AF3 Flashcards
Antithrombotic Options: AF
ASA, Warfarin, ASA + Clopidogre
summary
Efficacy: u ASA reduces risk of ischemic stroke by 19% u Warfarin reduces risk of stroke by 64% u ASA + Clopidogrel are more effective than ASA, but not as effective as warfarin
Safety: u Bleeding is higher with Clopidogrel + ASA than either ASA alone or Warfarin alone
ASA + Clopidogrel
not best treatment
options
compare DOACs tp warfarin
Dabigatran 150mg bid is
superior to warfarin with a
similar rate of major
bleeding; 110mg is noninferior with lower bleed
Rivaroxaban is non-inferior
to warfarin
with similar rates of
bleeding
Apixaban is superior to
warfarin with a
significantly lower rate
of major bleeding
Edoxaban 60mg daily is non-inferior to warfarin with a significantly lower rate of major bleeding
Role of Pharmacist in AF
Assessment of Patient with AF
Management of Medications
Is antithrombotic therapy indicated? q Is the treatment option effective? q Is the treatment option safe? q Is the patient able to be compliant? Monitoring of Medications and of Patient q How is the patient being monitored for safety and efficacy?
Major Goals and Expected Outcomes
Rapid Heart Rate
Loss of Atrial Kick:
Rapid Heart Rate: • Improvement of Symptoms, Functional Capacity and Quality of Life
Loss of Atrial Kick: • Prevent Complications such as LV Dysfunction
Rate Control Medications
Rate control agents prolong refractory period of the AV
node and act to slow AV node conduction
u βB and non-hydropyridine CCB (verapamil,
diltiazem)will prolong refractory period and slow heart
rate
u Digoxin prolongs refractory period of AV
node by enhancing vagal tone
u As vagal tone is withdrawn, digoxin is not usually
effective during exertion or stress
u Digoxin is therefore generally reserved for older or
sedentary patients or as an add-on to in patient
without adequate rate control on βB or CCB
Rhythm Control: Anti Arrhythmic Drugs (AAD)
IC:
PropafenoneFlecainide
III: amiodarone
dronedarone
III: sotalol
PropafenoneFlecainide
MOA
comments
MOA: • Strong Na+ blockers • Extended refractory period of AV node and accessory tracts
comment • AV node blocker (βB, diltiazem, verapamil) required concurrently/in advance to prevent rapid ventricular rate • Risk of Ventricular Tachycardia (VT)
III: amiodarone
dronedarone
MOA • Multichannel blocker (including K+ and β blockade) • Prolong action potential and refractoriness of slow and fast channel tissues
amiodarone:
• Extremely long t1/2 with increased risk of
extracardiac toxicities (skin, thyroid,
pulmonary, liver, neurologic)
• Prolong QT interval therefore have risk of TdP
• Many drug interactions
sometimes high loading doses
dronedarone: • Similar to amiodarone with shorter t1/2
• Increased risk of mortality in patients with HF
• Increased risk of hepatotoxicity
Sotalol
MOA • Increases AV node refractoriness at higher doses and β blockade at all doses
• Risk of TdP (torsades de pointes) due to QT
prolongation
• Accumulates in renal failure and can lead to
heart block
it is a BB but rarely used just for HTN/BB effects?
Rate vs. Rhythm
Anti Arrhythmic Drugs (AAD)
monitoring
Would it be better for a patient to be in SR? That would improve symptoms and reduce risk of stroke…
Efficacy Outcomes: • Improvement of symptoms/restoration of SR • Reduction in Stroke • Improve survival
Safety Outcomes:
• Side effects (including arrhythmias)
• Mortality
efficacy: not improving, should contact cardiologist and may increase dose, if no benefit, med should be discontinued
anticoagulantis continued
see slide 16
Rate Control vs. Rhythm Control:
AFFIRM
Patients > 65 years with AF + ≥ 1 other risk factor for stroke
Mean age = 70; no mean CHADS2 score reported – ~½ hypertensive, 23%
CHF, 5% valvular disease
Intervention / Comparator:
- Choice of rate control (by clinician)
Digoxin 70.6%
Beta blockers 68.1%
Non-hydropyridine CCB 62.9%
- Choice of rhythm control Amiodarone 39% Sotalol 33% Propafenone 10% Procainamide 6%
+ Anticoagulation with warfarin but it could be
stopped in rhythm control if SR (sinus rhythm) maintained
X 4 weeks
AFFIRM Outcomes:
Mortality
restoration of sr
prevention of stroke
1o End Point Mortality:
Rate Control: 25.9%
Rhythm Control 26.7%
rhythm control hgiher mortality
Efficacy: Restoration of SR
SR in Rate Group: <40%
SR in Rhythm Group: >60%
Efficacy: Prevention of Stroke
Stroke Incidence inRate Group:5.5%
Stroke Incidence inRhythm Group: 7.1%
Key Take-Aways:
u In older patients, rhythm controloffers no survivalbenefit over rate control
u Anti Arrhythmic therapy does not completely suppress AF
u Patients are still at risk of stroke and require stroke prevention therapy
Early Rhythm Control in Patients with AF:
EAST-AFNET 4 Trial
u Patients >18 years old with recent onset AF (<1 year prior to enrollment)
u CHAD2 score of > 2
u Excluded: not suited for rhythm control, severe mitral stenosis, prior AF ablation or
surgical therapy of AF, disease that limits life expectancy to < 1year
ntervention / Comparator:
® Early rhythm control
Usual Care – Initially rate control without rhythm control (rhythm control only used to mitigate uncontrolled AF symptoms during adequate rate control therapy
Outcomes: 10 outcome: composite of death from CV causes, stroke (ischemic or hemorrhagic), or hospitalization with worsening of HF or ACS 10 safety outcome: composite of death from any cause, stroke, or pre specified serious adverse effect Patients followed for 5 years
stroke: Early Rhythm
Control: 91.2%mreceived anticoagulation
Usual Care: 89.7% received anticoagulation
less death in early rhythm
Principles Guiding Rate or Rhythm
Control Selection:
Safety of Anti Arrhythmic Drugs (AAD):
u AAD have only been associated with beneficial effect when initiated in patients with recent onset AF (< 1 year)
u AAD are associate with many adverse effects and selection of AAD is driven by safety and tolerability
u If AAD not providing benefit, it should be discontinued
Efficacy of AAD:
u Long-term AAD may not completely suppress AF (i.e. patient may still have symptoms and would continue to have risk of stroke)
u Patients on both AAD and rate control need to
receiveantithrombotic stroke prevention therapy
Approach to Rate and Rhythm Management of AF
Paroxysmal AF
Self-terminating within 7 days
Low recurrence
burden: observe, if AFib do Pill-in-Pocket AAD
high recurrence burden: maintain AAD tx, keep them on normal sinus rhythm
catheter ablation is an option
Pill In Pocket Approach
which pts
which meds
Which Patients? u Paroxysmal AF, symptomatic with a sustained AF episode (e.g. > 2 hours) u AF usually occurs less frequently than monthly u Symptoms not severe or disabling that require ER visit (e.g. fainting, severe chest pain or breathlessness)
u Which medications?
u AV Nodal Blocker X 1 dose (Diltiazem 60mg X 1
Verapamil 80mg X 1 Metoprolol 25mg X 1)
u 30 minutes later – Class IC Anti Arrhythmic Drug (Flecainade 200 or 300mg X 1
Propafenone 450 or 600mg X1
(lower dose used if <70kg))
Pill In Pocket Approach
pt instructions
u Rest X 4 hours (laying down, seated) u Proceed to ER if: u AF does not terminate within 6- 8 hours u Feel unwell after taking medication u >1 episode in 24 hour period u Severe symptoms (e.g. fainting, severe chest pain or breathlessness) or symptoms of stroke
Non-Pharmacologic Conversion
Options: Catheter Ablation
u Catheter guided ablation of the re-entry loops causing the AF OR u Catheter guided AV node ablation so that rapid impulses in atria not carried to ventricles u Ventricular Pacemaker would be required
pt would be pt dependent
persistent AF flowchart
Persistent AF: > 7 days but <1 year
Long-standing Persistent: > 1 year,
rhythm control being pursued
slide 31
Initiate Rate-control and
consider Long-term treatment
Rhythm-Control preferred with: • Recently diagnosed AF (within 1 year)
• Highly symptomatic or significant QOL impairment
• Multiple recurrences
• Difficulty to achieve rate control
• Arrhythmia-induced cardiomyopathy
Non-Pharmacologic Conversion
Options: Cardioversion
u DC (Direct Current) cardioversion can be
used to electrically convert a patient from AF
to NSR
u Has shown to initially effective in converting >
80% of patients
u Patients must be therapeutically
anticoagulated for at least 3 weeks prior to
cardioversion and at least 4 weeks after
cardioversion (Exception: emergent situations)
see slide 33
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