Intrinsic Cardiac Conduction System

SA Node

AV Node

His Bundle

RBB & LBB

Purkinje Fibers
 Phases of action potential of myocytes

• Phase 0 rapid depolarisation (inflow

of Na+)
• Phase 1 partial repolarisation (inward
Na+ current deactivated, outflow of Phase 1
K+)
Phase 2
• Phase 2 plateau (slow inward calcium0 mV
current)
• Phase 3 repolarisation (calcium Phase 0
+
current inactivates, K outflow) Phase 3
• Phase 4 pacemaker potential (Slow
Na+ inflow, slowing of K+ outflow) -90mV Phase 4
‘autorhythmicity’
 Pacemaker Cells

Cells with natural automaticity; and do not have a

static resting potential
 Latent Pacemaker
Sinoatrial Node
Native Pacemaker;
Rate: 60 – 100x /min

Junctional
Latent / Ectopic
Pacemaker;
Rate: 40-60x /min

Ventricular
Latent/ Ectopic Pacemaker;
Rate: 30-40x /min

Latent Pacemaker will initiate impulses and take over the pacemaking function
if the SA node slows or fails to fire, or if conduction abnormalitites block the
normal wave of depolarization from reaching them (Escape Rhythm)
 Alterations in ↑ Sinus node automaticity
- symph stimulation
Sinus ↓ Sinus node automaticity
Automaticity - symph stimulation ↓
- parasymph ↑
- beta blockers
Escape Rhythms Initiated by latent PM
Altered Impulse SA,AV, Atrium sensitive to parasymp
Formation  ps ↑, shift to latent
↑ Automaticity - ↑ cathecolamine  rate of depol
of Latent exceeds sinus
Pacemaker - hypoxemia, ischemia, electrical
disturbance, digitalis tox.
Cardiac injury  sel sekitar jd
Abnormal spontaneously depol; ec. Cell
Mechanism Of Automaticity membrane leaky  resting potential
Arrythmia less (-)
Early afterdepol : TDPointes. In
Triggered phase 2/3 – different channel
activated. Also in conditions that
Activity prolong QT
Delayed afterdepol: high intracell
calcium, marked cath. Stim, digitalis
Altered Impulse Conduction
tox
Conduction Block Functional: still in refractory
Fixed: fibrosis / scarring

Fixed path – monomorphic VT.

Unidirectional Non fixed – Polymorph VT
6
Block & Reentry In normal conduction, need at least
10cm to re entry – SEE PICT
 Mechanism of Reentry

NORMAL UNIDIRECTIONAL BLOCK

NORMAL RETROGRADE SLOWED RETROGRADE

CONDUCTION VELOCITY CONDUCTION VELOCITY
BRADIARRYTHMIA
I. SA NODE
I.1 SINUS BRADYCARDIA
I.2 SICK SINUS SYNDROME

II. ESCAPE RHYTHM

II.1 JUNCTIONAL RHYTHM
II.2 VENTRICULAR ESCAPE RHYTHM

III. AV CONDUCTION SYSTEM

I.1 Sinus Bradycardia
 I.1 Sinus bradycardia--etiologies
• Decide : Normal / ≠ ?
– Underlying heart disease
– symptoms
– HR ↑ with exercise?
– Athletes  elevated vagal (normal)
– Aging
– disease of Atrium (ischemic, cardiomyopathy)
– medications (beta-block, ca-block)
– metabolic (hypothyroid)
 I.1 Sinus bradycardia--treatment
• Asymptomatic  No treatment

• Stop all drugs that may cause

• ER: Atropine if hemodynamic ↓, syncope, chest pain

• Pacing
 I.2 Sick Sinus Syndrome

Sinus node dysfunction, is a group of abnormal heart rhythms

(arrhythmias) presumably caused by a malfunction of the sinus node

Dobrzynski H, Boyett MR, Anderson RH (April 2007). "New insights into pacemaker activity: promoting understanding of
sick sinus syndrome". Circulation 115 (14): 1921–32
 I.2 Sick Sinus Syndrome
• Treatment:
– Acute: anticholinergic IV (atropine), B-adrenergic
agents (isoproterenol)  transiently accelerate HR

– Chronic  pacing
 I.2 Sick Sinus Syndrome
• Common in elderly

Susceptible to SVT (AF)

Combination: brady-tachycardia syndrome

Usually caused by Atrial
fibrosis – hit SA,
predisposed to AF &
flutter

Treat: combination of
antiarrythm & pace
maker
 II.1. JUNCTIONAL RHYTM
• SA impaired – rhytm from more distant latent PM
• Junctional beat / rhytm:
Retrograde P might P inverted in lead
from AV / Normal, Narrow Not followed by appear (retrograde II, III, aVF
proximal HIS QRS P wave wave from distal (activation from
PM to atrium)
inferior)
II.2. VENTRICULAR ESCAPE RHYTM

• From more distal point (RBB / LBB or More Distal)

• 30-40 bpm
• Widened QRS
• Morphology of QRS depends on site of origin
II.2. VENTRICULAR ESCAPE RHYTM
ESCAPE FROM ESCAPE
LBB FROM RBB

Depol. Left Depol. Right

first than right first than Left

RBBB QRS LBBB QRS

pattern pattern

• Treatment: similar to Sick Sinus Syndrome

 III.1. 1st degree AV block

• Prolongation of normal delay between

atrial & ventricular depol
• PR lengthened (>0.2s / 5 small boxes)
 III.1. 1st degree AV block

• Reversible cause:
– Vagal ↑
– Transient AV ischemia
– Drugs : Digitalis, B-blocker, Ca-ch antagonist,
antiarrythmic

• Structural Cause:
– Myocard infarction
– Chronic degenerative of conduction

• Benign, Asymptomatic, Does not need treatment

III.2.a. 2nd degree block Type I (Mobitz I / Weckenbach)

• AV delay gradually increase

• Almost always from impaired conduction in AV
• BENIGN – seen in children, athlete, increased vagal (sleep)
• During MI – vagal tone ↑ / ischemia of AV node  block
usually transient
• Treatment not necessary – except symptom (+)
 III.2.b. 2nd degree block Type II (Mobitz 2)

• Without gradual lengthening of PR interval

• Block may persist for 2/more beats – HIGH GRADE AV BLOCK
• Conduction block beyond AV Node – His / purkinje
• QRS often widened in pattern of RBBB / LBBB
• From: extensive MI involving septum, chronic degeneration of
His/purkinje
• DANGEROUS: indicating severe disease, may progress to 3rd without
warning. Treat with Pacemaker
 III.3. 3rd degree AV block

• Complete AV disassociation, HR is a ventricular rate

• Can degenerate to Vtach and Vfib
• Permanent pacemaker is necessary
TACHYARRYTHMIA
I. SUPRA VENTRICULAR ARRYTHMIA
I.1 SINUS TACHYCARDIA
I.2 ATRIAL PREMATURE BEATS
I.3 ATRIAL FLUTTER
I.4 ATRIAL FIBRILLATION
I.5 PAROXYSMAL SVT
I.5.1 AV NODAL RE ENTRANT
I.5.2 ATRIOVENTRIULAR RE ENTRANT TACH
I.5.2.1 VENTRICULAR PRE EXICATION SYNDROME (WPW)
I.5.2.2 CONCEALED ACCESSORY PATHWAY
I.5.3 ECTOPIC ATRIAL TACHYCARDIA
I.5.4 MULTIFOCAL ATRIAL TACHYCARDIA

II. VENTRICULAR ARRYTHMIAS

II.1 VENTRICULAR PREMATURE BEATS
II.2 VENTRICULAR TACHYCARDIA
II.3 VENTRICULAR FIBRILATION
 Sustained Tachycardia

Normal (narrow QRS

Wide QRS complex
complex)

No relationship
Irregularly irregular between P & QRS Constant relationship
Regular rhythm rhythm Ventricular of QRS & P
(constant P-P Tachycardia
interval) P upright in II,III,aVF
Sinus tachycardia SVT with abberancy
Reentrant SVT
Ectopic atrial
 3 P wave shapes
tachycardia No distinct P waves
Atrial Flutter Multifocal Atrial
Atrial Fibrillation
Tachycardia
 I.1. Sinus Tachycardia

• HR > 100 bpm, regular

• Normal P & QRS
• ↑symph / ↓ vagal
• Fever, hypoxemia, hyperthyroid, hypovolemia, anemia
 I.1. Sinus Tachycardia--treatment
• Verify it is sinus rhythm
• Evaluate/treat potential etiology :check TSH,
CBC, optimize CHF or COPD regimen, evaluate
recent OTC drugs
• If no etiology is found and is bothersome to
patients, can treat with beta-blocker
 I.2. Atrial Premature Beats

• Healthy / diseased hearts

• Atrial Focus outside SA – exacerbated by symphatic stimulation
• Asymptomatic, cause palpitations
• ECG: Earlier than expected P, abnormal shape, QRS normal
 I.2. Atrial Premature Beats
• Condition 1: BLOCKED APB

Blocked Premature P
Atrial focus AV still
impulse to not followed
fires very soon refractory
ventricle by QRS

• Condition 2: APB with WIDE QRS

Conduct
through AV, Conducted QRS
Atrial focus
encounter His impulse more abnormally
fires a bit later
/ purkinje still slowly wide
refractory
 I.3. Atrial Flutter

• Rapid, Regular – Rate 150-350 bpm

• SAWTOOTH appearance  large part of atrium depolarized
• Slower VENT RATE  mostly hit AV in refractory (ex: 2:1 block, Atrial Rate 300bpm, vent
rate 150 bpm)
• Vagal maneuvers  ↑AV block  better visualization of underlying atrial
 I.3. Atrial Flutter
• REENTRY OF LARGE ANATOMICALLY FIXED CIRCUIT

•Up interatrial septum

•Across roof
•Down free wall of RA
•Floor betwee tric. Valve &
inferior V.C

•Antiarrythmic can be dangerous  atrial conduction slower  block

become 1:1  faster ventricular rates
 I.4. Atrial Fibrillation

• Rate 350-600 bpm

• Unrecognize p wave
• Most of the wave hit AV in refractory period  randomly pass to Ventricle 
IRREGULARLY IRREGULAR
• Vent Rate 140-160bpm in untreated AF
 I.4. Atrial Fibrillation

• Involves multiple wandering reentrant

• Dangerous, for 2 reasons:

– CO↓
– absence of Atrial contraction 
thrombus formation

• Conditions for multiple reentry loops to

be sustained in AF:
– Minimum number of reentrant
– Enlarged Atrium

Treatment : 1. ventricular rate control

2. attempt to restore sinus rhythm
3. administration of anticoagulant
I.5. Paroxysmal Supraventricular Tachycardia

SVTs that have a sudden, almost immediate onset

1. Sudden onset & termination
2. Atrial rates 140-250bpm
3. Narrow QRS (unless abberant)

Most often etiology : Reentry of AV, atrium, accessory

Rarely : ↑ automaticity in atrium / AV
I.5.1 AV NODAL RE ENTRANT

I.5.2 ATRIOVENTRICULAR REENTRANT TACHYCARDIA

I.5.2.1 VENTRICULAR PRE EXITATION SYNDROME (WPW)
I.5.2.2 CONCEALED ACCESSORY PATHWAY

I.5.3 ECTOPIC ATRIAL TACHYCARDIA

I.5.4 MULTIFOCAL ATRIAL TACHYCARDIA

 I.5.1. AV NODAL REENTRANT

• Most common PSVT in adult

• ECG: - regular tachycardia Normal QRS complex
- P not apparent, retrograde depol occurs simultaneously with vent.
Depol; “P hidden in QRS”
- P might visible  superimposed on terminal QRS, inverted in II, III, aVF
 I.5.1. AV NODAL REENTRANT

• AV node: slow (shorter refractory period) & fast branch

• Uncommon AVNRT Retrograde Conduction on Slow  visible retrograde P
following QRS complex on ECG
• Well Tolerated - palpitations
 I.5.1. AV NODAL REENTRANT

Treatment:
- Lifestyle Modification
- Vagal Tone (Valsava / Carotid msg)
- I.V Adenosine – Impairs AV Nodal
- Ca-ch Blocker /B-Blocker
- Ablation
 I.5.2. Atrioventricular Reentrant Tachycardia

• Similar to AVNRT but not through slow & fast  through ACCESSORY
PATHWAY (1 in 1500 ppl have it)
• Allow impulse from atrial to ventricle, ventricle to atrial or both directions
• Depending on the pathway characteristic:
1. ventricular pre excitation syndrome (WPW)
2. concealed bypass tract
I.5.2. Atrioventricular Reentrant Tachycardia
I.5.2.1 Ventricular Pre excitation Syndrome (WPW)

• Conduction through accessory faster  ventricles pre excited

• ECG: - PR short (stimulation earlier than normal)
- QRS slurred rather sharp (delta wave)  initial is slower
- QRS widened (fusion of 2 excitation waves)
• Patient with WPW predisposed to PSVT
• Most common: orthodromic AVRT ; 10% antidromic
 I.5.2.2 Concealed Accessory Pathway

• Only capable of Retrograde condition

• Orthodromic AVRT
• Management:
– same as AVNRT  interrupt conduction to AV:
adenosine, verapamil, diltiazem, Beta-blocker
– Recurrent episodes:catheter ablation

*concealed: To keep from being seen, found, observed, or discovered

 I.5.3 Ectopic Atrial Tachycardia

• From automaticity of an atrial focus or re-entry

• P before QRS  p morphology is different 

depolarization of atrium from abnormal site

• Cause: digitalis toxicity, elevated sympathetic

tone

• Treatment: Vagal maneuvers not effective 

beta blocker, ca-ch blocker, IA, IC, III
 I.5.4 Multifocal Atrial Tachycardia

• Irregular rhytm
• At least 3 P waves morphologies
• Average atrial rate > 100bpm
• Isoelectric baseline (vs. chaotic baseline in AF) – distinguish MAT from AF
• Cause: abnormal automaticity in several foci within atria
• Occurs most often: severe pulm disease, hypoxemia
• MORTALITY RATE IS HIGH
• Treatment: causative disorder, verapamil often effective at slowing VR
 II.1 Ventricular Premature Beats

• Common among healthy, asymptomatic, benign

• Appear when ectopic fires action potential
• ECG: widened QRS  cell to cell conduction, slower than His – purkinje
• Every alternate beat  bigeminy; 2 normal – 1 VPB: Trigeminy
• Not dangerous without preceding heart disease
• Indication of underlying cardiac disorder
 II.2 Ventricular Tachycardia

• A series of 3 or more VPB

• QRS wide >0.12x, rate 100-200 bpm
 II.2 Ventricular Tachycardia
• Sustained VT: - persist >30s
- severe symptoms (syncope)
- requires termination by cardioversion / drug
- usually fall into VF
• Nonsustained VT: self-terminating episodes
• MONOMORPHIC VT – sustained monomorphic – indicates
structural abnormality
• POLYMORPHIC VT
– Multiple ectopic foci / continually changing circuit

TORSADES DE POINTES
 Distinguishing monomorphic VT from SVT w/ abberancy

• SVT w/ abberancy – wide QRS

– Patient has underlying abnormal condition – BBB
– Repetitive Ventricular stimulation during SVT  one of BB
refractory, impulse propagates abnormally to Ventricle  QRS
wide
– Accessory pathway – Antidromic tachycardi

• Differentiate:
– History of prior MI, CHF, LV dysfunction  more likely VT
– SVT  not responding to vagal maneuvers
– SVT morphology similar to patient’s ECG in normal condition

• More likely VT:

– No relationship between QRS & P
– QRS in every lead is similar (with positive / negative deflection)
All patients with wide QRS must be treated as VT unless proven otherwise
 Torsades De Pointes

• Polymorphic VT
• Twisting about baseline
• Produced by early afterdepol – in patients who
have prolonged QT
 Torsades De Pointes

• Etiology: - Electrical disturbance (hypokalemia/hypomagnesemia)

- Persistent bradycardia

- Drugs that block cardio potassium currents

- Drugs that prolong QT = phenothiazines, haloperidol

• Treatment: - IV magnesium

- Shortening QT: Phenothiazines, Haloperidol

 II.3 VENTRICULAR FIBRILLATION

• Life – threatening
• No coordinated contraction
• Start from VT  breakup of excitation waves into smaller
wavelets of re rentry
• ECG: chaotic irregular appearance without discrete QRS
• Treat: Defib
ANTIARRYTHMIC AGENT
 Vaughan Williams classification of
antiarrhythmic drugs

• Class I: block sodium channels

– Ia (quinidine, procainamide,
disopyramide) AP
– Ib (lignocaine) AP Phase 1
– Ic (flecainide) AP IV
• Class II: ß-adrenoceptor 0 mV
Phase 2
antagonists (atenolol, sotalol)
• Class III: prolong action potential
and prolong refractory period Phase I III
Phase 3
(suppress re-entrant rhythms) 0
(amiodarone, sotalol)
• Class IV: Calcium channel -80mV
antagonists. Impair impulse Phase 4
propagation in nodal and damaged II
areas (verapamil)
 • Reducing the slope of
spontaneous phase 4
Increased diastolic depolarization
automaticity
• Prolonging the effective
refractory period

• Lengthen tissue’s
refractory period
Reentrant • Additionally impair
pathways impulse propagation 
blockade Na+ for phase
depolarization

Triggered • Suppression of early

activity and delayed afterdepol
Proarrhythmia
• Ventricular
– Torsades de pointes (class IA, III)
– Sustained monomorphic VT (class IC)
– Sudden death in coronary disease (class
IC)
• Atrial
– Increased arrhythmias
– Conversion to atrial flutter (usually class
IC)
• Abnormal conduction/impulse formation
– Increased ventricular rate during AF (class
IA, IC)
– Sinus/AV-nodal dysfunction (nearly all
drugs)
• Altered defibrillation thresholds (class I)
TERIMA KASIH
 Atrial Fibrillation

• Irregular rhythm
• Absence of definite p waves
• Narrow QRS
• Can be accompanied by rapid ventricular response
 AF : A Common Clinical Problem
6%
6% PSVT
PVCs 18%
4% Unspecified
Atrial
Flutter

9% 34%
SSS Atrial
Fibrillation
Atrial fibrillation 8%
accounts for 1/3 of all Conduction
patient discharges Disease
with arrhythmia as 10% VT
3% SCD
principal diagnosis.
2% VF
Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.
 Pathophysiology of AF

 Multiple reentrant wavelets, that circulate

chaotically throughout the atria and drive
the ventricular rate in a typically rapid and
irregularly irregular fashion
 Multiple sites of reentry  rapid
depolarization: 300 – 400 /min
 No contraction of the atria as a whole
 No P Wave
 Transmission of multiple atrial impulses
through AV Node  Irregularly irregular
ventricular rate
Atrial Fibrillation Causes Several Types of Remodeling Over Time That
Have Adverse Physiologic Consequences

• Electrophysiologic changes
– Shortening of atrial refractory periods
– Loss of normal adaptation of atrial refractoriness
to heart rate

• Contractile changes
– Reduced atrial contractility

• Structural changes
– Left atrium and left atrial appendage enlargement
– Decrease in cardiac output
– Histologic changes

• Prothrombotic changes (increased propensity for clot formation)

– Atrial stasis
– Increases prothrombotic factors

Hobbs WJC et al. Circulation. 2000;101:1145-1151; Sanfilippo AJ et al. Circulation. 1990;82:792-797; Thijssen VLJL et al. Cardiovasc Pathol. 2000;9:17-28; Van
Gelder IC et al. Europace. 2006;8:943-949; Peters NS et al. Lancet. 2002;359:593-603.
Atrial Fibrillation Causes Histologic Remodeling of Atria as Early
as 4 Months

Myolysis
Sinus rhythm Atrial fibrillation

• Enlarged atrial cells

• Severe myolysis
• Glycogen accumulation

Connexin 40

• Reduction in connexin
40 expression

Ausma J et al. Circulation. 1997;96:3157-3163; Van der Velden HMW et al. J Cardiovasc Electrophysiol. 1998;9:596-607.
 Classification of AF
• Paroxysmal AF
– < a week (often less than 24 hours)
– Self terminate, recurrent
• Persistent AF
– Lasts > a week
– Doesn’t self terminate, recur after cardioversion
• Permanent AF
– Lasted > a year
– Refractory to cardioversion
• Lone AF
– Could be Paroxysmal, Persistent, or Permanent
– No Structural Heart Disease
Atrial Fibrillation—causes and associations

• Hypertension • Hypertrophic
• Hyperthyroidism and cardiomyopathy
subclinical hyperthyroidism • COPD
• CHF (10-30%), CAD • OSA
• Uncommon presentation of • ETOH
ACS • Caffeine
• Mitral and tricuspid valve • Digitalis
disease • Familial
• Congenital (ASD)
 Atrial fibrillation--assessment
• H & P—assess heart rate, sxs of SOB, chest pain,
edema (signs of failure)
• If unstable, need to cardiovert
• Echocardiogram to evaluate valvular and overall
function
• Check TSH
• Assess for RVR
• Assess onset of sxs—in the last 24-48 hours? Sudden
onset? Or no sxs?
 TREATMENT
• Evaluation Questions:
– Patient Unstable? Need Urgent Intervention?
– Impaired Ventricular Function?
– Pre-Excitation (WPW) Syndrome ?
– AF started
Unstable: Altered > 48 hours ago?
consciousness, hypotension, sign of shock,
ie. Severe pulmonary edema
WPW: existence of Delta Wave ?
AV Nodal Blocking Agents (Adenosine, Ca Blocker, Digoxin,
Beta-Blockers  Paradoxical Increase in Ventricular
Response to rapid atrial impulse
 Heart Rate Control Versus Rhythm Control in
Persistent AF

RACE1 AFFIRM2
100 30
P = .08
90 Rate control 25
Event-free Survival (%)

Cumulative Mortality (%)

80 20
Rhythm control
Rhythm control
70 15 Rate control

60 10

50 5

0 0
0 6 12 18 24 30 36 0 1 2 3 4 5
Months Years

No. at Risk No. of Deaths number (percent)

Rate control 256 239 232 222 212 99 25 Rate control 0 80 (4) 175 (9) 257 (13) 314 (18) 352 (24)
Rhythm control 266 243 224 218 207 85 24 Rhythm control 0 78 (4) 148 (7) 210 (11) 275 (16) 306 (21)

RACE = Rate Control Versus Electrical Cardioversion for Persistent AF; AFFIRM = AF Follow-up Investigation of Rhythm
Management.

1. Van Gelder IC, et al. N Engl J Med. 2002;347:1834-1840.

2. Wyse DG, et al. N Engl J Med. 2002;347:1825-1833.
 Sinus Rhythm Remains an Important
Therapeutic Objective

• Although RACE and AFFIRM confirmed no difference in

mortality between rate-control and rhythm-control
strategies, this may be due to broad ineffectiveness of the
rhythm-control methods that were used
– Rate control was compared with frequently inadequate rhythm
control
– Study designs may have excluded the patients with severe
symptoms who would benefit most from sinus rhythm
– Sinus rhythm developed spontaneously in 10% to 35% of patients
in the rate- control groups of RACE and AFFIRM
– Survival benefits of sinus rhythm were offset by the risks of drug
therapy
• It is incorrect to infer from these results that sinus rhythm
offers no benefit over AF, or that the pursuit of effective
treatments to maintain sinus rhythm should be abandoned

AFFIRM Investigators. N Engl J Med. 2002;347:1825-1833.

Van Gelder I, et al. N Engl J Med. 2002;347:1834-1840.
Verma A, Natale A. Circulation. 2005;112:1214-1231.
 Anticoagulant Therapy for AF
• Anticoagulant Therapy
– During restoration of normal sinus Rhythm
– Chronic Anticoagulation In Recurrent AF,
patient with Hypertension, Diabetes, CHF,
previous Embolic Event
– Anticoagulants: reduce stroke event
45 – 82%
• For CARDIOVERSION purpose :
– Unknown duration
– Valvular Heart Disease
– Left Ventricular Disfunction
– Prior Thromboembolism
 Antithrombotic Therapy for Patients With
AF

Risk Category Recommended Therapy

No risk factors Aspirin, 81 to 325 mg/d

One moderate-risk factor Aspirin, 81-325 mg/d, or warfarin
(INR 2.0-3.0, target 2.5)
Any high-risk factor or more than Warfarin (INR 2.0-3.0, target 2.5)*
1 moderate-risk factor
Less Validated or
Weaker Risk Moderate-Risk Factors High-Risk Factors
Factors
Female sex Age 75 y Previous stroke,
Age 65-74 y Hypertension TIA, or embolism
Coronary artery Heart failure Mitral stenosis
disease LV ejection fraction ≤35% Prosthetic heart
Thyrotoxicosis Diabetes mellitus valve
*If patient has a mechanical valve, target INR is >2.5.
INR = international normalized ratio; LV = left ventricular; TIA = transient ischemic attack.

Fuster V, et al. Circulation. 2006;114:e257-354.

 Catheter Ablation Therapy for AF
• Results better with paroxysmal > permanent
Afib
• Patients who have failed one or two anti-
arrhythmic drugs
• LA size < 55 mm
• Minimal underlying structural HD
• TEE to exclude LA thrombus
• Spiral CT for PV anatomy
 Surgery for AF

OPEN HEART vs MINI MAZE

Maze procedure involves a series of precise incisions made in

the atrium of the heart to create electrical barriers and specific
pathways for electrical activation of the heart. This allows for only
one major route for an electrical impulse to travel through both
atria of the heart—hence the term "maze."