THE SURGICAL CURE OF ATRIAL FIBRILLATION

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THE SURGICAL CURE OF ATRIAL FIBRILLATION

• Harold G. Roberts, Jr., M.D.

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Survival after CABG
Propensity matched groups of patients with or w/o
AF preoperative Kaplan Meier estimates _at_ five
years with 68 CI of pts remaining _at_ risk shown
in parenthesis
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DefinitionsACC AHA ESC

• Recurrent Atrial Fibrillation 2 or more
  episodes
• Paroxysmal atrial fibrillation
• Duration lt 7 days, terminates spontaneously
• Persistent Atrial Fibrillation
• Does not terminate spontaneously, requires
  electrical or pharmacolgoical intervention to
  create sinus rhythm
• Permanent Atrial Fibrillation
• SR cannot be sustained after cardioversion

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DEFINITIONS JL Cox

• Paroxysmal atrial fibrillation is intermittent
• Chronic atrial fibrillation is continuous
• A person who has Paroxysmal (intermittent) atrial
  fibrillation for a long time does not have
  Chronic atrial fibrillation
• Once atrial fibrillation is established, all
  atrial fibrillation is the same. The electrical
  events in the atrium during a bout of Paroxysmal
  aF are identical to those of Chronic AF

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Atrial Fibrillation-Maintenance

• Once atrial fibrillation is established
• 1. It is characterized by multiple
  simultaneous
  macro-reentrant circuits in both atria
• 2. It can spontaneously convert back to sinus
  rhythm (paroxysmal atrial fibrillation)
• 3. It can continue indefinitely (chronic
  atrial fibrillation
• Atrial Fibrillation begets atrial fibrillation

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Consequences of AF

• Impaired quality of life
• Thromboembolic complications (stroke)
• Progressive increase in atrial size
• Concealed and overt tachycardiomyopathy
• Overall Increased Mortality

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Risks Associated with Atrial Fibrillation

• A-Fib increases stroke rate 3 5 times
• A-Fib is responsible for 15 20 of all strokes
• A-Fib increases death rate 2 fold
• The longer a patient is in A-Fib, the more
  difficult it is to treat and eliminate the rhythm

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Percentages of Strokes Associated with Atrial
Fibrillation
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Symptomatic Presentation of Atrial Fibrillation
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AFFIRM TRIALRate Control vs. Rhythm Correction

• Currently available AADs are not associated with
  improved survival, which suggests that any
  beneficial antiarrhythmic effects of AADs are
  offset by their adverse effects. If an effective
  method for maintaining SR with fewer adverse
  effects were available, it might be beneficial.

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Conduction System ChangesResulting in Atrial
Fibrillation

• Abnormal Cardiac Conduction
• Cardiocytes lose ability to conduct in synchrony
• Triggers from pulmonary veins cause wavelets of
  A-Fib
• Wavelets form macro-reentry circuits that become
  self sustaining sources of A-Fib
• SA node no longer communicates with AV node
• Atrial tissue permanently changes

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Pulmonary Vein Triggers Paroxysmal AF
Right Atrium
Left Atrium
Septum
superior vena cava
31
fossa ovalis
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pulmonary veins
inferior vena cava
coronary sinus
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94 of triggers are in the PVs
Haissaguerre NEJM 1998 339659-66
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Causes of Atrial Fibrillation

• Most conditions are related to enlargement or
  dilation of the atrial tissues
• Mitral valve disease ( 30)
• Hypertension
• Ischemic heart disease
• Congestive heart failure
• Idiopathic (no known cause)

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Muscular sleeves extending from the atrium along
the pulmonary vein are the nexus for propagating
arrhythmia triggers
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Treatment Options for Atrial Fibrillation

• Medical
• Pharmacological
• Electrical
• Interventional Cardiology
• Surgical

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Drug Therapy for Atrial Fibrillation

• Efficacy poor at best 40-60 maintenance of
  sinus rhythm.¹, ²
• Proarrhythmia sinus and AV node dysfunction
• Toxicity liver, pulmonary fibrosis, peripheral
  neuropathy
• Patient issues quality of life and compliance

1Crijns HJ, et al. American Journal of
Cardiology. 199168(4)335-41. 2Antman EM, et al.
Journal of American College of Cardiology.
199015(3)698-707.
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Treatment Options for Atrial Fibrillation

• Electrophsyiological
• EP Cardiology peripheral based therapies
• Pulmonary vein isolation with fluoroguided
  catheters
• Radiofrequency (RF) and cyrothermic energy
  sources

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Cox-Maze III

• Maze Procedure developed by J. Cox, M.D. in 1987.
• Based on the principal that AF is caused by
  multiple reentrant circuits in the atria.
• Cut and sew technique which efffectively blocks
  the propagation of these renentrant circuits into
  dead ends and allows the normal propagation of SA
  node stimuli

Cox J, et al. J Thoracic Cardiovascular Surgery
1991101509-583.
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Catheter Ablation Challenges

• Technically challenging to create continuous
  lesion
• Transmurality not confirmed
• Poor long term outcomes
• Left Atrial Appendage not addressed
• Uncontrolled energy complications
• Esophgeal fistula, embolic events
• Prolonged fluoro-radiation exposure

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Radiofrequency Ablation

• Charring
• Thromboembolism
• Significant tissue disruption
• Difficult
• Transmural probe contact limited
• Lesion Depth
• Potential for Injury

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Shortcomings of the Cox Maze Procedure

• Requires cardiopulmonary bypass and an arrested
  heart
• Adds to cross-clamp time
• Few Surgeons perform the operation because of
  its complexity
• Can lead to increases in morbidity
• Increased length of stay
• Pacemaker requirements

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Left Atrial Anatomy
Ostia of Left Atrial Appendage
Mitral Valve
Left Superior Pulmonary Vein
Left Inferior Pulmonary Vein
Right Superior Pulmonary Vein
Right Inferior Pulmonary Vein
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Posterior View of Heart
SVC
Right Superior Pulmonary Vein
Left Superior Pulmonary Vein
Left Inferior Pulmonary Vein
Right Inferior Pulmonary Vein
IVC
Coronary sinus
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The AtriCure Bipolar Ablation System
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Optimimal tissue contact ensures a discrete,
transmural lesion
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Gross Pathology
Lesion through variable tissue thickness
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Histology
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MIS Approach Wolf Mini-MazeThe Next Step in
Evolution in Surgical Ablation

• Sole paroxysmal and persistent AF patients
• Bi-lateral pulmonary vein isolation 90
  success
• Close left atrial appendage to manage stroke
• Collaborate with EP partners with dual approach

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Oklahoma Group Observations

• Hyperactivity of autonomic ganglia at the
  PV-atrial junctions can induce APDs and rapid
  firing from adjacent PVs providing the drivers
  for AF
• Ablation of these ganglionic clusters can reduce
  the autonomic burden and thereby suppress the
  triggered firing as well as the substrate for
  converting PV ectopia into AF

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What is the Role of the Ganglionic Plexi in A-fib
Propagation?
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Working Hypothesis

• Ectopic beats arising in the PVs can be converted
  into AF by the activity of the autonomic ganglia
  located at the PV-atrial junctions
• Excessive release of cholinergic and adrenergic
  neurotransmitters can shorten refractoriness and
  induce triggered firing sufficient to cause AF

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SVC
R1
RSPV
R3
R2
RA
LA
R4
R5
Waterstons Groove
RIPV
R6
R7
R8
R9
R10
IVC
Ganglionic Plexi - Right
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Pulmonary Artery
L2
L1
LSPV
LA Appendage
L4
L3
Marshall Tract
L6
L5
LIPV
L8
LA
L7
LV
L10
L9
AV Groove
Ganglionic Plexi - Left
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Right PVs and Ganglionated Plexi
RSPV
Anterior Right GP
Head
Foot
RIPV
Inferior Right GP
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Left Pulmonary Veins and Location of Left GPs
Pulmonary Artery
Pericardial Insertion of Ligament of
Marshall (Region Superior Left GP)
Pericardium
LSPV
LIPV
Inferior Left GP
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PV potentials in AF
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Positive response to HFS
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Isolated no potentials
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Surgical Treatment of AF

• Bipolar RF Ablation Clinical Results
• Dr. Damiano
• Washington University
• 40 patients Modified Cox-Maze
• 23 patients with 6 mo follow-up
• 91 freedom A-Fib at 6 months

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Cryo MazeResults n40, (3-15.5 mo, Post-op, mean
10.3 mo.)

• Mini-maze 12
• Full Maze 8
• SR 35 (88)
• AF 2 ( 5) (RHD)
• PPM 2 ( 5)
• Mortality 0
• CVA TIA 1
• ARDS 1
• Bleeding 0
• EP Interventions 0
• Freedom from Recurrent AF 95

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Lateral Right Atrium
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Thank You