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Cardiology > Pharmacotherapy for Stable Ischemic Heart Disease > Flashcards

Pharmacotherapy for Stable Ischemic Heart Disease Flashcards

1
Q

What drugs are used to prevent SIHD?

A

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

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2
Q

What are to manage symptoms of SIHD?

A

Beta-blockers
Calcium channel blockers
Nitrates

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3
Q

What processes increases O2 demand at the heart?

A

increased heart rate
increased contractility
increased ventricular wall tension

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4
Q

What kind of drug is ASA?

A

antiplatelet

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5
Q

How does ASA prevent thrombosis?

A

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

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6
Q

Is ASA essential for all patients?

A

YES (prevention and management)

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7
Q

How does clodipogrel inhibit thrombosis?

A

inhibits platelet aggregation via P2Y12‐ADP receptor antagonism

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8
Q

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

A

T

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9
Q

Is clodipogrel essential?

A

NO –> only if ASA contraindicated

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10
Q

Which drug is termed vascular protective?

A

ACEi

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11
Q

Why do we give ACEi in SIHD?

A 
– decrease in progression of atherosclerosis
– plaque stabilization
– decrease in neointimal formation
– ventricular remodeling
– endothelial function
– fibrinolysis
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12
Q

When do we recommend ACEi?

A

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

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13
Q

What some adverse effects of ACEi?

A

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

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14
Q

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

A

T

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15
Q

What is the method of action for statins?

A
  • decrease cholesterol synthesis in liver

- increase LDL-C receptors

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16
Q

T or F: statins may cause GI issues and myopathy

A

T

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17
Q

What is the cardiac effects of beta blocker?

A 
↓Cardiac sympathetic tone:
– Chronotropy (heart rate)
– Inotropy (contractility)
– Dromotropy (electrical conduction)
– Lusitropy (relaxation)
18
Q

What are the vascular effects of beta blocker?

A

Vascular effects:

‐ Mild vasoconstriction (unopposed alpha effects)

19
Q

What is the effect of beta blocker on SIHD?

A

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

–> decreases death and recurrent MI

20
Q

What are the contraindication for BB?

A

Reactive airway disease like asthma
2 or 3 blocks
Decompensated HF

21
Q

What are adverse effects of BB?

A
  • fatigue
  • hypotension, bradycardia, decrease tolerance to exercise
  • bronchospasm
  • impotence
22
Q

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

A

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

23
Q

What’s the effect of CCB on the heart?

A

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)

24
Q

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

A

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

25
Q

Is BB or CCBs used for coronary spasms?

A

CCBs

26
Q

Is BB or CCB first line?

A

BB

27
Q

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

A

short acting

28
Q

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

A

T

29
Q

What are some adverse effects of CCBs?

A
  • Hypotension, brady‐/tachycardia, heart
    block, decreased exercise tolerance
  • Peripheral edema (DHP) (Dose related, 20%)
30
Q

What are some contraindications for CCBs?

A
  • 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])
31
Q

What drug interacts with CCB?

A

Digoxin and BB –> decreased BP

32
Q

T or F: CCB has effect on liver enzymes

A

T: 3A4 subtrate and inhibitor

33
Q

What is the mode of action of nitrates?

A

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

34
Q

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

A

– 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)

35
Q

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

A

T: CCB first line

36
Q

What should patents receive with angina at ER?

A

fast acting nitroglycerin

37
Q

T or F: nitrates tolerance does not occur

A

F:

occurs and requires an 8-12 hours nitrate free period

38
Q

What are instructions for fast acting NTG use?

A

– 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

39
Q

What are adverse effects of nitrates?

A

flushing
headache
hypotension

40
Q

What are contraindications for NTG?

A

– 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)

Cardiology (29 decks)

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