Comprehensive slides on the history, risk factors, pathophysiology, clinical features, diagnosis, management, complications and trials of Atrial Fibrillation(AF/AFib) for the use of Internal medicine residents or physicians

1. Atrial fibrillation
Presenting PG - Dr Raghav Agrawal, 2nd year
Guide - Dr Madhu Kumar, Assistant Professor, Dept of General Medicine, MMCRI, Mysuru

2. History
• In 2000 BC, the Yellow Emperor of China wrote in his book(Classics
of Internal Medicine) - "When the pulse is irregular and tremulous
and the beats occur at intervals, then the impulse of life fades."
• In 1775, William Withering demonstrated bene
fi
t of digitalis purpurea
(purple foxglove) in AF. In a patient with a weak and irregular pulse,
Digitalis resulted in a "more full and regular pulse"
• Known as 'the complete arrhythmia’ - all known arrhythmia
mechanisms including triggered activity, enhanced automaticity, and
re-entry are implicated in its pathophysiology
• ‘Ataxia of the pulse’, ‘delirium cordis’, and ‘pulsus irregularis
perpetuus’
• Einthoven published the
fi
rst ECG showing AF in 1906

3. • Form of disorganised rhythm - Supraventricular tachyarrhthymia
• Low-amplitude baseline oscillations (fibrillatory or f waves) and
an irregularly irregular ventricular rhythm and absent P waves
• f waves - 300 to 600 bpm, variable in amplitude, shape, and
timing - best seen in V1
• Rapid, irregular, uncoordinated electrical activity and atrial
contraction
• Decreased e
ff
ective atrial mechanical contraction
• Passed onto AVN - acts as speed braker - determines
Ventricular rate - 100-160/min. Beat to beat variability in
ventricular
fi
lling
Definition

4. • Excessively slow ventricular rate seen in AVN conduction
disease and in high vagal tone
• WPW - Ventricular rate >250/min
• Patients with sustained ventricular pacing, digitalis toxicity,
extremely rapid rate(>170bpm) and 3rd degree heart block with
regular escape rhythm - pseudo regularisation - diagnosis of AF
is based on the presence of f waves
• In some patients, f waves are very small and not perceptible on
the electrocardiogram, and the diagnosis of AF is based on the
irregularly irregular ventricular rhythm
• In RHD, the amplitude of the f waves exceeds 0.1 mV (coarse
fi
brillation), while in CAD, f waves are smaller (
fi
ne
fi
brillation)

7. Epidemiology
• Most common sustained arrhythmia in the world
• Most common arrhythmia treated in clinical practice
• Most common arrhythmia for which patients are hospitalized - 33%
• Global prevalence - 50 million in 2020
• >95% of AF patients are >60 years old
• Incidence and prevalence increasing
• Incidences doubles with each decade of life after age 55
• Prevalence is 10% in >80yrs
• 1 in 4 men over 40
• The average stroke rate - 1.5% and annual death rate- 3% in
anticoagulated AF patients

9. Overall and sex specific trends in incidence of AF between 1980 and 2000

10. Stroke risk related to various cardiac conditions - Framingham study

11. Issues
• Major public health issue
• Rising incidence - Multifactorial - aging population, rising obesity,
increasing detection, increasing longevity
• AF - 1.5- to 2-x mortality
• More frequent hospitalisations
• QoL - no change to marked reduction
• CHF - no change to severe (tachycardiomyopathy)
• Increased risk of adverse outcomes, - CVA - 5x (more severe), 1.5x
cognitive impairment/dementia, 1.5x MI, 2x SCD, 5x HF/
cardiomyopathy, increased MRI-detected asymptomatic embolic infarct
• Most important consequence of AF - increased risk of stroke,
accounting for ~25% of all strokes

12. Risk factors
• Age - AF is the price you pay for ageing
• Sex - M > F
• Race - Whites > blacks
• Height - tall stature
• Smoking
• Exercise - U shaped curve in males. Linear in females
• Alcohol - especially acute intoxication (Holiday heart syndrome)
• Excess ca
ff
eine
• Psychological stress
• Obesity. Epicardial fat - adipocyte infiltration. LEGACY study - sustained
weight loss and exercise can reduce AF burden

13. • Hypertension
• Diabetes - Metformin decreases risk
• Cardiac - CHF, CHD, IHD (esp AWMI),
cardiomyopathy(Hypertrophic/Dilated/Restrictive),
Myocarditis, Constrictive pericarditis, Cardiac
tumours eg atrial myxoma, Valvular HD especially
RHD - MS/MR, WPW syndrome, Sick sinus
syndrome, increased LA diameter/ED LA volume,
LVH, Prolonged PR interval, Cardiac surgery eg post
CABG, Posterior left pericardiotomy, AAA repair
• Electrocution

14. • Tachycardia- often have AVNRT or WPW syndrome
that degenerates into AF
• Respiratory - PTE, Severe pulm HTN, OSAS, COPD,
Pneumonia
• Endocrine - Hyperthyroidism, Phaechromocytoma
• Family history - familial AF - early onset - SCD
common
• Normal hearts a
ff
ected by high adrenergic states,
drugs (sympathomimetics), hypoxia, hypokalemia,
hypoglycemia, or sepsis

16. Electrophysiological mechanisms
• Triggers for onset + Substrate for maintenance
• Mechanism - triggered activity and re-entry
• Final common pathway - electrophysiological changes in the atrial tissue -
alteration in regulation of membrane channels and proteins - abnormal electrical
activity
• Most common site - pulmonary veins - Shorter refractory periods + Abrupt
changes in myocyte
fi
ber orientation + stretch activated channels
• Causes atrial ectopics - contribute to PACs - AT - AF
• Other ectopic sites - Muscular tissue sleeve within SVC, Coronary sinus, Remnant
of vein of Marshall
• Heterogeneity in ion channels between LA and RA further promotes
arrhythmogenicity.
• Prothrombotic changes - evident in LA, including increased endocardial
expression of vWF, VCAM-1 and MCP-1

18. • Sustained AF - in
fl
ammatory response - activation of
myo
fi
broblasts + cytokine release
• Remodelling - Atrial
fi
brosis(functional) + enlargement of
LA(anatomical) - correlates with progression of AF
• Myocyte apoptosis
• ECM generation
• Electrical and structural remodelling provides substrates for
maintenance - abnormal conduction - shortened refractory
period - more impulses conducted to ventricles - FVR
• Sustainance - increased automaticity + abnormal re entrant
circuits

22. Associated arrhythmias
• Atrial Tachycardia: regular atrial rhythm - constant rate of >100bpm + discrete
P waves + origin outside of SAN
• Focal ATs - single site within the LA/RA. AF - multiple sites/larger circuits
• Atrial Flutter and Macroreentrant AT : occur in same situations as AF
• Typical AFL or CTI-dependent AFL - macroreentrant circuit around tricuspid
annulus traversing the CTI on the right side of the heart - classic sawtooth
flutter waves in inferior leads when circuit goes in counterclockwise direction.
• Same circuit in the clockwise direction is called “reverse typical AFL”
• If the flutter involves a di
ff
erent circuit than tricuspid valve/isthmus, called
atypical AFL or nonCTI–dependent macroreentrant AT

28. AF - ECG Differentials
• 4 major fast, irregular patterns that may be mistaken for AF -
• (1) Artifact causing an irregular appearing baseline. Cause - poor electrode
contact or patient movement (eg tremor from PD)
• (2) Sinus rhythm with frequent premature atrial complexes (PACs)
• (3) Multifocal atrial tachycardia (MAT)
• (4) Atrial flutter or atrial tachycardia with variable AV conduction

29. • Atrial
flutter
waves
have a
rate of 250
to 350
bpm

30. Clinical features
• Asymptomatic - Trial of “diagnostic” cardioversion to
determine whether a patient feels better in SR. Valuable in a
patient < 80yrs presenting routinely and found to be in AF
• Palpitations (irregular)
• Syncope - decreased cerebral perfusion - uncommon
symptom of AF, can be caused by a long sinus pause on
termination of AF in a patient with the sick sinus syndrome
• Easy fatiguability, Exercise intolerance - decreased BP -
loss of atrial kick contribution
• Dyspnea - Diastolic
fi
lling time decreased - increased atrial
pressure and volume - back
fl
ow - Pulmonary edema

31. • Polyuria can occur because of release of ANP
• Worsens with underlying Cardiac disease - due to
increased LVEDP - increase LA pressure and LA
size - increased AF
• Stasis - thrombosis (LAA) - rupture - embolization -
CVA(embolic), Renal(ARF), GI(AMAE)
• Tachycardiomyopathy - Decreased LV function
• CHF - LA
fi
brosis - non contractile - non compliant
- increased LA pressure - Sti
ff
left atrial syndrome
• Exacerbation of underlying cardiac disease

32. Signs
• Hallmark of AF on physical examination is an irregularly
irregular pulse.
• Short R-R intervals - decrease LV diastolic filling - low SV
and the absence of palpable peripheral pulse - “pulse
deficit” - peripheral pulse is not as rapid as the apical rate
• Variable intensity of the S1
• JVP- absent a wave

34. • Old classification - based on duration - focused
on therapeutic interventions
• New classification - De
fi
nes AF as a progressive
disease, highlights the need to address it at the
earliest stages, emphasizing importance of
di
ff
erent strategies at di
ff
erent stages
• Optimal AF management - treatment of
comorbidities and risk factors, lifestyle changes
Classification

37. • A confounding factor in the classification
of AF is cardioversion and AAD

39. Paroxysmal AF
• Paroxysmal AF - classified clinically on the basis of the autonomic
setting in which it most often occurs
• 25% - vagotonic AF - high vagal tone - evening during relaxing,
post meal or sleep. Vagotonic drugs (e.g., digitalis) can aggravate,
and vagolytic drugs (e.g., disopyramide) used as prophylactic
therapy
• 15% - Adrenergic AF - high sympathetic tone - strenuous exertion.
Beta blockers - rate control, prevent AF episodes
• Most patients - mixed / random form - no consistent pattern of
onset

40. • Lone AF - <60 yrs age, no clinical/echo evidence of HTN/cardiopulmonary
disease, good prognosis, Thromboembolism is not an issue

42. Evaluation and detection
• An irregularly irregular pulse or irregular heart beat on auscultation should raise
suspicion
• ECG - irregular RR intervals, absent distinct P waves, low amplitude baseline
oscillations (f waves- 300 to 600/min)
• Any arrhythmia that has the ECG characteristics of AF and lasts su
ffi
ciently long for a
12-lead ECG to be recorded, or at least 30s on a rhythm strip, should be considered
as AF
• Holter (24-48hrs)
• Event monitors (upto 1 month)
• Dual chambers pacemakers and de
fi
brillators
• Implantable loop recorder (upto 3 yrs)
• A recent trial demonstrated that among patients with a cryptogenic stroke and no AF
seen on a 24-hour Holter monitor, AF was detected in 8.9% of patients who had an
implantable cardiac monitor within 6 months

44. • History taking - type, severity of symptoms, first onset,
triggers, whether episodes are random or at particular
times , frequency and duration, causes, and comorbidities
• Labs :CBC, BMP, TSH, LFT, CXR
• Echo : valvular, ventricular, atrial and congenital heart
diseases, LA dimensions
• Stress test : reasonable if signs/risk factors for CAD
• Routine testing for ischemia, ACS and PTE not performed
unless there are additional signs/symptoms suggestive

45. Evaluation and management
• Acute management
• 1) Handle risk factors
• 2) Symptomatic relief - rate or rhythm control,
cardioversion
• 3) Assessment and prevention of
complications

46. 4S-AF Scheme

47. Screening
for AF

50. • Pacemakers and ICDs are capable of detecting short episodes of asymptomatic AF
that are subclinical.
• Subclinical atrial tachyarrhythmias were independently associated with a 2.5x
stroke.
• Long-term intracardiac monitoring in patients with recently implanted pacemakers
or ICDs has detected subclinical AF (SCAF) in up to 50% of patients
• Common in older adults
• Whether anticoagulation lowers stroke risk in this subset of AF patients currently is
unknown
• The 2019 AHA/ACC/HRS AF Guidelines provides a class I LOE B recommendation
that the presence of recorded AHREs on an implanted device should prompt
further evaluation to document clinically relevant AF to guide treatment decisions.
• In the absence of data from clinical trials, most clinicians today would advise
anticoagulation for patients with device-detected AF who have episodes of at least
5 hours in duration and have an elevated stroke risk profile.

51. • Risk prediction model for newly diagnosed
AF is CHARGE-AF (Cohorts for Heart and
Aging Research in Genomic Epidemiology
for AF), while the C2HEST score was
derived and validated in Asian cohorts
• It is not yet established that patients at
high risk of developing AF by a validated
risk score bene
fi
t from screening and
interventions

54. CRUX
• Hemodynamically unstable - Electrical Cardioversion +
anticoagulation
• Hemodynamically stable -Rate/Rhythm control +
anticoagulation. Depends on symptoms, prior AF episodes, age,
LA size, and current AAD therapy.
• Refractory to medical management - Catheter ablation or
Surgery(Cox-Maze) or LAAOD
• Rhythm control - early(early symptom relief, less recurrence, no
need to anticoagulate before) vs delayed(TEE unavailable and
not anticoagulated, LA thrombus present, sponatenous
conversion chances present, reversible cause present).
Electrical vs pharmacological

55. • Pharmacological • Electrical
• Advantages • No anesthesia
requirement
• Pill in the pocket
approach
• Maybe repeated
immediately
• Immediate e
ff
ect
• Highly e
ff
ective even
in long standing
cases
• Safe in
hemodynamically
unstable patients
• Disadvantages • Negative ionotropic
• Pro arrhythmic
• Time consuming
• Only e
ff
ective is
• General anesthesia
required

56. Indications for emergency cardioversion
• New onset AF with hemodynamic instability(severe
hypotension)/Pulmonary edema/angina/evidence of coronary
ischemia
• Electrical - Synchronised DC Shock 150-200J with QRS
complexes preferably in sedated state
• Pharmacological - I.V. Class III antiarrhythmics eg Ibutilide,
Amiodarone
• For AF < 2 to 3 days, efficacy - 60% to 70% for ibutilide, 40%
to 50% for amiodarone, and 30% to 40% for procainamide

57. Whether to do cardioversion first or anticoagulant first
• AF< 48hrs / unstable patient - Cardioversion f/b anticoagulation.
Provided they are not at high risk of stroke - rheumatic MS/
HOCM with marked LAE or h/o embolic events
• AF in stable patient - unknown duration or >48hrs or high risk of
thromboembolism eg MS/HOCM - anticoagulant
fi
rst for 3
weeks f/b cardioversion OR anticoagulate with heparin, do TEE/
Cardiac CT angio to rule out LAA thrombus f/b Cardioversion
• Anticoagulation compulsory for 4 weeks post cardioversion -
CHADSVASc doesn’t matter - to allow for recover of atrial
mechanical function (stunning)

58. Management cascade

59. Anticoagulation
• Annual stroke risk without anticoagulation is
20%
• Anticoagulation reduces stroke risk by 2-3
times
• Anticoagulation only treatment shown to
decrease mortality
• Antiplatelet reduces stroke risk by 1/5th

60. CHADS2 Score
• Evolved from the AF investigators
• Rapid and easy to use for assessing stroke risk
• CHADS2 score of 0 - stroke rate of 1.9 per 100 pt yrs
• Stroke rate increased by a factor of 1.5 for each 1 point increase in score
• Recommendations :
• Low risk (score 0) - No anticoagulation
• Moderate (score 1) - Aspirin or OAC
• High risk (score >= 2) - OAC

61. CHADS2 score limitations
• Too many patients classi
fi
ed as
moderate risk
• Even patient at moderate risk
(CHADS2 = 1) bene
fi
t from OAC over
aspirin

62. CHA2DS2-VASc Score

67. • Direct relationship between the
CHA2DS2 VASc score and the annual
risk of stroke in the absence of OAC
therapy.
• The annual risk of stroke is 0 or close to
zero when the CHA2 DS2 -VASc score
is 0, compared with approximately 3%
when the CHA2DS2-VASc score is 3

71. HAS-BLED Score

74. • Rapid onset and o
ff
set
• Lower risk of IC bleed
• Limited in
valvular AF
• GI bleed

75. Warfarin
• DOC for Valvular AF
• TTR (Time in Therapeutic Range) >65-70% - SAMe-TT2R2 score
• Warfarin + drugs - Quinolones decreases e
ffi
cacy, NSAIDS
increases e
ffi
cacy
• Warfarin + food - Leafy vegetables rich in Vit K decreases e
ffi
cacy
• CHA2DS2-VASc Score of >=2 or + ESRD (CrCl < 15 mL/min) or
are on MHD, it is reasonable to prescribe warfarin
• VKA antidote - FFP/PCC/Vit K
• Narrow therapeutic index - Maintaining the INR at a level of 2.0 or
higher is important because even a relatively small decrease in
INR from 2.0 to 1.7 more than doubles the risk of stroke

77. Hart et al
• Stroke reduction
• Warfarin - 64%, ARR - 2.7% per year
• Aspirin - 19% non signi
fi
cant, ARR - 0.8% per year
• Warfarin vs antiplatelet therapy - 37%
• Major bleeding
• Warfarin vs aspirin - risk of IC haemorrhage doubled
• Absolute risk increase small - 0.2 % per year
• Mortality - Warfarin vs control - all cause mortality substantially reduced
(26%)

80. LMWH
• Longer half-life than UFH
• Predictable antithrombotic e
ff
ect attained with a fixed dosage
administered S/C
• Can be self-injected, is a practical alternative to UFH for initiation
of anticoagulation with warfarin
• Bridging therapy required
• High cost so rarely used as a substitute for long-term conventional
anticoagulation.
• Typically used as a temporary bridge to therapeutic anticoagulation
with warfarin or in high-risk patients eg h/o stroke/TIA/mechanical
valve during procedures when warfarin has been suspended

81. Dosing of NOACs

82. Dabigatran
• Direct Thrombin Inhibitor
• RE-LY Trial - 150 mg bd dose superior(35%)
to warfarin in preventing ischemic stoke with
no di
ff
erence(-20%) in bleeding
• Praxbind ® (Idarucizumab) is a speci
fi
c
reversal agent for Pradaxa

83. RE-LY - Randomized Evaluation of Long-Term
Anticoagulation Therapy

84. Rivaroxaban
• Oral factor Xa inhibitor
• Rocket AF: noninferior to warfarin for stroke
prevention(-21%)
• No signi
fi
cant di
ff
erence in risk of major bleeding
• Intracranial and fatal bleeding occurred less frequently
• Antidote: FDA approves AndexXa (Andexanet alfa)

85. ROCKET-AF - Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition
Compared with Vitamin K Antagonism for Prevention of Stroke and
Embolism Trial in AF

86. Apixaban
• Oral factor Xa inhibitor
• ARISTOTLE - superior to warfarin in
preventing stroke - by 21%
• Less bleeding - 31%
• Lower mortality - 11%
• Antidote - FDA approves AndexXa

87. Edoxaban
• Oral factor Xa inhibitor
• ENGAGE-AF study - Noninferior to
warfarin with respect to the prevention of
stroke or systemic embolism
• Signi
fi
cantly lower rates of bleeding and
death

94. Antiplatelets
• Aspirin is not e
ff
ective for preventing thromboembolic complications
in patients with AF
• A major update of the 2019 ACC/AHA/HRS AF Guidelines, as
compared with the 2014 Guidelines, was that aspirin is no longer
recommended for stroke prevention in AF patients
• In patients with a low CHA2 DS2 -VASc score, the recommended
options for stroke prevention are now an OAC v/s no therapy

100. Rate control
• Goal - Increase diastolic
fi
lling time - improve CO - improve
symptoms
• Long term e
ff
ect - decreases risk of CHF and
tachycardiomyopathy
• Exertional symptoms indicate inadequate rate control. HR should
be controlled even with exertion
• Resting HR <80bpm
• With light exertion eg walking - <100 bpm
• Accepted HR control <110 bpm provided no symptoms
• Rate control is reasonable for 1st episode of AF, LA size > 6 cm,
advanced age with asymptomatic AF, pulmonary/thyroid disease

103. In patients with SAN
dysfunction, use of a
beta blocker with intrinsic
sympathomimetic activity
(pindolol, acebutolol) may
provide rate control
without aggravating sinus
bradycardia.
Esmocard, Esocard,
Neotach, Miniblock

105. Eg. Amiodarone would be an appropriate choice for a patient with persistent AF,
heart failure, and reactive airway disease who cannot tolerate either a CCB or a
beta blocker and who has a RVR despite treatment with digitalis.

110. Rate vs rhythm control

112. Outcomes
• Mortality, hospitalisation, stroke - No bene
fi
t of rhythm control
• QoL - no di
ff
erences in QoL
• Rhythm-control strategy o
ff
ers no survival advantage over rate-control
• Lower risk of adverse drug e
ff
ects with the rate-control strategy
• EAST-AFNET 4 (Early Treatment of Atrial Fibrillation for Stroke
Prevention Trial - Early rhythm control strategy (within 1 year of
presentation) compared to standard rate control - reduction in
cardiovascular events, including death

113. • SR associated with decreased risk of death. In general, patients who maintain SR
have better survival than those who continue to have AF.
• AADs are not associated with improved survival, which suggests that any bene
fi
cial
e
ff
ects of AADs are o
ff
set by their adverse e
ff
ects - more hospitalization
• Low e
ffi
cacy - 40-60% for all except Amiodarone - 60-70%
• If an e
ff
ective method for maintaining SR with fewer adverse e
ff
ects were available,
it might be bene
fi
cial
• Warfarin use associated with decreased risk of death

118. Electric cardioversion
• E
ffi
cacy of transthoracic cardioversion > 95%
• Biphasic waveform shocks > monophasic waveform shocks. Allows the
use of lower energy shock - less skin irritation
• 1st-shock strength using a biphasic waveform - 200 J f/b higher output
shocks if needed
• If a 360-J biphasic shock is unsuccessful, IV ibutilide pretreatment
• May fail to restore SR
• An increase in shock strength, an infusion of ibutilide, or repeat CV with
greater pressure applied to the defibrillation patches can be tried.
• The second type of failure is an immediate AF recurrence within a few
seconds of successful conversion. Increase in shock strength is of no
value. Infusion of ibutilide helpful to prevent an immediate recurrence of AF

119. Principles of AAD therapy
• Treatment is to reduce AF-related symptoms
• E
ffi
cacy to maintain SR is modest
• If one AAD 'fails', a clinically acceptable response may be
achieved with another agent
• Proarrhythmia or extra-cardiac side e
ff
ects are frequent
• Safety rather than e
ffi
cacy considerations should guide the
choice
• Make sure patient has had adequate anticoagulation prior to
initiation or LA clot is ruled out

121. AV block,
Dyspnea,
Dizziness, HF
exacerbation
Visual
disturbances

122. Pill(s) in the pocket approach
• Acute pharmacologic cardioversion of AF also can be
attempted with oral drugs in patients without structural heart
disease.
• Most common oral agents used - propafenone and flecainide
• When flecainide is used, patients generally take a beta blocker
on AF onset and then take the flecainide one hours later
• Administered under surveillance upon first use, as patients may
have a pronounced postconversion pause
• If no adverse drug e
ff
ects are observed, the patient may then
be an appropriate candidate for episodic, self-administered
AAD therapy on OPD basis

128. Long term control

135. Dofetilide
• Pure Class Ill agent
• Dose 125 - 500 mg BID based on Cr Cl
• Proarrhythmia risk 3.3% highest in
fi
rst 72 hrs
• can be used in CAD and CHF
• Risk of QTc prolongation - continuous ECG
monitoring - initiate in hospital

141. • ATHENA: Reduction in hospitalization, deaths compared to
placebo. reduction
• ANDROMEDA: stopped prematurely increased mortality in pts
with advanced heart failure.
• PALLAS: increased rates of heart failure, stroke, and death

146. Catheter ablation
• Avoids requirement of AAD - Prevents drug toxicity and daily usage of
drugs
• Operator dependent
• Long term control of persistent AF - extensive area of ablation may be
required - less e
ff
ective
• Involves - Percutaneous venous access(femoral vein), transatrial septal
rupture, RFA, Cryoablation
• Detect and isolate arrhythmogenic LA regions present around PV antra
- abolish triggering foci and the substrate for re-entry
• Gaps in healed areas or emergence of new trigger sites may
necessitate repeat procedure in 10-30%
• Preferred modality in AF + CHF as AAD may be cardiotoxic

147. • Alternative energy sources - Laser beam radiation,
External beam radiation, Pulsed
fi
eld electroporation
• Single ablation - 70% reduction in AF in 1 year
• Multiple ablation - 90% reduction of AF in 1 year
• PVI - primary - requirement of repeated ablation or
AAD reduced
• Posterior LA wall ablation
• Thoracotomy f/b ablation
• OAC cover given

148. • Usually combined other surgery eg CABG/Valve repair.
Rarely done as standalone procedure
• Hybrid procedure - done in persistent AF. More e
ff
ective -
Surgical repair + Catheter ablation
• Strategy for selecting ablation target outside PV -
identi
fi
ed -
fi
re in response to high dose Isoproterenol
• Include areas of Atrial
fi
brosis (non PV foci), IVC and SVC
entry into RA, regions with repetitive activation during AF
• Require >1 ablative procedure to maintain SR because
they lack lesion durability (Complex atrial substrate)

151. Guidelines

152. • Primary endpoint ( Death + CVA + Bleeding + Cardiac arrest)
• Ablation therapy not superior to drugs for CV outcomes at 5 years
• Secondary endpoint - Signi
fi
cant reductions in death and CV
hospitalizations with ablation
• On treatment analysis, ablation demonstrated superior e
ffi
cacy

153. • Restoration of SR by catheter ablation in
CHF led to signi
fi
cant improvements in LVEF,
symptoms, exercise capacity, QoL

154. ]
• Catheter ablation more successful in maintaining SR
• Reduction in hospitalisations
• Reduction in mortality

161. AVN ablation
• AVN ablation + Permanent ventricular pacing - Ablate and
pace strategy
• Patients in whom rate and rhythm control with drugs or LA
ablation has failed
• Provides highly e
ff
ective control of ventricular rate
• Improves QoL, Decreases mortality
• Patients with reduced LV function may require biventricular
pacing after AVN
• Pacemaker -
• 1) Single chamber ventricular lead pacemaker - placed in
RV apex. Disadvantage - induces dyssynchronous
ventricular activation - reduces ventricular function
• 2) Biventricular pacing - direct pacing of Bundle of His or
LBB - minimises ventricular dyssynchrony

162. LAAOD
• LAA device placement - Watchman device,
Amplatzer cardiac device, Lariat plug -
seals LAA so thrombus formed will not
enter LA
• Anticoagulation is recommended for at
least 45 days, after which it can be
discontinued if there is no TEE evidence of
peridevice flow

163. Recommendations
• FDA approved for patients -
• 1) at increased risk of stroke and systemic
embolism based upon CHA2DS2-VASc scores
• 2) deemed by their physicians to be unsuitable for
OAC therapy
• 3) have an appropriate rationale to seek a
nonpharmacological alternative to OAC

165. • Watchman device only FDA approved
percutaneous LAA closure device
• semi-spherical nitinol frame with a
polyethylene terephthalate membrane
coating (fenestrated fabric)
• deployed transseptally using a
dedicated 14 Fr sheath usually under
TEE and
fl
uoroscopic guidance

168. • LARIAT plug - FDA approval for soft tissue
approximation (not stroke prevention).
Used o
ff
-label.
• A guidewire with a magnetic tip is inserted
into the LA - positioned at the tip of LAA.
It functions as a rail for an epicardial
snare. A snare with a pretied suture is
inserted and tightened to occlude the LAA

171. • Surgical excision of LAA is combined with Cox-Maze procedure
• Cox Maze procedure - cut and sew - Series of 12 incision/scars made +
atrial appendages excised - interrupts the abnormal electrical activity -
aborts re entry circuits. Resolution - 70-95%, Mortality - 1%
• Currently - Cox Maze 4 - bipolar clamp RF ablation tool to electrically
isolate the PV.
• Bi atrial maze incisions can also be done
• Performed during other open heart surgery, and in combination with
surgical ablation of AF or as a stand-alone thoracoscopic procedure - Mini
Maze
• Surgical ablation more e
ff
ective than catheter ablation - but with more
complications
Surgical ablation

173. • 707 pts with NV AF randomized to Watchman vs continued
warfarin
• Primary e
ffi
cacy endpoint stroke, systemic embolism and CV
death 3.0%(WATCHMAN) vs 4.3%(Warfarin) - noninferior
• Primary safety events 5.5% vs 3.6% (more safety events in
the Watchman arm) - less bleed

176. AF in specific settings

177. Pregnancy
• AF rare in pregnancy
• Rate control - BB, CCB, Digoxin - approved - lowest dose given
- crosses placenta
• Beta blockers - IUGR - preferably use after 1st trimester
• Amiodarone used for rhythm control in structurally abnormal
heart- fetal adverse e
ff
ects
• Fleicanide and sotalol used for rhythm control in structurally
normal heart - fetal arrhythmias
• Electric cardioversion - safe - risk of fetal distress
• Warfarin - Avoided in 1st trimester and 2-4 weeks before
delivery - use UFH/LMWH

178. HOCM
• Present in 25% cases
• AF increased mortality(3% vs 1%/yr)
• High stroke risk
• Rhythm control strategy preferred
• Severe LVH - increase risk of TdP with AAD

180. ACS
• Incidence of AF in patients with ACS -10-21%
• Increases with age and severity of MI
• Patients who develop AF during hospitalization have a worse prognosis
than those with AF on admission
• Independent predictor of poor long term outcome in patients with ACS
• NOAC recommended
• Urgent DC cardioversion of ACS presenting with new onset AF and
intractable ischemia, hemodynamic instablity or inadequate rate control
• IV beta blocker- rate control
• IV amiodarone
• ACE inhibitors

181. Antithrombotic therapy in AF after ACS

182. Antithrombotic in patients after elective PCI

183. WPW syndrome
• Very Rapid ventricular rates - 250-300/min - syncope,
VF, cardiac arrest
• Risk of AF over 10 years in patients with WPW-15%
• Preferred - Catheter ablation of AP
• Unstable - DC cardioversion
• Stable - IV Procainamide > Ibutilide - slow conduction
over AP, slow ventricular rate and might convert to SR

187. POSTOPERATIVE (CARDIAC AND
THORACIC SURGERY)
• Postop AF- 25-50% after open heart
surgery
• CABG- preop statin reduces AF

190. Heart failure
• AF seen in 10% in patients with NYHA I, Upto to 50% in NYHA IV
• May be the cause of HF in patients who present with a
nonischemic cardiomyopathy and AF with a RVR
• Stricter rate control target
• Due to RVR, irregular rates and loss of AV synchrony
• Systolic HF - Beta blockers, Digoxin +/- IV Amiodarone
• Diastolic HF - Beta blockers, CCBs, Digoxin +/- IV Amiodarone
• Rhythm control - Amiodarone, Dofetilide
• Catheter ablation - improvement in LVEF, improved QoL and
reduced mortality, stroke, and hospitalization - CASTLE AF
• AVN ablation + biventricular pacing

196. CKD
• Dose adjustments of NOAC and AAD
• Amiodarone - no dose modification needed
CLD
• Child-Pugh A or B - OAC therapy is reasonable in the absence of clinically
significant coagulopathy or thrombocytopenia

197. Cancers
• Increased risk of AF - related to increased
age, shared risk factors between cancer and
CVD (eg, obesity and inflammation),
coexistent comorbidities (eg, hypertension
and HF), cardiac involvement by the tumor,
medical therapeutics, Oncologic surgery,
especially thoracic RT.

198. Trials in AF

202. References
• Joglar A José et al. (2024) 2023 ACC/AHA/ACCP/HRS Guideline for the
Diagnosis and Management of Atrial Fibrillation: A Report of the American
College of Cardiology/ American Heart Association Joint Committee on
Clinical Practice Guidelines. Circulation 2024;149:e1–e156. DOI: 10.1161/
CIR.0000000000001193
• Calkins Hugh, Tomaselli F.Gordon, Morady Fred. 2021. “Atrial fibrillation :
Clinical features, mechanisms and management.” In BRAUNWALD’S HEART
DISEASE: A TEXTBOOK OF CARDIOVASCULAR MEDICINE, TWELFTH
EDITION edited by Libby et. al., 1272-1277. USA: Elsevier
• Sauer H.William, Zei C.Paul. 2022. “Atrial fibrillation.” In Harrison’s Principles
of Internal Medicine, edited by Loscalzo et. al. USA: McGraw Hill

203. THANK YOU