Atrial Fibrillation: Overview, practical and guidelines-directed approach

1. Atrial Fibrillation
Kerolus Shehata, MD

2. Objectives
• Identify the basic pathophysiologic mechanisms of AF
• Identify the types of AF and A-flutter
• Discuss the methods of rate and rhythm control strategies and the
potential merits for each approach.
• Identify the nonpharmacological options for the management of AF
including catheter ablation, device therapy and surgical options.
• Discuss the different options for stroke prevention in AF patients.

3. Overview
The most common cardiac arrhythmia
EKG: Irregularly irregular rhythm with no distinct P waves.
AF can have adverse consequences related to a reduction in cardiac
output and to atrial and atrial appendage thrombus formation.
Affected patients may be at increased risk for mortality regardless of
rate control.

4. Epidemiology
The prevalence of paroxysmal AF, which is more likely to be
detected with ambulatory monitoring, is much higher.
Infants and children: Rare. Always associated with structural
heart disease.
ATRIA study: The prevalence of AF ranged from 0.1% among
adults <55 years of age to 9% in those ≥80 years of age.
More prevalent in Men regardless of age group.
Race: Compared with Whites, Blacks (hazard ratio [HR] 0.84),
Hispanics (HR 0.78), and Asians (HR 0.78) each had a lower AF
risk after adjustment.
Subclinical AF: Asymptomatic episodes in a patient without a
prior history of AF, which are detected only by monitoring
techniques.
Go: JAMA, 2000

5. Risk Factors
Hypertension, CAD, heart failure, valvular heart disease, obesity, OSA, high levels of alcohol,
hyperthyroidism can cause AF.
Evidence for caffeine and energy drinks, while suspected, is questionable.
While exercise can be protective against AF, endurance athletics may be a cause for atrial fibrillation.
It is also well established that AF is more common in individuals who have a first-degree relative who
developed AF at a young age.
There are varieties of acute conditions that can initiate AF such as cardiac surgery, pulmonary embolus,
and inflammatory conditions (sepsis, covid..)

6. OSA and A-fib
Both entities are risk factors for ischemic stroke and both
conditions are linked with increased mortality.
OSA is associated with hypertension, heart failure, and AF.
OSA has been shown to increase the risk of stroke, independently
of other traditional stroke risk factors, such as hypertension,
diabetes, and AF
Mechanical effects of obesity and OSA can lead to increased
afterload, LVH, and left atrial fibrosis and remodeling. These
changes can result in an increased risk of AF development.
About 50% of AF patients also have OSA.
2019 guidelines stated class I indication for weight loss in obese
patients with AF.
OSA patients treated with CPAP had higher ablation success rates
than those not on CPAP.
Gami, et al. JACC2007,49:565-71
Patel D, et al. Circ Arrhythm Electrophysiol 2010;3:445–51

7. Alcohol and AF
ETOH is the most common trigger of atrial fibrillation reported by 35% of patients.
Earlier meta-analyses showed that alcohol was associated with a dose-related
increased risk of AF.
ETOH is associated with autonomic modulation with reduced heart rate variability,
sympathetic effects, and vagal stimulation.
Binge drinking has also been associated with acute cardiac inflammation.
Observational studies link regular ETOH consumption with dose-related increases in
LA size, impairments in atrial mechanical and reservoir function, and adverse
electrical remodeling.
Numerous studies have also reported higher rates of recurrence of AF after catheter
ablation among regular drinkers than among nondrinkers.
UCSF recent trial suggested that even just one glass of wine, beer or other alcoholic
beverage can double the chance of an AF event within the next 4 hours.

8. AF triggers and substrate
Trigger is a rapidly firing focus often arising in the pulmonary veins that can initiate AF.
Catheter ablation of AF depends in large part on the electrical isolation of the PVs from the remainder of the atrium.
Electrophysiologic evaluation of the PVs has identified myocardial tissue that can lead to repetitive firing or even the
presence of episodic reentrant activation in the veins
Stretch as in MR or CHF can increase the propensity for rapid firing from the PVs as a result of stretch sensitive ion
channels.
Non-PV triggers: The Vein of Marshall, SVC, coronary sinus or other supraventricular arrhythmias e.g., AVNRT, AVRT or
A-flutter
Substrate is the Mechanical and anatomic structure of the atria in which AF can occur.

9. AF begets AF

10. AF triggers
PACs typically from within or around the PVs (PVI is the
cornerstone of ablation strategies for AF)
Other trigger sites: LA posterior wall, LAA, IAS, Crista
terminalis, Eustachian ridge, SVC, Vein of Marshall and
CS.
Leak of Ca+2 from the sarcoplasmic reticulum during
diastole activates Na/Ca exchanger leading to influx of
Na+ inside the cell causing early or delayed
afterrepolarization.

11. AF substrate
structural and electrophysiologic abnormalities that promote re-
entry (e.g., atrial fibrosis, inflammation, reduced cell coupling, slow
conduction, short effective refractory period).
The multiple wavelet hypothesis supposes the existence of multiple
meandering re-entrant circuits that continually re-excite the atria.
The rotor hypothesis suggests that one or more functional re-entrant
circuits or rotors activate the atria rapidly enough to cause chaotic,
fibrillatory conduction.
Extrinsic influences, such as increased parasympathetic or
sympathetic tone, probably play a role in the initiation and even
maintenance of AF in some patients.
As AF persists, progressive changes and atrial remodeling can occur,
resulting in atrial dilatation and fibrosis that may preclude the
restoration and maintenance of sinus rhythm
AF begets AF.

12. AF
Pathophysiology

13. Types and Triggers of AF
Paroxysmal AF is associated with
triggering foci that are commonly
located in sleeves of muscle along the
pulmonary veins.
Persistent AF is often characterized by
some evidence of atrial remodeling
with electrophysiological changes in
the atrial myocytes, as well as fibrosis.
Triggering foci are also present.
In long-standing persistent AF, the atrial
remodeling, including fibrosis, is more
extensive and severe than in persistent
AF.

14. Flutter and Fibrillation are NOT the same
The elimination of the RA reentry circuit responsible for typical flutter
frequently does NOT eliminate the predisposition to AF that is
predominately a left-atrial problem in a large number of patients.
Studies have demonstrated that patients who undergo catheter
ablation of typical atrial flutter have a very high probability of
developing AF over the ensuing five years.
That has clinical implications when it comes to ablation,
anticoagulation strategies and patient follow-up.

15. Mechanisms of Maintenance of AF
A. Multiple wavelet
reentry, with
nonhierarchical wavelets
giving rise to fibrillatory
conduction.
B. Focal drivers either
inside or outside of the
pulmonary veins.
C. Rotor sources, or spiral
wave reentry giving rise to
a localized source, stable
gradients of activation,
and fibrillatory conduction
in the rest of the atrium.

16. The concept of “rotors” or “spiral wave re-entry”
The failure rate of PV isolation is as high as
40:60% at one year: The trigger(s) may have
been treated but not the abnormalities that
sustain AF once triggered.
A rotor is a similar form of functional
reentrant activity, but with a critical
difference: the curved wavefront and
wavetail meet each other, at a singularity,
and the tissue at the center is not refractory.
Rotors are “drivers” or organizing sources of
fibrillation, be it AF or VF, and a spiral wave is
more accurately a 2D representation of the
curved vortices generated by the spinning
rotor in its immediate surroundings.

17. Mechanism &
Pathogenesis
Enhanced Ca2+ loading during AF is believed to underlie most of the cellular pro-arrhythmic mechanisms (trigger
loop).
The main process in the electrical loop is an altered contribution of ion channels to the action potential
configuration that protects atrial myocytes against excessive Ca2+ loading.
Abbreviation of the action potential facilitates re-entry and thereby promotes AF.
In the structural loop, chronic atrial stretch activates numerous signaling cascades that produce alterations of the
extracellular matrix and conduction disturbances, also facilitating re-entrant mechanisms.
The main changes of the contractile properties of the heart are loss of atrial contractility which increases atrial
compliance and the development of a ventricular tachycardiomyopathy, both of which increase stretch in the atrial
wall.
The circular positive-feedback enhancement of these pathophysiological changes explains the general tendency of
AF to become more stable with time.
It should be noted that the different loops are interconnected by mechanisms that are part of more than one loop.
Increased Ca2+ loading enhances trigger activity (trigger loop) and also results in a change in the ion channel
population and activity (electrical loop).
Re-entrant mechanisms are promoted by both shortening of refractoriness (electrical loop) as well as by conduction
disturbances resulting from tissue fibrosis (structural loop).
Like in a system of meshing gear wheels, one loop will drive the other, leading to progression of the arrhythmia.
However, the proposed system of gear wheels does not start to move spontaneously. Structural heart diseases,
arrhythmias, aging, or inherited diseases are required to initiate movement of one or more of these wheels. When
the pathophysiological alterations eventually reach a certain threshold, AF will ensue.

18. Maintenance of AF – Other contributors
Atrial remodeling: fibrosis, or electrical changes, such as refractory-period dispersion or conduction display.
Electrical remodeling: results from the high rate of electrical activation, which stimulates the AF-induced changes in refractoriness.
Role of autonomic nervous system: exercise-induced AF may be sympathetically driven. The parasympathetic nervous system is thought to
contribute to AF in young patients with no structural heart disease. Bezold-Jarisch-like “vagal” reflexes can be elicited during radiofrequency
ablation and occur in and around the PVs. Vagal responsiveness also appears to decrease following ablation in the left atrium.
Role of Fibrosis: Patients with AF also display increased atrial fibrous tissue content, along with increased expression of collagen I and III, as
well as up-regulation of MMP-2 protein, and down-regulation of the tissue inhibitor of metalloproteinase, TIMP-1.
Role of Inflammation & Oxidative stress: Reactive oxygen species may be implicated not only in promoting AF but also in maintaining atrial
arrhythmia. Antioxidants such as vitamin C and n-acetylcysteine have been administered to patients undergoing cardiac surgery and have been
shown to decrease postoperative AF.
Reentrant mechanism: multiple wandering wavelets that rarely reenter themselves but can re-excite portions of the myocardium recently
activated by another wavefront, a process called random microreentry

19. Atrial structural & electrical remodeling
Rapid atrial rates increase potentially cytotoxic Ca2+ loading.
Autoprotective ICa,L reductions occur via rapidly developing functional
changes (ICa,L inactivation) and more slowly developing changes in gene
and protein expression.
Decreased ICa,L reduces Ca2+ loading but decreases APD. Diminished APD
shortens refractoriness and reduces the wavelength (WL), which allows for
smaller and more atrial reentry circuits, thus making AF unlikely to
terminate. Atrial tachycardia also increases inward-rectifier currents such
as IK1 and IK,ACh,c, which further reduces APD and promotes AF.
AF begets AF. Thus, the longer a patient has been in continuous AF, the
less likely it is to terminate spontaneously, and harder it is to restore and
maintain sinus rhythm.

20. The role of AV node in AF
AV nodal tissue consists of so-called "slow response" fibers, which depend on a mixed calcium/sodium current.
Unlike tissue generating a fast action potential that has an all-or-none response (i.e., the velocity of impulse conduction is similar at all
stimulation rates until block occurs), tissue that generates a slow action potential exhibits a graded or decremental response, in which the
velocity of impulse conduction slows as the stimulation rate increases.
The ventricular rate usually ranges between 90 and 170 beats/min.
Ventricular rates below 60 beats/min are seen with AV nodal disease, drugs that affect conduction, and high vagal tone as can occur in a well-
conditioned athlete.
Ventricular rates above 200 beats/min suggest catecholamine excess, parasympathetic withdrawal, or the existence of an accessory bypass
tract as occurs in the preexcitation syndrome.
The AV node is richly supplied and affected by both components of the autonomic nervous system.

21. Can AF generate a regular rhythm on ECG?
AF + CHB + regular escape rhythm
AF + AVN ablation + Pacing
Digoxin toxicity
Mistaken for fine A-flutter with
regular conduction

22. Classification of AF
N.B: Paroxysmal AF: <7 days WITH OR
WITHOUT intervention.

23. Basic thromboembolic stroke pathophysiology
90% of thrombi are in the LAA

24. AF related-thromboembolism
In patients with unexplained stroke, AF was detected by ILR in
25.5% (Cotter et al: Neurology,2013).
Mechanisms of thromboembolism in AF are multiple and
complex.
The components of CHA2DS2-VASc score could be independently
associated with thrombogenesis and high risk of embolism and
so, a high score in AF is associated with high risk of stroke.
AF appears to be associated with a hypercoagulable state.
AF is a syndrome and not merely a disease.

25. Stroke risk stratification in Non-valvular AF

26. HAS-BLED score

27. Rate control versus rhythm control in AFFIRM
No difference in Mortality or incidence of stroke.
Less hospitalization in rate control.
Conclusion: In patients with nonvalvular AF, there
is no survival benefit between rate and rhythm
control, but rhythm trends toward increased
mortality.
Wyse et al: NEJM, 2002; Van Gelder et al: NEJM, 2001

28. Rate and Rhythm control
Rate control: Consider in all patients
Rhythm control: Improves symptoms and
QOL, preferable if the patient is still
symptomatic despite rate control, or if the
patient is intolerant or failed rate control
measures. No date on decreasing incidence
of stroke.

29. Rate control in
AF/RVR

30. Oral agents for AF rate control

31. What NOT to do? – Class III

32. Rate control – What is the target HR in AF?
Resting HR <80: based on AFFIRM trial. Class IIa
Peak exercise HR < age predicted maximum HR: Class IIa
Resting HR <110: based on RACE II trial. Class IIb. If patient is asymptomatic and no HF.

33. How to Restore & Maintain the sinus rhythm?
Restoration of SR: Electrical or
pharmacologic cardioversion
Maintenance of SR: AADT or
ablation

34. Maintenance of SR

35. Pharmacologic
cardioversion

36. SR restoration –
NO structural
heart disease

37. SR restoration –
Structural heart
disease

38. Rhythm
Control in AF
patients

39. Key points in pharmacologic cardioversion of AF
A single oral loading dose of propafenone (450-600 mg) or flecainide (200-300 mg) can convert recent-onset AF in approximately
70% of patients.
A pill-in-the-pocket approach to achieve out-of-hospital conversion of AF, using flecainide or propafenone, appeared to be safe and
effective in some studies, but should be used only after it is observed to be safe in a monitored setting.
Because propafenone and flecainide can convert AF to slow atrial flutter, resulting in 1:1 AV nodal conduction and dangerously
rapid ventricular rates, an AV nodal blocking agent should be administered concomitantly.
Oral dofetilide and intravenous ibutilide are always administered in-hospital due to the risk of QT prolongation and TdP.
Conversion of AF to SR (via any means) is associated with an increased risk of stroke in nonanticoagulated patients, not only at the
time of cardioversion, but also for the ensuing weeks while atrial function is still depressed.

40. Overview of AF ablation
Catheter ablation of AF is more effective than antiarrhythmic drug therapy in maintaining sinus rhythm and improving AF symptoms.
Recent data from the CABANA trial showed no significant improvement in the outcomes of mortality or stroke when a strategy of AF ablation was compared
with drug therapy.
Electrical isolation of the PVs is the cornerstone of all ablation strategies in AF.
The most common energy source is radiofrequency (RF), delivered through an open-irrigated catheter, which causes cellular necrosis by tissue heating.
Cryoballoon ablation is another method to achieve PVI and is noninferior to RF ablation in paroxysmal AF.
In patients with persistent and longstanding persistent AF, the efficacy of PVI alone is limited, and adjunct ablation strategies to modify the atrial substrate.
A multisociety expert consensus statement on catheter and surgical ablation of AF recommends catheter ablation for patients with symptomatic paroxysmal
AF (Class I) or persistent AF (Class IIa) who are refractory or intolerant to at least one antiarrhythmic drug.
Anticoagulation should be maintained for ≥8 weeks after ablation for all patients. After this period, continuation of anticoagulation should be based on the
patient's thromboembolic risk profile (CHA2DS2-VASc score), even if the procedure is perceived successful.

41. Indications for AF
catheter ablation
Don’t ablate patients who can’t be
anticoagulated.
The primary indication for ablation should
NOT be obviating the need for AC.

42. Main complication of AF ablation
In a worldwide survey of 85 institutions performing 20,825 RF catheter ablations, major complications
occurred in 4.5% of ablations, including a 1.3% rate of cardiac tamponade, a 0.94% rate of stroke or TIA,
a 0.29% rate of PV stenosis, a 0.17% rate of phrenic nerve injury, a 0.04% rate of atrial-esophageal
fistula, and a 0.15% rate of death.
PV stenosis: Symptoms occur weeks to months after the procedure and include SOB, cough, and/or
hemoptysis. CXR may show localized consolidation, and the preferred diagnostic modalities are MRI or
CT. Mild PV stenosis is managed conservatively, whereas symptomatic patients may require PV
angioplasty and stenting.
Atrioesophageal fistula is one of the most serious complications and results in high lethality. It typically
presents 1-4 weeks after ablation with nonspecific symptoms (fever, dysphagia, nausea, chest
discomfort), sepsis, or neurologic events due to septic emboli. Evaluation is urgent and the preferred
diagnostic modality is a chest CT scan with contrast, which may demonstrate air in the LA. Treatment of
an atrioesophageal fistula is a medical emergency that requires urgent surgical repair.

43. Catheter Ablation of the AV node
Used to control ventricular rates in situations in which AF is refractory to pharmacologic rate control and is associated with improved
quality of life, exercise duration, and LVEF.
A potential downside to the AVN ablation is pacing-induced cardiomyopathy due to chronic (RV) pacing, so, in patients with LVEF <35%
and symptoms of HF, implantation of a biventricular pacing system is recommended.
BLOCK HF trial showed that even patients with LVEF <50% and >35% may benefit from biventricular pacing compared with RV apical
pacing. Upgrading to a biventricular pacing system should be considered in patients who develop a pacing-induced cardiomyopathy.
His bundle pacing has been proposed as an alternative to biventricular pacing in patients undergoing AVN ablation.
Sudden death secondary to TdP or VF has been rarely reported after AVN ablation due to increased dispersion of ventricular
refractoriness produced by sudden heart rate slowing and ventricular pacing. To minimize this risk, the ventricular pacing rate is usually
set between 90-100 bpm post-ablation and then gradually tapered over several months.

44. AADT for rhythm
control in HCM
Preferred: Amiodarone &
Disopyramide
Acceptable: Sotalol,
Dofetilide and Dronedarone.
Avoid: Flecainide &
Propafenone.

45. MAZE procedures
Class IIa: In patients undergoing cardiac
surgery for other indication.
Class IIb: Rarely used as a standalone
procedure for AF.

46. Rate vs Rhythm control in AF after cardiac surgery
Gillinov et al: NEJM 374:1911, 2016

47. Prophylaxis &
Management
of post-op AF

48. Weight loss as an effective anti-arrhythmic measure
Pathak et al: JACC 65:2159, 2015

49. Causes of post-ablation dyspnea

50. Pre-excited AF in WPW
Suspect if ventricular rate >200, Wide QRS complexes due to
abnormal ventricular depolarization via accessory pathway
and QRS complexes change in shape and morphology
IV digoxin, IV amiodarone, IV or oral beta blockers,
diltiazem, and verapamil are potentially harmful
In a hemodynamically unstable patient, urgent synchronized
DC cardioversion is required.
Medical treatment options in a stable patient include
procainamide or ibutilide, although DC cardioversion may be
preferred.

51. Pearls
Valvular AF: Rheumatic mitral stenosis, mitral valve repair,
Mecganical or bioprosthetic* valve. Do not apply CHA2DS2-
VASc score. Start Coumadin. Do NOT use NOAC.
AF+HCM: Do not apply CHA2DS2-VASc score. Start
Coumadin. Do NOT use NOAC.
All others: Use CHA2DS2-VASc score. No OAC if score is 0.
Use OAC if score if ≥2
The decision to anticoagulate is NOT altered by rate/rhythm
control.

52. NOACs Trials and mechanism of action

53. NOACs dosing, excretion and special considerations

54. NOACs drug interactions

55. NOACs Vs Warfarin
Ruff et al: Lancet 383: 955, 2014

56. Management
of bleeding on
NOACs

57. Cardioversion:
Anticoagulation
Management

58. No more ASA monotherapy
Hart et al: Ann Intern Med 146:857, 2007

59. Triple Therapy following PCI
Dewilde et al: Lancet 381:1107, 2013

60. AC Bridging

61. WATCHMAN – PREVAIL trial
Holmes et al: J Am Coll Cardiol 64(1):1, 2014

62. AC after LAA
closure

63. Overview of Atrial Flutter - I
Rapid, regular atrial depolarizations at characteristic rate of approximately 300 beats/min and a regular ventricular rate of
about 150 beats/min in patients not taking atrioventricular .
Atrial flutter may be a stable rhythm or a bridge arrhythmia between sinus rhythm and AF, or an organized rhythm in AF
patients treated with antiarrhythmic drugs(AV) nodal blockers.
Typical A-Flutter (CTI-dependent flutter): macroreentrant circuit traversing the cavo-tricuspid isthmus. The circuit is
usually a counterclockwise rotation around the tricuspid valve exhibiting a classic saw tooth appearance in the inferior
leads. If the circuit has a clockwise rotation, it will exhibit positive flutter waves in the inferior leads.
Atypical A-flutter (Not CTI-dependent): Can originate any region of the right or left atria, around areas of scar tissue due
to intrinsic heart disease or surgical/ablated scar tissue.
Surgical repair of congenital heart disease can lead to macroreentrant circuits causing either typical or atypical flutter.
LA scars after AF ablation can give rise to atypical flutter.
Flutter waves in V1 and inferior leads: Discordant in typical flutter (positive in V1 in counterclockwise circuits) and
concordant in atypical flutter.
A-tach with AVB can mimic A-flutter in EKG.

64. Overview of Atrial Flutter - II
Rarely occurs in a structurally normal heart.
Can be induced after initiation of AADT for AF (Flecainide, Propafenone, Amiodarone or Dronedarone).
Has the same triggers as those of AF.
Can occur after cardiac surgery: involves the isthmuses between natural barriers, incisions and scars.
Overall incidence of Flutter is much less than AF.
Even A:V flutter ratios (2:1/4:1) is more common than odd ratios (3:1).
If odd ratio, it usually reflects a bi-level AVB in the AVN.
If 1:1 conduction: suspect the presence of 1A/1C AADT, accessory pathway, catecholamine excess or parasympathetic
withdrawal.
Management options and for A-flutter are the same as for AF.
Digoxin is used less often because its major action is an enhancement of vagal tone, which is offset during exertion.
In general, it is more difficult to affect rate control in A-flutter, as compared with AF. While up-titration of AVN blocking
agents typically lowers the mean rate in AF, patients with A-flutter are frequently "stuck" at 2:1 AV conduction.

65. Overview of Atrial Flutter - III
Class IA and IC drugs risk causing rapidly conducted AF. They drugs can slow the atrial flutter rate, and in the absence of
AV nodal blocking agents, lead to 1:1 A:Vconduction and paradoxically faster rates than baseline flutter (generally with
2:1 A:V conduction). They can also "organize" atrial fibrillation and lead to "slow" atrial flutter, with the risk of 1:1 A:V
conduction.
Amiodarone and dronedarone can also slow the atrial flutter rate, but rarely lead to 1:1 A:V conduction because they also
slow AV nodal conduction.
Pharmacologic cardioversion of flutter: Ibutilide is the drug of choice, but carries risk of TdP due to QTc prolongation.
In patients with PMK (permanent or post-op epicardial atrial) who experience A-flutter, Atrial override pacing can convert
them back to SR. Use the same AC guidelines as those for cardioiversion.
Because of the high rate of recurrence in patients without a correctable cause, and because of its high success rate,
radiofrequency catheter ablation is generally preferable to long-term pharmacologic therapy in patients with typical atrial
flutter. The isthmus between the IVC and CTI is an obligatory route for typical flutter, and, as such, is the preferred
anatomic target for ablation.
Commonly, 4 weeks after successful ablation of isolated typical flutter (i.e, no prior AF history), anticoagulation is
discontinued. However, in patients with prior AF history, AC should be continued long term based on the CHADS-VASc
scoring system.

66. CTI-dependent flutter – Counterclockwise reentry -
2:1 conduction

67. CTI-dependent flutter – Clockwise reentry –
3:1 conduction – SR mimicker

68. CTI dependent flutter – Clockwise reentry –
Variable block

69. CTI-independent flutter post cardiac surgery
Note the flutter wave concordance in V1 and inferior leads.

70. Take home messages - I
For patients with AF and an elevated CHA2DS2-VASc score of 2 or greater in men or 3 or greater in women, OAC are
recommended.
NOACs (dabigatran, rivaroxaban, apixaban, and edoxaban) are recommended over warfarin in NOAC-eligible patients with AF
(except with moderate-to-severe mitral stenosis or a mechanical heart valve).
In patients with AF (except with moderate-to-severe mitral stenosis or a mechanical heart valve), the CHA2DS2-VASc score is
recommended for assessment of stroke risk.
For patients with AF who have mechanical heart valves, warfarin is recommended.
Selection of anticoagulant therapy should be based on the risk of thromboembolism, irrespective of whether the AF pattern is
paroxysmal, persistent, or permanent.
Renal function and hepatic function should be evaluated before initiation of a NOAC and should be reevaluated at least annually.
For patients with atrial flutter, anticoagulant therapy is recommended according to the same risk profile used for AF.
For patients with AF (except with moderate-to-severe mitral stenosis or a mechanical heart valve) who are unable to maintain a
therapeutic INR level with warfarin, use of a NOAC is recommended.

71. Take home messages - II
For patients with AF (except with moderate-to-severe mitral stenosis or a mechanical heart valve) and a CHA2DS2-VASc score of 0
in men or 1 in women, it is reasonable to omit anticoagulant therapy.
In patients with AF and end-stage CKD or on dialysis, the direct thrombin inhibitor dabigatran or the factor Xa inhibitors
rivaroxaban or edoxaban are NOT recommended because of the lack of evidence from clinical trials that benefit exceeds risk.
The direct thrombin inhibitor dabigatran should NOT be used in patients with AF and a mechanical heart valve.
Bridging therapy with unfractionated heparin or low-molecular-weight heparin is recommended for patients with AF and a
mechanical heart valve undergoing procedures that require interruption of warfarin. Decisions on bridging therapy should balance
the risks of stroke and bleeding.
Idarucizumab is recommended for the reversal of dabigatran in the event of life-threatening bleeding or an urgent procedure.
Andexanet alfa can be useful for the reversal of rivaroxaban and apixaban in the event of life-threatening or uncontrolled bleeding

72. Take home messages - III
Percutaneous LAA occlusion may be considered in patients with AF at increased risk of stroke who have contraindications to long-
term anticoagulation.
For patients with AF or atrial flutter of 48 hours’ duration or longer, or when the duration of AF is unknown, AC with warfarin (INR
2.0 to 3.0), a factor Xa inhibitor, or direct thrombin inhibitor is recommended for at least 3 weeks before and at least 4 weeks
after cardioversion, regardless of the CHA2DS2VASc score or the method (electrical or pharmacological) used to restore SR.
For patients with AF or atrial flutter of 48 hours’ duration or longer or of unknown duration who have not been anticoagulated for
the preceding 3 weeks, it is reasonable to perform TEE before cardioversion and proceed with cardioversion if no left atrial
thrombus is identified, including in the LAA, provided that anticoagulation is achieved before TEE.
For patients with AF or atrial flutter of less than 48 hours’ duration with a CHA2DS2-VASc score of 0 in men or 1 in women,
administration of heparin, a factor Xa inhibitor, or a direct thrombin inhibitor, versus no anticoagulant therapy, may be considered
before cardioversion, without the need for postcardioversion oral anticoagulation.

73. Take home messages - IV
AF catheter ablation may be reasonable in selected patients with symptomatic AF and HFrEF to potentially lower mortality rate
and reduce hospitalization for HF (IIb).
Urgent direct-current cardioversion of new-onset AF in the setting of ACS is recommended for patients with hemodynamic
compromise, ongoing ischemia, or inadequate rate control.
Intravenous beta blockers are recommended to slow a rapid ventricular response to AF in patients with ACS who do not display
HF, hemodynamic instability, or bronchospasm (I).
If triple therapy is prescribed for patients with AF at increased risk of stroke who have undergone PCI with stenting for ACS, it is
reasonable to choose clopidogrel in preference to prasugrel (IIa).
In patients with AF at increased risk of stroke who have undergone PCI with stenting for ACS, double therapy with a P2Y12
inhibitor (clopidogrel or ticagrelor) and warfarin is reasonable to reduce the risk of bleeding as compared with triple therapy (IIa).
In patients with AF at increased risk of who have undergone PCI with stenting for ACS, double therapy with clopidogrel and low
dose rivaroxaban 15 mg daily is reasonable to reduce the risk of bleeding as compared with triple therapy (IIa).

74. Take home messages - V
In patients with AF at increased risk of stroke who have undergone PCI with stenting for ACS, double therapy with clopidogrel and
dabigatran 150 mg twice daily is reasonable to reduce the risk of bleeding as compared with triple therapy (IIa).
If triple is prescribed for patients with AF who are at increased risk of stroke and who have undergone PCI with stenting (drug
eluting or bare metal) for ACS, a transition to double therapy at 4 to 6 weeks may be considered (IIb).
Administration of amiodarone or digoxin may be considered to slow a rapid ventricular response in patients with ACS and AF
associated with severe LV dysfunction and HF or hemodynamic instability (IIb).
In patients with cryptogenic stroke (i.e., stroke of unknown cause) in whom external ambulatory monitoring is inconclusive,
implantation of a cardiac monitor (loop recorder) is reasonable to optimize detection of silent AF (IIa).
For overweight and obese patients with AF, weight loss, combined with risk factor modification, is recommended (I).

75. A 34-year-old male presented on Wednesday morning to the emergency department after
a weekend of heavy drinking. He felt his heart racing when he woke up on Saturday
morning. The sensation has persisted. On assessment, he was in an irregularly irregular
rhythm with otherwise normal vital signs. He has no history of hypertension, diabetes
mellitus, stroke, or vascular disease. He was anticoagulated with IV unfractionated heparin.
He underwent transesophageal echocardiography followed by direct-current cardioversion.
The left atrial appendage was normal in size and there was no spontaneous
echocardiogram contrast seen. The left ventricular ejection fraction was normal and there
was trace mitral regurgitation. Which of the following is an appropriate anticoagulation
strategy upon discharge?
• A. Enoxaparin 1 mg/kg for 5 days.
• B. Aspirin 81 mg daily for 1 month.
• C. No additional therapy.
• D. Warfarin with international normalized ratio (INR) goal 2.0-3.0 for 1 month.
• E. Apixaban 5 mg BID for 1 month.

76. A 71-year-old woman with an ischemic CMP and permanent AF underwent Bi V ICD
implantation 6 months prior. She has NYHA III symptoms and continues to complain of very
limited functional capacity, with no change since resynchronization therapy was initiated.
She is currently taking carvedilol 25 mg BID, lisinopril 10 mg QD, furosemide 40 mg BID,
atorvastatin 40 mg QD, aspirin 81 mg QD, and warfarin 5 mg QD. Her vital signs in the office
were BP 90/60 mm Hg, heart rate 111 bpm, RR rate 20/m, and SaO2 94% RA. She was
afebrile. Her examination was significant for bibasilar rales, irregular heartbeat, and 1+
bilateral LE edema. Interrogation of her biventricular ICD revealed good pacing and sensing
thresholds. The battery status and lead impedances were adequate. There had been two
episodes of nonsustained ventricular tachycardia, up to 15 beats, but no shocks had been
required. She was 25% paced over the past 3 months. In addition to treatment of her heart
failure, which of the following should be the next step in her management?
• A. Add sotalol.
• B. Referral for heart transplant evaluation.
• C. Atrioventricular nodal ablation.
• D. Increase carvedilol dose.

77. A 30-year-old male with hypertrophic cardiomyopathy s/p DC-ICD for secondary prevention
of sudden cardiac death presented to your office for routine follow-up. He was on
metoprolol succinate 50 mg daily. ICD interrogation disclosed 3 episodes of atrial flutter in
the past 3 months, the longest lasting 2 hours. He has been asymptomatic during these
episodes.
What is the best next step?
• A. Aspirin 325 mg daily.
• B. Left atrial appendage occlusion device.
• C. No change in medications.
• D. Radiofrequency ablation.
• E. Rivaroxaban 20 mg daily.

78. A 75-year-old female with hypertension and AF presented to your office for consultation.
She felt well with no symptomatic palpitations or dyspnea. Her medications include
carvedilol 6.25 mg twice daily, lisinopril 10 mg daily, and rivaroxaban. On examination, her
BP was 105/70 mm Hg, her HR was 98 bpm, and she was afebrile. Cardiac examination
revealed irregularly irregular rhythm and the remainder of her examination was
unremarkable. Her EKG showed AF at approximately 100 bpm and LBBB. A nuclear
myocardial perfusion scan performed 6 months prior showed a normal LVEF without
perfusion defects. Which of the following is the most appropriate next step in the
management of this patient?
• A. Add dofetilide.
• B. No change in therapy.
• C. Add diltiazem.
• D. Add digoxin.
• E. Atrial fibrillation ablation.

79. A 50-year-old male with paroxysmal atrial fibrillation and CHADSVaSC 0 was
admitted with two weeks of symptomatic AF. While in the hospital, he
underwent a TEE guided DCCV, and was loaded on amiodarone.
Which of the following is the most appropriate anticoagulation regimen?
• A. No anticoagulation.
• B. Aspirin plus clopidogrel.
• C. Apixaban.
• D. Warfarin.
• E. Ticagrelor.

80. A 76-year-old woman has permanent AF. She has a history of HTN, DM, HLD, and
osteoarthritis. Her medications include apixaban 5 mg twice daily, metoprolol
succinate 25 mg twice daily, metformin 500 mg twice daily, and atorvastatin 40 mg
daily. She would like to stop anticoagulation because she bruises easily.
What is this patient's estimated annual stroke risk without anticoagulation?
• A. 21%.
• B. 7%.
• C. 1%.
• D. 15%.
• E. 3%.

81. A 76-year-old male with a history of AF, HTN, DM, CVA 2 months prior, and a
DC-PMK for tachy-brady syndrome was scheduled to undergo pacemaker
generator change. His medications include Lisinopril 20 mg daily, metformin
850 mg twice daily, metoprolol succinate 50 mg daily, and warfarin 5 mg daily.
Which of the following is the most appropriate periprocedure anticoagulation
management strategy?
• A. Hold warfarin 5 days prior.
• B. Replace warfarin with dabigatran (150 mg twice daily).
• C. Continue warfarin.
• D. Bridge with enoxaparin.
• E. Replace warfarin with aspirin (325 mg daily).

82. A 72-year-old female presented with complaints of weakness and fatigue. She has a past history
significant for AF managed with rate control strategy, PAD, and HTN. She recently was discharged from
the hospital following a recurrent episode of atrial fibrillation requiring cardioversion. She was unclear
what her home medications are, but knows she was taking several new medications for her heart. Upon
physical examination, she was confused and lethargic. Her blood pressure was 91/54 mm Hg and pulse
was 103 bpm. Physical examination was remarkable for a tachycardic rhythm and no murmurs. She
complained of blurred vision. An ECG was obtained in the ED. The recent addition of which of the
following medications to this patient's medication regime is most likely responsible for her clinical
findings and ECG changes?
• A. Amlodipine.
• B. Nadolol.
• C. Dronedarone.
• D. Labetalol.
• E. Apixaban.

83. A 60-year-old female has a history of PAF that has been symptomatic enough to warrant
treatment. She was started on sotalol 80 mg BID, which was titrated up to 120 mg BID
because of ongoing recurrences. She was started on HCTZ 25 mg QD 1 week ago for HTN.
She was brought by ambulance to the ED for multiple episodes of lightheadedness and
dizziness. Her blood pressure was 120/76 mm Hg and her serum K was 3.2 mEq/L. Her ECG
was obtained. Which of the following should be the next step in her management?
• A. Intravenous potassium and magnesium.
• B. Electrical cardioversion.
• C. Intravenous metoprolol.
• D. Temporary transvenous pacing.
• E. Intravenous amiodarone.

84. References
• January CT, Wann LS, Alpert JS, et al.; American College of Cardiology/American Heart Association Task Force on Practice
Guidelines. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am
Coll Cardiol 2014;64:e1-e76.
• Nattel S, Harada M. Atrial remodeling and atrial fibrillation: recent advances and translational perspectives. J Am Coll
Cardiol 2014;63:2335-45.
• Mayo clinic and Cleveland clinic cariology board review courses.
• ACC self-assessment program
• Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and
thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation.
Chest 2010;137:263-72.
• Ganesan AN, Shipp NJ, Brooks AG, et al. Long-term outcomes of catheter ablation of atrial fibrillation: a systematic review
and meta-analysis. J Am Heart Assoc 2013;2:doi: 10.1161/JAHA.112.004549.
• Calkins H, Hindricks G, Cappato R, et al. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter
and surgical ablation of atrial fibrillation. Heart Rhythm 2017;14:e275-e444.

85. Thank You