0
ByBy
Essam Mahfouz, MD
Professor of Cardiology, Mansoura University
AgendaAgenda
DefinitionDefinition
EpidemiologyEpidemiology
ClassificationClassification
Etiology & pathogenesisEtiology & ...
DefinitionDefinition
AF is a supraventricularAF is a supraventricular
tachyarrhythmia withtachyarrhythmia with
uncoordinat...
EpidemiologyEpidemiology
AF is the most common arrhythmia inAF is the most common arrhythmia in
adult populationadult popu...
EpidemiologyEpidemiology
The relative risk (RR) for death isThe relative risk (RR) for death is
1.51.5 for men,for men, 1....
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...
AF & CV riskAF & CV risk
5 fold increase risk of stroke5 fold increase risk of stroke
3 fold increase risk of HF3 fold inc...
1
Bialy D, Lehmann MH, Schumacher DN. JACC. 1992;19:41A
Impact on HealthcareImpact on Healthcare
Hospital Discharges by Ty...
Chronic comorbid conditionsChronic comorbid conditions
with AFwith AF
> 65y> 65y < 65y< 65y
HTNHTN 83%83% 81.1%81.1%
IHDIH...
ClassificationClassification
Term Definition
ParoxysmalParoxysmal
AFAF
• AF that terminates spontaneously or with
interven...
AF PathophysiologyAF Pathophysiology
Normal cardiac conduction isNormal cardiac conduction is
coordinated by rhythmiccoord...
AF PathophysiologyAF Pathophysiology (CONT’D)(CONT’D)
The hallmark of AF is chaotic atrial impulses leadingThe hallmark of...
AF PathophysiologyAF Pathophysiology (CONT’D)(CONT’D)
During AF, the atriaDuring AF, the atria
contract at a rate of 350co...
Mechanisms of AFMechanisms of AF
““AF Begets AF”AF Begets AF”
With time, remodeling of atrial tissueWith time, remodeling of atrial tissue
and the conducti...
A schema of theA schema of the
potential pathogenesispotential pathogenesis
of atrial tachycardiaof atrial tachycardia
rem...
Atrial RemodelingAtrial Remodeling
Potential basis forPotential basis for
suppression of AFsuppression of AF
in chronic CH...
Pathophysiology: Ectopic AFPathophysiology: Ectopic AF
FociFoci
1998 marks discovery1998 marks discovery
that AF couldthat...
From Marriot HJL. Practical Electrocardiography. 7th ed. Baltimore: Williams & Wilkins; 1983.
Atrial Fibrillatory Waveform...
Acute AFAcute AF
Acute AF = episode <48 hoursAcute AF = episode <48 hours
In two thirds of patients with acute AF,In two t...
AF Risk Factors and CausesAF Risk Factors and Causes
ElectrophysiologicElectrophysiologic
abnormalitiesabnormalities
Enhan...
AF Risk Factors and CausesAF Risk Factors and Causes
(CONT'D)(CONT'D)
DrugsDrugs
AlcoholAlcohol
CaffeineCaffeine
Changes i...
Independent Risk Factors for AF:Independent Risk Factors for AF:
the Framingham Heart Studythe Framingham Heart Study
In a...
Clinical Sequelae of AFClinical Sequelae of AF
Clinical sequelae of AF relate to loss of atrial “kick”Clinical sequelae of...
Clinical Sequelae of AFClinical Sequelae of AF (CONT'D)(CONT'D)
Tachycardia-induced cardiomyopathy resulting fromTachycard...
AF and Stroke – Pathophysiology:AF and Stroke – Pathophysiology:
LAA ThrombusLAA Thrombus
More than 90% of all cardioembol...
Left Atrial AppendageLeft Atrial Appendage (CONT’D)(CONT’D)
A.A. Example of a polylobed LAA with severe SEC and theExample...
Evaluation of Patients With AFEvaluation of Patients With AF
Minimum EvaluationMinimum Evaluation
History and physicalHist...
Evaluation of Patients With AFEvaluation of Patients With AF
(CONT’D)(CONT’D)
Minimum EvaluationMinimum Evaluation
TTE to ...
Evaluation of Patients With AFEvaluation of Patients With AF
(CONT’D)(CONT’D)
Additional TestingAdditional Testing
TEE:TEE...
Rapid AFRapid AF
Slow AFSlow AF
AF before 1 and after 2AF before 1 and after 2
IV adenosineIV adenosine
AF withAF with
WPWWPW
AF inAF in
? Pulmonary? Pulmonary
embolismembolism
Risk score definitionsRisk score definitions
Stroke risk stratificationStroke risk stratification
Af epidemiology and diagnosis
Af epidemiology and diagnosis
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Af epidemiology and diagnosis

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discuss the recent updates in AF guidelines 2014

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  • Atrial fibrillation is responsible for more hospital admissions than any other arrhythmia:
    It accounts for more than 1/3 of all patient discharges with arrhythmia as the principal diagnosis.
    1 Bialy D, Lehmann MH, Schumacher DN, et al. Hospitalization for arrhythmias in the United States: Importance of atrial fibrillation. JACC. 1992;19(3):41A
  • Transcript of "Af epidemiology and diagnosis"

    1. 1. ByBy Essam Mahfouz, MD Professor of Cardiology, Mansoura University
    2. 2. AgendaAgenda DefinitionDefinition EpidemiologyEpidemiology ClassificationClassification Etiology & pathogenesisEtiology & pathogenesis DiagnosisDiagnosis
    3. 3. 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
    4. 4. 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
    5. 5. 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
    6. 6. 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
    7. 7. 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
    8. 8. 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
    9. 9. 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%
    10. 10. 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.
    11. 11. 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
    12. 12. 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
    13. 13. 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
    14. 14. Mechanisms of AFMechanisms of AF
    15. 15. ““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.
    16. 16. 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 +
    17. 17. 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.
    18. 18. 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
    19. 19. 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
    20. 20. 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.
    21. 21. 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
    22. 22. 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.
    23. 23. 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)
    24. 24. 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
    25. 25. 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
    26. 26. 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
    27. 27. 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.
    28. 28. 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
    29. 29. 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.
    30. 30. 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.
    31. 31. Rapid AFRapid AF
    32. 32. Slow AFSlow AF
    33. 33. AF before 1 and after 2AF before 1 and after 2 IV adenosineIV adenosine
    34. 34. AF withAF with WPWWPW
    35. 35. AF inAF in ? Pulmonary? Pulmonary embolismembolism
    36. 36. Risk score definitionsRisk score definitions
    37. 37. Stroke risk stratificationStroke risk stratification
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