ByBy

Essam Mahfouz, MDProfessor of Cardiology, Mansoura University

Agenda Agenda DefinitionDefinition

EpidemiologyEpidemiology

ClassificationClassification

Etiology & pathogenesisEtiology & pathogenesis

Diagnosis Diagnosis

Definition Definition

AF is a supraventricular AF is a supraventricular tachyarrhythmia with uncoordinated tachyarrhythmia with uncoordinated atrial activation and consequently atrial activation and consequently ineffective atrial contractionineffective atrial contraction

ECG characteristics include: ECG characteristics include: 1.1. irregular R-R intervals irregular R-R intervals

2.2. absence of distinct repeating P waves, absence of distinct repeating P waves,

3.3. irregular atrialirregular atrial activity activity

January, CT et al.2 014 AHA/ACC/HRS A F Guideline

Epidemiology Epidemiology AF is the most common arrhythmia in AF is the most common arrhythmia in adult populationadult populationThe incidence of AF doubles with each The incidence of AF doubles with each decade of life; the prevalence of the decade of life; the prevalence of the disease increases as the longevity of disease increases as the longevity of the population increasesthe population increasesIn a large cross-sectional study (N = In a large cross-sectional study (N = 1.89 million), AF prevalence increased 1.89 million), AF prevalence increased from from 0.1%0.1% of adults of adults <55 years<55 years old to old to 9%9% of those of those 80 years80 years; ; 3.8%3.8% of of people older than people older than 60 years60 years had AF had AF

Epidemiology Epidemiology The relative risk (RR) for death is The relative risk (RR) for death is 1.51.5 for men, for men, 1.91.9 for women with for women with AF; the primary cause of death is AF; the primary cause of death is worsening heart failureworsening heart failure11

The annual incidence rate of The annual incidence rate of ischemic stroke is ischemic stroke is 5%5% among among people with nonvalvular AF, people with nonvalvular AF, 2 to 2 to 7 times7 times that of people without that 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

Prevalence of AF in a population of 1.89 million members of a large Prevalence of AF in a population of 1.89 million members of a large health maintenance organization in California. The numbers represent health maintenance organization in California. The numbers represent the number of men and women with AF in each age category.the number of men and women with AF in each age category.

9.1

7.2

5.0

3.4

1.71.0

0.40.1

11.1

10.3

7.3

5.0

3.0

1.7

0.90.2

0

2

4

6

8

10

12

<55 55-59 60-64 65-69 70-74 75-79 80-84 >85

Prev

alan

ce, %

Men Women

AF Prevalence by Age AF Prevalence by Age and Sexand Sex

Go AS, et al. JAMA. 2001;285:2370-2375.

Age, y

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 both 2 Fold increase risk of both dementia and mortality dementia and mortality

1Bialy D, Lehmann MH, Schumacher DN. JACC. 1992;19:41A

Impact on HealthcareImpact on HealthcareHospital Discharges by Type of ArrhythmiaHospital Discharges by Type of Arrhythmia11

Chronic comorbid Chronic comorbid conditions with AFconditions with AF

> 65y> 65y < 65y< 65yHTNHTN 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%Anemia Anemia 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%

Classification Classification Term Definition

Paroxysmal Paroxysmal AFAF

• AF that terminates spontaneously or with intervention within 7 d of onset.

• Episodes may recur with variable frequency.

Persistent Persistent AFAF

Continuous AF that is sustained >7 d.

LongstandinLongstanding persistent g persistent AFAF

Continuous AF of >12 mo duration.

Permanent Permanent 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.

Non-valvular Non-valvular AFAF

AF in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.

AF PathophysiologyAF PathophysiologyNormal cardiac conduction is Normal cardiac conduction is coordinated by rhythmic coordinated by rhythmic spontaneous depolarization of the spontaneous depolarization of the sinoatrial node (SAN)sinoatrial node (SAN)

SAN impulse causes atrial myocyte SAN impulse causes atrial myocyte contraction, and conduction spreads contraction, and conduction spreads across atrium toward the across atrium toward the atrioventricular node (AVN)atrioventricular node (AVN)

AVN slows conduction and AVN slows conduction and coordinates rapid depolarization of coordinates rapid depolarization of the His-Purkinje system through the the His-Purkinje system through the right and left bundle branches (RBB, right and left bundle branches (RBB, LBB)LBB)

Depolarization of endocardial to Depolarization of endocardial to epicardial surface ensues with epicardial surface ensues with synchronous ventricular contraction synchronous ventricular contraction and compressive ejection of stroke and compressive ejection of stroke volumevolume

SAN

AVN

RBB

LBB

AF Pathophysiology AF Pathophysiology (CONT’D)(CONT’D)

The hallmark of AF is chaotic atrial impulses leading The 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

AF Pathophysiology AF Pathophysiology (CONT’D)(CONT’D)

During AF, the atria During AF, the atria contract at a rate of 350 contract at a rate of 350 to 900 bpm, conducting to 900 bpm, conducting to the ventricles at 90 to to the ventricles at 90 to 170 bpm170 bpm

Traditional mechanism Traditional mechanism theory: AF is maintained theory: AF is maintained by migrating wavelets of by migrating wavelets of reentrant atrial reentrant atrial activationactivation

Wavelet collisions cause Wavelet collisions cause chaotic reexcitation and chaotic 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 ischaracterized 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

Mechanisms of AFMechanisms of AF

““AF Begets AF”AF Begets AF”With time, remodeling of atrial tissue With time, remodeling of atrial tissue and the conduction system causes and the conduction system causes chronic AF and makes conversion from chronic AF and makes conversion from AF to sinus rhythm more difficultAF to sinus rhythm more difficult

Lack of contraction leads to increased Lack of contraction leads to increased left atrial diameter; “mechanical left atrial diameter; “mechanical remodeling” may result from atrial remodeling” may result from atrial fibrosisfibrosis

AF may also be triggered by AF may also be triggered by premature atrial contractions, premature atrial contractions, repetitive firing from pulmonary veins, repetitive firing from pulmonary veins, or atrial flutteror atrial flutter

1995: elegant studies in the goat 1995: 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 experience The longer atrial tissues experience chaotic electrical activity, the more chaotic 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.

A schema of the A schema of the potential pathogenesis potential pathogenesis of atrial tachycardia of atrial tachycardia remodeling.remodeling.CaCa2+2+ loading due to loading due toincreased rates causesincreased rates causesa threat to cell viability,a threat to cell viability,which is prevented by which is prevented by short- and long-termshort- and long-termadaptations that reduce adaptations that reduce CaCa2+2+ entry, providing entry, providing protective negative protective negative feedback on Cafeedback on Ca2+ 2+

loading, APD loading, APD abbreviation, andabbreviation, andpositive feedback onpositive feedback onAF likelihood byAF likelihood byreducing ERP and WL.reducing ERP and WL.

Sinus rhythm(60/min)

AF(400-600/min)

10-fold rate increase

Cellular Ca2+ loadingThreat to cell viability

minutes hours-days

ICa inactivation

ICa mRNA

ICa protein

Prolonged Tachycardia Leads to CaProlonged Tachycardia Leads to Ca2+2+ Overload in Atrial Myocytes, Causing Overload in Atrial Myocytes, Causing

“Electrical Remodeling”“Electrical 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

+

Atrial RemodelingAtrial RemodelingPotential basis forPotential basis forsuppression of AFsuppression of AFin chronic CHF byin chronic CHF byACE inhibitorsACE inhibitorsand angiotensinand angiotensinreceptor blockersreceptor blockers

Pulmonary veinPulmonary veinablation therapyablation therapy

may target ectopicmay target ectopic

foci of AF andfoci of AF and

prevent recurrenceprevent recurrence

more effectively thanmore effectively thanrhythm-control rhythm-control drugsdrugs

Ectopicfocus

Thoracicveins

Multiple-circuitreentry

Single-circuitreentry

Fibrosis Substrate Trigger

TachycardiaTrigger Substrate

Angiotensin II

Congestiveheart failure

Angiotensinsystemantagonists

Antiremodelingdrugs

Calcium ionloading

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.

Pathophysiology: Ectopic Pathophysiology: Ectopic AF FociAF Foci

1998 marks discovery 1998 marks discovery that AF could that AF could be caused by a rapidly be caused by a rapidly firing focus (usually in firing focus (usually in the superior pulmonary the superior pulmonary veins) and eliminated veins) and eliminated by focal ablationby focal ablation

““Highest dominant Highest dominant frequency” may be the frequency” may be the factor, originating in factor, originating in the pulmonary vein, the pulmonary vein, inferior vena cava, or inferior vena cava, or right atrium, that drives right atrium, that drives the AF wave frontthe AF 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.

Superiorvena cava

Inferiorvena cava

PulmonaryVeins

17 31

116Coronary

sinus

Fossa ovalis

Right Atrium Left Atrium

Septum

From Marriot HJL. Practical Electrocardiography. 7th ed. Baltimore: Williams & Wilkins; 1983.

Atrial Fibrillatory Atrial Fibrillatory WaveformsWaveforms

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

Acute AFAcute AFAcute 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 occurs conversion to sinus rhythm occurs spontaneously within 24 hours, and in half spontaneously within 24 hours, and in half of the remaining third within 48 hoursof the remaining third within 48 hours11

Paroxysmal AF occurs in fits, accompanied Paroxysmal AF occurs in fits, accompanied by rapid ventricular conductionby rapid ventricular conduction

Permanent chronic AF is generally found to Permanent 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 first developing 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.

AF Risk Factors and AF Risk Factors and CausesCausesElectrophysiologic Electrophysiologic

abnormalitiesabnormalitiesEnhanced automaticity (focal Enhanced automaticity (focal AF)AF)

Conduction abnormality Conduction abnormality (reentry)(reentry)

Atrial pressure elevationAtrial pressure elevationM or T valve diseaseM or T valve disease

Myocardial diseaseMyocardial disease

Semilunar valvular disordersSemilunar valvular disorders

Ventricular hypertrophyVentricular hypertrophy

Systemic or pulmonary Systemic or pulmonary hypertensionhypertension

Pulmonary embolismPulmonary embolism

Intracardiac tumors or Intracardiac tumors or thrombithrombi

Atrial ischemiaAtrial ischemiaCoronary artery diseaseCoronary artery disease

Inflammatory or Inflammatory or infiltrative atrial infiltrative atrial diseasedisease

PericarditisPericarditis

AmyloidosisAmyloidosis

MyocarditisMyocarditis

Age-induced atrial Age-induced atrial fibrotic changesfibrotic changes

Endocrine disordersEndocrine disordersHyperthyroidism Hyperthyroidism

PheochromocytomaPheochromocytoma

AF Risk Factors and AF Risk Factors and Causes Causes (CONT'D)(CONT'D)

DrugsDrugs AlcoholAlcohol

CaffeineCaffeine

Changes in autonomic Changes in autonomic tonetone

Increased Increased parasympathetic parasympathetic activityactivity

Increased sympathetic Increased sympathetic activityactivity

Neoplasm in or adjacent Neoplasm in or adjacent to atrial wallto atrial wall

Postoperative Postoperative Cardiac, pulmonary, Cardiac, pulmonary, esophageal surgeryesophageal surgeryCongenital heart Congenital heart diseasedisease

NeurogenicNeurogenicSubarachnoid Subarachnoid hemorrhagehemorrhageMajor Major nonhemorrhagic nonhemorrhagic strokestroke

Idiopathic (lone AF)Idiopathic (lone AF)Familial AFFamilial AF

Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

Independent Risk Factors Independent Risk Factors for AF: for AF:

the Framingham Heart the Framingham Heart StudyStudy

In addition to traditional risk factors for AF, recent prospective In addition to traditional risk factors for AF, recent prospective studies show that the risk for developing AF is increased by the studies show that the risk for developing AF is increased by the induction of atrial myocyte fibrosis under stimulation by induction of atrial myocyte fibrosis under stimulation by angiotensin I and angiotensin II and by chronic inflammation as angiotensin 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 FactorRelative 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)

Clinical Sequelae of AFClinical Sequelae of AFClinical 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, with and 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, and Cardiac output typically falls 0.8-1.0 L/min, and pulmonary artery occlusion pressure rises 3-4 mm pulmonary artery occlusion pressure rises 3-4 mm Hg in human models of AF with rapid ventricular rate Hg in human models of AF with rapid ventricular rate versus paced atrial tachycardia (conserved atrial versus paced atrial tachycardia (conserved atrial contraction)contraction)

Hemodynamics may be compromised by preexisting Hemodynamics may be compromised by preexisting MS, LVH, restrictive cardiomyopathy, or diastolic MS, LVH, restrictive cardiomyopathy, or diastolic heart failure. These conditions are dependent on heart failure. These conditions are dependent on atrial contraction to maintain cardiac outputatrial contraction to maintain cardiac output

Clinical Sequelae of AF Clinical Sequelae of AF (CONT'D)(CONT'D)

Tachycardia-induced cardiomyopathy resulting from Tachycardia-induced cardiomyopathy resulting from

CaCa2+2+ toxicity toxicity

Rapid ventricular responses may be triggered by Rapid ventricular responses may be triggered by

fever, sepsis, volume depletion, gastrointestinal fever, sepsis, volume depletion, gastrointestinal

bleeding, medication noncompliance, or uncontrolled bleeding, medication noncompliance, or uncontrolled

hyperthyroidismhyperthyroidism

Patients with Wolfe-Parkinson-White syndrome are at Patients with Wolfe-Parkinson-White syndrome are at

risk for AF (15% to 20% of patients) with conversion risk for AF (15% to 20% of patients) with conversion

to ventricular fibrillation via relentless conduction to ventricular fibrillation via relentless conduction

across an accessory pathwayacross an accessory pathway

15% of patients with hypertrophic cardiomyopathy 15% of patients with hypertrophic cardiomyopathy

develop AF leading to rapid deteriorationdevelop AF leading to rapid deterioration

AF and Stroke – AF and Stroke – Pathophysiology: Pathophysiology:

LAA ThrombusLAA ThrombusMore than 90% of all cardioembolic strokes in More 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 of With 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) emptying wave (active) and E-wave (passive) emptying of the LAA, which are reduced with elevated of the LAA, which are reduced with elevated left ventricular end-diastolic pressuresleft ventricular end-diastolic pressures

Left atrial cavity thrombus was found by TEE Left atrial cavity thrombus was found by TEE in 2% of patients with chronic AF (Cleveland in 2% of patients with chronic AF (Cleveland Clinic study); LAA thrombus was found in Clinic study); LAA thrombus was found in 12% of patients and was strongly associated 12% of patients and was strongly associated with SECwith SEC

Left Atrial Appendage Left Atrial Appendage (CONT’D)(CONT’D)

A.A. Example of a polylobed LAA with severe SEC and the Example of a polylobed LAA with severe SEC and the corresponding pulsed Doppler of corresponding 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 of Example of an LAA ligated by the surgeon at the time of

mitral valvuloplasty. The ligature is incomplete and there mitral valvuloplasty. The ligature is incomplete and there is still flow between the LAA and the left atrial cavity.is still flow between the LAA and the left atrial cavity.

Adapted from Donal E, et al. Chest. 2005;128:1853-1862.

Evaluation of Patients Evaluation of Patients With AFWith AFMinimum EvaluationMinimum Evaluation

History and physical History and physical examinationexamination

Presence and nature of AF Presence and nature of AF symptomssymptoms

Clinical type of AF (first Clinical type of AF (first episode, paroxysmal, episode, paroxysmal, persistent, or permanent)persistent, or permanent)

Onset (first symptomatic Onset (first symptomatic attack or date of discovery attack or date of discovery of AFof AF

Frequency, duration, Frequency, duration, precipitating factors, and precipitating factors, and modes of termination of AFmodes of termination of AF

Response to any drugs that Response to any drugs that have been givenhave been given

Presence of underlying heart Presence of underlying heart disease or other reversible disease or other reversible condition condition

ElectrocardiogramElectrocardiogramRhythm (verify AF)Rhythm (verify AF)

P-wave duration and P-wave duration and morphology or fibrillatory morphology or fibrillatory waveswaves

PreexcitationPreexcitation

Bundle-branch blockBundle-branch block

Prior MIPrior MI

Other atrial arrhythmiasOther atrial arrhythmias

R-R, QRS, and QT R-R, QRS, and QT intervals in conjunction intervals in conjunction with antiarrhythmic drug with antiarrhythmic drug therapy therapy

Evaluation of Patients Evaluation of Patients With AF 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 pressure Peak RV pressure (pulmonary hypertension) (pulmonary hypertension)

LV hypertrophyLV hypertrophy

LA thrombus (low LA 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 is when ventricular rate is difficult to controldifficult to control

Additional TestingAdditional TestingSix-minute walk testSix-minute walk test

If adequacy of rate control is in If adequacy of rate control is in questionquestion

Exercise testingExercise testingIf adequacy of rate control is in If adequacy of rate control is in question (permanent AF)question (permanent AF)

To reproduce exercise-induced To reproduce exercise-induced AFAF

To exclude ischemia before To exclude ischemia before treatment of selected patients treatment of selected patients with a type IC anti-arrhythmic with a type IC anti-arrhythmic drugdrug

Holter monitoring Holter monitoring If diagnosis of the type of If diagnosis of the type of arrhythmia is in questionarrhythmia is in question

As a means of evaluating rate As a means of evaluating rate controlcontrol

Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

Evaluation of Patients Evaluation of Patients With AF With AF (CONT’D)(CONT’D)

Additional TestingAdditional TestingTEE:TEE:

To identify LA thrombus To identify LA thrombus (in the LA appendage)(in the LA appendage)

To guide cardioversionTo guide cardioversion

Electrophysiologic studyElectrophysiologic studyTo clarify the mechanism To clarify the mechanism of wide-QRS-complex of wide-QRS-complex tachycardiatachycardia

To identify a To identify a predisposing arrhythmia predisposing arrhythmia such as atrial flutter or such as atrial flutter or paroxysmal SVTparoxysmal SVT

To seek sites for curative To seek sites for curative ablation or AV conduction ablation or AV conduction block/modificationblock/modification

Chest radiograph,Chest radiograph,

toto evaluateevaluate

Lung parenchyma, Lung parenchyma, when clinical findings when clinical findings suggest an suggest an abnormalityabnormality

Pulmonary Pulmonary vasculature, when vasculature, when clinical findings clinical findings suggest an suggest an abnormalityabnormality

Fuster V, et al. ACC Guidelines Circulation. 2006;114:e257-e354.

Rapid AFRapid AF

Slow AFSlow AF

AF before 1 and AF before 1 and after 2 IV after 2 IV

adenosine adenosine

AF with AF with WPWWPW

AF in AF in ? ?

PulmonaryPulmonary embolism embolism

Risk score definitions Risk score definitions

Stroke risk stratification Stroke risk stratification