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Atrial fibrillationAF 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…
Autonomic tone
Atrial fibrillation is the most common arrhythmia & the incidence & prevalence increases with the age
The incidence
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
Introduction
CHF
RHD
HT
Stroke
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%
Pericarditis
Paraoxysmal AF - last < 7days (most<24hrs) self-terminating episodes
Persistent AF - last >7days requires electrical or pharmacologic cardioversion
Permanent AF - sustained >1yr & failed cardioversion
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
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
Mechanisms
Perpetuating factor - AF does not terminate spontaneously
Paraoxysmal AF - 95% of Triggering foci are mapped in pulmonary vein
Other foci - within SVC ,coronary sinus
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 alterations between type III & other types
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
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
Usually younger age group (30 – 50 years)
Mechanisms
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
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
Mechanisms
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
Three antiarrhythmic strategies
Acute pharmacologic termination
Control of ventricular rate
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)
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
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
Amiodarone
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
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 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
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
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
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
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
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
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%
Antithrombotic therapy
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
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 --- 0 -7%
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
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
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
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
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
Pacing & defibrillation therapies for treatment of AF & atrial tachycardias
Therapy for VT/VF
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 specified route
<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
Trigger ablation (Radiofrequency)
Focal pulmonary vein
Adverse effect
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
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
AF interspersed with periods of sinus rhythm & usually terminates spontaneously
Persistent AF
Chronic or permanent AF
No spontaneous conversion
Interventions to restore sinus rythum are either ineffectual or not tried
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
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)
Mechanisms
30%

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