1. Atrial fibrillation (AF) is an irregular heartbeat that can lead to blood clots, stroke, heart failure, and other complications. It is the most common arrhythmia and its prevalence increases with age. 2. AF occurs due to uncoordinated electrical signals in the atria that cause rapid and irregular beating. Risk factors include heart disease, high blood pressure, diabetes, sleep apnea, and thyroid problems. 3. Diagnosis involves an electrocardiogram to detect the irregular rhythm. Treatment depends on symptoms and includes rate or rhythm control medications, lifestyle changes, and sometimes procedures like ablation to restore normal rhythm.

2. ByBy
Essam Mahfouz, MD
Professor of Cardiology, Mansoura University

3. AgendaAgenda
DefinitionDefinition
EpidemiologyEpidemiology
ClassificationClassification
Etiology & pathogenesisEtiology & pathogenesis
DiagnosisDiagnosis

4. DefinitionDefinition
AF is a supraventricularAF is a supraventricular
tachyarrhythmia withtachyarrhythmia with
uncoordinated atrial activation anduncoordinated atrial activation and
consequently ineffective atrialconsequently ineffective atrial
contractioncontraction
ECG characteristics include:ECG characteristics include:
1.1. irregular R-R intervalsirregular R-R intervals
2.2. absence of distinct repeating P waves,absence of distinct repeating P waves,
3.3. irregular atrialirregular atrial activityactivity
January, CT et al.2 014 AHA/ACC/HRS A F Guideline

5. EpidemiologyEpidemiology
AF is the most common arrhythmia inAF is the most common arrhythmia in
adult populationadult population
The incidence of AF doubles with eachThe incidence of AF doubles with each
decade of life; the prevalence of thedecade of life; the prevalence of the
disease increases as the longevity ofdisease increases as the longevity of
the population increasesthe population increases
In a large cross-sectional study (N =In a large cross-sectional study (N =
1.89 million), AF prevalence increased1.89 million), AF prevalence increased
fromfrom 0.1%0.1% of adultsof adults <55 years<55 years old toold to
9%9% of thoseof those ≥≥80 years80 years;; 3.8%3.8% ofof
people older thanpeople older than 60 years60 years had AFhad AF

6. EpidemiologyEpidemiology
The relative risk (RR) for death isThe relative risk (RR) for death is
1.51.5 for men,for men, 1.91.9 for women withfor women with
AF; the primary cause of death isAF; the primary cause of death is
worsening heart failureworsening heart failure11
The annual incidence rate ofThe annual incidence rate of
ischemic stroke isischemic stroke is 5%5% amongamong
people with nonvalvular AF,people with nonvalvular AF, 2 to2 to
7 times7 times that of people withoutthat of people without
AFAF22
1. Benjamin EJ, et al. Circulation. 1998;98:946-952.
2. Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354

7. Prevalence of AF in a population of 1.89 million members of aPrevalence of AF in a population of 1.89 million members of a
large health maintenance organization in California. The numberslarge health maintenance organization in California. The numbers
represent the number of men and women with AF in each agerepresent the number of men and women with AF in each age
category.category.
9.1
7.2
5.0
3.4
1.7
1.0
0.4
0.1
11.1
10.3
7.3
5.0
3.0
1.7
0.9
0.2
0
2
4
6
8
10
12
<55 55-59 60-64 65-69 70-74 75-79 80-84 >85
Prevalance,%
Men Women
AF Prevalence by Age and SexAF Prevalence by Age and Sex
Go AS, et al. JAMA. 2001;285:2370-2375.
Age, y

8. AF & CV riskAF & CV risk
5 fold increase risk of stroke5 fold increase risk of stroke
3 fold increase risk of HF3 fold increase risk of HF
2 Fold increase risk of both2 Fold increase risk of both
dementia and mortalitydementia and mortality

9. 1
Bialy D, Lehmann MH, Schumacher DN. JACC. 1992;19:41A
Impact on HealthcareImpact on Healthcare
Hospital Discharges by Type of ArrhythmiaHospital Discharges by Type of Arrhythmia11

10. Chronic comorbid conditionsChronic comorbid conditions
with AFwith AF
> 65y> 65y < 65y< 65y
HTNHTN 83%83% 81.1%81.1%
IHDIHD 63.8%63.8% 64.5%64.5%
HyperlipidemiaHyperlipidemia 62.1%62.1% 60.6%60.6%
HFHF 51.4%51.4% 59.3%59.3%
DMDM 36.5%36.5% 53.1%53.1%
AnemiaAnemia 42.3%42.3% 45.6%45.6%
CKDCKD 32.3%32.3% 40.3%40.3%
COPDCOPD 23.2%23.2% 31.4%31.4%

11. ClassificationClassification
Term Definition
ParoxysmalParoxysmal
AFAF
• AF that terminates spontaneously or with
intervention within 7 d of onset.
• Episodes may recur with variable frequency.
PersistentPersistent
AFAF
Continuous AF that is sustained >7 d.
LongstandinLongstandin
g persistentg persistent
AFAF
Continuous AF of >12 mo duration.
PermanentPermanent
AFAF
• 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.

12. AF PathophysiologyAF Pathophysiology
Normal cardiac conduction isNormal cardiac conduction is
coordinated by rhythmiccoordinated by rhythmic
spontaneous depolarization of thespontaneous depolarization of the
sinoatrial node (SAN)sinoatrial node (SAN)
SAN impulse causes atrial myocyteSAN impulse causes atrial myocyte
contraction, and conduction spreadscontraction, and conduction spreads
across atrium toward theacross atrium toward the
atrioventricular node (AVN)atrioventricular node (AVN)
AVN slows conduction andAVN slows conduction and
coordinates rapid depolarization ofcoordinates rapid depolarization of
the His-Purkinje system through thethe His-Purkinje system through the
right and left bundle branches (RBB,right and left bundle branches (RBB,
LBB)LBB)
Depolarization of endocardial toDepolarization of endocardial to
epicardial surface ensues withepicardial surface ensues with
synchronous ventricular contractionsynchronous ventricular contraction
and compressive ejection of strokeand compressive ejection of stroke
volumevolume
SAN
AVN
RBB
LBB

13. AF PathophysiologyAF Pathophysiology (CONT’D)(CONT’D)
The hallmark of AF is chaotic atrial impulses leadingThe hallmark of AF is chaotic atrial impulses leading
to irregularly irregular ventricular contraction,to irregularly irregular ventricular contraction,
usually with incessant tachycardiausually with incessant tachycardia
Normal electrical pathways Abnormal electrical pathways
Normal sinus rhythm Atrial fibrillation
Sinus
(SA)
node
Atrioventricular
(AV) node

14. AF PathophysiologyAF Pathophysiology (CONT’D)(CONT’D)
During AF, the atriaDuring AF, the atria
contract at a rate of 350contract at a rate of 350
to 900 bpm, conductingto 900 bpm, conducting
to the ventricles at 90to the ventricles at 90
to 170 bpmto 170 bpm
Traditional mechanismTraditional mechanism
theory: AF is maintainedtheory: AF is maintained
by migrating waveletsby migrating wavelets
of reentrant atrialof reentrant atrial
activationactivation
Wavelet collisions causeWavelet collisions cause
chaotic reexcitation andchaotic reexcitation and
“multiple propagating“multiple propagating
wavelets”wavelets”
Adapted from Narayan SN, et al. Lancet. 1997;350:943-950.
AF compared with sinus rhythm. AF is
characterized by multiple electrical
wavelets in the atria. Disorders that
increase atrial size, decrease tissue
wavelength, or affect both may increase
the propensity for AF.
Sinus rhythm Atrial fibrillation
Sinus
node
Sinus node
inhibited
Coordinated activity
over atria
Migrating wavelets of
re-entrant activation

15. Mechanisms of AFMechanisms of AF

16. ““AF Begets AF”AF Begets AF”
With time, remodeling of atrial tissueWith time, remodeling of atrial tissue
and the conduction system causesand the conduction system causes
chronic AF and makes conversionchronic AF and makes conversion
from AF to sinus rhythm more difficultfrom AF to sinus rhythm more difficult
Lack of contraction leads to increasedLack of contraction leads to increased
left atrial diameter; “mechanicalleft atrial diameter; “mechanical
remodeling” may result from atrialremodeling” may result from atrial
fibrosisfibrosis
AF may also be triggered byAF may also be triggered by
premature atrial contractions,premature atrial contractions,
repetitive firing from pulmonaryrepetitive firing from pulmonary
veins, or atrial flutterveins, or atrial flutter
1995: elegant studies in the goat1995: elegant studies in the goat
model of AF prove that “AF begets AF”model of AF prove that “AF begets AF”
The longer atrial tissues experienceThe longer atrial tissues experience
chaotic electrical activity, the morechaotic electrical activity, the more
likely they are to remain in AFlikely they are to remain in AF
Wijffels MCEF, et al. Circulation. 1995;92:1954-1968.

17. A schema of theA schema of the
potential pathogenesispotential pathogenesis
of atrial tachycardiaof atrial tachycardia
remodeling.remodeling.
CaCa2+2+
loading due toloading due to
increased rates causesincreased rates causes
a threat to cell viability,a threat to cell viability,
which is prevented bywhich is prevented by
short- and long-termshort- and long-term
adaptations that reduceadaptations that reduce
CaCa2+2+
entry, providingentry, providing
protective negativeprotective negative
feedback on Cafeedback on Ca2+2+
loading,loading,
APDAPD
abbreviation, andabbreviation, and
positive feedback onpositive feedback on
AF likelihood byAF likelihood by
reducing ERP and WL.reducing ERP and WL.
Sinus rhythm
(60/min)
AF
(400-600/min)
10-fold rate
increase
Cellular Ca2+
loading
Threat to cell viability
minutes hours-days
ICa inactivation
↓ ICa mRNA
↓ ICa protein
Prolonged Tachycardia Leads to CaProlonged Tachycardia Leads to Ca2+2+
OverloadOverload
in Atrial Myocytes, Causing “Electricalin Atrial Myocytes, Causing “Electrical
Remodeling”Remodeling”
↓ ICa ↓ ICa
APD = action potential duration; ERP = effective refractory period; WL = wavelength.
Adapted from Shiroshita-Takeshita A, et al. J Interv Card Electrophysiol. 2005;13:181-193.
↓ APD
−
↓ ERP, ↓ WL
+

18. Atrial RemodelingAtrial Remodeling
Potential basis forPotential basis for
suppression of AFsuppression of AF
in chronic CHF byin chronic CHF by
ACE inhibitorsACE inhibitors
and angiotensinand angiotensin
receptor blockersreceptor blockers
Pulmonary veinPulmonary vein
ablation therapyablation therapy
may target ectopicmay target ectopic
foci of AF andfoci of AF and
prevent recurrenceprevent recurrence
more effectively thanmore effectively than
rhythm-controlrhythm-control
drugsdrugs
Ectopic
focus
Thoracic
veins
Multiple-
circuit
reentry
Single-
circuit
reentry
Fibrosis Substrate Trigger
Tachycardia
Trigger Substrate
Angiotensin II
Congestive
heart failure
Angiotensin
system
antagonists
Antiremodeling
drugs
Calcium ion
loading
↓ ICa ↓ RP, ↓ WL
Rapid atrial tachycardia causes atrial remodeling by down-regulating L-type calcium
channel function (ICa), thereby accelerating atrial repolarization, reducing the refractory
period and wavelength, and promoting reentry. Remodeling may also be able to promote
ectopic activity in the thoracic veins. CHF activates the RAS and causes atrial fibrosis.
Specific drug therapy might attenuate tachycardia-induced and fibrotic atrial remodeling
and help prevent AF.
Shiroshita-Takeshita A, et al. J Interv Card Electrophysiol. 2005;13:181-193.

19. Pathophysiology: Ectopic AFPathophysiology: Ectopic AF
FociFoci
1998 marks discovery1998 marks discovery
that AF couldthat AF could
be caused by a rapidlybe caused by a rapidly
firing focus (usually infiring focus (usually in
the superior pulmonarythe superior pulmonary
veins) and eliminatedveins) and eliminated
by focal ablationby focal ablation
““Highest dominantHighest dominant
frequency” may be thefrequency” may be the
factor, originating in thefactor, originating in the
pulmonary vein, inferiorpulmonary vein, inferior
vena cava, or rightvena cava, or right
atrium, that drives theatrium, that drives the
AF wave frontAF wave front
Adapted from Haissaguerre M, et al. N Engl J Med. 1998;339:659-666.
Diagram of the sites of 69 foci triggering AF in 45 patients. Note
the clustering in the pulmonary veins, particularly in both
superior pulmonary veins. Numbers indicate the distribution of
foci in the pulmonary veins.
Superior
vena cava
Inferior
vena cava
Pulmonary
Veins
17 31
116
Coronary
sinus
Fossa
ovalis
Right Atrium Left Atrium
Septum

20. From Marriot HJL. Practical Electrocardiography. 7th ed. Baltimore: Williams & Wilkins; 1983.
Atrial Fibrillatory WaveformsAtrial Fibrillatory Waveforms
Coarse (A), medium (B), and fine (C) atrial fibrillation,Coarse (A), medium (B), and fine (C) atrial fibrillation,
each with irregular ventricular response.each with irregular ventricular response.
A
B
C

21. Acute AFAcute AF
Acute AF = episode <48 hoursAcute AF = episode <48 hours
In two thirds of patients with acute AF,In two thirds of patients with acute AF,
conversion to sinus rhythm occursconversion to sinus rhythm occurs
spontaneously within 24 hours, and in halfspontaneously within 24 hours, and in half
of the remaining third within 48 hoursof the remaining third within 48 hours11
Paroxysmal AF occurs in fits, accompaniedParoxysmal AF occurs in fits, accompanied
by rapid ventricular conductionby rapid ventricular conduction
Permanent chronic AF is generally found toPermanent chronic AF is generally found to
be a frequent outcome of paroxysmal AF,be a frequent outcome of paroxysmal AF,
developing within a few years of the firstdeveloping within a few years of the first
arrhythmic episodearrhythmic episode22
Danias PG, et al. J Am Coll Cardiol. 1998;31:588-592.
Kerr CR, et al. Am Heart J. 2005;149:489-496.

22. AF Risk Factors and CausesAF Risk Factors and Causes
ElectrophysiologicElectrophysiologic
abnormalitiesabnormalities
Enhanced automaticityEnhanced automaticity
(focal AF)(focal AF)
Conduction abnormalityConduction abnormality
(reentry)(reentry)
Atrial pressure elevationAtrial pressure elevation
M or T valve diseaseM or T valve disease
Myocardial diseaseMyocardial disease
Semilunar valvularSemilunar valvular
disordersdisorders
Ventricular hypertrophyVentricular hypertrophy
Systemic or pulmonarySystemic or pulmonary
hypertensionhypertension
Pulmonary embolismPulmonary embolism
Intracardiac tumors orIntracardiac tumors or
thrombithrombi
Atrial ischemiaAtrial ischemia
Coronary artery diseaseCoronary artery disease
Inflammatory orInflammatory or
infiltrative atrial diseaseinfiltrative atrial disease
PericarditisPericarditis
AmyloidosisAmyloidosis
MyocarditisMyocarditis
Age-induced atrialAge-induced atrial
fibrotic changesfibrotic changes
Endocrine disordersEndocrine disorders
HyperthyroidismHyperthyroidism
PheochromocytomaPheochromocytoma

23. AF Risk Factors and CausesAF Risk Factors and Causes
(CONT'D)(CONT'D)
DrugsDrugs
AlcoholAlcohol
CaffeineCaffeine
Changes in autonomicChanges in autonomic
tonetone
IncreasedIncreased
parasympatheticparasympathetic
activityactivity
Increased sympatheticIncreased sympathetic
activityactivity
Neoplasm in or adjacentNeoplasm in or adjacent
to atrial wallto atrial wall
PostoperativePostoperative
Cardiac, pulmonary,Cardiac, pulmonary,
esophageal surgeryesophageal surgery
Congenital heartCongenital heart
diseasedisease
NeurogenicNeurogenic
SubarachnoidSubarachnoid
hemorrhagehemorrhage
MajorMajor
nonhemorrhagicnonhemorrhagic
strokestroke
Idiopathic (lone AF)Idiopathic (lone AF)
Familial AFFamilial AF
Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

24. Independent Risk Factors for AF:Independent Risk Factors for AF:
the Framingham Heart Studythe Framingham Heart Study
In addition to traditional risk factors for AF, recent prospectiveIn addition to traditional risk factors for AF, recent prospective
studies show that the risk for developing AF is increased by thestudies show that the risk for developing AF is increased by the
induction of atrial myocyte fibrosis under stimulation byinduction of atrial myocyte fibrosis under stimulation by
angiotensin I and angiotensin II and by chronic inflammation asangiotensin I and angiotensin II and by chronic inflammation as
marked by elevated serum CRP levels.marked by elevated serum CRP levels.
Heist EK, Ruskin JN. Prog Cardiovas Dis. 2006;48:256-269.
Risk FactorRisk Factor
Relative Risk (95% CI)Relative Risk (95% CI)
MenMen WomenWomen
Heart failureHeart failure
Age (per decade)Age (per decade)
Valve diseaseValve disease
HypertensionHypertension
Diabetes mellitusDiabetes mellitus
Acute MIAcute MI
4.5 (3.1-6.6)4.5 (3.1-6.6)
2.1 (1.8-2.5)2.1 (1.8-2.5)
1.8 (1.2-2.5)1.8 (1.2-2.5)
1.5 (1.2-2.0)1.5 (1.2-2.0)
1.4 (1.0-2.0)1.4 (1.0-2.0)
1.4 (1.0-2.0)1.4 (1.0-2.0)
5.9 (4.2-8.4)5.9 (4.2-8.4)
2.2 (1.9-2.6)2.2 (1.9-2.6)
3.4 (2.5-4.5)3.4 (2.5-4.5)
1.4 (1.1-1.8)1.4 (1.1-1.8)
1.6 (1.1-2.2)1.6 (1.1-2.2)
1.2 (0.8-1.8)1.2 (0.8-1.8)

25. Clinical Sequelae of AFClinical Sequelae of AF
Clinical sequelae of AF relate to loss of atrial “kick”Clinical sequelae of AF relate to loss of atrial “kick”
and inadequate time for ventricular filling, withand inadequate time for ventricular filling, with
reduced cardiac outputreduced cardiac output
AF may lower stroke volume as much as 20%AF may lower stroke volume as much as 20%
Cardiac output typically falls 0.8-1.0 L/min, andCardiac output typically falls 0.8-1.0 L/min, and
pulmonary artery occlusion pressure rises 3-4 mmpulmonary artery occlusion pressure rises 3-4 mm
Hg in human models of AF with rapid ventricular rateHg in human models of AF with rapid ventricular rate
versus paced atrial tachycardia (conserved atrialversus paced atrial tachycardia (conserved atrial
contraction)contraction)
Hemodynamics may be compromised by preexistingHemodynamics may be compromised by preexisting
MS, LVH, restrictive cardiomyopathy, or diastolicMS, LVH, restrictive cardiomyopathy, or diastolic
heart failure. These conditions are dependent onheart failure. These conditions are dependent on
atrial contraction to maintain cardiac outputatrial contraction to maintain cardiac output

26. Clinical Sequelae of AFClinical Sequelae of AF (CONT'D)(CONT'D)
Tachycardia-induced cardiomyopathy resulting fromTachycardia-induced cardiomyopathy resulting from
CaCa2+2+
toxicitytoxicity
Rapid ventricular responses may be triggered byRapid ventricular responses may be triggered by
fever, sepsis, volume depletion, gastrointestinalfever, sepsis, volume depletion, gastrointestinal
bleeding, medication noncompliance, or uncontrolledbleeding, medication noncompliance, or uncontrolled
hyperthyroidismhyperthyroidism
Patients with Wolfe-Parkinson-White syndrome are atPatients with Wolfe-Parkinson-White syndrome are at
risk for AF (15% to 20% of patients) with conversionrisk for AF (15% to 20% of patients) with conversion
to ventricular fibrillation via relentless conductionto ventricular fibrillation via relentless conduction
across an accessory pathwayacross an accessory pathway
15% of patients with hypertrophic cardiomyopathy15% of patients with hypertrophic cardiomyopathy
develop AF leading to rapid deteriorationdevelop AF leading to rapid deterioration

27. AF and Stroke – Pathophysiology:AF and Stroke – Pathophysiology:
LAA ThrombusLAA Thrombus
More than 90% of all cardioembolic strokes inMore than 90% of all cardioembolic strokes in
patients with AF arise from LAA thrombipatients with AF arise from LAA thrombi
With TEE, assess LAA size; presence ofWith TEE, assess LAA size; presence of
spontaneous echo contrast (SEC),spontaneous echo contrast (SEC),
representing turbulent blood pooling; and A-representing turbulent blood pooling; and A-
wave (active) and E-wave (passive) emptyingwave (active) and E-wave (passive) emptying
of the LAA, which are reduced with elevatedof the LAA, which are reduced with elevated
left ventricular end-diastolic pressuresleft ventricular end-diastolic pressures
Left atrial cavity thrombus was found by TEELeft atrial cavity thrombus was found by TEE
in 2% of patients with chronic AF (Clevelandin 2% of patients with chronic AF (Cleveland
Clinic study); LAA thrombus was found inClinic study); LAA thrombus was found in
12% of patients and was strongly associated12% of patients and was strongly associated
with SECwith SEC

28. Left Atrial AppendageLeft Atrial Appendage (CONT’D)(CONT’D)
A.A. Example of a polylobed LAA with severe SEC and theExample of a polylobed LAA with severe SEC and the
corresponding pulsed Doppler ofcorresponding pulsed Doppler of
LAA flows.LAA flows.
B.B. Second example of polylobed LAA.Second example of polylobed LAA.
C.C. Example of an LAA ligated by the surgeon at the time ofExample of an LAA ligated by the surgeon at the time of
mitral valvuloplasty. The ligature is incomplete and there ismitral valvuloplasty. The ligature is incomplete and there is
still flow between the LAA and the left atrial cavity.still flow between the LAA and the left atrial cavity.
Adapted from Donal E, et al. Chest. 2005;128:1853-1862.

29. Evaluation of Patients With AFEvaluation of Patients With AF
Minimum EvaluationMinimum Evaluation
History and physicalHistory and physical
examinationexamination
Presence and nature of AFPresence and nature of AF
symptomssymptoms
Clinical type of AF (firstClinical type of AF (first
episode, paroxysmal,episode, paroxysmal,
persistent, or permanent)persistent, or permanent)
Onset (first symptomaticOnset (first symptomatic
attack or date of discovery ofattack or date of discovery of
AFAF
Frequency, duration,Frequency, duration,
precipitating factors, andprecipitating factors, and
modes of termination of AFmodes of termination of AF
Response to any drugs thatResponse to any drugs that
have been givenhave been given
Presence of underlying heartPresence of underlying heart
disease or other reversibledisease or other reversible
conditioncondition
ElectrocardiogramElectrocardiogram
Rhythm (verify AF)Rhythm (verify AF)
P-wave duration andP-wave duration and
morphology or fibrillatorymorphology or fibrillatory
waveswaves
PreexcitationPreexcitation
Bundle-branch blockBundle-branch block
Prior MIPrior MI
Other atrial arrhythmiasOther atrial arrhythmias
R-R, QRS, and QTR-R, QRS, and QT
intervals in conjunctionintervals in conjunction
with antiarrhythmic drugwith antiarrhythmic drug
therapytherapy

30. Evaluation of Patients With AFEvaluation of Patients With AF
(CONT’D)(CONT’D)
Minimum EvaluationMinimum Evaluation
TTE to identifyTTE to identify
Valvular heart diseaseValvular heart disease
LA and RA sizeLA and RA size
LV size and functionLV size and function
Peak RV pressurePeak RV pressure
(pulmonary hypertension)(pulmonary hypertension)
LV hypertrophyLV hypertrophy
LA thrombus (lowLA thrombus (low
sensitivity)sensitivity)
Pericardial diseasePericardial disease
Blood tests of thyroid,Blood tests of thyroid,
renal, and hepatic functionrenal, and hepatic function
For first episode of AF,For first episode of AF,
when ventricular rate iswhen ventricular rate is
difficult to controldifficult to control
Additional TestingAdditional Testing
Six-minute walk testSix-minute walk test
If adequacy of rate control isIf adequacy of rate control is
in questionin question
Exercise testingExercise testing
If adequacy of rate control isIf adequacy of rate control is
in question (permanent AF)in question (permanent AF)
To reproduce exercise-To reproduce exercise-
induced AFinduced AF
To exclude ischemia beforeTo exclude ischemia before
treatment of selectedtreatment of selected
patients with a type IC anti-patients with a type IC anti-
arrhythmic drugarrhythmic drug
Holter monitoringHolter monitoring
If diagnosis of the type ofIf diagnosis of the type of
arrhythmia is in questionarrhythmia is in question
As a means of evaluatingAs a means of evaluating
rate controlrate control
Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

31. Evaluation of Patients With AFEvaluation of Patients With AF
(CONT’D)(CONT’D)
Additional TestingAdditional Testing
TEE:TEE:
To identify LA thrombusTo identify LA thrombus
(in the LA appendage)(in the LA appendage)
To guide cardioversionTo guide cardioversion
Electrophysiologic studyElectrophysiologic study
To clarify the mechanismTo clarify the mechanism
of wide-QRS-complexof wide-QRS-complex
tachycardiatachycardia
To identify a predisposingTo identify a predisposing
arrhythmia such as atrialarrhythmia such as atrial
flutter or paroxysmal SVTflutter or paroxysmal SVT
To seek sites for curativeTo seek sites for curative
ablation or AV conductionablation or AV conduction
block/modificationblock/modification
Chest radiograph,Chest radiograph,
toto evaluateevaluate
Lung parenchyma,Lung parenchyma,
when clinical findingswhen clinical findings
suggest ansuggest an
abnormalityabnormality
PulmonaryPulmonary
vasculature, whenvasculature, when
clinical findingsclinical findings
suggest ansuggest an
abnormalityabnormality
Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

32. Rapid AFRapid AF

33. Slow AFSlow AF

34. AF before 1 and after 2AF before 1 and after 2
IV adenosineIV adenosine

35. AF withAF with
WPWWPW

36. AF inAF in
? Pulmonary? Pulmonary
embolismembolism

37. Risk score definitionsRisk score definitions

38. Stroke risk stratificationStroke risk stratification