1
Q
systolic injury current
A
- shortening of AP causes intracellular potential of ischemic cells to be more negative than normal cells (they don’t depolarize enough)
- intracellular positive current flows from normal cells to ischemic ones
- occurs during systole (phases 2 and 3)
2
Q
Aspirin
A
- antiplatelet drug
- irreversibly inhibits platelet COX –> blocks thromboxane A2 formation
- uses: stable angina, unstable angina, acute MI, prophylaxis
3
Q
Ticlopidine
A
- antiplatelet drug
- alternative to asprin
- inhibits platelet aggregation induced by ADP
- also reduces blood viscosity by decreasing plasma fibrinogen and increases red cell deformability
- hasn’t shown decrease in adverse events in PTs with stable angina
- induces neutropenia and rarely TTP (need to draw blood regularly) –> not really used anymore
4
Q
Clopidogrel (Plavix)
A
- antiplatelet drug
- irreversibly inhibits binding of ADP to platelet receptor –> blocks activation of gpIIb/IIIa complex
- greater antithrombotic effect than ticlopidine but higher risk of bleeding
5
Q
Prasugrel (Effient)
A
- antiplatelet drug (alternative to clopidogrel)
- irreversibly binds P2Y12 receptor (chemoreceptor for ADP)
- reduces thrombotic events in those with PCI (stent)
- more potent/efficaious than clopidogrel but greater risk of bleeding
- limited to PTs <75 y/o, >60 kg, no hx of TIA or stroke
6
Q
Ticagrelor
A
- antiplatelet (clopidogrel alternative)
- similar in structure to adenosine –> reversibly blocks ADP receptors
- more potent that clopidogrel but greater risk of bleeding
- no hepatic activation required –> faster onset of action and elimination than clopidogrel or prasugrel
- black box warning: doses of aspirin > 100 mg decrease effectiveness of ticagrelor
7
Q
Dipyridamole
A
- antiplatelet agent
- increases platelet cAMP –/ phosphodiesterase –> adenylate cyclase –/ uptake of adenosine
- uses: adjunct tx in PTs with peripheral vascular disease, stress test
- use is limited bc it vasodilates coronary aa which can enhance exercise-induced ischemia due to coronary artery stealing
8
Q
Cilostazol (Pletal)
A
- quinolone antiplatelet drug
- inhibits phosphodiesterase like dipyridamole
- uses: tx for claudication with peripheral vascular disease due to vasodilationr effects (don’t want it to act centrally on coronary aa –> coronary artery stealing)
9
Q
Lipid-lowering agents
A
- LDL-reducing agents decrease risk of adverse ischemic events in patients with established CAD
- 4S trial showing that treating with statin reduced mortality and major coronary events by 30-35% in PTs with known CAD
- everybody gets a statin now but the question is when to start it in the setting of primar prevention
10
Q
ACE Inhibitors
A
- captropril (shortest acting- dose 3x/day), enalapril, lisinopril, ramipril, quinapril, fosinopril
- HOPE trial showed that ACEI reduced incidence of cardiovascular death, MI and stroke in PTs at high risk for or had vascular disease
- BP was only slightly reduced in these PTs
11
Q
SE of ACEI
A
- dry cough (10-30%)
- hypotension
- hyperkalemia (decreased aldo)
- angioedema (0.1%)
12
Q
BBs
A
- decrease contractility and HR —> myocardial O2 demand is decreased (limit the amount of ischemia when you already have limited supply)
- most BB used in CAD are beta-1 selective
- beta2 has some vasodilation –> blockage results in small degree of vasoconstriction
- also class II antiarrhythmic agent
- increase survival immediately post-MI (likely a result of their anti-ischemia and anti-arrhythmic effects –> MIs can trigger arrhythmias)
--\> no real role for long-term use in the setting of CAD
13
Q
contraindications to use of BBs
A
- severe bradycardia
- high degree AV block (ie: PR =420 ms)
- sick sinus syndrome
- unstable LV failure (will only decrease contractility further)
- asthma and bronchospastic disease
- severe depression
- peripheral vascular disease (raynaud’s)
14
Q
SE of BBs
A
- fatigue and lethargy (via decreased HR and contractility)
- decreased exercise tolerance
- insomnia (they make you tired but you can’t sleep)
- worsening claudication (leg cramping)
- impotence (cardiologists prescribe the most viagara!)
15
Q
Nitrates (mech)
A
- converted to NO intracellularly –> smooth muscle cGMP –/ Ca influx –> vasodilation
- cause dilation of coronary aa
- venou dilation predominates (decrease preload –> decrease ventricular wall stress –> decreases O2 demand)
- NO inhibits platelet aggregation and leukoycyte-endothelial cell interactions
- oral: isosorbide dinitrate
16
Q
contraindications of nitrates
A
- hypertrophic cardiomyopathy and severe aortic stenosis (both rely on high preload to generate CO)
- significant hypotension
- use of phosphodiesterase inhibitors like Viagara (too much cGMP)
17
Q
SE of nitrates
A
- tolerance
- headaches (vasodilation)
- hypotension
- can activate Bezold Jarisch reflex causing bradycardia
18
Q
CCBs
A
- dihydropyridines are vasoselective –> relieve coronary vasospasm and peripheral vasoconstriction
- non-hydropyridines are selective for myocardium –> negative inotropy, chronotropy
- Net effect: increased O2 delivery and decreased O2 demand
19
Q
CCB contraindications
A
- overt decompensated HF
- bradycardia, sinus node dysfunction or high degree AV block
20
Q
initial interventions
A
- aspirin
- non-coated and chewable for faster absorption
21
Q
unstable angina/non-STEMI
A
- give heparin and gpIIb/IIIa
- **these will prevent the clot from forming!
22
Q
STEMI in the absence of PCI
A
- thrombolytics (plasminogen activators)
- the clot has already formed at this point!
23
Q
comparing the “grel’s”
A
- clopidogrel –> prasugrel –> ticagrelor
- both prasugrel and ticagrelor or more potent than clopidogrel but associated with higher risk of bleeding
- unlike clopidogrel and prasugrel, ticagrelor has a faster onset of action and is eliminated faster (based on its metabolism)
- however, ticagrelor has block box warning about concomitant use with aspirin
24
Q
what drugs have shown a mortality benefit (reduce recurrent MI and death) ?
A
- aspirin
- ACEI
- BB
- Statins
unit 4 pharm
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