Does the MET reduce cardiac arrest
Download
Report
Transcript Does the MET reduce cardiac arrest
Atrial fibrillation and DM
Stephen Byrne and Fiona Barton Cardiology CNS
Aims and objectives
What is AF?
How is AF diagnosed?
Why do we care?
Treatment options?
Pharmacology of AF
Case Studies
Questions?
Definition of atrial fibrillation
Atrial fibrillation is an atrial arrhythmia characterised
by predominantly uncoordinated atrial activation with
consequent deterioration of atrial function.
• NICE 2008
Atrial fibrillation
Sinus rhythm
Atrial fibrillation
Multiple foci causing
fibrillation waves
AV node slows conduction to ventricles
A Fib
Atrial flutter
SA node
A single irritable focus
Diagnosing AF
Pulse checks
3 lead monitor, 12 lead ECG, 24/48 hour 7 day Holter monitor
If found
History Clinical examination
CXR ECHO
Labs electrolytes thyroid renal hepatic function FBC BNP is some.
ECG
Classification
Paroxysmal (23%)
Self-terminating (<7 days)
Persistent (38%)
Lasting longer than 7 days
Permanent (39%)
Episodes > 1 year or unresponsive to reversal
Non valvular AF is AF in the absence of rheumatic mitral stenosis, a
mechanical or bioprosthetic heart valve, or mitral valve repair
Epidemiology
Most common presenting arrhythmia in cardiology
Affects 2% of the population
Incidence of AF increasing (13% in last 20years)
Stewart et al Population, prevalence, incidence and predictors of atrial
fibrillations. Heart 2001 86:516-521
Increasing Prevalence with age. Approx 1% of those <60 years
whereas 12% of those in the 75 to 84 year age range.
AHA/ASC Guidelines for management of AF JACC 2014
Why do we care?
Impact of Atrial Fibrillation on the Risk of Death The Framingham
Heart Study
Conclusions—In subjects from the original cohort of the Framingham
Heart Study, AF was associated with a 1.5- to 1.9-fold mortality risk
after adjustment for the preexisting cardiovascular conditions with
which AF was related. The decreased survival seen with AF was
present in men and women and across a wide range of ages.
Circulation 1998:946-952
Rotterdam Study - Ommoord
7983 participants over age 55 years
1990 – 1999
209 cases of AF noted on inception
167 developed new AF over course of study
Over all incidence 5.5%
Prevalence increasing with age
55 – 60yrs 0.7%
85yr and above 17.8%
Heeringa et al 2006 EHJ 27: 949 - 953
Etiology of AF
Atrial dilatation and micro fibrosis are the most important factors
contributing to the occurrence and maintenance of AF
AF is associated with increase in connective tissue between cardiac
cells
Leads to increase deposits of collagen and fibronectin causing fibrosis
Fibrosis within atrial tissues leads to the development of arrhythmias
The appearance of AF is often associated with exacerbation of
underlying heart disease.
Decompensation
Loss of atrial contraction may markedly decrease cardiac output
particularly if diastolic ventricular filling is impaired by mitral stenosis
hypertension hypertrophic or restrictive cardiomyopathy.
Sympathetic activation and vagal withdrawal such as with exertion or
illness accelerate the ventricular response.
Contributing factors
Obesity
15% increase in obesity equates to
a 7.5% increase in AF
Congestive heart failure (41%)
COPD (11%)
Hypertension (71%)
Sleep apnoea
Valvular heart disease (63%)
Ageing
Diabetes mellitus (20%)
Thyroid dysfunction (10%)
Coronary artery disease (36%)
Renal disease (13%)
EORP-AF study Europace 2014;16(3):308-319
Blood clot in the LAA
Risk of Stroke.
Associated with a 5 fold increase risk of stroke and stroke risk
increases with age.
AF related strokes are likely to be more severe then non AF strokes
AHA/ACC/HRS Guidelines JACC 2014
Observed absolute stroke rates for nonanticoagulated patients with
single independent risk factors were in the range of 6 to 9% per year
for prior stroke/TIA, 1.5 to 3% per year for history of hypertension, 1.5
to 3% per year for age >75, and 2.0 to 3.5% per year for diabetes.
Neurology August 7 2007 Vol 69 No 6 546-554
AF non a benign issue!
5 fold increase in Stroke
3 fold increase in Heart Failure
2 fold increase in Dementia
Patients with AF are hospitalized twice as often as patients without
AF: Are three times more likely to have multiple admissions and 2.1%
of patients with AF died in hospital compared to 0.1% without it.
Diabetes patients are at higher risk of AF
Diabetes Mellitus is a strong independent risk
factor for atrial fibrillation atrial flutter.
Control
10.3% A Fib
2.5% A Flutter
DM
14.9% A Fib
4% A Flutter
International Journal of Cardiology Vol 105 Issue 3 P315-318 2005
Symptoms
Symptoms can range from non existent to severe.
Chronic fatigue
Breathlessness on exertion
Palpitations
Syncope/ pre syncope
Chest pain/ tightness on exertion
Tachycardia induced cardiomyopathy
Embolic stroke (5 fold risk of stroke)
Acute Management
Stable or unstable?
Unstable
transfer to hospital
Stable
Rate control
Consider Anticoagulation
Refer for Cardiology opinion.
Initial aims of treatment
Reduce symptoms
Rate control
Beta blockade/ calcium channel blockade
Determine LV function - Echocardiogram
Antiarrhythmic selection
DC Cardioversion
Performed under G.A. (propofol)
Synchronised electrical shock
AP position of pads
Success rate >95%
Risks 1-2%
cardiac arrest (VF/VT) – beware digoxin/ over use of rate control
Stroke
Skin burns
Aspiration
Awake within 5-10min, If fails – proceed to chemical then immediate
DC cardioversion
Post Discharge
Anticoagulation monitoring for further 6 - 8 weeks
If CHADS2VA2Sc score < 2 aspirin 75mg od
If > 2 warfarin, dabigatran or rivaroxaban life-long
Antiarrhythmic continues (long term)
Advice for patients
Avoid alcohol (specifically spirits)
Avoid caffeine
Avoid eating large meals
If palpitations reoccur – get to hospital immediately
C oronary AD
H ypertension
A2 ge >75
D iabetes
S2 troke
V ascular Disease
A ge >65
S ex category (F)
Sites of AF
Radio frequency ablation of AF
The Watchman device to close the left
atrial appendage.
Rate Control and
Pharmacotherpay Options
The management cascade for patients with AF
ACEI = angiotensin-converting enzyme inhibitor; AF = atrial fibrillation; ARB = angiotensin receptor blocker;
PUFA = polyunsaturated fatty acid; TE = thrombo-embolism.
Available Drugs
Vaughan Williams Classification
Class I-Sodium channel blockers
quinidine, disopyramide,
lignocaine
flecainide, propafenone
Class II-Beta blockers
propranolol, atenolol, metoprolol, bisoprolol, nebivolol
Class III- Potassium channel blockers
sotalol, amiodarone, ibutilide
Class IV-Calcium channel blockers
verapamil, diltiazem
Others-Digoxin, Adenosine
Class 1 drugs-Sodium channel blockers
1a-Disopyramide-anticholinergic side effects,
occasionally torsades des pointes-dose is 250mg SR bd
Quinidine-not used anymore as high chance of
torsades des pointes. Procainamide-lupus like
syndrome without renal involvement, torsades.
1b-Lignocaine-toxicity usually in elderly patients with heart failure
manifest by confusion and convulsions
Class 2. Beta blockers
Class 3.-Potassium channel blockers
Amiodarone, Sotalol, Ibutilide, Bretylium
• Nausea, hypothyroidism, less commonly
hyperthyroidism, skin discolouration-blue-gray,
photosensitive rash-use sunblock, corneal depositsnight driving, hepatitis-cumulative with oral
preparation, allergic with intravenous preparation,
pulmonary fibrosis, torsades (unusual)
Use minimum dose, usually 200mg/d
Check TFTs and LFTs and CxR at intervals
Class 4-Calcium channel blockers
Verapamil-constipation, hypotension, ankle and finger
oedema, facial flushing, headache
Diltiazem-as above but less likely to cause side-effects
Digoxin, and adenosine are not classified in VaughanWilliams classification
Types of rhythm correction
DC cardioversion (20%)
Chemical cardioversion (36%)
Ibutilide
Vernakalant
Amiodarone
Radiofrequency ablation (7%)
EORP-AF study Europace 2014;16(3):308-319
Depends on
Whether paroxysmal, persistent or chronic
Presence or absence of other heart disease
Presence of diabetes, hypertension, CVA, age >
75 years
Severity of symptoms
Reversible precipitant
Response to medication
Treatment Journey (Onset > 48hrs)
Anticoagulation with warfarin*/ sinthrome*/
rivaroxaban/ dabigatran/ apixaban for at least 4
weeks (*INR 2.0 – 3.0)
Commence antiarrhythmic drugs prior to
cardioversion (need echocardiogram)
DC cardioversion (day case or in-pt)
Anticoagulation for at least 6 weeks
post procedure
OPD follow-up
appointment
C oronary AD
H ypertension
A2 ge >75
D iabetes
S2 troke
V ascular Disease
A ge >65
S ex category (F)
Ischemic Stroke Risk - CHA2DS2-VASc
Lip et al Stroke 2010
Ischemic Stroke Risk
(Clinical Application)
ESC Guidelines 2011
Bleeding Risk
Bleeding Risk
Diagnostic Evaluation
Time of onset
Patients in AF with signs of HF require immediate rate control,
cardioversion and echocardiogram
Assess for stroke risk – CHADS2VA2Sc
TFT’s, FBC, U&E, BP, ECG, fasting glucose, LFT’s
AMADEUS Trial
Chronic kidney disease is associated with hypo and
hypercoagulability
Impact of renal function on outcomes of anticoagulated AF
patients
4576 patients
Mean age 70 years
Apostolakis et al Eur Heart J. 2013;34 (46):3572-3579
AMADEUS conclusion
Mild renal impairment (CrCl 60mL/min) doubles the risk of
stroke and increased the risk of bleeding by almost 60% in
anticoagulated patients with AF.
Patients with a CHA2DS2VASc 1-2 with CrCl 60mL/min
Associated with an 8 fold higher stroke risk
New Oral Anticoagulants (NOACs)
Emerged as alternative to VKAs (warfarin) for thrombo-embolic
prevention in non-valvular AF
Predicable effect without need for monitoring
Fewer drug interactions
Shorter plasma half life
Improved efficacy/ safety ratio
New anticoagulants
Dabigatran
Rivaroxaban
Apixaban
Action
Direct thrombin inhibitor
Xa inhibitor
Xa inhibitor
Dose
150mg bd
20mg od
5mg bd
110mg bd
15mg od
2.5mg bd
RE-LY
ROCKET-AF
ARISTOTLE
Clinical trial
NOAC plasma levels
Dabigatran
Rivaroxaban
Apixaban
Plasma peak level 2hrs after ingestion 2-4 hrs after ingestion
1-4 hrs after ingestion
Plasma trough
12-24hr after
ingestion
16-24hrs after
ingestion
12-24 hrs after
ingestion
PT
Cannot be used
Prolonged
Cannot be used
INR
Cannot be used
Cannot be used
Cannot be used
Dosing
Dabigatran
Rivaroxaban
Apixaban
Fraction renally
excreted
80%
35%
27%
Normal dosing
150mg bd
20mg od
5mg bd
>80yrs 110mg bd
Dosing and CrCl
150mg bd
15mg od
CrCl 30 – 49 ml/min CrCl 15 – 49 ml/min
110mg bd if high risk
of bleeding
2.5mg bd
CrCl 15 – 49 ml/min
Not recommended
CrCl <30ml/min
CrCl <15ml/min
CrCl <15ml/min
Drug – Drug interactions
These are new agents so thee jury is still out on drug –
drug interactions, some are listed in the respective SPC
E.g. Dabigatran – diclofenac risk of haemorrhage
E.g. Rivaroxaban – enzyme inducers, phenytoin and
carbamazepine
All side effects and suspected Drug-drug interactions
should be reported to the IMB
Management of bleeding in patients
on dabigatran or rivaroxaban
There is currently no reversal agent or antidote for these medications.
Vitamin K is not effective.
In an acute overdose (<1hr) activated charcoal may be helpful.
Supportive care and control of bleeding site are the mainstays of managing
bleeding.
Possible options
Red cell concentrate
Platelet transfusions if the patient has also received anti-platelet agents.
Haemodialysis may be effective in removing dabigatran but not rivaroxaban.
Coagulation factors
Management of bleeding in patients
on dabigatran or rivaroxaban
There is currently no reversal agent or antidote for these medications.
Vitamin K is not effective.
In an acute overdose (<1hr) activated charcoal may be helpful.
Supportive care and control of bleeding site are the mainstays of managing
bleeding.
Possible options
Red cell concentrate
Platelet transfusions if the patient has also received anti-platelet agents.
Haemodialysis may be effective in removing dabigatran but not rivaroxaban.
Coagulation factors
Swallowing Difficulties
Pradaxa (Dabigatran) should be swallowed as a
whole with water, with or without food.(1)
Patients should be instructed not to open the capsule
as this may increase the risk of bleeding.(1)
The oral bioavailability may be increased by
75 %
compared to the reference capsule formulation when
the pellets are taken without the
Hydroxypropylmethylcellulose (HPMC) capsule shell..
Common Side effects
(other than bleeding)
Dabigatran
Abdominal pain
Diarrhoea
Nausea
Dyspepsia
Rivaroxaban
GI side effects - Abdominal pain,
diarrhoea, nausea,
dyspepsia,constipation
Pruritus, rash (allergy uncommon)
Fever
Peripheral oedema
Fatigue
Headache, dizziness, syncope
Tachycardia, hypotension
Switching to/ from warfarin
Warfarin to Dabigatran:
Stop warfarin and start dabigatran when INR less than 2.
Warfarin to Rivaroxaban:
Stop warfarin and start rivaroxaban when INR less than 3 (n.b.
rivaroxaban can cause false high INR)
Dabigatran to Warfarin:
If CrCl >50ml/min – start warfarin 3 days before stopping dabigatran
If CrCl 30-50ml/min – start warfarin 2 days before stopping dabigatran
Rivaroxaban to Warfarin
Give both agents concurrently until INR is 2 or greater
Test INR prior to next dose of rivaroxaban during this period
Missed Doses
Dabigatran
Take dose if up to 6 hours late.
Omit dose if over 6 hours late
Do not double up next dose.
Rivaroxaban
Take the tablet when you remember
Do not take more than 1 tablet in 1 day
Predictors for long term SR
Short duration of AF
Antiarrhythmic therapy
Left atrial size
Avoidance of triggers
Upstream therapy
Upstream therapy to prevent fibrosis
ACE inhibitors
Statins
Angiotension receptor blockers (ARBs)
??Omega 3
Questions??
Thank you