Pharmacotherapy for Stable Ischemic Heart Disease Flashcards
What drugs are used to prevent SIHD?
Anti-platelets
ACEi
Statins
(beta blockers for those with previous MI)
What are to manage symptoms of SIHD?
Beta-blockers
Calcium channel blockers
Nitrates
What processes increases O2 demand at the heart?
increased heart rate
increased contractility
increased ventricular wall tension
What kind of drug is ASA?
antiplatelet
How does ASA prevent thrombosis?
inhibits platelet aggregation via thromboxane A2 being not produced from arachnodoic acid (COX-1 inhibition)
Is ASA essential for all patients?
YES (prevention and management)
How does clodipogrel inhibit thrombosis?
inhibits platelet aggregation via P2Y12‐ADP receptor antagonism
T or F: there is increased bleeding with dual antiplatelet therapy
T
Is clodipogrel essential?
NO –> only if ASA contraindicated
Which drug is termed vascular protective?
ACEi
Why do we give ACEi in SIHD?
– decrease in progression of atherosclerosis – plaque stabilization – decrease in neointimal formation – ventricular remodeling – endothelial function – fibrinolysis
When do we recommend ACEi?
-in all patients esp in those with post-MI, systolic heart failure, DM neuropathy
What some adverse effects of ACEi?
lightheadedness, angioedema, hypotension (othostasis), renal dysfunction, hyperkalemia
T or F: Do not put someone on ACEi if they have angioedema, bilateral renal stenosis, or is pregnant
T
What is the method of action for statins?
- decrease cholesterol synthesis in liver
- increase LDL-C receptors
T or F: statins may cause GI issues and myopathy
T
What is the cardiac effects of beta blocker?
↓Cardiac sympathetic tone: – Chronotropy (heart rate) – Inotropy (contractility) – Dromotropy (electrical conduction) – Lusitropy (relaxation)
What are the vascular effects of beta blocker?
Vascular effects:
‐ Mild vasoconstriction (unopposed alpha effects)
What is the effect of beta blocker on SIHD?
Delays or eliminates angina during exercise
– limits in HR & BP during exercise (allows for proper diastolic filling of coronaries)
–> decreases death and recurrent MI
What are the contraindication for BB?
Reactive airway disease like asthma
2 or 3 blocks
Decompensated HF
What are adverse effects of BB?
- fatigue
- hypotension, bradycardia, decrease tolerance to exercise
- bronchospasm
- impotence
Which areas do calcium channel blockers target and what is their mode of action?
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
What’s the effect of CCB on the heart?
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)
What the main difference between non-dihydropyridines and dihydropyridines CCBs?
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
Is BB or CCBs used for coronary spasms?
CCBs
Is BB or CCB first line?
BB
Is the short or long acting DHPs responsible for increasd CV risk from drop of BP?
short acting
T or F: long acting DHPs are used for managing SIHD symptoms
T
What are some adverse effects of CCBs?
- Hypotension, brady‐/tachycardia, heart
block, decreased exercise tolerance - Peripheral edema (DHP) (Dose related, 20%)
What are some contraindications for CCBs?
- 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])
What drug interacts with CCB?
Digoxin and BB –> decreased BP
T or F: CCB has effect on liver enzymes
T: 3A4 subtrate and inhibitor
What is the mode of action of nitrates?
– Vasodilation:
• Converted to nitric oxide by vascular endothelium
• Activates cGMP ‐> decreased cellular calcium ‐> smooth muscle relaxation and vasodilation
How does nitrates improve exercise tolerance and time to onset of angina and ischemic threshold?
– 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)
T or F: nitrates are second line and okay for vasospasms
T: CCB first line
What should patents receive with angina at ER?
fast acting nitroglycerin
T or F: nitrates tolerance does not occur
F:
occurs and requires an 8-12 hours nitrate free period
What are instructions for fast acting NTG use?
– 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
What are adverse effects of nitrates?
flushing
headache
hypotension
What are contraindications for NTG?
– 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)
