AF recent advances

2. Atrial Fibrillation
 AF is a supraventricular tachyarrhythmia
characterized by uncoordinatedatrial activation with
consequent deterioration of atrial
mechanical function.

3.  A rapid, irregular, sustained, wide-QRS-
complextachycardia strongly suggests AF with
conduction over an accessorypathway or AF with
underlying bundle-branch block. Extremelyrapid rates
(over 200 beats per minute) suggest the presenceof an
accessory pathway or ventricular tachycardia.

4.  Prevalence:
In US <1% ‘ve AF;
Varies with age –
 Rare in children & young adults.
 Is also rare < 60 yrs.
 > 8% in > 80 yrs.
 Median age 75 yrs.

6.  Presence of very irregular & disorganized atrial activity
represented - as Fibrillatory waves; aka “F” waves,
 These are due to several independent reentrant wavelets
within atria

7.  F waves - fine or coarse ; varying morphologies
 F waves may not be present; flat line with irreg irreg R-R
seen.
 A. rate - ≥350 bts/min.
 V. rate- irreg irreg & depends on # of atrial impulses
conducted through AVN.
 QRS complexes are narrow unless - BBB, aberrant
conduction, or preexcitation

8.  Coarse f waves –
 RHD MV ds,
 Thyrotoxicosis,
 Emphysema,
 Hypertensive CVD
 Fine f waves – Arteriosclerotic hrt dis.

11. 6 Sec time lines:
 6 sec = 30 large blocks.
 # QRS in 6-sec time X 10= HR/min
 1st QRS - not counted; serves as baseline.

12. 10 Sec time lines:
 If HR very slow- longer interval -10 sec taken.
 10 Sec = 50 large blocks.
 # QRS in 10-sec X 6 = HR/min.

14. AF
Paroxysmal
Persistent
Permanent
Recurrent

15. First detected: AF detected for 1st time, regardless of
duration or previous episodes.
Recurrent: If >2 episodes ‘ve occurred- may be paroxysmal
or persistent.
Paroxysmal: When recurrent AF has sudden onset & abrupt
termination.
 AF that terminates spontaneously or with intervention
within 7 d of onset.
 Episodes may recur with variable frequency.

16. Persistent: if AF is >7 days.
Longstanding Persistent AF: continuous AF lasting >1 year.
 Not self terminating,
 But terminated with pharmacologic/ electrical cardioversion.
 Permanent: Permanent AF is used when there has been a joint
decision by the patient and clinician
 to cease further attempts to restore and/or maintain sinus rhythm.
 · Acceptance of AF represents a therapeutic attitude on the part of
the patient and
 clinician rather than an inherent pathophysiological attribute of the
AF.
 · Acceptance of AF may change as symptoms, the efficacy of
therapeutic interventions,
 and patient and clinician preferences evolve.

17. Nonvalvular AF: in absence of RHD – MV ds, prosthetic
valve, or MV repair.
Valvular AF: - a/w RHD MS, prosthetic valve, or post valve
repair.
Lone AF: AF in age > 60 yrs - with structurally normal hrt,
non HT, no e/o pulmonary dis.

19. AF -mistaken for SVT:
When V. rate is unusually rapid - R-R interval may
look regular because of very close QRS clustering -
thus mistaken for SVT
Diagnosis of AF ascertained by slowing V. rate with
vagal maneuvers eg- CS pr. – showing irreg-irreg R-
R interval with fibrillatory/ undulating baseline b/w
QRS

20. AF mistaken for MAT:
F waves, esp when coarse- mistaken for P waves.
When these “F” waves inscribed before QRS- may be
mistaken for MAT

21. AF with regular R-R intervals:
V. rate in AF is irregularly irregular.
But it becomes regular when there is
complete AV dissociation or
complete AV block.

22. AF with regular R-R intervals:
Complete AV dissociation:
 Frequently due to digitalis toxicity.
 Here, V. are no longer controlled by AF, but rather
by separate pacemaker, usually AV jnx with regular
rate > 60 bpm.

23. AF with regular R-R intervals:
Complete AV Block :
 Fibrillatory impulses not conducted to ventricles.
 AV junctional/ ventricular escape rhythm usually
comes to rescue
 Here V rate is slow & regular- mid to low 40s

25. Ashman phenomenon:
In AF, R-R intervals are irreg-irreg.
Some R-R are longer & other shorter.
When R-R increased, HR is decreased, RP of
conduction tissues becomes increased.
When R-R decreased or HR increased, RP is
decreased.

27. Ashman phenomenon:
If long R-R is f/b short R-R (long/short cycle), atrial
impulse may find RBB still refractory from previous
impulse & will conduct with wide QRS.
This aberrantly conducted complex is 2nd complex
(complex with short cycle following long cycle).
This variability in RP is k/a Ashman phenomenon

28. Atrial fibrillation & WPW Sx
 WPW Sx – Impulses from A to V via AVN + AP.
 Unlike AVN, which has >RP; AP has much <RP.
 Thus, during AF, rapid A. impulses that are delayed/
blocked at AVN d/t its > RP, are conducted via AP,
resulting in very rapid V rate.

29. Atrial fibrillation & WPW Sx
 AVN blocking agents are standard drugs for
controlling V. rate in AF.
 H/e These are C/I in WPW sx - they enhance
conduction across AP resulting in rapid V rate &
hemodynamic collapse

31. Pathophysiological Mechanisms

32. Atrial Pathology as a Cause of
Atrial Fibrillation
 The most frequent patho anatomic changes in AF are
atrial fibrosisand loss of atrial muscle mass.
 Patientswith mild or moderate fibrosis responded
more successfully tocardioversion than did those with
severe fibrosis, which was thought to contribute to
persistent AF in cases of valvularheart disease

33.  Atrial fibrosis may be caused by genetic defects like
laminAC gene mutations . Other triggers of fibrosis
include inflammationas seen in cardiac sarcoidosis
and autoimmune disorders.
 Autoimmune activityis suggested by high serum levels
of antibodies against myosinheavy chains in patients
with paroxysmal AF who have no identified heart
disease

34.  Fibrosis is alsotriggered by atrial dilation in any type
of heart disease associatedwith AF, including valvular
disease, hypertension, HF, or coronaryatherosclerosis.

35. Stretch
RAAS
TGF-beta1
connective tissue growth factor
Fibrosis

36.  Transition of AV reentry into AF in patients with the
Wolff-Parkinson-White(WPW) syndrome can
produce a rapid ventricular response thatdegenerates
into ventricular fibrillation, leading to death .
 Intravenous administration of drugs such as
digitalis,verapamil, or diltiazem, which lengthen
refractoriness and slowconduction across the AV
node, does not block conduction overthe accessory
pathway and may accelerate the ventricular rate.

38.  A, Focal activation. The initiating focus (indicated by
the star) often lies within the region of the pulmonary
veins. The resulting wavelets represent fibrillatory
conduction, as in multiple-wavelet reentry.
 B, Multiple-wavelet reentry. Wavelets (indicated by
arrows) randomly reenter tissue previously activated
by the same or another wavelet.

39. Etiologies and Factors
Predisposing Patients to AF

41. Atrial Fibrillation
-- Prevalence in associated diseases --
 Hypertension – increased relative risk of only 1.42; however prevalence
of hypertension accounts for the high association
 CAD – AF is transient in 6-10% of MI patients; however it is almost
never in isolation to other ECG findings of ACS (Zimetbaum et al. Incidence and
predictors of myocardial infarction among patients with atrial fibrillation. J Am Coll Cardiol 2000;
36;1223)
Incidence in chronic, stable CHD is 0.6%
 Valvular heart disease
 High prevalence with Rheumatic heart disease
 MS + MR – 52%
 MS alone – 29%
 MR alone - 16%
 AS alone – 1%
 Degenerative MR incidence 5% per year

42. Atrial Fibrillation
-- Prevalence in associated diseases, cont. --
 Heart Failure – 10-30%
 Pulmonary embolism – 10-14 % (rarely the only sign or
symptom)
 Hyperthyroidism – low TSH in 5.4%; clinical
hyperthyroidism present in 1%
 COPD
 Post cardiac surgery
 Pericarditis
 Obstructive sleep apnea ( for patients with AF and OSA, incidence of AF
recurrence is 2X for those not treated with CPAP)
 Congenital heart disease
 Peripartum cardiomyopathy
 “Holiday Heart”

43. Atrial Fibrillation
-- Pathogenesis --
 Underlying heart disease of any cause that is complicated
by:
 heart failure
 atrial enlargement
 elevated atrial pressure
 inflammation or infiltration of the atria
 Echocardiographic risk factors
 increased left ventricular wall thickness
 left atrial diameter > 4 cm
 reduced left ventricular fractional shortening
 Triggering event
 majority related to atrial premature beat
 minority related to atrial flutter or atrial tachycardia

47. Atrial Fibrillation
-- Management and Disposition --
 Which category?
 Recent onset AF
 Recurrent paroxysmal AF
 Recurrent persistent AF
 Permanent (Chronic) AF
and patient condition, determines
 Which primary option
 Rate control
 Urgent cardioversion
 Delayed cardioversion
 Rhythm control / maintenance if converted
 Systemic embolization prevention

48. Atrial Fibrillation
-- Management and Disposition --
“Elective” cardioversion in the ED
 duration clearly identified less than 48 hrs
 No reversible cause
 low risk of intra-cardiac thrombus formation

49. Atrial Fibrillation
-- ED Cardioversion in the stable patient --Burton, John H. et al. Electrical cardioversion of ED patients with Atrial
Fibrillation. Annals of Emergency Medicine 2004;44: 22-30
Retrospective, consecutive
cohort
42 months,
Oct 1998 – March 2002
4 institutions
3,688 AF encounters
Excluded: Cardioversion for unstable patients
hypotension, dyspnea, ischemic chest pain, altered
consciousness, CHF, acute MI
No standardized protocol at any of the study sites
388 stable AF encounters
(10.5%)
Mean age = 61 +/- 13 yrs
332 successful (86%)
56 unsuccessful (14%)
91% discharged
55% discharged
9% admitted
45% admitted

50. Atrial Fibrillation
-- Management and Disposition --
“Urgent” or “Emergent” cardioversion in the ED
What are the indications?
What are the contraindications?

51. Atrial Fibrillation
-- Management and Disposition --
Urgent cardioversion
Restoration of sinus rhythm takes precedence over mitigation of thromboembolic risk
Indicated if any of the following is present:
• Active ischemia
• Significant hypotension where LV dysfunction (systolic or diastolic) or valvular
disease is a factor
• Severe CHF
• Pre-excitation syndrome (eg WPW)
“Relative” Contraindications to urgent cardioversion
 Duration of episode > 48hrs or uncertain duration
 Associated mitral valve disease, cardiomyopathy or CHF (known EF < 50%)
 Prior history of thromboembolic event

54. Rate V Rhythm control first?
 Rate
Over 65
Coronary artery disease
Unsuitable cardioversion
Unsuitable for
antiarrhythmics
 Rhythm
Under 65
Lone AF
CCF
Secondary to treated
trigger
Paroxysmal AF

55. Rate control

56. Atrial Fibrillation
-- Antiarrhythmic agents --

57. Fast Channel (Na+)
Action Potential
Purkinje fibers
Slow Channel (Ca++)
Action Potential
Sinus / A-V Nodes
0
1
2 3
4
2
0
Myocardial Cellular Electrophysiology
Class 1 antiarrhythmics
-Slowing of conductance
-Phase 0 is determined by Na+ channel
-Slowing of conduction velocity
and decreased excitability
Class 4 antiarrhythmics
-Slowing of AV nodal conductance
-Phase 0 is determined by Ca++ channel
-Slowing of conduction velocity in
sinus and AV nodes

58. -- Antiarrythmic Agent Classification—
Vaughn-Williams Classification
(Journal of Clinical Pharmacology, 1984)
Class 1- depression of Na+conductance during phase 0; slowed conduction
velocity and decreased excitability
 1a: moderate depression of Na+ conductance in resting and depolarized tissue;
depression of K+ currents and prolongation of repolarization
 Quinidine, Procainamide, Disopyramide
 1b: depression of Na+ conductance in depolarized fibers only;
 Lidocaine, Tocainide, Phenytoin
 1c: marked depression in Na+ conduction; no effect on repolarization
 Encainide, Flecainide, Propafenone
Class 2- β-adrenergic receptor blockers
 Atenolol, Metoprolol
Class 3- prolongation of action potential duration by varied effects
 Bretylium, Sotolol, Amiodarone, Ibutilide, Dofetilide
Class 4- depression of Ca+-dependent slow channels
 Diltiazem, Verapamil

59. Atrial Fibrillation
-- Management and Disposition --
Delayed cardioversion
 AF duration of 48 hours or duration unknown
 Associated mitral valve disease, cardiomyopathy or CHF
 Prior history of thromboembolic event
 Anticoagulate with a goal INR of 2.0 to 3.0 for at least
three weeks before and four weeks after either electrical
or pharmacologic cardioversion.

60. Atrial Fibrillation
-- Management and Disposition for Delayed ECV --
 Strategy 1 (Conventional)
 Oral anticoagulation with Warfarin
 Target INR 2.0 – 3.0
 No antiarrythmics
 Rate control as needed – hospitalization usually necessary if rate control needed
 Metoprolol
 Diltiazem
 Digoxin (useful only in presence of CHF)
 Scheduled ECV after minimum of 3 weeks of anticoagulation
 4 weeks of anticoagulation after ECV
 Strategy 2
 Indication
 recent onset but > 48 hrs
 useful for hospitalized patients (rate control, associated complications) and stable patients for
which earlier timing is useful
 Patients with increased risk of hemorrhage with anticoagulation
 Screening Transesophageal echocardiography (TEE)
 No anticoagulation
 No antiarrhythmics
 Rate control as needed
 ECV if no thrombi seen

61. Atrial Fibrillation
-- Indications for hospitalization --
 For the treatment of an associated medical
problem, which is often the reason for the
arrhythmia
 For elderly patients who are more safely treated for
AF in hospital
 For patients with underlying heart disease who
have hemodynamic consequences from the AF or
who are at risk for a complication resulting from
therapy of the arrhythmia

62. Atrial Fibrillation
-- Rate control alone vs rhythm control--
Rhythm control strategy
 Advantages:
 Better exertional capacity
 Improved cardiac function for CHF patients
 Mitigation of other arrhythmic related symptoms (eg palpitations)
 Disadvantages:
 frequent recurrences of AF – 50% of patient recurr in 3-6 months
 repeated need for electrical cardioversion;
 adverse effects of prophylactic antiarrhythmic drugs including life-threatening
events related to proarrhythmic effects
 No clear benefit of either approach for patients over 65 years of age;
trend for increased mortality in rhythm control (AFFIRM trial, NEJM 2002,
> 4,000 patients)
 Rate control with anticoagulation is acceptable in patients 65 yrs or
greater
 Strategy is weighed for acutely symptomatic patient with new onset of
Atrial fibrillation, particularly if < 65 yrs

63. Atrial Fibrillation
-- Rate control alone vs rhythm control --
VanGelder, et al, A Comparison of Rate Control and Rhythm Control in
Patients with Recurrent Persistent Atrial Fibrillation, NEJM
2002;347:1834-40
522 Patients with persistent AF after
previous electrical cardioversion
Mean age 68 +/- 8
Mean duration of AF diagnosis 315 d
Mean duration of presenting episode 32 d
No history of heart disease 21%
Primary Endpoints:
Death
CHF
TE event
Bleeding
Pacer
severe drug adverse event
Primary endpoint:
Rhythm control = 23%
Rate control = 17%
Follow up period of at least 2 yrs
Rhythm control Rate control
Entry: ECV + Sotolol
1st recurrence: ECV +
Flecanide or Propafenone
2nd recurrence: Amiodarone load +
ECV + Amiodarone main.
Target HR < 100
Digoxin, Diltiazem,
β blocker – alone or
In combination
All patients anticoagulated: could be discontinued if
In NSR 4 weeks after ECV

64. Atrial Fibrillation
-- Rate control alone vs rhythm control --
VanGelder, et al, A Comparison of Rate Control and Rhythm
Control in Patients with Recurrent Persistent Atrial
Fibrillation, NEJM 2002;347:1834-40
Factors related to lack of risk reduction with rhythm control strategy
•Tachycardia induced cardiomyopathy and heart failure also are
likely reduced with rate control (incidence of CHF similar in
the two arms of the study)
•Patients with risk factors for stroke are still at risk for stroke even
when sinus rhythm is maintained (17% of the thromboembolic
events occurred after cessation of anticoagulant therapy and in
5 of 6 cases the patient was in sinus rhythm at the time of the event)
•Senescent conduction disease is occasionally unmasked by rhythm
control strategy

65. Atrial Fibrillation
-- Maintenance of Sinus Rhythm after Chemical or Electrical Cardioversion --
Canadian Trial of Atrial Fibrillation Investigators
Roy, et al Amiodarone to Prevent Recurrence of Atrial Fibrillation, NEJM,
2000;342:913-920403 patients; 19 centers
201 Amiodarone 202 Propafenone ; Sotolol
101 Propafenone 101 Sotolol
Mean 16 month follow-up
35% recurrence for Amiodarone 63% recurrence for Propafenone or Sotolol

66. Atrial Fibrillation
-General Management Principles-
-- Pharmacologic Cardioversion -- Semi – urgent (hospitalization or Obs Unit)
 Class 1c
 used only if no pre-existant heart disease
 monitoring for rapid conducting At. Flutter
 Flecainide
 Propafenone
 Class 3
 monitoring for QT prolongation; Torsade
 Dofetilide
 Ibutilide
 Out-patient / Ambulatory scenario
 Class 1c “Pill-in-the-Pocket”
 Flecainide
 Propafenone
 Used only when demonstrated effective under as in-patient
 Must have AV nodal blockade with β blockade or Ca++ channel blocker to prevent 1:1
AV conduction if Atrial flutter occurs
 Class 1c Extended dosing
 Amiodarone –particularly with patients with pre-existing heart disease

67. Atrial Fibrillation
-General Management Principles-
-- Maintenance of Sinus Rhythm after Chemical or Electrical Cardioversion –
ACC / AHA / ESC anticoagulation recommendations

68. Atrial Fibrillation
-General Management Principles-
Assessment of Thromboembolic Risk

69. Atrial Fibrillation
-- Risk for Thromboembolism --
Go, AS, Hylek, EM, Chang, Y, et al, JAMA 2003
Risk assessment – CHADS2
 CHF – any history (1)
 Hypertension – prior history (1)
 Age > 75 (1)
 Diabetes mellitus (1)
 Stroke, TIA or systemic embolic event (2)

70. Atrial Fibrillation
-- Risk for Thromboembolism --
Risk assessment – CHADS2
Go, AS, Hylek, EM, Chang, Y, et al, JAMA 2003
Score (risk) Event rate (% / yr)
Warfarin Without Warfarin NNT
0 (low) 0.25 0.49 417
1 (interm) 0.72 1.52 125
2 (interm) 1.27 2.50 81
3 (high) 2.2 5.27 33
4 (high) 2.35 6.02 27
5,6 (high) 4.6 6.88

71. Atrial Fibrillation
-- Prevention of Thromboembolism --
ACC / AHA / ESC anticoagulation recommendations
Age < 60 + heart disease but no other risks: Aspirin
Age 60 – 75 with no risks: Aspirin
Age 65 – 75 with heart disease or DM: Warfarin
Women > 75: Warfarin
Men > 75: Warfarin or Aspirin
Age > 65 with CHF: Warfarin
EF < 35% + Hypertension Warfarin

72. CHA2DS2-VASc acronym
 Congestive HF
 Hypertension
 Age ≥75 y
 Diabetes mellitus
 Stroke/TIA/TE
 Vascular disease (prior MI,
PAD, or aortic plaque)
 Age 65–74 y
 Sex category (i.e., female sex
 Maximum Score
 1
 1
 2
 1
 2
 1
 1
 1
 9

73. Risk-Based Antithrombotic
Therapy: Recommendations

75. Atrial Fibrillation
-- Summary –
 Patients with new onset atrial fibrillation of less than 48 hrs duration, who
have normal ventricular function, no known mitral valvular disease and no
history of thromboembolic event can be considered for cardioversion in the
ED
 Up to 90% of atrial fibrillation episodes are asymptomatic with
approximately 20% of such episodes longer than 48 hrs (Select your
cardioversion cases carefully!)
 If the episode is greater than 48hrs, rate control, anticoagulate and refer for
delayed cardioversion
 TSH and free T4 are essential in the evaluation of initial onset
 AF is transient in 6-10% of MI patients; however it is almost never in
isolation to other ECG findings of ACS
 AF is transient in 6-10% of MI patients; however it is almost never in
isolation to other ECG findings of ACS

76.  The following are 10 points to remember about the 2014 guideline for the
management of patients with nonvalvular atrial fibrillation (AF):
1. In assessing risk of stroke in a patient with nonvalvular AF, the writing
committee recommends (Class I) the usage of the CHA2DS2-VASc (C=congestive
heart failure; H=hypertension; A2=age ≥75 years [doubled]; D=diabetes mellitus;
S2=stroke, transient ischemic attack, or thromboembolism [doubled];
V=vascular disease; A=age 65-74 years; Sc=sex category, i.e., female gender)
score, as opposed to the CHADS2 score.
2. For nonvalvular AF patients with a history of stroke or transient ischemic
attack, or a CHA2DS2-VASc score ≥2, oral anticoagulation is recommended
(Class I). Options for oral anticoagulation include warfarin, dabigatran,
rivaroxaban, and apixaban.
3. For patients with nonvalvular AF and a CHA2DS2-VASc score of 0, it is
reasonable to omit antithrombotic therapy (Class IIa).
4. The following options may be considered with a patient with nonvalvular AF
and a CHA2DS2-VASc score of 1: no antithrombotic therapy, oral
anticoagulation, or aspirin (Class IIb).

77. 5. None of the novel oral anticoagulants (dabigatran, rivaroxaban, or apixaban) are
recommended to be used in patients with AF and a mechanical or bioprosthetic heart
valve (Class III harm).
6. As in the earlier guidelines, the committee recommends against the use of certain
antiarrhythmic medications (flecainide, propafenone, dofetilide, and sotalol) in patients
with severe left ventricular hypertrophy (LVH). In the current guidelines, severe LVH is
now defined as wall thickness exceeding 1.5 cm.
7. Oral anticoagulation should be prescribed to patients with hypertrophic
cardiomyopathy and AF irrespective of the CHA2DS2-VASc score (Class I).
8. A randomized trial suggested that a lenient (<110 bpm) rate control strategy was as
effective as a strict strategy (<80 bpm) in patients with persistent/permanent AF.
However, the writing committee still advocates for the latter (Class IIa), as the results of
this single trial were not thought to be definitive.
9. Catheter ablation is useful in patients with symptomatic, paroxysmal AF who have not
responded to or tolerated antiarrhythmic medications (Class I).
10. Catheter ablation is also reasonable in selected patients with symptomatic, paroxysmal
AF prior to a trial of medical therapy, provided that it can be performed at an experienced
center (Class IIa).

78. THANK YOU