Atrial Fibrillation: Discussed by - DR Kunwar Sidharth Saurabh

You might also like

Download as pptx, pdf, or txt
Download as pptx, pdf, or txt
You are on page 1of 45

ATRIAL FIBRILLATION

DISCUSSED BY –
DR KUNWAR SIDHARTH SAURABH

REFERENCES – AHA GUIDELINES 2014/2019


DEFINITION
• AF is a supraventricular tachyarrythmia with uncoordinated atrial
activation and consequently ineffective atrial contraction.
• Most common sustained cardiac arrythmias
• Incidence increases with age.
• Men > Women
• White > Black
• Increased risk of stroke, heart failure, dementia , tachycardia induced
cardiomyopathy and mortality are some of the major ill effects.
CLASSIFICATION
Also it can be..

VAGOTONIC AF

ADRENERGIC AF
HAEMODYNAMIC
CONSEQUENCES
• Loss of coordinated atrial contraction
• Suboptimal ventricular rate control
• Beat to beat variability in ventricular filling
• Sympathetic activation
• Decreased cardiac output
• Increase in filling pressures
Clinical Features
Mechanism of AF
PATHOPHYSIOLOGY
• Any change of atrial architecture potentially increases susceptibility of
AF e.g. inflammation/fibrosis/hypertrophy etc.
• Even in patients of paroxysmal AF (Asymp), biopsies have revealed
atrial wall inflammation consistent with myocarditis and fibrosis.
• The atria are sensitive to profibrotic signalling and harbour a greater
number of fibroblast than the ventricles. Atrial stretch activates RAAS
which generates multiple downstream profibrotic factors including
TGF.
• Late Gadolinium enhanced MRI can quantitate atrial fibrosis.
Triggers of AF
• Ectopic focal discharges.
• Most commonly from LA myocardial sleeves that extend into
pulmonary veins  Cornerstone for Pulmonary Vein Isolation by
Catheter Ablation
Triggers of AF
• Most commonly from pulmonary vein site, but can also arise
elsewhere including posterior LA, Ligament of marshall, Coronary
sinus, Cavotricuspid isthumus (usually Atrial Flutter)
• Abnormal intracellular calcium handling owing to calcium leak from
sarcoplasmic reticulum can trigger delayed after-depolarisations.
Maintenance of AF
1. Multiple re-entrant wavelets associated with heterogenous
conduction and refractoriness.
2. >1 rapidly firing foci
3. > 1 rotors or spiral re-entrant circuits
4. Multiple other unknown mechanisms
ROLE OF AUTONOMIC NERVOUS
SYSTEM
• ANS can provoke AF  both parasympathetic and sympathetic.
• Action related to the calcium channels
• Plexi of autonomic ganglia are located in epicardial fat near
pulmonary vein –LA junction and ligament of marshall.
• In some patients during conditions of High Parasympathetic tone , e.g.
SLEEP, can precipitate AF and is known as Vagally mediated AF.
Avoidance of drugs such as digoxin which increases parasympathetic
tone has been suggested in these patients.
PATHOPHYSIOLOGY
• Atrial remodelling – “AF begets AF”
• Inflammation and oxidative stress
• Plasma concentration of CRP and IL-6 are elevated in these patients
• Rising CRP may indicate relapse after successful cardioversion
• RAAS system –
• Components of this are synthesised in the atrium
• Patients of primary hyperaldosteronism, incidence of AF is high 
spironolactone is helpful in these patients.
Clinical Evaluation
• ECG
• CHEST X RAY
• 2D ECHO
• ELECTROPHYSIOLOGICAL STUDY-
• Usually in patients having delta wave
On ECG indicating pre-excitation.
• BNP
• CRP
• Rhythm monitoring, Stress testing
TREATMENT STRATEGY
• PREVENTION OF THROMBOEMBOLISM
• RATE CONTROL
• RHYTHM CONTROL
Prevention of Thromboembolism
Prevention of Thromboembolism
Salient points -
• In oral anticoagulants, For Warfarin – Level of evidence A
• For others – B, C
• Non valvular AF increases the risk of stroke 5 times and AF in the
setting of mitral stenosis increases by 20 times.
• CHA2DS2- VASc score which includes vascular disease and sex
category, both, is now preferred over CHADS2.
Salient Points

• Bleeding risk scores to quantify haemorrhage risk include HAS-BLED,

RIETE , HEMORR2HAGES & ATRIA

• HAS-BLED(Hypertension, Abnormal Renal/Liver Function, Stroke,

Bleeding Predisposition, Labile INR, Elderly, Drugs/Alcohol) is most

commonly used. Score >3 predicts potentially “high risk” for bleeding.
Salient Points
• BAFTA (Birmingham atrial fibrillation treatment of the aged) study
evaluated warfarin, and concluded that it was superior in preventing
stroke or systemic embolism without a significant increase in bleeding
risk.
• Dabigatran followed by Rivaroxaban were the others approved by
FDA.
• Both are renally excreted – precaution in patients of CKD.
• Apaxiban – elimination by Hepatic route.
Consideration in selecting
anticoagulants
• New agents are more expensive than warfarin
• Benefits over warfarin – less drug interaction, more predictable
pharmacological effects, less risk of intracranial bleeding. They have
rapid onset and offset of action, hence bridging therapy with heparin
is usually not required. Hence even missing 1 dose can have
significant effects.
• MORE BLEEDING in patients undergoing valve surgery put on
dabigatran – Class III (harm)
• Warfarin has the advantage of available reversal agents, and long half
life. Also it can be safely given in patients of CKD
UPDATE
Percutaneous approaches to
occlude LAA
Devices Available
Watchman Amplatzer cardiac Plug LARIAT
Rate Control Recommendations
Salient Points
• In hemodynamically unstable patient, Electrical cardioversion is indicated
e.g decompensated HF, Ongoing MI, hypotension etc
• Orally administered beta blockers are the first line agents. Can be given IV
in acute situations.
• Diltiazem and verapamil have direct AV nodal effects, blocking calcim
channels, and are used for ventricular rate control in both acute and
chronic AF.
• Diltiazem and Verapamil SHOULD NOT BE USED in patients with LV systolic
dysfunction and decompensated HF because of negative inotropic effects.
They should also NOT be used in patients with pre-excitation & AF.
Salient Points
• DIGOXIN is NOT usually the first line drug for rate control, as the onset
of action requires >1hr and the effect doesnot peak upto 6 hrs. hence
not ideal choice in acute setting.
• Combined with beta blockers, its effective.
• Association between digoxin and mortality (serum levels >0.9 ng/ml)
raise concern about its use, particularly in long term.
• Amiodarone can be used in patients to attain rate control although its
less effective than CCB.
AV NODAL ABLATION
• Leads to pacemaker dependency
• Done 3-4 weeks after pacemaker implantation.
• In patients with EF <35%, biventricular pacing is recommended.
RHYTHM CONTROL
DIRECT CURRENT
CARDIOVERSION
SALIENT POINTS
• Attempt to restore a normal sinus rhythm improve the quality of life.
• No RCT has proven the benefit of Rhythm control over Rate Control.
• Persistent symptoms due to AF is the most common indication for
rhythm control.
• Anticoagulation should always be initiated well before electrical
cardioversion which is usually done under the sedation ad TEE
guidance.
• Drugs like IBUTILIDE lower the cardiversion shock threshold.
Salient Points
• Patients with recent onset AF, IV IBUTILIDE restored sinus rythm in
>50%. Major risk is excessive QT prolongation leading to VF.
• Ibutilide should be avoided in patients of EF <30%.
• Catheter ablation procedure are not well studied in patients of
chronic AF
THANKS

You might also like