recent updates about diagnosis and management of atrial fibrillation

2. Atrial fibrillation – Diagnosis and
Management
Dr K V pradeep babu.
Post graduate ,
Internal Medicine,
PSIMS &RF

3. Clinical features of AF

4. • It is estimated that approximately 25% of patients with AF
are asymptomatic
• Among those that are, symptoms associated with AF are
variable.
• Typical symptoms include palpitations, tachycardia, fatigue,
weakness, dizziness, lightheadedness, reduced exercise
capacity, increased urination, or mild dyspnea.
• The history should focus on obtaining the following
information:
• A description of the symptoms: onset or date of discovery,
the frequency and duration, severity, and qualitative
characteristics.

5. • More severe symptoms include dyspnea at rest,
angina, presyncope, or infrequently, syncope.
• In addition, some patients present with an
embolic event or the insidious onset of rightsided heart failure (as manifested by peripheral
edema, weight gain, and ascites).
• Precipitating causes: exercise, emotion, or
alcohol.
• Polyuria can occur because of release of atrial
natriuretic hormone.

6. • Syncope is an uncommon symptom of AF, most often
caused by
a long sinus pause on termination of AF in a patient with
the sick sinus syndrome.
Less commonly, syncope occurs with a rapid ventricular
rate either because of neurocardiogenic (vasodepressor)
syncope that is triggered by the tachycardia
a severe drop in blood pressure due to a sudden
reduction in cardiac output, mostly in AS, HOCM.

7. • The presence of the following disease
associations should be noted :
• cardiovascular or cerebrovascular disease
• Diabetes
• Hypertension
• Chronic obstructive pulmonary disease
• potentially reversible causes (eg,
hyperthyroidism, excessive alcohol ingestion).

9. Clinical findings in AF
• The hallmark of AF on physical examination is an irregularly
irregular pulse.
• Short R-R intervals during AF do not allow adequate time
for left ventricular diastolic filling, resulting in a low stroke
volume and the absence of palpable peripheral pulse.
• This results in a “pulse deficit,” during which the peripheral
pulse is not as rapid as the apical rate.
• Other manifestations of AF on the physical examination are
irregular jugular venous pulsations and variable intensity of
the first heart sound.

10. Clinical Evaluation of Atrial
Fibrillation

11. • Minimum Evaluation :

16. The electrocardiogram in
atrial fibrillation

17. Findings on ECG
• Lack of discrete P waves.
• Fibrillatory or f waves are present at a rate that is
generally between 350 and 600 beats/minute
• the f waves vary continuously in amplitude,
morphology, and intervals.
• The variability in the intervals between QRS complexes
is often termed “irregularly irregular.”

18. • The ventricular rate usually ranges between 90 to
170 beats/min.
• The QRS complexes are narrow unless AV conduction
through the His Purkinje system is abnormal due to
• Functional (rate-related) aberration
• Pre-existing bundle branch or fascicular block
• ventricular preexcitation with conduction down the
accessory pathway.

19. AF is associated with the following
changes on ECG
AF with f waves

20. AF without f waves

21. ATRIAL ACTIVITY in AF
• In AF there is no regular or organized atrial activity
• Numerous micro-reentrant circuits within the atria generate
multiple waves of impulses which often compete with or even
extinguish each other.
• No uniform activation of the atrial tissue and no distinctive P
waves are generated or recognized on the surface ECG.
• The sinus node is suppressed or not able to be expressed .

22. F waves
• When the AF is of recent onset, the f waves are often
coarse (>2 mm).
• “Coarse” AF in which the amplitude of the f waves is
large (especially in lead V1) is more common in recent
onset AF and can be confused with atrial flutter or
multifocal atrial tachycardia.
• The f waves are usually fine (<1 mm) with AF of greater
duration.

25. • The f waves are of greater amplitude when there is
hypertrophy of left atrial myocardium and become
smaller with increasing atrial scarring and fibrosis.
• The amplitude of the fibrillatory waves does not
correlate with the actual atrial size.

26. • In some cases, there are no recognizable deflections of
the baseline in any ECG lead (more common in
longstanding AF) .
• AF is inferred because of the absence of P waves and
the irregularly irregular ventricular rate.
• If present, f waves are best seen in the inferior leads
and in V1.

27. VENTRICULAR RATE in AF
• The atrial rate is very rapid and depends upon the
electrophysiologic characteristics of the atrial myocardium.
• The ventricular response rate is dependent upon the
properties of the atrioventricular node (AV) and His Purkinje
system.
• The ventricular rate (especially in the absence of nodal
blockade) usually ranges from 90 to 170 beats/min.
• However, many factors determine the rate at any moment in
any individual.

28. Why irregular ventricular rate??
• Refractoriness of AV Node due to bombardment of the
AV node with impulses in rapid succession.
• The large number of atrial impulses arriving at the
node compete with each other, interfering with their
penetration into and through the node, leaving this
tissue variably refractory.
• The frequency of bombardment can lengthen
conduction time, and these impulses that reach the AV
node but do not conduct are said to lead to concealed
conduction within the AV node.

29. When VR is increased ?
Increases in the ventricular response rate to over 200
beats per minute may occur if the refractory period of
the AV node is shortened:
• With sympathetic stimulation
• Increase in circulating catecholamines
• conduction down an accessory pathway if present

30. When VR is decreased ?
• A decrease in the ventricular response rate occurs
when the refractory period of the node is increased .
• Happens with aging.
• Intrinsic AV nodal disease in combination with
sympathetic blockade
• Direct depression of the AV node with some drugs
• Enhanced vagal tone.

31. Regularization of atrial fibrillation
• Due to the complete blockade of AV nodal
conduction .
• Subsequently there will be development of a
junctional (narrow QRS) or ventricular (wide QRS)
escape rhythm.
• Also, at very fast rates of conduction, the ventricular
response rate can appear to be regular

33. • In some cases, regularization in rate is due to
conversion of AF into atrial flutter with a fixed ratio of
conduction.
• Drugs that impair nodal conduction (such as digoxin,
beta or calcium channel blockers) or AV nodal disease
may result in the development of slowing and
regularization of the ventricular response.
• Digoxin is the most likely to do so.

34. Regular is not always right !!??
• So , regular rhythm in patient with AF after
digoxin may be more ominous , for it may
indicate complete Heart block !

35. AF in accessory pathway
• When AF is associated with a preexcitation syndrome
(ie, the presence of an antegrade conduction accessory
pathway), the ventricular response rate may be very
rapid, often in excess of 280 to 300 beats per minute.
• Here impulse conduction bypasses the atrioventricular
node, as conduction from the atria to the ventricles
occurs by an accessory or intranodal pathway.
• If the refractory period of this pathway is very short,
impulse conduction can be very rapid

36. Why conduction is rapid in accessory
tract ??
• The tissue of accessory pathways does not have the
same characteristics as the AV node
• It does not exhibit postrepolarization refractoriness
• Conducts rapidly as the tissue is not dependent on
calcium conduction
• Rather it’s dependent on sodium conduction similar
to atrial and ventricular muscle.

37. • In such cases, the QRS complex is usually
aberrant (and wide) and may be confused
with ventricular tachycardia, although the
rhythm is still irregularly irregular.
• This rhythm may also be confused with AF
with aberrancy; but with standard aberration,
the morphology is more typical of a left or
right bundle branch block.

38. • Conduction via an accessory pathway often shows a slurred QRS
upstroke (“Delta” wave)
• This morphology depends on the location of the pathway and
wherein inserts into the ventricular myocardium.
• During so-called preexcitation syndromes, conduction can proceed
through the AV node and/or the accessory pathway.
• The more conduction proceeds through the accessory pathway,
the more QRS appearance is “aberrant.”
• A distinguishing feature of this entity of AF with preexcitation is the
relationship between heart rate and QRS duration; the faster the
rate, the wider the QRS width.

40. DIFFICULTIES IN DIAGNOSIS of ECG
• The f waves may be inapparent on the standard and
precordial leads . This is most likely to occur when AF
is of long duration.
• The f and u waves may have sufficient amplitude to
look like P waves.
• Extracardiac artifacts, such as those seen in patients
with Parkinson disease and tremors, may simulate f
waves

41. • Other rhythms in which the R-R intervals are
irregularly irregular. These include :
•
•
•
•
Multifocal atrial tachycardia (MAT)
Wandering atrial pacemaker (WAP)
Multifocal atrial premature beats
Atrial tachycardia or atrial flutter with varying
AV block.

42. • The R-R interval may be regular with AV
dissociation or block, a setting in which a lower
junctional, subjunctional, or ventricular pacemaker
assumes control of the ventricles. Example :
advancing digitalis toxicity .

43. • Atrial fibrillation with rapid ventricular rates may
be misdiagnosed as paroxysmal supraventricular
tachycardia patients are commonly treated
with adenosine, which will not convert patients
with AF .
• AF with a wide QRS complex, as occurs in patients
with either preexcitation or aberrancy, may make
it difficult to determine if the rhythm is AF or
ventricular tachycardia.

44. Morphology of the QRS complex
• The QRS complex usually maintains its normal
narrow configuration in AF, since activation
through the infranodal conduction system is
intact.
• There are settings in which widening of the
QRS complex occurs

45. • These include:
• a pre-existing conduction defect (left or right bundle
branch block)
• Functional (generally rate-related) block in a portion of
the infranodal conduction system that results in
asynchronous or aberrant activation and, for example,
a right bundle branch block (RBBB) pattern
• Preexcitation through an atrioventricular (AV) bypass
tract which is capable of antegrade conduction.

46. • Aberration following a long-short cycle in AF is
often called the Ashman or Gouaux-Ashman
phenomenon .
• Ecg of ashman phenomena

47. Effect of high degrees of AV nodal block
and exit block on ventricular response
• May occur with digitalis toxicity or progressive AV nodal disease),
impulses from the fibrillating atria fail to reach the infranodal
conduction system.
•
As a result, a pacemaker below the level of the block assumes
control of the ventricles.
•
The pacemaker is usually located in the AV junction above the
bifurcation of the bundle branches.
• Leads to a QRS complex that has the same morphology as if it had
been conducted from the atria through the AV node.
• This pacemaker has a characteristic rate of about
60 beats/min,unless it is accelerated or depressed due to
pathology, ischemia, or drugs.

48. • Less commonly, the pacemaker is
subjunctional or ventricular.
• In this setting, the QRS complex will be wide
and, unless accelerated, the ventricular rate
will be relatively slow at 30 to 50 beats/min.

49. SUMMARY —ECG in AF
• Absence of discrete P waves.
• Fibrillatory or f waves are present at a rate that is generally between
350 and 600 beats/minute; the f waves vary in amplitude, morphology,
and intervals.
• The RR intervals follow no repetitive pattern; they have been labeled
as “irregularly irregular.”
• The ventricular rate usually ranges from 90 to 170 beats/min.
• The QRS complexes are narrow unless AV conduction is abnormal due
to functional (rate-related) aberration, pre-existing bundle branch or
fascicular block, or ventricular preexcitation .
• Although ECG findings described above usually allow the diagnosis of
AF to be made easily, there are several pitfalls in correct identification
of the rhythm.

50. Role of echocardiography in atrial
fibrillation

51. Echo may be helpful in assessing …
• Helpful in determining the conditions
associated with AF
• Risk for recurrent AF following cardioversion.
• Identification of patients at increased risk for
thromboembolic complications of AF before
cardioversion and in patients with chronic AF

52. Two varieties of Echo
• TTE : Transthoracic echocardiogram
• TEE : Trans esophageal echocardiographic

53. Usually TTE is done
It is useful for evaluating :
• left atrial size
• left ventricular systolic function
• Mitral valve morphology and function.

54. Left atrial size
• The normal left atrial dimension in adults is less
than 4.0 cm (or <2.0 cm/m2 body surface area).
• Left atrial enlargement is common in AF,
particularly in patients with mitral valve disease,
left ventricular dilation, annular calcification, or
hypertension.
• sustained AF itself can lead to a further increase
in left atrial size, an effect that is reversible after
cardioversion and maintenance of sinus rhythm.

55. Why LA status should be assessed ??
• Left atrial enlargement is important
prognostically.
• It decreases the probability that long-term
maintenance of sinus rhythm will be
successful .
• Patients with chronic (more than one year) AF,
rheumatic mitral valve disease, and severe left
atrial enlargement (dimension greater than
6.0 cm) are at greatest risk for recurrent AF

56. Mitral valve function
• Mitral stenosis in the adult may initially present with
AF, often in the setting of acute thromboembolism.
• In this setting, long-term anticoagulation
with warfarin is indicated even if cardioversion to
sinus rhythm is successful.
• Long-term maintenance of sinus rhythm is unlikely
unless the mitral stenosis is corrected (by surgery
or percutaneous balloon mitral valvuloplasty).

57. • Moderate to severe mitral regurgitation
appears to protect against clinical
thromboembolism in chronic AF, presumably
by minimized stasis in the left atrium and
atrial appendage and less coagulation activity.
• However, it does not appear to protect from
the formation of left atrial appendage
thrombus as identified on TEE

58. Left ventricular function
• Assessment of left ventricular systolic function helps to
guide the choice of pharmacologic therapy for ventricular
rate control in chronic AF.
• A beta blocker or a calcium channel blocker
(diltiazem or verapamil)  patients with preserved left
ventricular systolic function.
• Patients with depressed left ventricular systolic function
may be best treated  digoxin.
• Patients with overt heart failure due to systolic dysfunction
 both a beta blocker to improve survival and digoxin to
control symptoms, independent of the presence or absence
of AF.

59. • Left ventricular dysfunction, as determined from the
TTE, independently predicts an increased risk of a
stroke in patients with AF.
• Analysis of 1066 patients entered into three
prospective clinical trials evaluating the role of
anticoagulation in nonvalvular AF (BAATAF, SPINAF, and
SPAF) found that, the incidence of a stroke was 9.3
percent per year in patients with moderate to severe
left ventricular dysfunction compared to 4.4 percent
per year in those with normal or mildly abnormal left
ventricular systolic function .

60. Left atrial thrombi
• The ability of TTE to identify or exclude left
atrial or atrial appendage thrombi is limited,
with a reported sensitivity of 39 to 63
percent largely to poor visualization of the
left atrial appendage.

61. TEE in a more selected subgroup
• May benefit evaluation for left atrial thrombi
to allow for early cardioversion, if no thrombi
are identified.
• The Stroke Prevention in Atrial Fibrillation
(SPAF) investigators confirmed the usefulness
of transesophageal echocardiography (TEE) for
predicting thromboembolism, study involved
786 patients with nonrheumatic AF.

62. Results of SPAF study
The rate of stroke was :
1. increased over threefold when TEE evidence of
dense spontaneous echocontrast was present.
2. Increased by threefold for reduced left atrial
appendage peak flow velocity and for left atrial
appendage thrombus
3. Increased by fourfold by complex aortic plaque.

63. • TEE permits detection of thrombus in both
the left atrium and the left atrial appendage
• TEE evidence of left atrial thrombi is seen in
approximately 13 percent of patients
presenting with nonrheumatic AF of more
than three days duration

67.  The prevalence is increased in high-risk
patients with :
• Mitral stenosis (33 percent in one series)
• Left ventricular systolic dysfunction,
enlargement of the left atrium or left atrial
appendage
• Spontaneous echo contrast, a recent
thromboembolic event (43 percent in one
report) , and high CHADS2 score

68. • The sensitivity and specificity of TEE for left atrial thrombi
(in patients in whom the left atrium was directly examined
at surgery) are 93 to 100 percent and 99 to 100 percent,
respectively.
• Cardioversion should not be attempted in patients with TEE
evidence for atrial thrombi, even if thrombi appear
"adherent" to the wall of the appendage.
• Such patients are typically given warfarin therapy for at
least four weeks before cardioversion as are patients who
do not undergo TEE.
• Resolution of thrombi occurs in approximately 75 percent
of patients with nonrheumatic AF with no formation of new
thrombi

69. Spontaneous echo contrast
• Spontaneous echo contrast (SEC or "smoke")
refers to the presence of dynamic, smoke-like
echoes seen during TEE in the left atrium or
atrial appendage .
• SEC is thought to reflect increased erythrocyte
aggregation caused by low shear rate due to
altered atrial flow dynamics and
uncoordinated atrial systole

70. • Erythrocyte aggregation is mediated by plasma
proteins, especially fibrinogen, which promotes
red cell rouleaux formation by moderating the
normal electrostatic forces (due to negatively
charged membranes) which keep erythrocytes
from aggregating.
• SEC is a strong risk factor for and may be the
preceding stage to thrombus formation and
thromboembolic events

71. Warfarin, which leads to thrombus resolution and a
lower incidence of thromboembolism, does not
affect the presence of SEC, since it does not
change the underlying hemodynamic abnormality .

72. Mechanisms of thrombogenesis in
atrial fibrillation

73. • Atrial fibrillation (AF) is associated with
substantial mortality and morbidity, largely
due to thrombo embolism, particularly stroke.

74. Risk factors
• Pooled data from a meta-analysis have
demonstrated that independent clinical risk
factors for stroke in nonvalvular AF include a
history of hypertension and diabetes .
• Patients with heart failure are also at high risk,
particularly those with left ventricular systolic
dysfunction or aneurysm formation

76. Question we need to think over !!!
Why the great majority of embolic events in
patients occur within the first 10 days after
cardioversion ???
Why even after the restoration of sinus
rhythm ????

77. How cardioversion causes thromboembolism ??
• Risk  particularly if patients are not
anticoagulated before, during, and after
cardioversion.
• In addition to dislodgement of pre-existing
thrombi, embolization may result from de
novo thrombus formation induced by
impaired left atrial systolic function.

78. • The transient atrial contractile dysfunction is
also known as atrial "stunning," and can occur
whether sinus rhythm is restored
spontaneously, by external or internal DC
(electric) cardioversion, or by drugs.

79. • Pulsed Doppler studies have shown that the
time to recovery of atrial mechanical function
is directly related to the duration of AF
• In Patients with AF for ≤2 weeks , mechanical
recovery within 24 hours
• In those with AF for more than six weeks, up
to one month

80. Paroxysmal atrial fibrillation
Is the incidence of stroke is higher with
paroxysmal AF or Chronic AF ???
Is the risk of stroke is higher with paroxysmal
AF or Paroxysmal supra ventricular
tachycardia????

81. • Reports from the Framingham study and
Montreal Heart study had suggested
thromboembolic rates for paroxysmal AF that
were intermediate between those associated
with chronic atrial fibrillation and sinus
rhythm.

82. Paroxysmal AF :abnormal haemostasis
• Levels of beta-thromboglobulin and platelet
factor 4 (markers of platelet activation) were
significantly increased during episodes more
than 12 hours in duration
• There was also a trend toward an elevation in
fibrinogen levels in these patients.
• Intermediate values of fibrinogen and fibrin Ddimer between sinus rhythm and chronic AF.

83. Left ventricular dysfunction
• Heart failure by itself confers a risk of stroke
and thromboembolism
• What is the percentage increase in risk of
stroke for % decrease in ejection fraction ???

84. SAVE TRIAL
• Every 5 percentage point decrease in left
ventricular ejection fraction (LVEF) was
associated with an 18 percent increase in the
risk of stroke.

85. LV aneurysm
• A left ventricular aneurysm has both diastolic and
systolic bulging or dyssynergy which result in
severe stasis of blood .
• Patients with heart failure and left ventricular
aneurysm, also demonstrate abnormalities of
blood rheology, coagulation, and endothelial
function.
• As an example, both plasma fibrinogen and von
Willebrand factor concentrations may be elevated
in heart failure

86. paroxysmal supraventricular tachycardia
• These patients retain active atrial contraction
• Have a low risk of stroke
• Had levels of hemostatic markers that were
similar to controls in sinus rhythm.

87. Hypertension
• It increases the risk of stroke associated with
AF twofold.
• Hypertension may be associated with a
hypercoagulable state due in part to
abnormalities in blood rheology and
endothelial function

88. Valvular disease
• Especially mitral stenosis, increases the risk of
stroke in atrial fibrillation 17-fold.
• some evidence that the presence of mitral
regurgitation is protective against embolism.
• SPAF trail :Even in the presence of left atrial
enlargement, severe mitral regurgitation is
associated with a lower incidence of embolism.

89. FACTORS PROMOTING
THROMBOEMBOLISM in AF
Almost 150 years ago, Virchow proposed that three
conditions should be present for development of
thrombosis [1]:
• Abnormalities in blood flow
• Abnormalities in the blood vessel wall
• Interaction with blood constituents
• Abnormalities in blood flow and vessels (the first two
components of Virchow's triad) can be related to the
presence of structural heart disease or extrinsic
interventions such as cardioversion.

90. The third component !
Is AF a hypercoaguable state ???

91. IN patients with AF , the following observations
suggesting hypercoaguable state are made :
• Increased plasma concentrations of markers of platelet
activation (beta-thromboglobulin and platelet factor 4)
• Increased plasma markers of thrombogenesis
(thrombin-antithrombin complexes, D-dimers)
• Evidence of endothelial damage/dysfunction (elevated
plasma and endocardial levels of von Willebrand factor,
which is released from damaged endothelium)

92. Anticoagulation in AF alters the hypercoagulable state as illustrated by the
following observations:
• Fibrin D-dimer levels are increased in patients
with AF.
• In one study, fibrin D-dimer levels were
highest in patients who were not receiving any
antithrombotic therapy, intermediate in those
on aspirin, and lowest in those treated
with warfarin

93. In a substudy from the AFASAK trial
• 100 patients with chronic AF were randomized to
treatment with
fixed minidose warfarin 1.25 mg daily alone
 combination with aspirin 300 mg/day and conventional
warfarin therapy with dose adjusted to maintain an
International Normalized Ratio (INR) between 2.0 and
3.0
Aspirin 300 mg daily.
• Patients treated with warfarin at any dose demonstrated
a significant rise in the INR with a corresponding
reduction in prothrombin fragment F1 + 2 [52].

94. The degree of anticoagulation
with warfarin appears to be important!
• In one report, ultra low-dose warfarin (1 mg/day) did
not significantly alter plasma fibrin D-dimer or betathromboglobulin levels .
• A second study found that treatment with aspirin (300
mg daily) plus low-dose warfarin (1 or 2 mg daily) or
low-dose warfarin alone (2 mg daily) did not
significantly reduce any of the hemostatic markers
• In contrast, there was a significant reduction of
fibrinogen and fibrin D-dimer with dose-adjusted
warfarin .

95. Is AF a hypercoaguable state ???
yes. Beyond any doubt
How and why it is a hypercoaguable state ??

96. Sluggish, slow flow within the atria
Endothelial disturbance in the pulmonary
vasculature
stimulation of lung macrophages to produce
hepatocyte stimulating factor ( IL-6)
Increase in hepatic synthesis of fibrinogen,
perhaps in a similar manner to smoking.
Proposed mechanism of hypercoaguability in AF

97. SILENT CEREBRAL ISCHEMIA
• Silent cerebral ischemia (SCI) is said to occur in a patient who
has specific lesions on cerebral magnetic resonance imaging
(or other tests) in the absence of clinical complaints or
findings.
• The prevalence of SCI and its potential relationship to
cognitive performance in patients with AF was better studied
in a registry that included 90 patients.
• Cognitive impairment was significantly greater in persistent
and paroxysmal AF patients compared to controls.

98. Antithrombotic therapy to prevent
embolization in atrial fibrillation

99. Risk Vs benefit ratio
• Embolization of atrial thrombi can occur with any form (ie,
paroxysmal, persistent, or permanent) of atrial fibrillation
(AF).
• chronic antithrombotic therapy with either oral
anticoagulation (ie, a vitamin K antagonist, direct thrombin
inhibitor, or factor Xa inhibitor) or antiplatelet therapy is
considered for most of these patients.
• As antithrombotic therapy is associated with an increased
risk of bleeding, its use must take both benefit and risk into
account.

100. • Historically, the CHADS2 risk score is the most
popular and has been best validated in
different patient populations
• The main advantage of the CHADS2 score
compared to other risk models is its simplicity

101. • Using the CHADS2 or CHA2DS2-VASc (for
those with CHADS2 of 0 or 1) score for
evaluating risk of stroke and arterial
embolization.
• Antithrombotic prevention is recommended
when the benefits outweigh the risks.

104. Prevention approach by CHADS2 score

105. • Warfarin is remarkably effective at
reducing stroke risk in patients with AF.
• This was clearly demonstrated by a metaanalysis by the AF Investigators of five
randomized, controlled clinical trials
comparing warfarin versus placebo in patients
with AF

106. Break through RCT’s in AF

107. Effects of warfarin versus placebo on risk of stroke in six
randomized, placebo-controlled clinical trials in nonvalvular AF

108. Annualized incidence of stroke or intracranial
hemorrhage according to the INR.
Note that when the INR decreases to <2.0, there is
a steep rise in the odds ratio (OR) for stroke; but

109. Effects of aspirin versus placebo on risk of stroke in five
randomized, placebo-controlled trials in nonvalvular AF.
AFASAK I (1), The Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulant Therapy Study;
CI, confidence interval; EAFT (9), European Atrial Fibrillation Trial; ESPS II (14), European
Stroke Prevention Study; LASAF (13), Alternate-Day Dosing of Aspirin in Atrial Fibrillation
Pilot Study Group; SPAF I (3), Stroke Prevention in Atrial Fibrillation; UK-TIA (16), United
Kingdom Transient Ischaemic Attack Trial.

110. Effects of aspirin versus warfarin on risk of stroke in five
randomized, controlled clinical trials in nonvalvular AF.
AFASAK I (1) and AFASAK II (2), The Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulant Therapy Study;
EAFT (9), European Atrial Fibrillation Trial; PATAF (15), Primary Prevention of Arterial Thromboembolism in
Nonrheumatic Atrial Fibrillation; SPAF II (3), Stroke Prevention in Atrial Fibrillation.

111. Risk with warfarin
• Bleeding risk — The major safety concern with
the use of warfarin (and all oral anticoagulants) is
the risk of major bleeding.
• Major bleeding includes bleeding that requires
hospitalization, transfusion, surgery, or involves
particularly sensitive anatomic locations.
• Intracranial hemorrhage (ICH) is the most serious
bleeding complication with warfarin

114. Other anticoagulants
• Overall, the trials, demonstrate equal or superior
thromboembolism efficacy and major bleeding safety of these
newer anticoagulants compared to warfarin.
• Additional advantages of dabigatran, apixaban, rivaroxaban, and
edoxaban (compared to warfarin) include no need for international
normalized ratio monitoring and less susceptibility to dietary and
drug interactions .
•
Disadvantages include twice-daily dosing (dabigatran, apixaban),
higher pharmaceutical cost, lack of an antidote/reversingagent, the
potential need for dose adjustment in patients with chronic kidney
disease, and lack of long-term safety and “real world” data.

115. Dual anti platelet therapy
• Dual antiplatelet therapy may be a reasonable
alternative to therapy with aspirin alone in the
occasional high-risk patient with AF who CANNOT be
treated with anticoagulation .
• It should be kept in mind that as dual antiplatelet
therapy and oral anticoagulation have similar bleeding
risks, a patient who would not be a candidate for oral
anticoagulation because of bleeding risk is also not a
candidate for dual antiplatelet therapy.

116. Management of new onset atrial
fibrillation

117. • There is overlap between “new onset,”
“acute,” and “first identified” atrial fibrillation,
but each represents a distinct clinical
presentation with unique features .

118. Decisions need to be made soon after a patient
presents with new onset AF:
• Is cardioversion indicated and if so should it be urgent?
• When and how should rate control be carried out?
• Who should be anticoagulated immediately and how?
• Does the patient need hospitalization?
• Are there any correctable causes of atrial fibrillation?
• What should be done with the patient who spontaneously
converts to sinus rhythm?

119. Important first steps
• A complete history and physical examination
should be performed in all patients with new
onset AF.
• Old records should be searched for evidence
of a prior episode of AF or other atrial
tachyarrhythmias

120. Is cardioversion indicated and if so
should it be urgent?

121. Four circumstances for which urgent or
emergent cardioversion may be needed:
• Active ischemia (symptomatic or electrocardiographic
evidence).
• Evidence of organ hypoperfusion.
• Severe manifestations of heart failure (HF) including
pulmonary edema.
• The presence of a preexcitation syndrome, which may lead
to an extremely rapid ventricular rate due to the presence
of an accessory pathway.

123. • In a patient with any of these indications for
urgent cardioversion, the need for restoration
of NSR takes precedence over the need for
protection from thromboembolic risk.

124. Are there any correctable causes of
atrial fibrillation?

125. • There should be a quick assessment for an underlying
cause, such as heart failure (HF), pulmonary problems,
poorly controlled blood pressure, or hyperthyroidism.
• Therapy for a precipitating cause should be initiated prior to
cardioversion in stable patients and may result in reversion
to sinus rhythm.

126. What are the tests ,in addition to the
electrocardiogram, should be performed on
patients with new onset AF??

127. • Vital signs including oxygen saturation (in the ER setting and beyond)
• Thyroid stimulating hormone (TSH) and free T4. (since the risk of AF is
increased up to threefold in patients with subclinical hyperthyroidism )
• Serum electrolytes and assessment of renal function
• Complete blood count
• A transthoracic echocardiogram should be performed to screen for cardiac
causes of new onset atrial fibrillation, even in the face of a normal physical
examination.
• Chest x-ray
•
Evaluation of myocardial infarction with serial troponin measurements,
especially in patients with electrocardiogram (ECG) changes, hypotension,
symptoms, history, or additional risk factors only .(AF rare manifestation of
MI)

129. Who should be anticoagulated
immediately and how?

130. • If the duration of AF is known to be less than 48 hours,
cardioversion can be performed without anticoagulation
• For most patients in whom the duration of new onset AF is
suspected to be more than 48 hours (or when the duration
is unknown), the risk of embolization is measurably
increased.
• If the time of onset of AF is unclear, for the sake of safety,
the AF duration should be assumed to be more than 48
hours.

131. • Regardless of whether cardioversion is performed
pharmacologically or electrically, therapeutic anticoagulation
is necessary for 3 weeks or more before, if the AF has been
ongoing for more than 48 hours.
• These patients should be therapeutically anticoagulated for 4
weeks after cardioversion to prevent thromboembolic
complications that may occur because of atrial stunning
• When warfarin is chosen as the anticoagulant, the
recommended target International Normalized Ratio (INR) is
2.5 (range 2.0 to 3.0)

132. When and how should rate control be
carried out?

133. • In patients with mild to moderate symptoms, concurrent with
the initiation of the appropriate anticoagulation treatment,
the initial therapy includes slowing the ventricular rate
without an immediate strategy to restore sinus rhythm.
• Slowing the ventricular rate often results in significant
improvement or even resolution of symptoms.
• Attempting to get the rate below 110 beats per minute is
reasonable.

134. • This can be achieved with beta blockers, calcium
channel blockers ,verapamil and diltiazem
• Occasionally, intravenous (IV) amiodarone may be
needed for patients with poor left ventricular
function.
• The drug selected and the route of administration
(oral versus intravenous) are dictated by the clinical
presentation

135. • Beta blockers or verapamil or diltiazem are the
preferred drugs in the absence of heart failure.
• Intravenous amiodarone may help control rate when
the other drugs are ineffective or cannot be given.
• Digoxin is the preferred drug only in patients with AF
due to HF.

136. Rate control in pre excitation
• Procainamide IV is recommended for rate control
and for attempt to cardiovert atrial fibrillation
with preexcitation when urgent cardioversion is
not available or recommended.
• IV amiodarone is an alternative option.
• IV AV nodal blockers in particular Beta blockers
and CCB’s are contraindicated in AF with
preexcitation .

138. Choice of drug for rate control
• The choice between a beta blocker, diltiazem, and verapamil is
frequently based upon physician preference and patients status.
• Beta blockers are particularly useful when the ventricular response
increases to inappropriately high rates during exercise, after an acute
MI, and when exercise-induced angina pectoris is also present,
especially after cardiac surgery.
• a calcium channel blocker is preferred in patients with chronic lung
disease
• The use of both a beta blocker and calcium channel blocker is
reasonable when rate control is not adequate with single therapy

140. Why it is recommended to control
ventricular Rate immediately ???

141. The prevention of tachycardia-mediated
cardiomyopathy is a principle reason for this
recommendation.

142. Why rate control is prefered over
rhythm control ???

145. Patient had rate control , haemodynamically stable ,
what is the next probable step ???

146. To decide whether an attempt will be made to
cardiovert the patient and if so when.
Most patients with symptomatic new onset atrial
fibrillation should have at least one attempt at
cardioversion (either electrical or chemical) to sinus
rhythm, particularly after reversible causes have been
identified and corrected.
The rationale for cardioversion is that some patients
will never have a second episode, or will have very
infrequent episodes
Cardioversion will likely improve symptom status,
particularly in young people.

147. It is reasonable to not attempt cardioversion in a
patient with new onset AF in :
• Patients who are completely asymptomatic, particularly those
who are very elderly (>80 years) with multiple comorbidities,
where risks of undergoing cardioversion and/or pharmacologic
rhythm control may outweigh the benefits of restoring sinus
rhythm.
• A patient with a high CHADS2 score who has a bleeding risk
and cannot be anticoagulated during and after cardioversion.

148. Cardioversion --Electrical or pharmological ??
• The choice of electrical or pharmacologic cardioversion
depends upon the comfort of the clinician to use one or the
other approach.
• Longer durations of the arrhythmia are less likely to
respond to antiarrhythmic drug therapy for conversion
• For patients with paroxysmal episodes of atrial fibrillation,
drug therapy is preferred if they will have sinus rhythm
maintained with long-term antiarrhythmic drug therapy
• For persistent episodes, electrical cardioversion is
preferred.

149. What should be done with the patient who
spontaneously converts to sinus rhythm?

150. • New onset AF often spontaneously reverts to normal
sinus rhythm, with the incidence of reversion related to
the duration of the arrhythmia.
• This was illustrated in a study of 1822 patients
admitted to the hospital because of AF.
• Two-thirds of those with spontaneous reversion had AF
duration of less than 24 hours, which was the only
predictor of spontaneous reversion
• Choice of anticoagulation depending on CHADS2 score.

151. INDICATIONS for RHYTHM CONTROL
There are three settings in which a rhythm control strategy for the
maintenance of sinus rhythm should be considered
• Persistent symptoms (palpitations, dyspnea, lightheadedness,
angina, syncope, and heart failure) despite adequate rate control
• An inability to attain adequate rate control (to prevent tachycardiamediated cardiomyopathy).
• Patient preference. Some patients will strongly prefer to avoid either
paroxysmal or persistent AF.

154. Paroxysmal AF

155. Survival in paroxysmal AF
• Whether patients with paroxysmal AF have worse
survival than the general population has been studied
from the Stockholm cohort study of atrial fibrillation
(SCAF) were followed for a mean of 4.6 years.
• The standardized mortality ratio was significantly
increased at 1.6 percent .
• This excess mortality was principally from
cardiovascular causes.
• Patients treated with warfarin appeared to do better
than those not treated.

156. MANAGEMENT OF THE ARRHYTHMIA
• Acute therapy : same as in new onset AF
• Prevention of recurrence :
Catheter-based pulmonary vein isolation (PVI) is
generally viewed as being more effective than
antiarrhythmic medications.
Surgical-based techniques such as the MAZE procedure
are still being used and are often performed in
conjunction with other cardiac surgical procedures.

157. Non pharmacological methods to
prevent recurrent AF
• . The two most common nonpharmacologic
approaches are:
• Radiofrequency catheter ablation (RFA)
• surgery

158. Surgery and RAF are directed at
• Elimination of the triggers of AF – Triggers are usually eliminated
by disrupting the conduction of electrical activity between the
tissues that contain these arrhythmogenic triggers .
• Most commonly the ostial portion of the pulmonary veins, and the
atrial myocardium.
• Less commonly, triggers within the atrial myocardium can be
directly ablated.
• Modifying the atrial substrate(s) responsible for the maintenance of
AF.

159. Recommendations for the use of
radiofrequency catheter ablation (RFA)
•
The American College of Cardiology Foundation /American Heart Association
/Heart Rhythm Society guidelines on the management of patients with atrial
fibrillation (AF):
•
•A strong recommendation for RFA for patients with symptomatic, paroxysmal
atrial fibrillation (AF) who have failed treatment with an antiarrhythmic drug.
•
•A weak recommendation for RFA for patients with symptomatic, persistent AF.
•
•A very weak recommendation was made for RFA for patients with symptomatic
paroxysmal AF in patients with significant left atrial dilatation or with significant
left ventricular dysfunction.

160. RFA
• PULMONARY VEIN ISOLATION PROCEDURE
• The pulmonary veins are the most common
source for the initiation of AF
• The LAA was the only source of the arrhythmia in
about one third.
• The two principal techniques are :
• segmental ostial (PV) ablation
• Circumferential ablation of left atrial tissue.

161. The three principal goals of surgical strategies
• Interrupting the electrophysiologic substrate
propagating the arrhythmia in both the right and
left atria.
• Reestablishment or maintenance of
atrioventricular synchrony.
• Restoration and preservation of atrial mechanical
function in order to improve diastolic filling.

162. MAZE OPERATION
• Developed in the 1990s
• Aims to surgically create a “maze” of
functional myocardium within the atrium
• This allows for propagation of atrial
depolarization while reducing the likelihood of
microreentry

163. • The procedure has evolved over the last 20 years.
• Originally involved several small incisions around
the sino-atrial (SA) node as well as one to the
atrial-superior vena caval junction (Maze I)
• unintentionally resulted in chronotropic
incompetence resulted in the Maze II
procedure

164. • The final version (Maze III) reduced the
frequency of chronotropic incompetence,
improved atrial transport function, and
shortened procedure times.
• The maze procedure meets the three criteria
for an ideal treatment of atrial fibrillation (AF)

165. Other surgical approaches
• Radial approach
• Pulmonary vein isolation
• CORRIDOR OPERATION

168. Thank you !