MT2_9_Chronic Stable Angina Flashcards
What is significant CAD defined as?
- CAD greater than or equal to 70% diameter stenosis of one major epicardial artery
- greater or equal to 50% diameter stenosis from left main coronary artery
- vasospasm, uncontrolled HTN, valvular heart disease, hypertrophic cardiomyopathy
Define stable angina
- predictable, not changing in frequency, intensity, or duration
Define unstable angina
- presents as rest
- new onset (less than 2 months)
- severe pain that is more frequent, longer duration, lower threshold
What are the considerations for high risk unstable angina?
- more than 20 min
- pulmonary edema
- hypotension
- angina at rest w ST elevation
- worsening MR murmur
- s3, new worsening rales
Lifestyle modifications for CAD?
- reduce cholesterol
- reduce saturated fat
- increase unsaturated fat
PE requirement
Lipid Management
Diabetes management
- moderate intensity 30-60min 5d/week, or vigorous for 20min, 3d/week
- lipid management goal LDL less than 70, or high intensity statin
- diabetes: HbA1C less than 7
Explain how NSAIDs and Aspirin work
- at low doses, aspirin inhibits cox-1, inhibiting clots from forming and sparing PG anti-thrombotic properties. The higher the dose, the more thrombotic patient will get.
Safest COX2 inhibitor?
Pain management strategy in CVD?
- avoid, but naproxen is ok
- apap, ASA, opioids, then non COX2 selective NSAIDs
What is the general approach to treating CSA?
- balance O2 supply and demand (increase supply, decrease demand)
- slow progression of the disease
- provide prophylaxis against thrombus formation
therefore, use
- an antiplatelet
- abtianginal/antiischemic
- disease modifying therapy
Common anti platelets used?
- aspirin
- clopidogrel
- prasugrel
- ticlopidine
- ticagrelor, cangrelor, voraxapar
What to monitor for when patient is on aspirin?
- CBC
- Platelets
- Bleeding (GI)
When is clopidogrel most effective regarding use?
- additive benefit when used in combo with aspirin for UA/NSTEMI or post-PCI
- only used as an alternative to ASA for monotherapy in patients with CAD
Monitoring for clopidogrel?
- CBC
- Bleeding
- DDI
- DC 5 days prior surgery
So what is the recommendation for clopidogrel use?
- when ASA is absolutely CI (75mg daily)
- combo with aspirin post PCI, refractory anginal issues despite revascularization attempts
- anginal issues, not a candidate for revasc.
- ACS
Prasugrel efficacy/use?
Monitor
Dose
CI
DC
BBW
- ONLY inpatients with ACS + PCI.
- more effective than clopidogrel, but higher risk of bleeding
- monitor: bleeding, CBC, plt
- dose 60mg loading, then 10mgQD
- CI: pts with a hx of stroke/TIA
- DC 7-10 days before surgery
- BBW: bleeding
Why is ticlopidine no longer used?
- agranulocytosis ,plt, bleeding risk
Is ticagrelor a prodrug?
What does it do? reduces the rate of ____events and vascular death in ____ vs. clopidogrel, with more ____
no
- thrombotic CV events
- ACS
- higher major bleeding
For ticagrelor, avoid aspirin DC ADR DDI AVOID Pregnancy Dose
- doses higher than 100
- 5 days before surgery
- bleeding/dyspnea
- DDI w 3A4/5 substrate
- avoid in severe hepatic impairment
- category C
- 180mg PO load, 90 PO BID
Cangrelor monitoring and ADRs
Dose
- monitor for bleeding, do not give with clopidogrel or prasugrel
- preg C
NOT FOR CSA
30mcg/kg IV bolus, then 4
Vorapaxar MOA Indication CI DDI
- par1 receptor antagoinst
- oral, competitive reversible binding
- reduce the risk of heart attacks, stroke, death, in patients with PREVIOUS MI or PAD
- CI in CVA or TIA
- DDI: 3A4 inhibitors and inducers
What are the main drugs NOT recommended in CSA? (3)
- ASA + clopidogrel + warfarin (only for CAD), or in patients who had a PCI with a need for warfarin
- dipyridamole (increases induced ischemia)
ticolpidine
CSA anti platelet recommendations?
- Aspirin
- Clopidogrel, only when ASA is CI
- clopidogrel + ASA in refractory ischemia or post PCI
- ticagrelor (only if started on when pt had ACS)
- vorapaxar for refractory patients
What is the main role of antianginals? Name them
Increasing supply
- BB, CCB, Nitrates, Ranolazine
Non cardioselective BBs
- ptns (propanolol, timolol nadolol, sotalol)
Cardioselctive BBs
maa
metoprolol, atenolol, acebutolol
ISA BBs
acebutolol, pindolol, oxyprenolol
Lipophilicity of BBs
propanolol>metoprolol>atenolol
How do BBs work?
- decrease demand by decreasing HR and contractility
- increase supply by increasing diastolic time and decreasing after load
- blocks sympathetic effects
What to monitor when pt is on a BB?
- CP
- HR (goal is 55-60) to lower the MVO2
- BP due to rebound HTN
- EKG
- Bronchospasm (if pt is on a steroid and a LABA) no BB! not even a cardioselevtive one!
- cocaine alpha 1 is vasoconstriction, avoid BB because it inhibits only beta, leaving alpha
Should CAD patients get a BB?
Depression
Renal issues
When is a BB CI?
- yes, w/wo prior hx of MI
- all patients w IHD should get a BB
- no propanolol
- no atenolol
- acute ischemia caused by cocaine/stimulant OD
For CCBs, what do we monitor for?
- HR
- BP
- DDI (d and v)
- peripheral edema
- constipation
- HA, flushing, dizziness
For nonDHP CCB, what to look out for? CI?
- bradycardia
- heart block
- do not use if LVEF is less than 40%
- CI in heart failure and severe AV block
For DHP CCB, look out for…
- reflex tachycardia
- peripheral edema
Sp, when are CCB indicated?
- substitute for BB or add w BB if tx is unsuccessful with a BB, no difference if DHP or NDHP
- avoid short acting DHP (nifedipine)
What is the DOC for ischemia secondary to vasospasm. (prinzmetal) or due to cocaine/stimulant use?
CCBs!
What is the MOA of nitroglycerin?
- decrease in demand by decreasing preload and/or after load, decreasing wall stress
- coronary artery vasodilatation, increase supply
Compared to BB and CCB, do nitrates affect long term outcomes?
- reduce in anginal frequency, and increase in exercise tolerance
- no effect on long term patient outcomes though
What to monitor for nitro?
- BP
- HR
- Headache
- nitrate free interval
What is the recommendation for immediate relief of angina? regarding nTG
- spray
- substitute for BB or add on
- SL Nitro 0.4mg q5min once, then ER if doesn’t work
How does ranolazone work?
- inhibits late sodium from going into the cell, to decreses contractility, HR, decreasing demand.
- is preferred bc it has no effects on HR and BP, so pt with a low BP may use it
What to monitor for ranolazine?
Cyps
PGP
- ADR: constpiation, NV, headache, QTc prolongation
- caution in cyp3A4 inhibitors with will increase ranolazine levels (dilt,verap, azaleas, macrolides)
- pgp substrates like digox will increase ranolazine levels
- avoid use with other meds that cause QTc prolongation (antiarrhythmics)
When to recommend ranolazine? Dose?
- adjunct therapy for STABLE patients with REFRACTORY angina OR as monotherapy
- dose initially 500mg PO2x, then 1000mg 2x
What meds are used to modify the artherosclerotic process?
ACE, ARBs, lipid lowering therapy
What is the MOA of ACE inhibitors?
- counteracts effects of vasoconstriction, fluid retention, cardiac remodeling, inhibiting ACEI or blocking the AT1 receptor
- increases bradykinin (vasodilatory)
What have ACEI been shown to improve?
- long term outcomes post MI
When should patients recieve an ACE?
- stable CAD + DM and/or LV dysfunction
including those w HTN,DM, CKD
What to monitor for in ACE/ARB?
- BP
- Renal fx
- serum K
- angioedema
cough, dysguesia
When should an ACE be initiated?
- all patents post MI, continued indefinitely
- early in stable high risk patient
When is an ACE inhibited?
- AKI (significant increasing SCr trend)
- severe chronic kidney disease (SCr greater than 3.0)
What are the lipid goals in patient with CAD?
- LDL less than70 (high risk)
- TG less than 150
HDL greater than 40(m), 50(w) - TC less than 200e
- high-intensity statin is recommended in ALL CAD PATIETNS regardless of LDL
What to monitor for a statin?
- LFT
- Myopathy
- CK
- DDI
