Management of new onset atrial fibrillation involves assessing risk factors, controlling the ventricular rate, and determining an anticoagulation strategy. Rate control can be achieved acutely with intravenous medications like metoprolol or verapamil, with a target rate of 80-100 bpm. Pharmacological cardioversion with medications like ibutilide, flecainide or amiodarone may be considered. For anticoagulation, the CHA2DS2-VASc score is used to determine risk of stroke, and the HASBLED score evaluates bleeding risk. Long-term management focuses on preventing thromboembolism, symptom relief, managing underlying conditions, and rate or rhythm control.

1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Atrial fibrillation management

2. Management of New onset AF
-A complete history and physical examination should be
performed in all patients with new onset AF (for disease,
comorbidities, complications). Old records should be
searched for evidence of a prior episode of AF or other
atrial tachyarrhythmias
-Detect time of onset
-Assess risk of stroke: Most patients with acute AF will
require anticoagulation unless they are at low risk and no
cardioversion is necessary (e.g. AF terminates within 24–
48 h).
-Most patients who present with AF will require slowing of
the ventricular rate to improve symptoms then longterm
plan

4. --Acute rate control:
Stable oral b-blockers or nondihydropyridine CCB
Severely compromisedi.v. verapamil or metoprolol
Target ventricular rate should usually be 80–100 bpm.
Severely depressed LV functionamiodarone, digoxine
In pre-excitationclass I antiarrhythmic drugs or
amiodarone.
AF with slow ventricular ratesatropine (0.5–2 mg i.v.),
urgent cardioversion or placement of a temporary
pacemaker

5. --Pharmacological CV of recent AF:
-Flecainide:
i.v. less than 24 h
2 mg/kg over 10 min.
Rarely effective for termination of atrial flutter or
persistent AF.
Avoided in abnormal LV function, ischaemia.
May prolong QRS duration, and hence the QT interval
May inadvertently increase the ventricular rate
due to conversion to atrial flutter and 1:1 conduction

6. --Ibutilide:
1 mg i.v. over 10 min—repeated 1 mg i.v. over 10 min
after waiting for 10 min
Can cause prolongation of the QT interval and torsades
de pointes
Will slow the ventricular rate.

7. --Propafenone:
2 mg/kg i.v. over 10 min, or 450–600 mg p.o.
Not suitable for patients with marked structural heart
disease; may prolong QRS duration; will slightly slow
the ventricular rate
May inadvertently increase the ventricular rate due to
conversion to atrial flutter and 1:1 conduction to the
ventricles.

8. --Vernakalant:
3 mg/kg i.v. over 10 min
Second infusion of 2 mg/kg i.v. over 10 min after15
min rest
So far only evaluated in clinical trials; recently
approved

10. --Amiodarone:
5 mg/kg i.v. over 1 h –follow up dose50 mg/h
Phlebitis, hypotension.
Will slow the ventricular rate.

11. --Recent onset AFhaemodynamic instability—CV
nostructural heart disease—Amiodarone no
i.v. flecainide or
i.v. propafenone
i.v. ibutilide
--In selected patients with recent onset AF and no
significant structural heart disease, a single high oral dose
of flecainide(200-300mg) or propafenone(450-600mg)
{{the ‘pill-in-the-pocket’ approach}} should be considered,
provided this treatment has proven safe during previous
testing in a medically secure environment (IIa)
--Digoxin, verapamil, sotalol, metoprolol are ineffective in
CV

12. --OAC therapy (INR 2.0–3.0) is recommended for at least
3 weeks prior to and for 4 weeks after cardioversion
(longterm in high risk for thromboembolism)
--If TOE detects a thrombus in the left atrium or LAA, VKA
(INR 2.0–3.0) treatment is required for at least 3 weeks
repeat TOE
thrombus resolutioncardioversion can be performed,
and post-cardioversion OAC is continued lifelong.
thrombus is still evidentrate control strategy,
especially when AF-related symptoms are controlled, since
there is a high risk of thrombo-embolism if cardioversion is
performed

13. INDICATIONS FOR URGENT CARDIOVERSION
•Active ischemia (symptomatic or electrocardiographic
evidence)
•Evidence for organ hypoperfusion
•Severe manifestations of heart failure (HF) including
pulmonary edema
•preexcitation syndromeextremely rapid ventricular
rate
--heparin (i.v.UFH bolus followed by infusion, or
weight-adjusted therapeutic dose LMWH), but it
should not cause a delay in emergent cardioversion

14. Direct current cardioversion
--Pre-treatment with amiodarone, flecainide, propafenone, ibutilide,
or sotalol should be considered to enhance success, prevent recurrent
AF.
--Contraindicated in patients with digitalis toxicity
--AP electrode placement is more effective than anterolateral
placement
--At least 3 h of ECG and haemodynamic monitoring are needed after
--Complications:
1–2% risk of thrombo-embolism
Skin burns
Prolonged sinus arrest without an adequate escape rhythm especially
in elderly patients with structural heart disease
Dangerous arrhythmias hypokalaemia, digitalis intoxication, or
improper synchronization
hypoxic or hypoventilate from sedation

15. If PPM
-At least 8 cm from the pacemaker battery
-The AP paddle positioning is recommended
-Biphasic shocks are preferred because they require
less energy
-In pacemaker-dependent patients, an increase in
pacing threshold should be anticipated
-After cardioversion, the device should be interrogated

17. Factors that predispose to AF recurrence:
-age
-AF duration before cardioversion
-Number of previous recurrences
-Increased LA size or reduced LA function
-Presence of coronary heart disease or pulmonary or
mitral valve disease

18. Long-term management
(1) Prevention of thrombo-embolism.
(2) Symptom relief.
(3) Optimal management of concomitant
cardiovascular disease.
(4) Rate control.
(5) Correction of rhythm disturbance.

19. Antithrombotic management
Assessing the risk of embolization =CHADS2
Congestive heart failure (any history)=1
Hypertension (prior history)=1
Age ≥75 years =1
Diabetes mellitus=1
Secondary prevention in patients with a prior ischemic
stroke or a transient ischemic attack; most experts also
include patients with a systemic embolic event=2
{0=low risk, 1-2= intermediate risk, 3-6=high risk}

20. Risk factor-based approach for non-valvular AF =
CHA2DS2-VASc
Congestive heart failure/LV dysfunction= 1
Hypertension= 1
Age >75= 2
Diabetes mellitus= 1
Stroke/TIA/thrombo-embolism= 2
Vascular disease= 1
Age 65–74= 1
Sex category (i.e. female sex)= 1

22. HASBLED score
H Hypertension(uncontorlled, systolic blood pressure>160
mmHg)= 1
A Abnormal renal and liver function (1 point each)=
1 or 2
S Stroke= 1 (previous history, particularly lacunar)
B Bleeding(previous bleeding history and/or predisposition to
bleeding, e.g. bleeding diathesis, anaemia)= 1
L Labile INRs= 1
E Elderly (e.g. age >65 years)= 1
D Drugs (antiplatelet agents, non-steroidal anti-inflammatory
drugs) or alcohol (1 point each)= 1 or 2
{≥3 indicates ‘high risk’}

23. CHA2DS2-VASc > 2 OACa
CHA2DS2-VASc=1 Either OACa or aspirin 75–325
mg daily {Preferred: OAC rather than aspirin} XX
CHA2DS2-VASc =0Either aspirin 75–325 mg daily
or noantithrombotic therapy {Preferred: no
antithrombotic therapy rather than aspirin}.
--N.B.female patients aged <65 years with
no other risk factors, aspirin may be considered rather
than OAC therapy

26. --Stroke risk in paroxysmal AF is not different from
that in persistent or permanent AF
--Antithrombotic therapy is recommended for patients
with atrial flutter as for those with AF.
--Combination therapy with aspirin 75–100 mg plus
clopidogrel 75 mg daily, should be considered for
stroke prevention in patients refusing to take OAC
therapy or a clear contraindication to OAC therapy,
where there is a low risk of bleeding.

29. INR
--Cohort studies suggest a 2-fold increase in stroke risk at INR 1.5–2.0
and, therefore, an INR <2.0 is not recommended
--In patients with AF who sustain an ischaemic stroke despite adjusted
dose VKA (INR 2.0–3.0), raising the intensity of anticoagulation to a
higher INR range of 3.0–3.5 may be considered {appreciable risk in
major bleeding only starts at INRs >3.5}
--At least 2.5 in the mitral prosthesis and at least 2.0 for an aortic
--Treatment should be interrupted 5 days before surgery to allow the
INR to fall<1.5
--If still elevated, administer low-dose oral vitamin K (1–2 mg)
--mechanical heart valve or high risk ‘bridging’ anticoagulation with
therapeutic doses of either LMWH or unfractionated heparin
--resumption of OAC therapy ‘usual’ maintenance dose (without a
loading dose) on the evening of (or the next morning after) surgery,
assuming there is adequate haemostasis.

30. -Foods that increase the INR include fish oil,
mango, grapefruit juice, and cranberry juice. Foods
and supplements that reduce the INR
include high vitamin K–content food, enteral feeds,
soy milk, ginseng, and sushi containing
seaweed.

32. PCI
--Triple therapy seems to have an acceptable risk–
benefit ratio provided it is kept short (e.g. 4 weeks in
BMS, 3m in olimus, 6m in paclitaxel)
--DES should be avoided in HASBLED>3 and triple
therapy (VKA, aspirin, and clopidogrel) used in the
short term, followed by longer therapy with VKA plus a
single antiplatelet drug (either clopidogrel or aspirin)
--An uninterrupted strategy of OAC is preferred in very
high risk of thrombo-embolism, and radial access
should be used as the first choice in ACS
--INR range of 2.0–2.5 if triple therapy

34. the 2012 ACCP guidelines:
-Recommend against routine vitamin K administration unless the INR is
more than 10.
-For INRs less than 4.5 without bleeding, the guidelines recommend lowering
the dose or holding the next dose with frequent INR monitoring until the INR
is within the therapeutic range and then resuming a lower dose.
-For INRs 4.5 to 10 without bleeding, the 2012 ACCP guidelines recommend
omitting 1 to 2 doses, frequent INR monitoring, and resuming a lower
warfarin dose when the INR is within the therapeutic range.
-When the INR is greater than 10 without overt bleeding, the 2012 ACCP
guidelines recommend low-dose (5 mg or less) oral vitamin K.
-For patients experiencing minor bleeding with an elevated INR, oral vitamin
K is recommended at a dose of 2.5 to 5 mg, repeated at 24 hour intervals until
the INR is within the therapeutic range and then resuming a lower dose of
warfarin.

37. Direct thrombin inhibitors
--(RE-LY) study:
Dabigatran 110 mg b.i.d. was non-inferior to VKA for the prevention of stroke and
systemic embolism with lower rates of major bleeding,
Dabigatran 150 mg b.i.d. was associated with lower rates of stroke and systemic
embolism with similar rates of major haemorrhage, compared with VKA.
--Where oral anticoagulation is appropriate therapy, dabigatran may be considered
(i) If a patient is at low risk of bleeding (e.g. HAS-BLED score of 0–2, dabigatran 150
mg b.i.d. may be considered
(ii) If a patient has a measurable risk of bleeding (e.g. HAS-BLED score of ≥3),
dabigatran 110 mg b.i.d. may be considered
--In patients with one ‘clinically relevant non-major’ stroke risk factor, dabigatran 110
mg b.i.d. may be considered, in view of a similar efficacy with VKA in the prevention of
stroke and systemic embolism but lower rates of intracranial haemorrhage and major
bleeding compared with the VKA and (probably) aspirin
--Antidotes have not been developed yet for these drugs, although strategies for
overdose treatment and bleeding (e.g., charcoal therapy and hemodialysis in
dabigatran overdose) have been proposed.

38. Oral factor Xa inhibitors (rivaroxaban, apixaban, edoxaban,
betrixaban)
(AVERROES) study:
Was stopped early due to clear evidence of a reduction
in stroke and systemic embolism with apixaban 5 mg
b.i.d. compared with aspirin 81–324 mg once daily in
patients intolerant of or unsuitable for VKA, with
an acceptable safety profile.

42. There is early research suggesting that the
preferred coagulation test for determining
accumulation
of dabigatran concentrations may be the
dilute thrombin time (dTT), with trough
dTT concentrations of
more than 200 ng/mL suggesting
increased bleeding risk.
Because apixaban and rivaroxaban are
factor Xa inhibitors, the preferred
monitoring test measures
anti–factor Xa activity levels, but tests are
not readily available and there is no
guidance on interpretation
of their results at this time.

43. -At this time, there is insufficient data and experience to recommend any methods of
reversing the anticoagulant effects of dabigatran etexilate, apixaban, or rivaroxaban.
-Administration of activated charcoal is recommended if less than 2 hours has passed since the
anticoagulant has been ingested.
-Hemodialysis removes about 60% of dabigatran over a 2 to 3 hour dialysis session and should be
initiated immediately for life-threatening bleeding in a patient with recent dabigatran exposure.
-Administration of fresh frozen plasma alone is ineffective and not recommended.
-A four-factor prothrombin complex concentrate (PCC) containing clotting factors II, VII, IX, and
X, has shown reversal of prolonged PTs in healthy volunteers given rivaroxaban, and in animal
models with dabigatran. However, the only available PCC in the U.S. at this time is a three-factor
PCC, which has a lower concentration of factor VII. Recombinant factor VIIa (rVIIa)
administration has demonstrated partial reversal of thrombin generation due to rivaroxaban in an
in vitro model but does not reverse the effects of dabigatran.
-Low-dose anticoagulant inhibitor complex (factor VIII inhibitor bypassing activity FEIBA NF;
Baxter Bioscience, Deerfield, Ill.) has demonstrated reversal of endogenous thrombin
potential, maximum concentration, lag-time, and time to reach maximum concentration of
thrombin after both dabigatran and rivaroxaban administration
in an ex vivo healthy volunteer study. However, higher doses of FEIBA increased thrombin
generation in this study, and administration of any clotting factor heightens all thromboembolic
risk.
-So the best advice in the case of significant bleeding associated with any of the new oral
anticoagulants is to discontinue the anticoagulant and consult with a hematology anticoagulation
specialist.

45. --New score (SAMe-TT2R2), which is a newly described score to predict those who
would do well on Vitamin K antagonists (SAMe-TT2R2 score 0-1) or those who are
likely to have poor anticoagulation control with VKA (SAMe-TT2R2 score ≥2)
where a novel OAC could be a better option.

46. Non-pharmacological methods to prevent stroke
--Occlusion of the LAA {considered the main site of atrial
thrombogenesis} may reduce the development
of atrial thrombi and stroke in patients with AF
--The 2006 American College of Cardiology/American
Heart Association (ACC/AHA) guidelines on the
management of valvular heart disease recommended
amputation of the LAA at the time of mitral valve surgery
to reduce the likelihood of postoperative thromboembolic
events
--Composite endpoint of stroke, cardiovascular death, and
systemic embolism of the WATCHMAN device was
considered non-inferior to that of VKA

48. Thank you