atrial fibrillation
TRANSCRIPT
Atrial Fibrillation
Current Approachesto Management
BY: Dr . P. Raveendran
Chief Interventional Cardiologist ,KMC
Atrial fibrillation accounts for 1/3 of all
patient discharges with arrhythmia as principal diagnosis.
2% VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
34% Atrial
Fibrillation
18% Unspecified
6% PSVT
6% PVCs
4% Atrial Flutter
9% SSS
8% Conduction
Disease3% SCD
10% VT
Camm AJ. Am J Cardiol. 1996;78(8A):3-11.
Total Hospitalization Days Based on Presenting Arrhythmia
900
800
700
600
500
400
300
200
100
0
AF
Atrial Flutter
Cardiac arrest
Conduction disease
Junctional
Premature beats
Sick sinus syndrome
VF
VT
Unspecified
Presenting Arrhythmia
Atrial Fibrillation
Common and age-dependent2 - 4% over age 60
Significant risk of stroke4% per year (Framingham Study)
High risk of embolism with cardioversion
Atrial Fibrillation (AF)
Chaotic and disorganized atrial activity Irregular heartbeat Can be paroxysmal, persistent or
permanent (chronic) Most common sustained arrhythmia Can be symptomatic or asymptomatic Incidence increases with age
Atrial Fibrillation
Conover: Electrocardiography. 4th ed. Mosby 1998; 68.
Mechanism
Mechanism: – Multiple wavelets of reentry– Ectopic focus
Induction: – Rapid atrial pacing
Termination:– Pharmacologic therapy– Cardioversion– Spontaneous
ECG Recognition
Atrial Rate: > 300 bpm Rhythm: Irregular Ventricular Rate: Variable
– Dependent upon:• AV node conduction properties
• Sympathetic and parasympathetic tone
• Drugs
Recognition: Absence of P waves
ECG Recognition
Absence of discrete P waves Chaotic atrial activity Ventricular rate irregular
ECG Recognition
ECG used with permission of Texas Cardiac Arrhythmia, P.A.
Other Characteristics
Lost atrial kick and decreased filling times can result in congestive heart failure
Ventricular rates < 100 bpm suggest AV conduction disease
Irregular ventricular rhythm > 180 bpm– Suggest an accessory pathway (broad QRS)– Enhanced AV nodal conduction (narrow QRS)
Tachycardia-Induced Tachycardia
One tachycardia degenerates into another Examples:
– Atrial flutter and atrial tachycardia into AF– AV node reentry and AV reentry into AF– Ventricular tachycardia into VF
Treating the initiating tachycardia can help prevent future episodes of AF an VF
Atrial Fibrillation: Causes
Cardiac
Non-cardiac
“Lone” atrial fibrillation
Atrial Fibrillation: Cardiac Causes Hypertensive heart disease Ischemic heart disease Valvular heart disease
– Rheumatic: mitral stenosis
– Non-rheumatic: aortic stenosis, mitral regurgitation
Pericarditis Cardiac tumors: atrial myxoma Sick sinus syndrome Cardiomyopathy
– Hypertrophic
– Idiopathic dilated (? cause vs. effect)
Post-coronary bypass surgery
Atrial Fibrillation: Non-Cardiac Causes
Pulmonary
– COPD
– Pneumonia
– Pulmonary embolism
Metabolic
– Thyroid disease: hyperthyroidism
– Electrolyte disorder
Toxic: alcohol (‘holiday heart’ syndrome)
“Lone” Atrial Fibrillation
Absence of identifiable cardiovascular, pulmonary, or associated systemicdisease
Approximately 0.8 - 2.0% of patients with atrial fibrillation (Framingham Study)1
In one series of patients undergoing electrical cardioversion, 10% had lone AF.2
1 Brand FN. JAMA. 1985;254(24):3449-3453.
2 Van Gelder IC. Am J Cardiol. 1991;68:41-46.
Atrial Fibrillation: Clinical Problems
Embolism and stroke (presumably due to LA clot)
Acute hospitalization with onset of symptoms
Anticoagulation, especially in older patients (> 75 yr.)
Congestive heart failure
– Loss of AV synchrony
– Loss of atrial “kick”
– Rate-related cardiomyopathy due to rapid ventricular response
Rate-related atrial myopathy and dilatation
Chronic symptoms and reduced sense of well-being
Atrial Fibrillation and Stroke
Risk: 5 - 8% per year in high-risk patients
Anticoagulant therapy is clearly indicated and beneficial in rheumatic atrial fibrillation.
In non-rheumatic atrial fibrillation, major randomized trials have provided useful guidelines for identifying and treating patients at risk.
Treatment Options
Restoration/maintenance of sinus rhythm– Pharmacologic therapy– Surgery (Maze procedure)– Catheter ablation – Atrial pacing– Device therapy– Cardioversion
Treatment Options
Rate control during AF– Pharmacologic therapy– Catheter ablation
• AV junction ablation (ablate and pace)
• AV nodal modification
Prevention of thromboembolism– Pharmacologic therapy
• Warfarin
• Aspirin
Major Clinical Trials in Atrial Fibrillation
SPAF1 Stroke Prevention in Atrial Fibrillation
BAATAF2 Boston Area Anticoagulation Trial for Atrial Fibrillation
CAFA3 Canadian Atrial Fibrillation Anticoagulation
AFASAK4 Copenhagen Investigators
SPINAF5 Stroke Prevention in NonrheumaticAtrial Fibrillation
1 Circulation. 1991;84:527-539.2 N Engl J Med. 1990;323:1505-1511.3 J Am Coll Cardiol. 1991;18:349-355.
4 The Lancet. 1989;1:175-178.5 N Eng J Med. 1992;327:1406-1412.
SPAF BAATAF CAFA AFASAK SPINAF
Number of Patients 1330 420 378 1007 571
Drug Used Warfarin ASA Warfarin Warfarin Wafarin ASA Warfarin(INR 2-4.5) 325 mg (PT 1.2-1.5x (INR 2-3) (INR 2.8-4.2) 75 mg (INR 1.2-1.5)
Control)
Embolic Rate (%)
Treatment 2.3 3.6 0.41 3.5 1.5 6.0 4.3Control 7.4 6.3 2.98 5.2 6.2 6.2 0.9
Risk Reduction (%)(95% confidence) 67 42 86 45 — — 79
Major Bleeding Complications (%)
Treatment 1.5 1.4 0.9 2.5 6.3 0.6 1.5Control 1.6 1.9 0.5 0.5 0.0 0.0 0.9
Predictors of Thromboembolic Risk in Atrial Fibrillation
History of hypertension
Prior stroke or TIA
Diabetes
Recent heart failure
Age > 65 years
Atrial Fibrillation Investigators. Arch Intern Med. 1994;154:1449-1457.
SPAF III
SPAF III study evaluated the benefit of
adjusted-dose warfarin vs. low-intensity, fixed-
dose warfarin (INR 1.2 - 1.5) plus ASA
in high-risk patients with atrial fibrillation.
SPAF Investigators. Lancet. 1996;348:633-638.
Relative Risk of Adjusted-Dose Warfarin and Combination Therapy
SPAF Investigators. Lancet. 1996;348:633-638.
Combinationtherapy
Adjusted-dosewarfarin
Combinationtherapy
Adjusted-dosewarfarin
p = 0.007 p = 0.002
Intracranial hemorrhage
Disabling ischemic stroke
Non-disabling ischemic stroke
Eve
nt
rate
(%
per
yea
r)
0
2
4
6
8
10
12
14
16
No previous thromboembolism Previous thromboembolism
Relative Risk of Adjusted-Dose Warfarin and Combination
Therapy
SPAF Investigators. Lancet. 1996;348:633-638.
Combination therapy
Adjusted-dose warfarin
<1.2 1.2-1.5 1.5-1.9 1.9-2.4 >2.5
INR
An
nu
al e
ven
t ra
te (
95%
CI)
0
5
10
15
20
Event rates for ischemic stroke or systemic embolism at start of follow-up
Recommendations Regarding Anticoagulation for Atrial Fibrillation
Clinical Background
Rheumatic heart disease,age < 75 yr.
“Lone” atrial fibrillation,age < 65 yr.
High risk, age < 75 yr.
High risk, age > 75 yr.
Patients with major contraindications to warfarin:
– Intracranial hemorrhage
– Unstable gait/falls/syncope
– Poor compliance
Treatment
Warfarin (INR 2.0 - 3.0)
ASA 325 mg/day
Warfarin (INR 2.0 - 3.0)
Warfarin (INR 1.5 - 2.5)
ASA 325 mg/day
Treatment
Warfarin (INR 2.0 - 3.0) 4 wks. before and 4 wks. after cardioversion
– Hold warfarin for 3 days
– Stop warfarin 7 days prior to surgery
Daily INR when < 1.5
Start SQ heparin 10,000u every 12 hours and follow PT/PTT
Stop heparin 12 hours beforesurgery
Guidelines Regarding Anticoagulation for Atrial Fibrillation
Clinical Background
Elective cardioversion
Elective surgery for anticoagulated patient:
– Minor surgery
– Major surgery
Current Recommendations for Anticoagulation Therapy
for Atrial Fibrillation INR 2.0 - 3.0 for appropriate patients1,2
or
Warfarin (INR 2.0 - 3.0) or ASA 325 mg/dayin patients without clinical orechocardiographic risk factors
1Blackshear JL. Mayo Clin Proc. 1996;71:150-160.2Hylek EM. N Eng J Med. 1996;335:540-546.
Echocardiographic Risk Factorsfor Stroke Factors in Patients with
Atrial Fibrillation
LV systolic dysfunction
Increased LA size
SPAF Investigators. Ann Intern Med. 1992;116:6-12.
Role of Echo in Atrial Fibrillation
Identify structural heart disease
Identify LVH
Identify LA size
Detect “smoke”
Detect clot in LA
Role of TEE in Atrial Fibrillation
Transesophageal echo is more sensitive (92%) and specific (98%) for detecting left atrial clot.
Thromboembolic event is presumably due to left atrial clot.
Most clots are in left atrial appendage but poorly visualized by transthoracic surface echo.
Manning WJ. N Engl J Med. 1993;328:750-755.
Manning WJ. N Engl J Med. 1993;328:750-755.
A Left Atrium B Left Atrial Appendage Clot
Rationale for Precardioversion TEE
Absence of clot on TEE may obviate need for anticoagulation.
Avoiding delay necessary for prolonged anticoagulation prior to cardioversion increases likelihood of successful cardioversion and maintenance of normal sinus rhythm.
Increase in Spontaneous Echo Contrast (“Smoke”) Following Electrical Cardioversion
Grimm RA. J Am Coll Cardiol. 1993;22(5):1359-1366.
Left atrial appendage (LAA) before (A) and after (B) cardioversion
Precardioversion TEE
ACUTE: Assessment of Cardioversion Using Transesophageal Echocardiography.
Large-scale randomized clinical trialson the role of precardioversion TEE are still pending.
Chronic1 month coumadin cardioversion (CV)
Uncertain durationStable 1 month coumadin CVUnstable TEE CV
Acute
Timing of Cardioversion for Atrial Fibrillation
coumadin repeat TEE CV
no clot
clot
Heparin TEE
CV coumadin
Therapeutic Approaches to Atrial Fibrillation
Anticoagulation
Antiarrhythmic suppression
Control of ventricular response
– Pharmacologic
– Catheter modification/ablation of AV node
Curative procedures
– Surgery (maze)
– Catheter ablation
AtrialFibrillation Duration of atrial
fibrillation may predict likelihood of remaining in normal sinus rhythm after cardioversion
Dittrich HC. Am J Cardiol. 1989;63:193-197.
< 3 Months3 - 12 Months> 12 Months
100
80
60
40
20
0Initial One month
post-CVSix months
post-CV*P = <0.02
Pat
ien
ts in
sin
us
rhyt
hm
(%
)
Length of timein AF prior tocardioversion
*
Control of Ventricular Rate in Atrial Fibrillation
Digoxin
Calcium channel blockers
Verapamil, diltiazem
Beta blockers
Antiarrhythmic Drugs to SuppressAtrial Fibrillation
Class I agents
– IA: quinidine, procainamide, disopyramide
– IC: flecainide, propafenone
Class III agents
– amiodarone, sotalol
Medication for Rate Control in Atrial Fibrillation
Adapted from Blackshear JL. Mayo Clin Proc. 1996;71:150-160.
Agent ActionImmediate
IV dose
Oralmaintenance
therapy Avoid use in
Digoxin Cardiac 0.5 mg + 0.125-0.5 mg/day; WPW, HCMglycoside 0.25 mg in 4-6 h + renal
0.25 mg in 4-6 h
Diltiazem Calcium 20 mg (or 25-35 120-360 mg/day; WPW, constipation,channel mg/kg) over 2 min hepatic peripheral edema,blocker + 2nd bolus CHF allowed after 20 min + 5, 10,
15 mg/h infusion
Verapamil Calcium 5-10 mg every 120-240 mg/day; Same as diltiazem,channel 30 min or 5 mg/h hepatic risks with CHF blocker
possibly greater
Medication for Rate Control in Atrial Fibrillation
Adapted from Blackshear JL. Mayo Clin Proc. 1996;71:150-160.
Agent ActionImmediate
IV dose
Oralmaintenance
therapy Avoid use in
Propranolol ß-blocker 0.5-1.0 mg every 40-320 mg/day; Bronchospastic5 min up to 5 mg hepatic lung disease,total CHF
Metoprolol ß-blocker 5 mg every 5 min 50-200 mg/day; Same asup to 15 mg total hepatic propranolol
Esmolol ß-blocker 0.5 mg/kg/min None Same asload over 1 min propranolol + 0.05-0.3 mg/kg/min
Medication for Rhythm Control in Atrial Fibrillation
Class IAQuinidine gluconate 324-648 mg Q 8-12 hr Chronic renal failure CHF, liver failure
Procainamide 0.5-1.5 g Q 12 hr* Men, short-term therapy Renal failure, CHF, joint disease
Disopyramide 200-400 mg Q 12 hr Women Older men at risk for urinary retention, CHF, glaucoma, renal failure
Class ICFlecainide 75-150 mg Q 12 hr Failure of Class IA drugs CHF, CAD
Propafenone 150-300 mg Q 8 hr Failure of Class IA drugs CHF
Class IIISotalol 80-240 mg Q 12 hr Failure of IA or IC drug Where beta blockade is
May be used with mild- contraindicated moderate LV dysfunction
Amiodarone 1200 mg QD for 5 days Severe LV dysfunction, Young patients, followed by 400 mg QD for failure of other drugs, pulmonary disease 1 month, then 200-400 mg QD CHF, renal failure Many alternative dosing regimens
* For newer preparation.Adapted from Gilligan DM. Am J Med. 1996;101:413-421.
Drug Oral Dose Useful in Avoid in
Recommendations for Management of Atrial Fibrillation < 48 Hours
Adapted from Golzari H. Ann Intern Med. 1996;125:311-323.
Atrial Fibrillation < 48 hours
Prompt electrical or pharmacologic
conversion
Control ventricular rateConsider antithrombotic therapy
Observe for spontaneous conversion
Antiarrhythmic therapyif
No antiarrhythmic therapyif
Unstable hemodynamics or frequent recurrences
Stable hemodynamics, infrequent
recurrences, or first episode
Adapted from Golzari H. Ann Intern Med. 1996;125:311-323.
Recommendations for Management of Atrial Fibrillation > 48 HoursAtrial Fibrillation > 48 Hours
Control ventricular rateStart antithrombotic therapy
(heparin and/or warfarin or aspirin)
Duration < 1 year Duration > 1 year
Warfarin therapy 3-4 weeks
Cardioversion or pharmacologic conversion
Antiarrhythmic therapyif
No antiarrhythmic therapyif
Unstable hemodynamics or frequent recurrences
Stable hemodynamics,infrequent recurrences, or
first episode
Continue warfarin 1-2 monthsMonitor for recurrences
Chronic antithrombotic therapy
Assure control of ventricular rate
or
Disadvantages
– High recurrence rate
– High long-term cost
– Noncurative
– Adverse effects
– Potential proarrhythmia
Antiarrhythmic Therapy for Atrial Fibrillation
Advantages
– High efficacy for somepatients, at leastinitially (< 50% of all patients)
– Low initial cost
– Noninvasive
Rate Control for Atrial Fibrillation
Some “idiopathic” cardiomyopathies are due to
atrial fibrillation with rapid ventricular response.
When rate control is achieved, LV function often
improves dramatically.
In some patients, pharmacologic therapy is
ineffective for rate control, and catheter ablation and
permanent pacing are indicated.
Improved EF of36-year-old malewho presented withAF (HR 140 bpm) 1 week prior toinitial echo
60
40
20
0Initial 4 days 2 months 8 months
AF 75* SR 80 SR 80 SR 60Heart rate(bpm)
* Heart rate 140 one week earlier
30 29
4852
EF
(%
)Case Study
Grogan M. Am J Cardiol. 1992;69:1570-1573.
Primary Rx: DC cardioversion
Other Rx: digoxin and quinidine
Grogan M. Am J Cardiol. 1992;69:1570-1573.
60
40
20
0Initial 1 month 4 months 8 months
AF 120 AF 70 AF 76 AF 70Heart rate(bpm)
30
40
60 60
EF
(%
)Case Study
Improved EF in80-year-old femalewith chronic AFbut with improvedrate control
Primary Rx: digoxin and propranolol
Grogan M. Am J Cardiol. 1992;69:1570-1573.
60
40
20
0Initial 3 months 51 months 56 months
AF 150 AF 75 AF 140 SR 80Heart rate(bpm)
20
61
20
52
EF
(%
)Case Study
Markedly improved EF in 55-year-old female with both rate control& NSR, with reversion to AF (HR 140 bpm) and subsequent decrease in EF
Primary Rx: amiodarone
Other Rx: digoxin and lisinopril
AV Nodal Modification by Intracardiac Ablation
RAO LAO
Catheter Ablation of AV Nodal Conduction and Permanent Pacemaker Implantation
Treatment for patients with atrial fibrillation with a rapid ventricular response
Maze Procedure
Concept involves open heart surgery on the atria to restore sinus rhythm and prevent AF
Multiple atrial incisions are made to direct sinus impulses through a path or a “maze” to reach the AV node
This “maze” compartmentalizes the atria utilizing scar tissue
Approximately 5% require permanent pacemaker post-op
Kawaguchi AT. J Am Coll Cardiol. 1996;28:985-990.
AtrialFibrillation
CurativeProcedures:
Surgical Maze
Efficacy ofSurgical MazeProcedure for
Atrial Fibrillation
Kawaguchi AT. J Am Coll Cardiol. 1996;28:985-990.
0
10
20
30
40
50
60
70
80
90
100
0 1 2 3
Fre
edo
m f
rom
atr
ial f
ibri
llati
on
(%
)
Post-op years
Control
Maze
Haïssaguerre M. J Cardiovasc Electrophysiol.
1994;5:1045-1052.
Catheter MazeProcedure for
Atrial Fibrillation
RF Ablation
Maintenance of sinus rhythm:– Endocardial linear lesions are made to
compartmentalize the atria creating a maze-like result
Rate control:– AV node ablation (ablate and pace)
• Catheter ablation of the AV junction that results in complete heart block
– AV node modification• Catheter ablation on the AV node (slow pathway) to prevent rapid
ventricular rates
AV Junction Ablation
Indications:– Permanent, symptomatic atrial fibrillation– Suppression of AV node conduction
• Paroxysmal atrial fibrillation
• Atrial tachycardia
• Atrial flutter
AV Junction Ablation
AVJ ablation (ablate and pace)– Right and left sided catheter approaches utilized – Creates complete heart block (CHB)– Permanent pacing is required– Warfarin therapy is indicated
AV Junction Ablation
Singer: Interventional Electrophysiology. Williams & Wilkins 1997; 328.
AV Node Modification
Indications: – Suppression of AV node conduction
• Atrial fibrillation
• Atrial tachycardia
• Atrial flutter
May prevent need for permanent pacing Modify AV node conduction Ablation of slow pathway potentials
Atrial Fibrillation: Areas of Research AFFIRM study
– National Heart Institutes atrial fibrillation study
– Heart rate control and anticoagulation vs. rhythm control with antiarrhythmic drugs
Patient-activated or automatic atrial defibrillator
Dual-site and biatrial pacing
Atrial pacing therapies for AF prevention
Catheter ablation therapies for AF
– Catheter “maze” procedure
– Ablation for “focal” AF
Permanent Pacing and Atrial Fibrillation: Findings
With Atrial Pacing:
Less atrial fibrillation
Less thromboembolic risk
Less incidence of AV block
Andersen HR. Lancet. 1994;344:1523-1528.
Incidence of Chronic Atrial Fibrillation in Patients Randomized to Atrial & Ventricular Pacing
Andersen HR. Lancet. 1994;344:1523-1528.
0
10
20
30
40
50
3 months 1 2 3 4 5
AtrialVentricular
Years after implantation
Ch
ron
ic a
tria
l fib
rilla
tio
n (
%)
0
5
10
15
20
25
Incidence of Thromboembolic Events in Patients Randomized to Atrial or Ventricular Pacing
Andersen HR. Lancet. 1994;344:1523-1528.
Nu
mb
er o
f p
atie
nts
Years after implantation
0 3 months 1 2 3 4 5 6
Ventricular
Atrial
Permanent Pacing for Prevention of Atrial Fibrillation
1 Andersen HR. Lancet. 1994;344:1523-1528.2 Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
Evidence that AAI pacing is associatedwith less atrial fibrillation than VVI pacing.1
Chronic dual-site right atrial pacing may also prevent recurrent atrial fibrillation.2
CXRs of Pacemaker with Dual-Site Atrial Pacing and Single Ventricular Lead
Courtesy of Dr. Sanjeev Saksena
Permanent Pacing for Prevention of AF:Results
Marked decline in AF recurrence withatrial pacing
With dual-site pacing & optimal drug regimen, no AF recurrence
With single-site pacing, 5 recurrences in12 patients
Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
Permanent Pacing for Prevention of AF:Results
Mean arrhythmia-free interval increasedfrom 14 days before pacing to 89 days(dual-site) & 76 days (single-site) after pacing.
Mean antiarrhythmic drug use declinedfrom 4 drugs before pacing to 1.5 drugsafter pacing.
Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
Mean Arrhythmia-Free Intervals
Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
0
P < 0.001
p = 0.10
Days
14
89
76
20
40
60
80
100
120Preimplantation period
Dual-site pacing
High right atrial pacing
Number of Symptomatic Episodes Before and After Initiation of Pacing
Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
0
p = 0.09
p – NS
1
2
3
4
5
6
7Episodes per Week
Preimplantation period
Dual-site pacing
High right atrial pacing
Mean Number of Antiarrhythmic Drugs Before and After Initiation of Pacing
Saksena S. J Am Coll Cardiol. 1996;28(3);687-694.
0
p < .001
p < .005
1
2
3
4
5
6
7# Drugs Before Pacing After Pacing
Drugs of all classes
Class I and III
Transvenous Atrial Defibrillation
Prospective multicenter trial to define efficacy and safety of low-energy shocksfor atrial defibrillation
Delivery of shocks between right atrial and coronary sinus electrode catheters
141 patients enrolled
Levy S. J Am Coll Cardiol. 1997;29:750-755.
Catheter Position for Intracardiac Atrial Defibrillation
Levy S. J Am Coll Cardiol. 1997;29:750-755.
Atrial Defibrillation: Conclusions
Atrial defibrillation using transvenous intracardiac leads can be highly efficacious and requires relatively low energies.
The optimal waveform characteristics of delivered energy to minimize patient discomfort during defibrillation continues to be evaluated.
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