Pharmacotherapy for Stable Ischemic Heart Disease

Question 1

What drugs are used to prevent SIHD?

Answer 1

Anti-platelets
ACEi
Statins
(beta blockers for those with previous MI)

Question 2

What are to manage symptoms of SIHD?

Answer 2

Beta-blockers
Calcium channel blockers
Nitrates

Question 3

What processes increases O2 demand at the heart?

Answer 3

increased heart rate
increased contractility
increased ventricular wall tension

Question 4

What kind of drug is ASA?

Answer 4

antiplatelet

Question 5

How does ASA prevent thrombosis?

Answer 5

inhibits platelet aggregation via thromboxane A2 being not produced from arachnodoic acid (COX-1 inhibition)

Question 6

Is ASA essential for all patients?

Answer 6

YES (prevention and management)

Question 7

How does clodipogrel inhibit thrombosis?

Answer 7

inhibits platelet aggregation via P2Y12‐ADP receptor antagonism

Question 8

T or F: there is increased bleeding with dual antiplatelet therapy

Answer 8

T

Question 9

Is clodipogrel essential?

Answer 9

NO –> only if ASA contraindicated

Question 10

Which drug is termed vascular protective?

Answer 10

ACEi

Question 11

Why do we give ACEi in SIHD?

Answer 11

– decrease in progression of atherosclerosis
– plaque stabilization
– decrease in neointimal formation
– ventricular remodeling
– endothelial function
– fibrinolysis

Question 12

When do we recommend ACEi?

Answer 12

-in all patients esp in those with post-MI, systolic heart failure, DM neuropathy

Question 13

What some adverse effects of ACEi?

Answer 13

lightheadedness, angioedema, hypotension (othostasis), renal dysfunction, hyperkalemia

Question 14

T or F: Do not put someone on ACEi if they have angioedema, bilateral renal stenosis, or is pregnant

Answer 14

T

Question 15

What is the method of action for statins?

Answer 15

• decrease cholesterol synthesis in liver

- increase LDL-C receptors

Question 16

T or F: statins may cause GI issues and myopathy

Answer 16

T

Question 17

What is the cardiac effects of beta blocker?

Answer 17

↓Cardiac sympathetic tone:
– Chronotropy (heart rate)
– Inotropy (contractility)
– Dromotropy (electrical conduction)
– Lusitropy (relaxation)

Question 18

What are the vascular effects of beta blocker?

Answer 18

Vascular effects:

‐ Mild vasoconstriction (unopposed alpha effects)

Question 19

What is the effect of beta blocker on SIHD?

Answer 19

Delays or eliminates angina during exercise
– limits in HR & BP during exercise (allows for proper diastolic filling of coronaries)

–> decreases death and recurrent MI

Question 20

What are the contraindication for BB?

Answer 20

Reactive airway disease like asthma
2 or 3 blocks
Decompensated HF

Question 21

What are adverse effects of BB?

Answer 21

• fatigue
• hypotension, bradycardia, decrease tolerance to exercise
• bronchospasm
• impotence

Question 22

Which areas do calcium channel blockers target and what is their mode of action?

Answer 22

Competitive antagonist of L‐type calcium channels
• vascular smooth muscle, cardiac myocytes, nodal tissue
(SA and AV node)
• MOA: decreased calcium available for contractile elements,
smooth muscle relaxation and vasodilation

Question 23

What’s the effect of CCB on the heart?

Answer 23

Depending on the agent may have:
– decrease in inotropy (demand)
– decrease in chronotrophy (supply and demand)
– decrease in dromotropy, conduction velocity (supply and demand)
– vasodilation, coronary and systemic (supply and demand)

Question 24

What the main difference between non-dihydropyridines and dihydropyridines CCBs?

Answer 24

NDHP –> SA/AV superior decrease conduction
DHP –> only vasodilates peripheral more than coronary

The dihydropyridines are more vascular selective and the non-dihydropyridines are more myocardial selective and tend to reduce the heart rate.

The dihydropyridines, which are predominantly vasodilators and generally have limited chronotropic and inotropic effects, and the non-dihydropyridines, which are less potent vasodilators and also slow cardiac contractility and conduction

Question 25

Is BB or CCBs used for coronary spasms?

Answer 25

CCBs

Question 26

Is BB or CCB first line?

Answer 26

BB

Question 27

Is the short or long acting DHPs responsible for increasd CV risk from drop of BP?

Answer 27

short acting

Question 28

T or F: long acting DHPs are used for managing SIHD symptoms

Answer 28

T

Question 29

What are some adverse effects of CCBs?

Answer 29

- Hypotension, brady‐/tachycardia, heart block, decreased exercise tolerance - Peripheral edema (DHP) (Dose related, 20%)

Question 30

What are some contraindications for CCBs?

Answer 30

- 2nd or 3rd degree heart block or sick sinus syndrome without a pacemaker (NDHP) • Hypotension • Bradycardia (NDHP) • Heart failure with reduced ejection fraction [HFrEF] (except amlodipine [DHP])

Question 31

What drug interacts with CCB?

Answer 31

Digoxin and BB --> decreased BP

Question 32

T or F: CCB has effect on liver enzymes

Answer 32

T: 3A4 subtrate and inhibitor

Question 33

What is the mode of action of nitrates?

Answer 33

– Vasodilation: • Converted to nitric oxide by vascular endothelium • Activates cGMP ‐> decreased cellular calcium ‐> smooth muscle relaxation and vasodilation

Question 34

How does nitrates improve exercise tolerance and time to onset of angina and ischemic threshold?

Answer 34

– Systemic vasculature: • Vasodilation: – Venodilation: decrease venous pressure and preload – Vasodilation: decrease arterial pressure (small effect) – Cardiac • decrease preload/afterload = decrease wall stress = decrease O2 demand – Coronary • decrease vasospasm • Vasodilation (primary epicardial vessels) = ↑subendothelial perfusion = ↑ O2 delivery (minor mechanism)

Question 35

T or F: nitrates are second line and okay for vasospasms

Answer 35

T: CCB first line

Question 36

What should patents receive with angina at ER?

Answer 36

fast acting nitroglycerin

Question 37

T or F: nitrates tolerance does not occur

Answer 37

F: | occurs and requires an 8-12 hours nitrate free period

Question 38

What are instructions for fast acting NTG use?

Answer 38

– Stop and sit down (avoids presyncope/ syncope) – After one dose, if NO relief or gets worse → call 911 – If improves, but does not resolves wait 5 minutes, take a second dose, if NOT resolved in 5 minutes → call 911 and take another dose – Can continue to take q5min until EMS arrives

Question 39

What are adverse effects of nitrates?

Answer 39

flushing headache hypotension

Question 40

What are contraindications for NTG?

Answer 40

– Severe aortic stenosis (pre‐load dependent) - Use of sildenafil (Viagra®, Revatio®), vardenafil (Levitra®), tadalafil (Cialis®) • Inhibits the breakdown of NO by PDE5 inhibitor • coadmin = increased risk of life‐threatening hypotension (very high NO)