombinant mutant of t-Pa)

Question 24

The Canadian Cardiovascular Society (CCS) classification of angina

Answer 24

Grade I. Angina with extreme exertion
Grade II. Angina with more than two flight of stairs
Grade III. Angina with less than two flights of stairs
Grade IV. Angina at rest (unstable angina)

Question 25

New York Heart Association Classification of Heart Failure (NYHA)

Answer 25

I. symptoms with extreme exertion
II. symptoms with moderate exertion
III. symptoms with mild exertion
IV. symptoms at rest

symptoms: shortness of breath

Question 26

Management of stable angina (CCS I–>III)

Answer 26

• Management is conservative and medical
• Conservative includes lifestyle changes (diet, exercise, stress)
• Medical includes anti-hypertensives, anti-platelets (ASA), perhaps B-blockers and acute treatment of nitroglycerin

Question 27

Is management of unstable angina (CCS IV), NSTEMI, STEMI conservative, medical or invasive/surgical?

Answer 27

Usually medical (see other cards) and invasive.

Percutaneous Catheter Intervention can result in angioplasty, drug-eluting stents, or subsequent CABG

Question 28

DDx of chest pain

Answer 28

1. Cardiovascular (acute MI, pericarditis, aortic dissection, aortic rupture)
2. MSK (costochondral syndrome, cervical radiculitis)
3. GI (GERD, peptic ulcer disease, esophageal spasm, biliary colic)
4. Pulmonary (pulmonary thromboembolism, pneumothorax, pneumonia)

Question 29

How to differentiate NSTEMI and unstable angina

Answer 29

• they cannot be distinguished on initial presentation

- UA will not have necrosis, so the cardiac enzymes will distinguish them

Question 30

How to differentiate ACS from other forms of chest pain

Answer 30

History- may have previous history

Pain quality, location, length (pain will be tightness, pressure, squeezing, may radiate up to the jaw, down the arm, and to the epigastrium, MI pain lasts about 1/2 an hour)

ECG

Cardiac enzymes (troponin I or T, CK-MB, lactate dehydrogenase)

Question 31

ACC/ AHA Staging of Heart Failure

Answer 31

Stage A: high risk
Stage B: structural heart disease, but no Sx
Stage C: structural heart disease with symptoms (previous or current)
Stage D: structural disease requiring special intervention

Question 32

Mechanisms of nitroglycerin action

Answer 32

• decreased preload due to venodilation
• increased perfusion pressure due to decreased preload and therefore decreased LVEDP
• decreased afterload due to systemic vasodilation
• increased flow due to coronary vasodilation (at higher doses)