Atrial Fibrillation in the Era of the Accountable Care Organization

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Transcript Atrial Fibrillation in the Era of the Accountable Care Organization

John Windle MD
October 18, 2013
Professor and Chief of Cardiology
University of Nebraska Medical Center
“Ha ha ha, Biff. Guess what? After we go to the drugstore
and the post office, I’m going to the vet’s to get tutored.”
Conflict of Interest
 I have no relevant conflicts. Just lots of opinions
Atrial Fibrillation in the Era of the
Accountable Care Organization
 A Quick Review of the Basics
 The importance of Definitions
 The importance of atrial transport
 The clinical trials that drive the guidelines
 Filling in the Gaps
 Rate Control versus Rhythm Control issues
 Perspectives on bleeding versus stroke but not discussing
new therapies.
 Musings on how this might work in an ACO model
Atrial Fibrillation
 Most common sustained symptomatic
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tachyarrhythmia. Over 3,000,000 Americans suffer
from atrial fibrillation.
Incidence  with age and presence of structural
heart disease
Slightly more common in men than women
15%(75,000 per year) of all strokes occur in AF
patients
One of the top causes of hospitalizations and
extension of stays in Hospitals
Bialy et al. Journal of the American College of Cardiology 1992; 19(3):41A.
Prystowsky et al. Circulation. 1996; 93(6):1262-1277.
Wolf et al. Archives of Internal Medicine. 1987; 147(9):1561-1564.
Incidence of Atrial Fibrillation
(Framingham Study)
Chronic AF
14-
Paroxysmal AF
1412.9
12.7
6-
5.4
4.8
42.2
2-
-
-
30-39
64.8
4-
1.5
0.7
0
Women
8-
2-
0.9
-
0-
0.5
40-49
50-59
60-69
70-79
Age
Kannel et al. American Heart Journal. 1983;106(2):389-396.
9.2
0-
0.5
0
0
30-39
0.4
1.9
0.6
0.5
-
6.7
Men
-
Women
8-
10-
-
Men
-
10-
2-yr Incidence (per 1000)
12-
-
2-yr Incidence (per 1000)
12-
40-49
50-59
60-69
70-79
Age
Consequences of Atrial Fibrillation
 Arrhythmia-associated symptoms, look at exertional
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symptoms of shortness of breath, exertional dyspnea
and decreased exercise tolerance.
 LV function: Impact of atrial transport and diastolic
function.
Tachycardia-mediated cardiomyopathy (heart rates
over 130 b/m)
2-fold  in cardiac mortality
5-fold  in risk of stroke
“Why do I feel like crap?”
Myocardial and Hemodynamic Consequences of Atrial
fibrillation
 Loss of atrial contraction decreases cardiac output
 9% drop in C.O. in canine model
 15% drop in C.O. in irregular response vs. same average rate
pacing.
 Decrease in coronary blood flow with irregular ventricular
rhythm.
 Tachycardia-induced cardiomyopathy (heart rate >130 for
several weeks).
 LVH (diastolic dysfunction) accentuates the importance atrial
contraction.
The impact of atrial contribution by cardiac doppler
Atrial Fibrillation-The 3 Ps
 Paroxysmal-Self-limited, often occurring in
structurally normal hearts
 Persistent-Requiring intervention, either chemical
(antiarrhythmic drugs) or electrical to restore sinus
rhythm
 Long-standing persist-a term created by cardiac
electrophysiologists to “not give up”.
 Permanent-”Uncardiovertable”
Atrial Fibrillation Guidelines
Paroxysmal Atrial Fibrillation
 Vasovagal-nocturnal, triggered by stress, meals or
alcohol
 Self-limited but shortened duration with
propafenone or flecainide
 Often have pulmonary vein foci
 Amenable to Ablative therapy
Persistent Atrial Fibrillation
 Need an intervention to restore sinus rhythm
 More likely to involve structural heart disease: Cardiac
effects of hypertension and LVH, prior myocardial
damage such as MI
 Try to figure out the symptom trigger: Rate, regularity
or Atrial synchrony and atrial transport.
Permanent Atrial Fibrillation
 Un-cardiovertable atrial fibrillation
 Duration
 Left atrial size
 Comorbidities
 Absence of Symptoms
Decision Points for Atrial Fibrillation
Prevention of Thromboembolism
Ventricular Rate Control
Conversion
to NSR
Maintenance of NSR
Short Term
NSR = normal sinus rhythm
Time
Long Term
Rate Control Therapy
 A-V Nodal Agents (slow ventricular response)
 Digoxin-increases vagal tone, reduces resting heart rate
but not exercise rate
 Beta Blockers-underutilized but most effective
 Calcium Channel Agents

Diltiazem and verapamil not nifedipine
 Adenosine
 A-V Node Ablation with pacemaker placement
 Single versus Bi-V device
Rhythm Control Therapy
Atrial Muscle Agents (restoration and maintenance of sinus
rhythm)
 Procainamide and Quinidine-What we learned about in
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School but of limited use and availability now
Propafenone, Flecainide-Good for acute conversion and
normal hearts (Pill-in-the Pocket)
Disopyramide-Still in good option for some, decreases vagal
tone
Sotalol and Dofetilide-Torsades de Pointes but otherwise
great agents
Dronederone-very limited use.
Amiodarone*
*The Vaughn-Williams Classification system is easy but wrong.
The Affirmed Trial
 The Affirmed Trial-Rate Control versus Rhythm
Control in Patients with Atrial Fibrillation
 Critical Study: Randomized Control Trial
 Rhythm Control no better than Rate Control
 Rate control less costly
The Affirmed Trial: Part II
 Short follow-up on “elderly”, asymptomatic patients
 Based on an “intention to treat”
 “Failure” based on first recurrence versus time spent in
desired rhythm
 Very high overlap in assigned patients in their actual
rhythm (sinus rhythm versus atrial fibrillation).
 Not a comparison of atrial fibrillation versus sinus
rhythm (The sinus rhythm patients did significantly
better)
Atrial Fibrillation; now what?!
No significant improvement in quality of life with “rhythm control” strategy in
multiple trials above. STAF and HOT CAFÉ showed increase in exercise
tolerance.
It’s just AF; it won’t KILL ME.
Excess mortality in AF patients
compared to matched (non-AF).
Framingham Heart Study (1983);
The Regional Heart Study
Whitehall Study
Manitoba Study (1995)
 HF promotes AF, AF
exacerbates HF, and
patients with either who
develop the other, share
a poor prognosis.
 Stroke in AF averages 5%
per year!
 1.5% annual in 50-59y to
23% annual in 80-89 yrs.
Framingham Data.
My Take Home Messages:
 Yep-Sinus rhythm and rate controlled atrial fibrillation
equivalent in asymptomatic, elderly patients followed
over 3-5 years.
 Yep-Lower utilization of resources with rate control
strategy
 But,
 Didn’t answer sinus versus rate control
 Most of my patients are not truly asymptomatic
 Atrial fibrillation causes a 5-10% drop in EF in most
patients, what do you think will happen over time?
Anticoagulation
Anticoagulation is recommended for
ALL patients with atrial fibrillation,
except those with “LONE AF” or
contraindications.
Anticoagulation with a vitamin K
antagonist is recommended for
patients with more than 1 moderate
risk factor
Aspirin 81-325 mg for low-risk patients,
or those with CI to oral
anticoagulation
Anticoagulation for atrial flutter is
recommended as per AF.
Long term anticoagulation with
vitamin K antagonist is NOT
recommended for primary strike
prevention in patients <60 yrs of age
without heart disease.
CHADS2 Score
EF <35%
Circulation. 2006;114:e257-e357.
Why anticoagulation to a target of 2.0 to 3.0?
Warfarin vs. Aspirin
Why not everyone with AF?
Atrial Fibrillation: Interventions
 Cardioversion: Medical versus Electrical
 Dual Chamber Pacing (Bradycardic-dependent
arrhythmias)
 AV Node Ablation and Ventricular Pacing
 EF <45%
 Pacing over 40%
 Pulmonary Vein Isolation Ablation
 Surgical MAZE Procedure
Dilbert
Dilbert
All roads lead to catheter ablation!
Catheter Ablation for AF
 Rationale:
 Triggers within the pulmonary veins and other sites
(SVC, LM, CS, CT)
 Isolation of the pulmonary veins eliminates AF in many
patients with PAF.
 Alteration of substrate in Persistent AF patients
dramatically reduces symptoms of AF, and frequently
reduces or eliminates the need for antiarrhythmic
medications to control the rhythm.
History of AF Ablation
 Initial procedure mimicked the surgical maze
procedure. Success rate was 40-50% and complication
rate high. (Prior to 1998).
 Automaticity within the pulmonary veins was then the
target…
Pulmonary Vein Isolation
 ~95% of the triggers for AF are suspected to be in the
pulmonary veins.
 Additional triggers at sites of “Complex Fractionated
Atrial Electrograms” (CFAEs)
 In PAROXYSMAL atrial fibrillation, pulmonary vein
isolation is effective in 80-85% of cases at “CURING”
atrial fibrillation.
 Currently, “Symptomatic atrial fibrillation refractory to
or intolerant of medical therapy” is the primary
indication for PVAI.
Ultrasound
Reconstruction of
The Left Atrium
with
CartoSound/ICE
WHAT FOR:
Mapping veins, appendage
Mitral annulus/valve
Velocities, evaluate for PFO
Map coronary arteries
CONTINUOUSLY EVALUATE
FOR PERICARDIAL
EFFUSION
CT scan merged with ultrasound image (right).
Pulmonary vein isolation for paroxysmal AF
Atrial fibrillation persists within the RSPV, but sinus rhythm is present elsewhere
What about “Non-Paroxysmal” AF?
 More complex disease entity from an ablation
standpoint.
 PVAI is not sufficient for elimination of atrial fibrillation
in many patients.
 Additional lesions include approximation of the maze
lesion set with ablation at the roof, mitral annulus,
cavotricuspid isthmus, and svc.
 The addition of CFAE ablation is of unclear benefit and
remains controversial.
Complications:
 Perforation with pericardial tamponade
 ~1% of cases of PVAI (up to 5% depending on series)
 Usually self-limiting, requiring a drain
 Rarely can require surgical drainage/repair.
 Cerebrovascular accidents
 0.5 to 2.5% of cases
 Dramatically reduced with higher ACT
 Phrenic Nerve Injury
 0.1 to 0.48% of cases
 Recovery in 66% of cases, can be permanent
 Radiation related
 Fluoroscopy times can be prolonged.
 Pulmonary vein stenosis
 1 to 2% with current techniques
 (15-20% historically)
 Atrio-Esophageal fistula
New Ablation Tools and Techniques
 CryoBalloon (Arctic Front)
 Ablation Frontiers Catheter
 High-Intensity Focused Ultrasound
 Laser ablation
 And more…. Just around the corner.
Where Do We Go From Here?
 3,000,000 patients how do we divide up the work?
 Base-rate theory: EP>Cardiology>Primary Care
 Team-based Care
 Decision-making
 Rate versus rhythm control
 Antithrombotic Care
Where do we go from here: the ACO
 In my “perfect-world”
 EP physicians would consult (either actual or virtually)
on all patients at presentation of their atrial fibrillation
 The EP physician, the primary care provider and the
patient would develop a consensus treatment plan with
all three holding accountability for the outcome.
 If anti-thrombotic therapy was initiated it would be
managed by a non-physician team member under
protocol.
 Cardiologists would be involved in atrial fibrillation
management.
Questions?
New Drugs
 Dronedarone: a non-iodinated amiodarone analog.
 Trials have compared the medication to placebo and
amiodarone.
 Euridis and Adonis (European and American) trials showed
efficacy relative to placebo.
 ANDROMEDA study showed higher death rate in NYHA
Class IV patients.
 ATHENA trial demonstrated stroke risk reduction.
 Currently, approval is for “treatment of patients with a history
of, or recurrent atrial fibrillation to reduce their risk of
cardiovascular hospitalization due to this condition.”
Azmilide
 Not yet approved
 Potassium blocker similar to dofetilide or sotalol, but
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blocks both iKr and iKs.
Does not perform as a beta-blocker.
LONG HALF-LIFE of up to 4 days.
In a trial to assess its efficacy in MI patients with EF 1535%, (ALIVE), a higher proportion of patients in the
treatment arm were in sinus rhythm at the end of the
study…
Placebo-controlled trial is in the works.