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Introduction…
AF is characterised by wavelets propagating in different
directions causing disorganized atrial depolarization without
effective atrial contraction
Electrical activity of atrium can be detected in ECG as small
irregular baseline undulations of variable amplitude &
morphology (f waves) at rate of 350 to 600
Ventricular response is irregularly irregular, & in untreated
patients with normal AV conduction, is usually between 100 to
160
WPWsyndrome ventricular rate may be rapid >300 due to
conduction over accessory pathway( short antegrade refractory
periods)
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Introduction…
ventricular rate during AF is altered due to
Autonomic tone
Property of AV node
Effect of drugs on AV conduction
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Introduction
Atrial fibrillation is the most common arrhythmia & the
incidence & prevalence increases with the age
The incidence
<0.5% below 50Yrs
2% in age 60-69
4.6% in age 70-79
8.8% in age 80-89
Men were 1.5 times more likely to develop AF than
women
Whites were more likely to develop AF than blacks
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Relative risk of stroke - 6 fold in non
rheumatic AF
Relative risk of stroke - 17 fold in
rheumatic AF
Annual risk of stroke in pt aged 50-
59:1.5%
Annual risk of stroke in aged 80-89:23.5%
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Classification of Atrial
fibrillation
First detected AF -usually <48hr in
AF during diagnosis
Paraoxysmal AF - last < 7days
(most<24hrs) self-terminating episodes
Persistent AF - last >7days requires
electrical or pharmacologic
cardioversion
Permanent AF - sustained >1yr &
failed cardioversion
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Mechanisms
It was first thought that irregular contractions of the atria are
caused by either single or multiple foci
In 1924, Garry had suggested reentry to be the mechanism
behind the AF
In 1960, Moe suggested the “multiple wavelet hypothesis ”
AF is characterized by fragmentation of a wavefront into
multiple, independent daughter wavelets that move randomly
throughout the atrium, giving rise to new wavelets that collide
with each other & mutually annihilate, or that give rise to new
wavelets in a perpetual activity that resembles Brownian motion
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Mechanisms
Stability of AF is a function of several factors
Non-uniform distribution of refractory periods
Specially large tissue area
Either a relatively brief refractory period or a relatively
slow conduction velocity of the impulse, or both
Average no. of the wavelets
Allessie et al, estimated the critical no. of wavelets
to sustain AF was approximately 4 - 6
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Mechanisms
Trigger factor - self-terminating AF
Perpetuating factor - AF does not
terminate spontaneously
Paraoxysmal AF - 95% of Triggering foci
are mapped in pulmonary vein
Other foci - within SVC ,coronary sinus
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Mechanisms
Waldo et al divided AF into 4 types according atrial
electrogram
• Type – I --- ECG showed discrete complexes of variable
morphology separated by a clear isoelectric baseline
• Type – II --- ECG characterized by discrete atrial
complexes with variable cycle lengths and morphology,
the baseline is not isoelectric
• Type – III --- ECGs were highly fragmented, showing no
discrete complexes or isoelectric intervals
• Type – IV --- Fibrillation was characterized by
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Mechanisms
“ f” waves
They do not represent total atrial activity but depict only the
larger vectors generated by the multiple wavelets of
depolarization that occur at any given time
Why ventricular response is irregularly irregular?
Large no. of atrial impulses that penetrate the AV node, makes
it partially refractory to subsequent impulses
These effect of non conducted atrial impulses to influence the
response of subsequent atrial impulse is called as “concealed
conduction”
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Mechanisms
Electrical remodelling
It means long term changes in refractory periods resulting from
prolonged changes in atrial rate
EPS --- ↓ERP,↓Action potential, ↓ amplitude of AP plateau
Mechanisms --- Structural , cellular or ion channels It
encompasses diverse structural changes in the myocardium
-interstitial fibrosis
Alteration in quantity or properties of ion channel proteins in
sarcolemma
Microscopic changes in cell size , content & extra cellular matrix
leads to irreversible macroscopic changes
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Maladoptations of atrial refractionaries – cause of chronic AF
Atrial remodelling
Caused by atrial ischemia & stretch leads to AF due to ↑
automaticity & reentry
After AF has continued for a long time, atria are not only
electrically remodelled, but atrial contractile function is also
disturbed
Recovery of atrial transport function may depend upon
duration of AF
After sinus rhythm is restored, it may take several weeks
before atrial contractility fully returns
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Mechanisms
Modulating factors
The onset & persistence of AF may be modulated by
autonomic nervous system
Coumel et al distinguished vagal & adrenergic AF
(distinction is not clear)
Vagally mediated AF
Occurs more frequently in men than in women
Usually younger age group (30 – 50 years)
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Mechanisms
Predominantly occurs in the absence of structural heart disease
Rarely progresses to permanent AF
Attacks occur at night, end of the morning
Neither emotional stress nor exertion trigger the arrhythmia
Rest, postprandial state, & alcohol are other precipitating
factors
Mechanism may relate to vagally induced shortening of the
atrial refractory period
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Mechanisms
Adrenergic AF
More frequently associated with structural heart disease (IHD)
Occurs during the day time, & it is precipitated by stress,
exercise, tea, coffee or alcohol
The underlying mechanism is unknown
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Hemodynamic effect
Loss of atrial contraction
Rapid ventricular rate - ↓duration of
diastole & ventricular filling
irregular ventricular rhythm - ↓ CO &
coronary blood flow
Loss of AV synchrony - ↓LVEDP - ↓SV
AF causes hypotension or pulmonary
oedema in the setting of restrictive
physiology
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Antiarrhythmic therapy of atrial fibrillation
Three antiarrhythmic strategies
Acute pharmacologic termination
Prevention of recurrence after cardioversion
Control of ventricular rate
Acute conversion of paroxysmal AF
Pharmacologic cardioversion
Most effective if initiated within 7 days after onset of AF
Restoration of sinus rhythm can be achieved in 70% of the
patients
First choice : Propafenone & flecainide (po & iv), ibutilide,
dofetilide
Second choice : Amaiodarone (high dose, iv +oral) &
Qunidine (po)
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Antiarrhythmic therapy of atrial
fibrillation
Class IC drugs – Restore sinus rhythm with in a short
period of time ( 1 hour) – conversion rate up to 90% (PAFIT-3)
Ibutilide
It acts twice more effectively for conversion of atrial flutter than
atrial fibrillation (63% v 31%)
Efficacy decreased significantly with AF of >7 days
Studies, enrolled patients with mild to moderate underlying
disease, so these results may not be generalizable to patients
with markedly depressed LVF
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Antiarrhythmic therapy of atrial
fibrillation
Dofetilide
DIAMOND-CHF
Study of 1518 patients with symptomatic heart failure (EF
<35%)
Therapy with 1000mic.g was associated with a greater rate of
conversion to sinus rhythm (44% v14%)
SAFIRE-D
Study of 325 patients with persistent AF &/or atrial flutter
Cardioversion rates were 6.1%,9.8% & 29.9% for 125, 250 &
500mic.g bid compared with 1.2% of conversion with placebo
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fibrillation
Amiodarone
Produce sinus rhythm in 80% within 24hours (late conversion)
Advantages
It lowers ventricular rate before conversion (IC drugs increase
the rate)
Recommended in hemodynamically compromised patients
since it is less negatively inotropic
Prefered in pts with LVF, LVH, IHD
IV amiodarone is moderately effective in converting AF
compared with placebo (63% v 44%), with maximum effect at
24hours (74% v 55%) --- 12 meta-analysis
Higher than usual dose & combination of IV & oral
administration may enhance the cardioversion rate
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fibrillation
Quinidine
Usually administered in conjunction with B-Blocker
Cumulative dose of up to 1350mg has shown to cardiovert 50-
77% of patients with recent onset AF
Sotalol
It is ineffective in acute conversion
It is effective for the prevention of AF
This discrepancy relates to its property to prolong the refractory
period predominantly at lower atrial rates, but not during rapid
AF
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Antiarrhythmic therapy of atrial
fibrillation
Availability of studies on the efficacy of procainamide &
disopyramide is limited, precluding definite conclusions
Digitalis, B-Blockers, & CCBs are ineffective for acute conversion
of AF
DAAF study (Digoxin in acute AF)
There was no difference in cardioversion rates at 16 hours
between IV digoxin & placebo (51% v 46%)
Digoxin can facilitate AF due to its cholinergic effects which may
cause a non-uniform reduction in conduction velocity & effective
refractory periods of the atria, and to delay the reversal of
remodelling after restoration of sinus rhythm
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Antiarrhythmic therapy of atrial
fibrillation
Prevention of paroxysmal AF
No need for prophylactic AAD
After first episode of AF which may self terminate or require
electrical or pharmacologic cardioversion
Patients with infrequent, self limiting & well tolerated paroxysms
of AF
Prophylactic AAD are recommended if
Occurs frequently (1 episode per 3 months)
Associated with significant symptoms
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Antiarrhythmic therapy of atrial
fibrillation
Prophylactic AAD are recommended if…
Worsening of LV function
In the presence of left atrial enlargement, LVD, underlying
CVS pathology, long duration of AF, advanced age
B-blockers
Effective in adrenergic dependent AF (class IA & IC are
ineffective)
It prevents the recurrence of persistent AF after
cardioversion
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Antiarrhythmic therapy of atrial
fibrillation
Control of ventricular rate during paroxysmal AF
Digitalis, B-blockers, CCBs are useful
Addition of rate controlling drugs is necessary with class IA & IC
drugs (not needed with amiodarone or sotalol)
Control of ventricular rate in the setting of SSS may be
impossible without implanting pacemaker
In WPW syndrome complicated by AF – acute rate control &
conversion to SR may be achieved by procainamide or
flecainide
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Antithrombotic therapy
Whether AF is persistent or intermittent ---
Predisposes to stroke
Non valvular AF
Most common cardiac disease associated with
cerebral embolism
The risk of stroke is 5-7 times greater when
compared to control group
Risk factors that predicts stroke
Previous stroke or TIA
Diabetes mellitus
Systemic hypertension
Increasing age
CAD
CHF
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Antithrombotic therapy
LV dysfunction & left atrial size > 2.5cm/sq.m --- associated
with thromboembolism
Age - 60-65, normal echo, no risk factors --- Extremely low
risk for stroke (1% per year)
Results from 5 large anticoagulation trails
Annual rate of stroke in control group --- 4.5%
Annual rate of stroke in warfarin-treated group --- 1.4%
(68% risk reduction)
Aspirin 325mg/d produced a risk reduction of 44%
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Antithrombotic therapy
Annual rate of major hemorrhage
Control group --- 1%
Aspirin group --- 1%
Warfarin group --- 1.3%
No difference was noted in stroke risk, when patients with
paroxysmal (intermittent) AF were compared with chronic AF
Anticoagulation was 50% more effective than aspirin in
preventing ischemic stroke
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Antithrombotic therapy
Risk factors for stroke
Prior stroke or TIA
Significant valvular heart disease
Hypertension
Diabetes mellitus
Age >65 years
Left atrial enlargement
CAD
Congestive heart failure
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Antithrombotic therapy
Lone AF
Age <60years, no risk factors ---No antithrombotic therapy
Age - 60-75 years (risk-2%per year) ---Aspirin
Age > 75 years --- Anticoagulation (INR – 2.0)
Any patients with AF + Risk factors for stroke --- Treated with
warfarin anticoagulation (INR – 2 to 3)
Patients with contraindication to anticoagulation (or) unreliable
individual (or) no risk factors --- Aspirin
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Antithrombotic therapy
Risk of embolism after cardioversion
Risk --- 0 -7%
Risk is independent of mode of cardioversion
High risk patients are
Prior embolism, Mechanical valve prosthesis, Mitral stenosis
In AF (>2d) --- Warfarin for 3 weeks before cardioversion + 3-4
weeks after reversion to sinus rhythm
Alternate strategy --- TEE (to exclude LA thrombus) + heparin
before cardioversion + followed by warfarin for 4weeks
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Risk of embolism after cardioversion…
For emergency cardioversion (TEE cannot be obtained) ---
heparin before cardioversion + followed by warfarin for
4weeks
Low risk patients
Age <65 years without risk factor for stroke in nonvalvular AF
Anticoagulation may not be necessary before cardioversion
but aspirin is indicated
It is important to emphasize that suggestions must be
individualized for a given patient
Absolute contraindication for anticoagulation -
ICH,SDH,GI bleed
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Non – pharmacologic therapies
Rhythm control strategies
Device therapy
Single site pacing --- High right atrial & septal
In many patients with SSS, atrial pacmaker allows higher dose
of AAD since sinus node dysfunction is treated
In patients with paroxysmal AF, there is evidence for intraatrial
conduction delay
Atrial pacing may decrease the frequency of recurrent AF in
patients who have SSS
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Non – pharmacologic therapies
Incidence of AF is lower in patients treated by atrial
pacing than ventricular pacing (prospective studies)
Multisite pacing --- Biatrial synchronous & Dual site
atrial pacing
In addition to the high RA lead, another atrial lead is
placed just outside the CS ostium for stability & LA
synchronization
These pacing cause resynchronization of atrial
depolarisation & helpful in patients with intra atrial
conduction delay
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Non – pharmacologic therapies
Usually performed in patients with recurrent,
symptomatic & drug refractory AF
ECG showed biphasic ‘p’ wave in inferior leads with
abbreviation of ‘P’ wave duration
Implantable atrial defibrillator
Automatic atrial defibrillator
• It detect AF by means of implanted RA, CS & RV
leads
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Non – pharmacologic therapies
• It delivers ‘R’ wave synchronization shock of 6J after
a minimal preceding R-R interval of 500 ms
• Unfortunately this device in its current form is not in
use
Atrial-ventricular defibrillator/pacemaker
• It has dual chamber algorithm-based arrhythmia
detection
• Pacing & defibrillation therapies for treatment of AF
& atrial tachycardias
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Non – pharmacologic therapies
Ablation therapy --- surgical
His bundle ablation (surgical ligation, mechanical,
cryothermia) + Pace maker implantation
Corridor surgery
Creating an isolated strip of muscle to isolate the SA & AV
nodes, thus driving ventricular rate via AV node-His bundle
complex
But, atrial areas outside of narrow RA corridor continued to
fibrillate with persistent loss of atrial transport function &
persistent risk of thromboembolism
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Non – pharmacologic therapies
Maze procedure
The principle is compartmentalize both atria so that AF
cannot be maintained
Right & left atrial appendages were resected,
pulmonary vein ostia are isolated, linear RA & LA
lesions are connected to anatomic structures to form
an “electrical maze” --- “Maze 3”
Appropriately placed atrial incisions not only interrupt
the conduction routes of reentrant circuits, but they
also direct the sinus impulse from SA to AV along a
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Maze procedure
90% pt cured of AF with operative mortality <1
<10% requires PPI due to sinus node dysfunction
Transient fluid retention due to
↓atrial natriuretic
peptide must be treated with diuretics
The entire atrial myocardium was electrically
activated & atrial transport function is preserved
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Non – pharmacologic therapies
Rate control strategy
Catheter AV junctional modification (radiofrequency)
Principle --- Posterior inputs of AV node have shorter ERP, their
ablation slows the ventricular response during AF
Patient who becomes symptomatic due rapid ventricular
response will benefit
Currently, AV node modification is usually reserved for patients
who require non-pharmacologic control but are opposed to
pacemaker implantation
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Non – pharmacologic therapies
Catheter ablation (DC shock or radiofrequency) +
Pacemaker
It is performed in patients with unmanageable symptoms
related to rapid ventricular response
DC current ablation is highly dangerous --- produce electrical
arcing & barotrauma ( cardiac perforation, tamponade, acute
depression of LV, proarrhythmia & sudden death
Radiofrequency ablation ---avoid complications
Disadvantages
Dependence on pacemaker
Atria will continue to fibrillate --- need long term
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Non – pharmacologic therapies
Choice of pace maker type --- determined by the current phase
of AF
Chronic AF --- VVIR + AV nodal ablation
Paroxysmal AF ( usually in sinus rhythm between episodes) ---
Dual-chamber pacemaker with mode switching
Stroke prevention strategy
Percutaneous LA appendage transcatheter occlusion
(PLAATO)
Involves insertion of an occlusion device by catheter into the LA
appendage via trans septal puncture
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site, the sharp PVPs are seen in the first two beats but
are absent during the last two beats
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Introduction
Paroxysmal AF
Short lasting < 1 hour
Long lasting >1; < 48 hours
AF interspersed with periods of sinus rhythm & usually
terminates spontaneously
Persistent AF
Occur between 2days - weeks
Intervention is needed to restore the sinus rythum
Chronic or permanent AF
Persists for months to years
No spontaneous conversion
Interventions to restore sinus rythum are either ineffectual or
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Mechanisms
Type – I --- Activation consisted of single, broad wavefronts
propagating without conduction delay & either only short arcs of
conduction block or small areas of slow conduction that did not disrupt
the main course of propagation
Type – II --- Activation consisted of either the presence of 2 wavelets
or of single wave (with either considerable conduction block or slow
conduction or both)
Type – III --- Activation was characterized by 3 or more wavelets
combined with areas of slow conduction & multiple arcs of conduction
block
As the fibrillation changed from type I to III, AFs frequency & irregularity
increased, creating a higher incidence of continuous electrical activity &
reentry
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Mechanisms
Familial AF
• Genetic predisposition – is a hypothesis
• Defect linked to chromosome 10q (21 of 49 members from 3
spanish families presented with AF)
• Missense mutation in the lamin A/C gene (In DCM – associated
with AF)
• Missense mutation Arg663His ( In specific phenotype of HCM –
associated with 47% of AF)