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Atrial Fibrillation:Rate Control, Rhythm Control, Anticoagulation & Ablation. What Are My Options?
ROBERT T ROGERS MSN, ACNP-BC, AACC
NORTON HEART SPECIALISTS
HEART RHYTHM CENTER
Speaker Disclosure
None to report
How Atrial Fibrillation is like a bear?
What is Atrial Fibrillation?
Incidence of AF
Index Age, yrs Men Women
40 26.0% (24.0 – 27.0) 23.0% (21.0 – 24.0)
50 25.9% (23.9 – 27.0) 23.2% (21.3 – 24.3)
60 25.8% (23.7 – 26.9) 23.4% (21.4 – 24.4)
70 24.3% (22.1 – 25.5) 23.0% (20.9 – 24.1)
80 22.7% (20.1 – 24.1) 21.6% (19.3 – 22.7)
Lifetime Risk for AF at Selected Index Ages by Sex
Lloyd-Jones DM, et al. Circulation. 2004 Aug 31;110(9):1042-6. Pub Med PMID: 15313941.
1 in 4 Men & women>40 Yearswill develop AF
Lifetime risk if currently free of AF
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Incidence of AF Atrial fibrillation is the most prevalent cardiac arrhythmia
Untreated Atrial Fibrillation increases mortality
Cost
AFib Costs and Consequences
More than 750,000 hospitalizations occur each year because of AFib. The condition contributes to an estimated 130,000 deaths each year. The death rate from AFib as the primary or a contributing cause of death has been rising for more than two decades.3,4
AFib costs the United States about $6 billion each year. Medical costs for people who have AFib are about $8,705 higher per year than for people who do not have AFib.1,2
Causes of AF Hypertension (usually with LVH)
Ischemic heart disease
Dilated cardiomyopathy
Restrictive cardiomyopathies such as amyloidosis, constrictive
Pericarditis
Cardiac tumors
Severe pulmonary hypertension
Obesity and obstructive sleep
Excessive alcohol intake (holiday heart),
Open heart or thoracic surgery,
Myocarditis
Pulmonary embolism.
Hyperthyroidism
Pathophysiology
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How do you feel with AF?
Complications- Heart and Brain Diagnosis of AF
ECG
Holter monitor
Event monitor (ILR)
Echocardiogram
Stress test
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Management :Time to wrestle the bear…
Management- What do we do?
2 things must be done regardless of rate and rhythm control
1. Change their ways
Lifestyle changes
Weight control
Heart Healthy Diet
Exercise
Sleep hygiene
Stress reduction
Treat underlying Medical Conditions
Sleep apnea
High blood pressure
Diabetes control
Thyroid disease
2. Protect their brains!
How do we save the brain?
How to save the brain
Anticoagulation
Warfarin
NOACs/DOACs
Eliquis, Xarelto, Pradaxa and Savaysa
Mechanical Occlusion
Watchman device
How do we save the heart?
Rate Control
Controls symptoms in some people
Rhythm Control
Anti-arrhythmic medications
Daily vs “pill in the pocket”
Catheter ablation
Surgical ablation
Anticoagulant drugs
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Who should be anticoagulated?
Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Chest. 2010 Feb;137(2):263-72. Pub Med PMID: 19762550.
Bleeding Risk Scores in AF
ATRIA HAS-BLED HEMORR2HAGES
Anemia1 3 Hypertension4 1 Hepatic10 or Renal disease2
11
Severe renal disease2 3 Abnormal Renal5 or Liver function6
11 Ethanol abuse 1
Age ≥75 yrs 2 Stroke 1 Malignancy 1
Any prior hemorrhage 1 Bleeding 1 Older Age (>75 yrs) 1
Hypertension3 1 Labile INR8 1 Reduced platelet number or function11 1
Elderly (>65 yrs) 1 Rebleeding12 2
Drugs9 or Alcohol
11 Hypertension4 1
Anemia13 1
Genetic factors14 1
Excessive fall risk15 1
Stroke 1
Apostolakis S, Lane DA, Guo Y, Buller H, Lip GY. J Am Coll Cardiol 2012;60:000–000. 2012 Jul 24. [Epub ahead of print] Online Appendix. PMID: 22858389.
1. Hemoglobin <13 g/dl men; <12 g/dl women2. Estimated glomerular filtration rate <30 ml/min or dialysis-dependent3. Diagnosed hypertension4. Systolic blood pressure >160 mmHg5. Presence of chronic dialysis or renal transplantation or serum creatinine ≥200 mmol/L6. Chronic hepatic disease (eg cirrhosis) or biochemical evidence of significant hepatic derangement (eg bilirubin 2 x upper
limit of normal, in association with aspartate aminotransferase/alanine aminotransferase/alkaline phosphatase >3 x upper limit normal, etc.)
8. Unstable/high INRs or poor time in therapeutic range (eg <60%)9. Concomitant use of drugs, such as antiplatelet agents, non-steroidal anti-inflammatory drugs, or alcohol abuse etc. 10. Cirrhosis, two-fold or greater elevation of AST or APT, or albumin <3.6 g/dl11. Platelets <75,000, use of antiplatelet therapy (eg daily aspirin) or NSAID therapy; or blood dyscrasia12. Prior hospitalization for bleeding13. Most recent hematocrit <30 or hemoglobin <10 g/dl14. CYP2C9*2 and/or CYP2C9*315. Alzheimer's dementia, Parkinson's disease, schizophrenia, or any condition predisposing to repeated falls
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Anticoagulants
Vitamin K Antagonists
Coumarin
Warfarin
Factor Xa Inhibitors
Heparins
Low molecular heparins
Apixaban (DOAC)
Rivaroxaban (DOAC)
Edoxaban (DOAC)
Direct Thrombin Inhibitors
Argatroban
Ximelagatran
Lepirudin
Bivalirudin
Dabigatran (DOAC)
1930s
Heparin
1950s 1990s 20021970s
Warfarin LMWHs Factor Xa inhibitor
DTIs
ArgatrobanBivalirudinLepirudinIprivask
FondaparinuxEnoxaparinDalteparinTinzaparin
1980s 2010-current
DTI and Factor Xainhibitors
DabigatranRivaroxaban
ApixabanEdoxaban
Developmental History –Current FDA Approved Anticoagulants
Warfarin- the old standby
DOSING
Usual dose is 5 mg/day (1-20 mg) Lower doses require in
Elderly Pt on increased risk of bleeding eg. Pt on aspirin Heart failure Liver disease Renal impairment Malnutrition Thyrotoxicosis (Opposite in Myxedema) Asian patients: Explained by genetic variation in hepatic enzymes
(CYP3C9 & VKORC1 Polymorphism) High intake dietary Vit-K (green vegetables e.g. broccoli)
reduces the efficacy of Warfarin. Practically best time to give warfarin is ~ 6 PM.
Commencement of oral anticoagulant therapy
If the baseline INR≤1.3 the patient will receive 5mg of warfarin once daily on days 1 and 2. The INR is checked on day 3 and 4 and the warfarin dose is adjusted according to the schedule.
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Caution with VITAMIN K containing food
It is okay to eat food with different levels of vitamin K, but because vitamin K can interfere with blood-thinning effects of warfarin, it is important to eat the same amount from day to day. Do not eat a lot one day and none the next
Vitamin K foods
Factors that affect warfarin effectiveness Side effects of Warfarin
Bleeding
Skin necrosis
Purple toe syndrome
Teratogenicity
Osteoporosis
Others: Agranulocytosis, leukopenia, diarrhea,
nausea, anorexia.
It’s a Brave New World of Anticoagulation….NOAC/DOAC…
Whatever you call them they are new and better than we had before
NOAC vs Warfarin
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NOAC vs WarfarinNOAC vs Warfarin
NOACs approved or under evaluation for prevention of systemic embolism or stroke in patients with non-valvular AF
Dabigatran Apixaban Edoxaban Rivaroxaban
Action Direct thrombin inhibitor
Activated factor Xa(FXa) inhibitor
Activated factor Xa (FXa) inhibitor
Activated factor Xa(FXa) inhibitor
Dose150 mg BID
110 mg BID
5 mg BID
2.5 mg BID
60 mg QD
30 mg QD
15 mg QD
20 mg QD
15 mg QD
Phase III clinical trial RE-LY 1ARISTOTLE 2
AVERROES 3ENGAGE-AF 4 ROCKET-AF 5
1. Connolly et al, N Engl J Med 2009; 361:1139-51 4. Ruff et al, Am Heart J 2010; 160:635-412. Granger et al, N Engl J Med 2011; 365:981-92 5. Patel et al, N Engl J Med 2011;365:883-913. Connolly et al , N Engl J Med 2011; 364:806-17
Drug-drug interactions and pharmacokinetics of NOACs
Absorption and metabolism of NOACs
Absorption and metabolism of NOAC
Dabigatran Apixaban Edoxaban Rivaroxaban
Bioavailability 3-7% 50% 62% 66% (w/o food) ~100% with food
Prodrug yes no no no
Clearance: non-renal/renal of adsorbed dose if normal renal function
20%/80% 73%/27% 50%/50% 65%/35%
Liver metabolism: CYP3A4 no yes (elimination; minor CYP3A4)
minimal (<4% of elimination)
yes (elimination)
Absorption with food no effect no effect 6-22% more +39%
Intake with food? no no no official recommendation yet
mandatory
Absorption with H2B/PPI plasma level -12 to -30% no effect no effect no effect
Asian ethnicity plasma level +25% no effect no effect no effect
GI tolerability dyspepsia 5-10% no problem no problem no problem
Elimination half-life 12-17h 12h 9-11h 5-9h (young)/11-13h (elderly)
Possible drug-drug interactions –Effect on NOAC plasma levels part 1
Dabigatran Apixaban Edoxaban Rivaroxaban
Atorvastatin P-gp/ CYP3A4 +18% no data yet no effect no effect
Digoxin P-gp no effect no data yet no effect no effect
Verapamil P-gp/ wk CYP3A4+12–180%
no data yet+ 53% (slow release)
minor effect
Diltiazem P-gp/ wk CYP3A4 no effect +40% No data minor effect
Quinidine P-gp +50% no data yet +80% +50%
Amiodarone P-gp +12–60% no data yet no effect minor effect
Dronedarone P-gp/CYP3A4 +70–100% no data yet +85% no data yet
Ketoconazole; itraconazole; voriconazole; posaconazole;
P-gp and BCRP/ CYP3A4 +140–150% +100% no data yet up to +160%
Red – contraindicated; orange – reduce dose; yellow – consider dose reduction if another yellow factor present; hatching – no data available; recommendation made from pharmacokinetic considerations
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Possible drug-drug interactions –Effect on NOAC plasma levels part 2
Interaction Dabigatran Apixaban Edoxaban Rivaroxaban
Fluconazole CYP3A4 no data no data no data +42%
Cyclosporin; tacrolimus
P-gp no data no data no data +50%
Clarithromycin; erythromycin
P-gp/ CYP3A4 +15–20% no data no data +30–54%
HIV protease inhibitors
P-gp and BCRP/ CYP3A4
no data strong increase no data up to +153%
Rifampicin; St John’s wort; carbamezepine; phenytoin; phenobarbital
P-gp and BCRP/ CYP3A4/CYP2J2
-66% -54% -35% up to -50%
Antacids GI absorption -12-30% no data no effect no effect
Red – contraindicated; orange – reduce dose; yellow – consider dose reduction if another yellow factor present;hatching – no data available; recommendation made from pharmacokinetic considerations
Switching between anticoagulant regimensVKA to NOAC INR <2.0: immediate
INR 2.0–2.5: immediate or next day INR >2.5: use INR and VKA half-life to estimate time to INR <2.5
Parenteral anticoagulant to NOAC:Intravenous unfractioned heparin(UFH)Low molecular weight heparin (LMWH)
Start once UFH discontinued (t½=2h). May be longer in patients with renal impairmentStart when next dose would have been given
NOAC to VKA Administer concomitantly until INR in appropriate rangeMeasure INR just before next intake of NOACRe-test 24h after last dose of NOACMonitor INR in first month until stable values (2.0–3.0) achieved
NOAC to parenteral anticoagulant Initiate when next dose of NOAC is due
NOAC to NOAC Initiate when next dose is due except where higher plasma concentrationsexpected (e.g. renal impairment)
Aspirin or clodiprogel to NOAC Switch immediately, unless combination therapy needed
Summary of the NOACThe Brain is now safe, how about the Heart?
Which to choose? Trials of Rate vs Rhythm Control
ACC/AHA/ESC Guidelines 2006
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AFFIRMBaseline Characteristics
Age = 69.7 ± 9.0 yrs
39% female
> 2 days of AF in 69%
CHF class > II in 9%
Symptomatic AF in 88%
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Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) Trial (n=522)
Van Gelder, I. et al. N Engl J Med 2002;347:1834-1840
CV death, HF, thromboembolic complications, bleeding, pacemaker, and SAEs.
Based on the data, why try for rhythm control at all?
LIMITATIONS of Trials: AGEGuideline Statement
ACC/AHA/ESC Guidelines 2014
LIMITATIONS 1
- The mean ages in AFFIRM and RACE were 70 and 68 years, respectively. -The RACE and AFFIRM trials did not address AF in younger, symptomatic patients with little underlying heart disease, in whom restoration of sinus rhythm by cardioversion antiarrhythmic drugs or non-pharmacological interventions still must be considered a useful therapeutic approach.
One may conclude from these studies that rate control is a reasonable strategy in elderly patients with minimal symptoms related to AF.
LIMITATIONS 2
Approximately one-half of patients in AFFIRM who had a detailed history had symptomatic episodes of AF that occurred less often than once per month.
Such patients would be expected to derive little symptomatic benefit from rhythm control, and the results may not directly apply to patients with frequent episodes of symptomatic AF
LIMITATIONS of Trials: SYMPTOMS
LIMITATIONS 3
Both trials allowed for cessation of anticoagulant therapy four weeks after documentation of SR, leading to a higher rate of stroke.
It has been postulated that continued anticoagulation might have led to a lower mortality in the rhythm control group
LIMITATIONS of Trials: ANTICOAGULATION
LIMITATIONS 4
The use of antiarrhythmic drugs in AFFIRM was associated with a significant increase in mortality (HR 1.49), which was due to non-cardiovascular causes, while the presence of SR was associated with a significant reduction in mortality (HR 0.53).
A similar benefit from being in sinus rhythm (relative risk 0.44) was noted in the DIAMOND trial that compared dofetilide to placebo in patients with reduced left ventricular systolic function
LIMITATIONS of Trials: DRUGS
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LIMITATIONS
One interpretation of these data is that maintenance of SR might be beneficial if there were a safer and more effective approach than current antiarrhythmic drugs:
The AFFIRM and RACE data were largely gathered before catheter ablation was common. The potential impact of this procedure (versus chronic antiarrhythmic therapy) remains incompletely explored
LIMITATIONS of Trials: DRUGS Bottom Line: Rate versus Rhythm Control for AF
The AFFIRM, RACE and AF-CHF trials have shown no mortality benefit from a rhythm control strategy compared to a rate control strategy.
Therefore, a rate control strategy, without attempts at restoration or maintenance of sinus rhythm (SR), is reasonable in some patients with AF, especially those who are elderly and asymptomatic.
If rate control offers inadequate symptomatic relief, restoration of SR may become a long-term goal.
Restoration and maintenance of SR continues to be a reasonable treatment approach in many patients with AF.
68
Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed.
Rate ControlVentricular Rate Control
Principles of a Rate Control Strategy: Adequate control of the ventricular response during AF can significantly improve
symptoms and is critical to avoid tachycardia-mediated cardiomyopathy. Most patients managed using a rhythm control strategy also require medications for
rate control. Rate control during atrial flutter tends to be more difficult than during AF.What is Adequate Rate Control? Control of the ventricular rate during AF is important both at rest and with exertion.
No standard method for assessment of heart rate control has been established.
Criteria for rate control vary with patient age but usually involve achieving ventricular rates between 60 and 80 bpm at rest and between 90 and 115 bpm during moderate exercise.
For the AFFIRM trial, adequate control was defined as an average HR up to 80 bpm at rest and either an average rate up to 100 bpm during Holter monitoring with no rate above 100% of the maximum age-adjusted predicted exercise HR, or a maximum HR of 110 bpm during a 6-min walk test.
In the RACE trial, rate control was defined as less than 100 bpm at rest.
Only about 5%of patients from these trials required AV ablation to achieve HR control.
70Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed.
Ventricular Rate Control:Drugs to Control the Ventricular Response
Beta blockers are the most effective drug class for rate control.
Calcium channel antagonists (non-dihydropyridine) are good choices for patients with asthma or COPD requiring beta agonist inhaler therapy.
Digoxin provides relatively poor rate control during exertion and should be reserved for patients with systolic HF.
Digoxin does not convert AF to SR and may perpetuate AF.
Digoxin is marginally effective as a sole agent, but may prove useful in combination with beta blocker or calcium channel antagonists, particularly in hypotensive patients.
71
Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed. with modifications.
How controlled is controlled?
No strict definition of rate control
Rest – 60-80/min
Holter – Mean 80 - 100/min
Moderate exercise – 90-115/min
Peak exercise – 20-30% reduction of age predicted heart rate
Treatment to achieve strict heart rate control (<80 at rest or <110 during 6 minute walk) IS NOT BENEFICIAL compared with treating a resting heart rate <110 in patients with normal LV function
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Ventricular Rate Control:Drugs to Control the Ventricular Response
A combination of a beta blocker and either a calcium channel antagonist or digoxin may be needed to control the HR.
The choice of medication should be individualized and the dose modulated to avoid bradycardia.
Beta blockers and calcium channel antagonists should be used cautiously in patients with HF.
AV nodal blocking drugs at doses required to control the ventricular response can cause symptomatic bradycardia that requires pacemaker therapy.
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Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed.
Ventricular Rate Control:Drugs to Control the Ventricular Response
Some antiarrhythmic drugs that are used to maintain sinus rhythm, such as sotalol, dronedarone (multaq), and amiodarone, also provide some control of the ventricular response when patients are in AF.
Amiodarone should rarely be used for rate control because of its potential for toxicity.
IV digoxin or non-dihydropyridine calcium channel antagonists given to patients with AF and WPW may accelerate the ventricular response and are not recommended.
74
Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed.
Ventricular Rate Control:AV Nodal Ablation
Ablation of the AV conduction system and permanent pacing (the “ablate and pace” strategy) is an option for patients who have rapid ventricular rates despite maximum medical therapy and often yields remarkable symptomatic relief.
There is growing concern about the negative effects of long-term RV pacing.
Biventricular pacing, on the other hand, may overcome many of the adverse hemodynamic effects associated with RV pacing and is preferred when systolic dysfunction is present.
Catheter ablation of the AV node should not be attempted without a prior trial of medication to control the rate.
75
Knight, et al, Practical Rate and Rhythm Management of Atrial Fibrillation, January 2010 ed. with modifications.
Rate Control AgentsRate Control Agents
Calcium Channel blockers-non-dihydropyridine agents
IV diltiazem-initial dose 10 mg IV over 2 minutes
Can increase dose to 20mg IV if needed
Maintenance diltiazem 30mg PO q6hrs (short acting) or can transition to total long acting diltiazem
Can also use 10mg IVP q6 hrs prn
Start PO dose at same time as IV dosing, so PO can kick in by time IV dosing wears off
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Rate Control Agents
Beta blockers Metoprolol- Initial dose: 5mg IVP q5 minutes x3 doses and q6hrs
prn Maintenance Dose: 25 mg PO BID, can uptitrate to 100mg
PO BID max Start PO at same time as IV medication
Esmolol –Initial dose: 500mcg/kg IV over 1 min, can repeat in 5 minutes
Maintenance drip: 50-300 mcg/kg per min IV continuous infusion
Used only in ICU: Advantage: short duration of action, easy to titrate to
heart rate goal
Rate Control Agents
Digoxin can be used in acute setting but rarely as monotherapy Initial loading dose: 0.5mg IVthen 0.25mg IV in 6
hrs0.25 mg IV 6 hours afterMaintenance dose: 0.125mg daily POCaution in elderly patients and those with renal
failure TREAT-AF study-increased risk in mortality in elderly patients by >20% on digoxin
Indicated in patients with LVEF<30% (inotropic agent)
Rate Control Agents
Amiodarone- both a rate control and rhythm control agent Initial loading dose: 150 mg IV over 10 minutes,
then 1 mg/min x 6 hrs, then 0.5mg/min x18 hrsMaintenance dose: can change to oral 100mg-
200mg dailyCan promote cardioversion-so need to be on
anticoagulationPreferred agent in WPW to prevent AF impulses
down accessory pathway leading to promotion of VF
Rhythm Control
With AF Rhythm Control, timing is everything… AF Begets AF
AF causes changes in atrial electrophysiology that promote AF maintenance
AF causes changes in atrial electrophysiology that promote AF maintenance
Wijffels Circulation 1995; 92: 1954-68Wijffels Circulation 1995; 92: 1954-68
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Spontaneous Conversion of Patients with AF Scheduled for Electrical CardioversionAn ACUTE Trial Ancillary Study
Tejan-Sie J Am Coll Cardiol 2007;42:1638-1643
Conversion According to Duration of Pre-existing AF
Daily Conversion According to Strategy
Cardioversion: Forcing the issue.
Direct Current Cardioversion
Chemical Cardioversion
Some things to consider with DCCV
Anticoagulation and Cardioversion
• Afib < 48 hours:
– Cardioversion (CV)
– No anticoagulation indicated
• Afib > 48 hours:
– Anticoagulate for 3-4 weeks before CV
– OR get TEE
– Anticoagulate for 1 month after CV
DCCV
Atrial Fibrillation: DC Cardioversion
• Advantage- Highly effective
Disadvantage-
Risk of Thromboembolism (1-7%)
Requires conscious sedation
Arrhythmia (Sinus Arrest , Bradycardia - VF, VT)
Recurrence
• Complete shock failure and immediate recurrence – 25%
• Subacute recurrence in 2 wk – 25%
• 70% in NSR at 24 hour after cardioversion
• High chance of recurrences- old age, long duration of AF
DCCV
Atrial Fibrillation: DC Cardioversion
Method –
Synchronized DC shock- External
Biphasic preferred ( high success- 79-84%)
Monophasic- 100 J- 14% success
200 J- 39% success
360 J- 95% success
Initial 200 J is recommended with monophasic
100 J with biphasic [ Jogler et al, AJC 2000, 86: 348]
[ Mittal et al, Circ 2000, 101:1282]
[ Page et al , JACC 2002,39:1956]
Chemical Cardioversion
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Cardioversion with Amiodarone
AMIODARONE [ IIa] • Efficacy - 18-80%
• 150 mg IV bolus, 1mg/min for 6 hours then .5mg/min for 18 hours
• Tab Amiodarone 200 mg TDS x 1 wk 200 mg BD x 3 wk
• Efficacy–48.5%at 30 days vs placebo 0% - 82% if LA size < 45 mm
- 76 % if AF duration < 1 month[ Kochiadakis et al AJC 1999, 83: 58]
Cardioversion with Amiodarone
Ibutilide and Dofetilide
IBUTILIDE [CORVERT] Class III agent Efficacy-45-60% If f/b DC Cardioversion – 100% Only IV 1 mg bolus [ 0.01 mg/kg] Risk-TDP[1.7-4%] DOFETILIDE [TIKOSYN] Class III • Efficacy-30%
• Only oral 500 microgram BD • Risk-TDP
Flecainide
FLECAINIDE [ TAMBOCOR] – Class 1C
• Efficacy- 75-91% for recent onset AF
• Should be avoided in patients with underlying organic heart disease with LV dysfunction
• Dose – 200-300 mg PO-maintenance 50mg– 150mg BID
• Side effects- TDP, Reduce LV contractility, exacerbation of sinus node dysfunction
Propafenone
PROPAFENONE [ RYTHMOL] Class 1C Useful for recent onset AF Efficacy- 56-83% Dose- 600 mg PO - 1.5 – 2 mg/kg over 10-20 min Should be used cautiously or not at all in patients
with HF or severe COPD. Side effects- Atrial Flutter, VT, Hypotesion,
Bradycardia, Intraventricular conduction defects.
Electrical
More effective (90%)
Quick
One procedure with TEE
Cardioversion itself safe
Pharmacological
Works well for recent onset, for atrial flutter
Avoid sedation
Less expensive
Early maintenance enhanced by some drugs
Electrical vs Chemical
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Pill in the pocket approach
“PILL IN THE POCKET APPROACH” • A single oral bolus dose of propafenone or flecainide
(‘pill-in-the-pocket’) –terminate persistent AF outside the hospital if treatment was safe in hospital previously.
For selected patients without Sinus or AV node dysfunction, Bundle-branch block, QT interval prolongation, the Brugada syndrome, or
structural heart disease. Before antiarrhythmic medication is initiated, • A beta blocker or ccb should be given to prevent
rapid AV conduction in the event atrial flutter occurs.
Maintenance AAD’s
Maintenance of Sinus Rhythm in Specific Patient Populations
99
Maintenance of Sinus Rhythm
No (or minimal) Heart Disease
HypertensionCoronary Artery
DiseaseHeart Failure
FlecainidePropafenone
SotalolDronedarone
DofetilideSotalol
Dronedarone
AmiodaroneDofetilide
Substantial LVH
No Yes
Amiodarone
Dofetilide CatheterAblation
CatheterAblation
Amiodarone
CatheterAblation
AmiodaroneDronedarone
CatheterAblation
Amiodarone
Dofetilide
FlecainidePropafenone
SotalolDronedarone
Catheter
Ablation
Abbreviation: LVH, left ventricular hypertrophy. Modified from Fuster, V. et al. J. Am. Coll. Cardiol. 48, e149–e246 (2006).
Antiarrhythmic drugs
Antiarrhythmic Drugs to Maintain Sinus Rhythm
Recommendations COR LOEBefore initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended.
I C
The following antiarrhythmic drugs are recommended in patients with AF to maintain sinus rhythm, depending on underlying heart disease and comorbidities:
a. Amiodaroneb. Dofetilidec. Dronedaroned. Flecainidee. Propafenonef. Sotalol
I A
The risks of the antiarrhythmic drug, including proarrhythmia, should be considered before initiating therapy with each drug.
I C
Antiarrhythmic Drugs to Maintain Sinus Rhythm (cont’d)
Recommendations COR LOEBecause of its potential toxicities, amiodarone should only be used after consideration of risks and when other agents have failed or are contraindicated.
I C
A rhythm-control strategy with pharmacological therapy can be useful in patients with AF for the treatment of tachycardia-induced cardiomyopathy.
IIa C
It may be reasonable to continue current antiarrhythmic drug therapy in the setting of infrequent, well-tolerated recurrences of AF when the drug has reduced the frequency or symptoms of AF.
IIb C
Antiarrhythmic drugs for rhythm control should not be continued when AF becomes permanent,… III:
Harm
C
…including dronedarone.B
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Antiarrhythmic Drugs to Maintain Sinus Rhythm (cont’d)
Recommendations COR LOEDronedarone should not be used for treatment of AF in patients with New York Heart Association class III and IV HF or patients who have had an episode of decompensated HF in the past 4 weeks.
III: Harm B
Enough suppression, lets get rid of this thing: Catheter Ablation
It must be symptomatic Atrial Fibrillation
Paroxysmal Atrial fibrillation
Early Persistent Atrial fibrillation
Ablation compared with Medication
100
80
20
40
% P
atie
nts
Fre
e o
f Sy
mp
tom
atic
AF
2 4 6 8 10 12
Months
60 Amiodarone*
Sotalol**Propafenone**
Hx of Two Failed Drugs***
* Roy et al NEJM, 2000**Antman et.al., JACC 1990***Crijns et. al., AJC 1991
Ablation…
Ablation SitesMRA of LA
Multiple Foci from Multiple
Veins
Success ~ 70-80% paroxysmal~ 50-70% persistent
Radiofrequency - Fire
RadioFrequency Ablation – RFA
Vs.
Cryoablation
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Complications of RF ablation:
Systemic embolism/CVA (1-2%)
PV stenosis < 1-3%
Pericardial effusion/cardiac tamponade (1%)
Proarrhythmia (intra-atrial reentry tachycardia/left atrial flutter)
Atrial-esophageal fistula (very rare)
Need for multiple procedures (10 to 30%) to achieve clinical efficacy
CRYO- Ice
Complications of Cryo-ablation
Systemic embolism/CVA (1-2%) PV stenosis < 1-3% Pericardial effusion/cardiac tamponade
(1%) PN palsy 1-3% Atrial-esophageal fistula (very rare) Need for multiple procedures (10 to > 30%)
to achieve clinical efficacy
Surgical Ablation
Coronary Artery Disease
Valvular Heart Disease
Structural Heart Disease
More persistent AF
Atrial Fibrillation Ablation Outcomes
Paroyxsmal– 70-80% success at freedom from atrial fibrillation at one year off
anti-arrhythmic therapy.– 30% of patients required 2 procedures to achieve this result.– Most utilized pure-pulmonary vein isolation approach
Persistent– Similar success rates in persistent patients with similar end-point and
need for repeat procedure– More commonly requires substrate modification (targeting of CFAE)
and linear ablation Long-Standing Persistent
– Utilizing stepwise approach (PV isolation Linear ablation CFAE), some studies have demonstrated 70-80% freedom from atrial fibrillation at one year off anti-arrhythmic therapy
Calkins et al. HeartRhythm 2007; HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation; 4: 1-46
Atrial Fibrillation Ablation Outcomes Randomized Trials:
– Paroxysmal Atrial Fibrillation (Flecainide or Sotalol vs Ablation)
One year freedom from atrial fibrillation (AF)
37% freedom from AF in anti-arrhythmic arm
87% freedom from AF in ablation arm
– Persistent Atrial Fibrillation (Ablation vs. Cardioversion)
One year freedom from AF or atrial flutter
74% freedom from AF in ablation arm
58% freedom from AF in cardioversion arm
Calkins et al. HeartRhythm 2007; HRS/EHRA/ECAS Expert Consensus Statement on Catheter and Surgical Ablation of Atrial Fibrillation; 4: 1-46
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Atrial Fibrillation Ablation Outcomes
Randomized Trials:– Paroxysmal or Persistent Atrial Fibrillation
One year freedom from AF (ablation vs. anti-arrhythmic (AA) drug)
9% freedom from AF in the AA arm
56% freedom from AF in the ablation arm– Paroxysmal Atrial Fibrillation
One year freedom from AF (ablation vs anti-arrhythmic (AA) drug)
22% freedom from AF in AA arm
86% freedom from AF in ablation arm
Stabile et al. European Heart Journal 2006; 27: 216-221
Atrial Fibrillation Ablation Outcomes
Paroxysmal Atrial Fibrillation
– One year freedom from AF (ablation vs anti-arrhythmic (AA) drug)
– 22% freedom from AF in AA arm
– 86% freedom from AF in ablation arm
Paroxysmal and Persistent Atrial Fibrillation
– One year freedom from AF (ablation vs. anti-arrhythmic (AA) drug)
– 7% freedom from AF in AA arm
– 75% freedom from AF in ablation arm
– 63% of AA treated patients crossed over
Stabile et al. European Heart Journal 2006; 27: 216-221
Final Summary for AF Ablation Identifying appropriate ablation candidates
Failing medical therapy Refusing medical therapy Need for symptoms Young patients
Differences in approach for paroxysmal and persistent patients Lesion set Utility of isuprel post ablation Likelihood of recurrence / need for additional procedures (see Cappato,
Circulation, AF registry outcomes paper) Definition of success / likelihood of success Managing atypical flutter / need for confirmation of block across lines
Surgical based ablation Relative efficacy vs. catheter based Rationale / benefit of appendage ligation / resection Cox III – the “gold standard” Efficacy of other lesion sets, modalities (bipolar RF, cryo, HIFU) vs. Cox
Bottom Line
Surgical Reduction in Stroke
Left Atrial Appendage Occlusion
High Stroke risk and high bleed risk
Watchman Device
Atri-Clip
Usually with other surgery, but not always
Surgical procedure vs catheter based procedure
Longer recovery
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Questions?