Atrial fibrilation

http://cardiologysearch.blogspot.in/

Atrial fibrillation
(Classification, Mechanism &

Management)


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)


Introduction…
 ventricular rate during AF is altered due to
 Autonomic tone
 Property of AV node
 Effect of drugs on AV conduction


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


 Framingham heart study ---cardiac factor
predicting AF
• CHF
• RHD
• HT
• Stroke
• Left atrial enlargement
• Increased LV wall thickness
• Decreased LV fractional shortening


 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%

Underlying causes of AF
 CVS
 Tumors
 Rheumatic heart disease  WPW syndrome
 ASD  Systemic
 Cardiac surgery  Alcohol (holiday heart
 Cardiomyopathy syndrome)
 Hypertrophic
 CVA
 Idiopathic
 Infiltrative
 COPD
 Hypertension  Defibrillation
 CAD (Acute & chronic)  Effort
 MVPS  Electrocution
 Non rheumatic mitral or tricuspid
valve disease
 Electrolyte abnormalities
 Pericarditis  Fever
 Tacycardia-bradycardia syndrome  Hypothermia


Underlying causes of AF…

 Pneumonia  Congenital

 Pulmonary embolism  Multiple sclerosis

 Sudden emotion  Muscular dystrophy

 Thyrotoxicosis  Pheochromocytoma

 Trauma  Right atrial cold injections

 Rare  Swallowing

 Acute hypovolemia  Tyramine foods


Classification of Atrial fibrillation

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


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

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


Mechanisms


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


Anatomic distribution of focal
trigger in Paraoxysmal AF

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


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”


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

Mechanisms http://cardiologysearch.blogspot.in/

 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


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)


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


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


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

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)

Antiarrhythmic to maintain sinus rhythm in AF

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

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


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


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

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


Conversion of paroxysmal AF(<3days)

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

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

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

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

 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%

 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


 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


 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

 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


 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


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

 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

 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

• 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


 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

 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


Indication for maze procedure
 Symptomatic AF
 Refractory to AAD
 Recurrent systemic embolism despite
anticoagulation

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

 Tans catheter ablation therapy
 Linear atrial ablation (Radiofrequency)
 It is employed in LA & RA for substrate compartmentalization

 Trigger ablation (Radiofrequency)
 Focal pulmonary vein
 Pulmonary vein isolation - transseptal puncture followed by
pulmonary venography to define anatomy

 Adverse effect
 Stroke
 Phrenic nerve injury
 Pericardial effusion & tamponade
 Pulmonary vein stenosis


Indication for ablation
 Symptomatic AF
 Refractory to AAD
 Without structural heart disease


 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

 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

 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

A circular mapping catheter is in the ostium of the left lower
PV and an ablation catheter with a large-tip electrode is
recording a PV potential from the nearby strand.

During radiofrequency ablation near Lasso-8 recording
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

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


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)


Rate control in atrial fibrillation


Antiarrhythmic therapy of atrial fibrillation


30%

Atrial fibrilation

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