ACS NSTEMI med tx Flashcards

1
Q

med therapy of NSTEMI

A
ASA
anticoag
} Beta blockers
} ACE inhibitors
} Statin therapy
} Nitroglycerin (long-acting vs rescue)
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2
Q

beta blockers

A

} Anti-ischemic
} Reduction of tachyarrhythmias
} Prevention of adverse remodelling

} Oral beta blockade to be started within the
first 24 hours unless:
◦ Heart failure
◦ Risk for shock or evidence of low output state
◦ Contraindications – i.e. heart block
◦ In these cases, beta blocker initiation may need to
be delayed to when the patient is more stable

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3
Q

Who should continue oral beta blockers

long-term?

A

◦ All patients with heart failure or left ventricular
systolic dysfunction (LVSD)
◦ All others, except those at low risk (by score or
assessment at follow-up) or with contraindications
} Target doses if tolerated:
◦ metoprolol 100mg BID
◦ carvedilol 25mg BID
◦ bisoprolol 10mg daily

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4
Q

ACEi and NSTEMI

A

} Continued indefinitely for cardiovascular protection, if no contraindications
◦ Dosing from different trials in stable CAD
} Heart failure or left ventricular systolic dysfunction (LVSD)
} Hypertension, diabetes or stable chronic kidney disease
} ARBs for those intolerant of ACEi
} Hypotension, hyperkalemia and renal dysfunction

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5
Q

statin therapy and NSTEMI

A

} Acute management of unstable atheroma
} Early and intensive statin therapy (in comparison to
placebo) significantly decreased combined endpoint of death, MI, cardiac arrest and recurrent ischemia
} Initiate high intensity statin therapy
◦ Atorvastatin 80mg po daily
◦ Rosuvastatin 40mg po daily

} For ACS, more intensive statin therapy long-term decreased clinical events
} Intensive vs less intensive comparisons rather than specific LDL level achieved

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6
Q

nitroglycerin and NSTEMI

A

} Long-Acting
◦ No benefit on clinical outcomes
◦ Useful for recurrent angina if treatment does not preclude beta blockers
◦ Importance of nitrate free interval

} Useful chronically for symptomatic management of stable angina

} Sublingual for rescue
◦ All patients should have available

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7
Q

recommendations for MRAs and PPIs

A

MRAs are recommended in patients with heart failure with reduced LVEF (<40%) in order to reduce all-cause and cardiovascular mortality and cardiovascular morbidity.

Proton pump inhibitors
Concomitant use of a proton pump inhibitor is recommended in patients receiving aspirin monotherapy, DAPT, DAT, TAT, or OAC monotherapy who are at high risk of gastrointestinal bleeding in order to reduce the risk of gastric bleeds

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8
Q

secondary prevention recommendations for ACS

A

} Referral to a comprehensive outpatient
cardiovascular rehabilitation program
} Reasonable to screen for depression
} Annual influenza vaccination and pneumococcal vaccination initially and at 5 years

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9
Q

tobacco use

pharmacist role

A
} At every visit:
◦ Ask about tobacco use
◦ Advise users to quit
◦ Assess willingness to quit
◦ Assist by counselling and development of plan for
quitting – including pharmacotherapy and/or
referral as required
◦ Arrange follow-up
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10
Q

bleed risk with low dose ASA

A

} ASA vs placebo
◦ Risk of any major bleed 1.71 (1.41-2.08)
◦ Risk of major GIB 2.07 (1.61-2.66)
NNH=833 at one year

Doub;les risk of bleed from placebo

} 5 year observational cohort from Denmark
◦ RR of hospitalization for upper GIB with low-dose
ASA alone 2.6 (2.2-2.9)
◦ No difference with enteric coated and uncoated ASA

Baseline bleed risk is quite low so baby ASA a day is ok
Dual antiplatelet further increases the risk
Intracranial bleeding

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11
Q

bleed risk with dual antiplatelet
tic + ASA more bleeding than ASA alone
dual tx with tic + ASA does not sig increase major b leeding compared to clop + ASA

A

ASA vs ASA/clopidogrel (CURE)
◦ Risk of any major bleed RRR 0.27 (0.12-0.40)
◦ Risk of major GIB RRR 0.44 (0.20-0.61)
◦ Risk of intracranial bleed NS

} Clopidogrel vs ASA/clopidogrel (MATCH)
◦ Risk of any major bleed RRR 0.58 (0.45-0.68)
◦ Risk of major GIB RRR 0.66 (0.49-0.77)
◦ Risk of intracranial bleed NS

further increases bleeding

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12
Q

TIMI majopr bleeds
one type of scoring system
cohorts

A

◦ Any intracranial bleeding
◦ Bleeding that results in death
◦ Clinically overt signs of hemorrhage associated with
a drop in Hgb of >50
} Rates of 2-3% with dual antiplatelet therapy

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13
Q

nuisance bleeding with dual antiplatelet tx

A

} Single center observational study of 2360
patients with DES implantation
} Bleeding events included superficial – easy
bruising, bleeding from small cuts, petechia,
ecchymosis, as well as internal and alarming
} Telephone follow-up or office visit
} Bleeding events self-reported

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14
Q

diff tyoes of bleeding events (3)

A

} 32.5% of patients reported bleeding events
} Most bleeding events were classified as
} Nuisance – 85.7%
} Internal – 13.6%
} Alarming – 0.7%

rates of d/c tx high in intrnal bleeding vs nuisance, highest dropout in clopidogrel
least with both therapy

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15
Q

chronic DAPT therapy

considerations

A

} Careful patient hx, physical examination
and assignment to therapy
◦ Individual patient’s risk factors
◦ Impact of non-cardiac concomitant therapies
} Appropriate duration of antithrombotic
regimens
} Consider use of proton pump inhibitors for
mitigating GI bleed risk
} Consider more frequent monitoring and
closer follow-up in high risk patients

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16
Q

Factors associated with increased
bleeding risk

} Patients need to be aware of the signs of
serious bleeding and understand when they
need to seek medical attention
} Patients need to know to contact a health
care professional to ensure appropriate
management if they experience side effects
that may be due to antiplatelet therapy,
rather than just stopping the medication

A
  1. Need for OAC in addition to DAPT
  2. Advanced age (> 75 years)
  3. Frailty
  4. Anemia with hemoglobin < 110 g/dL
  5. Chronic renal failure (creatinine clearance < 40 mL/min)
  6. Low Body Weight (< 60 kg)
  7. Hospitalization for bleeding within last year
  8. Prior stroke/intracranical bleed
  9. Regular need for NSAIDS or prednisone
17
Q

what are otehr AE of ticagrelor

A

◦ Mild and usually self-limiting dyspnea
◦ 1/3 of patients will have resolution within a week
◦ Considered reversible upon discontinuation
◦ Need for investigation of new, prolonged or
worsening dyspnea
◦ Limited data in patients with asthma and COPD

dysnea higher with tica than clopid

18
Q

what are otehr AE of clopid

A
~4% of patients
◦ Pruritic macular erythematous confluent rash on
trunk
◦ Usually presents on day 6 of therapy
} Ticagrelor as alternative
19
Q
clopid responsiveness
2 factors (20
A

} Genetic
◦ Polymorphism

} Pharmacokinetic
◦ Prodrug
◦ Reduced generation of active metabolites due to
variability in intestinal absorption and CYP450 2C19
availability / activity

20
Q

interaction b/w clopid and PPI

A

We recommend selective use of PPIs in patients
receiving DAPT at high risk of upper
gastrointestinal bleeding

We suggest that prescribing a PPI that minimally
inhibits CYP2C19 (e.g. pantoprazole) be considered
in patients receiving a PPI with clopidogrel
21
Q

ticagrelor admined with CYP34a inhibitors

A

} Concurrent administration with ketoconazole
increased the Cmax of ticagrelor 2.4-fold and
AUC 7.3-fold
} Cmax of the active metabolite reduced 89%
and AUC of active metabolite reduced 56%
} Co-administration of any strong 3A4
inhibitor is contraindicated

22
Q

ticagrelor admined with CYP34a inducers

A

} Concurrent administration with rifampin decreased the Cmax of ticagrelor 73% and AUC 86%
} AUC of active metabolite reduced 46%
} Platelet aggregation inhibition reduced by 27%
} Co-administration of any strong 3A4 inducer
is contraindicated

23
Q

pharmacodynamic of tic

A

Increased risk of bleeding when combined
with other agents that also increase this risk
} Addition of oral anticoagulants (including
DOACs) likely increase bleed risk two-fold
} Caution re multiple prescribers and intent

24
Q

predictors of discontinution

A

Older
} Less likely to have completed high school
} Less likely to be married
} More likely to avoid health care due to cost
} Pre-existing cardiovascular disease
} Anemia at presentation
} Less likely to have been given discharge
instructions re medications
} Less likely to have been referred to cardiac
rehab

25
Q

discontinuation and one-year mortality

A
} All cause mortality 7.5% for patients who
discontinued clopidogrel within 30 days
compared to 0.7% for those who continued
therapy (P<0.0001)
} After adjustment, HR 9.02 (1.3-60.6)

Non-adherence to medication is associated with increased mortality
} Education level (possibly health literacy) appears to be a risk factor for discontinuation of therapy
} Health policy can also impact patient compliance

26
Q

what pharmacists can do to improve adherence

A
Patient education
} Pharmacists should address cost issues
} DAPT should be included in automated
follow-up systems
} If antiplatelet agents are discontinued for a
procedure, patients should receive clear
written and verbal directions on when to
resume therapy
27
Q

key educational messages for dual antiplatelet therapy

A

} ASA is lifelong therapy
} Patients should know the duration of their
DAPT and the potential consequences of early
discontinuation or non-adherence
} Patients should know to inform other HCP that they are taking antiplatelet agents and that they should not stop their ASA or antiplatelet agents without speaking with their cardiologist
} pt need to be aware of the signs of serious bleeding and understand when they need to seek medical attention
} pt need to know to contact a HCP to ensure appropriate management if they experience side effects that may be due to antiplatelet therapy, rather than just stopping the medication