Download A6 Chronic AA

Chronic Atrial Arrhythmias
Objectives - 3
1. Summarize pathophysiologic mechanisms underlying normal heart conduction and major atrial
arrhythmias
2. Describe major atrial arrhythmia sign and symptom complex
3. Characterize each class of antiarrhythmic drug according to effects on ion channels
4. Discuss the decision to anticoagulant in atrial fibrillation using CVA prediction tools
5. Highlight rate and rhythm control strategies in atrial fibrillation
6. Outline pharmacotherapy for each of the following arrhythmias: paroxysmal supraventricular
tachycardia (PSVT) and atrial fibrillation/flutter (treated the same with the majority of the data
discussing AFib)
Action Potential - 4
Normal occurrence of Atria and Ventricular cardiac
myocytes
• Phase 0 – rapid depolarization – Na+ rushes into the cell
• Na+ in
• Phase 1 – initial repolarization – Ca++ rushes into the cell
and K+ rushes out initiating the plateau phase
• K+ out
• Phase 2 – plateau phase – Ca++ continues rushing into the
cell and K+ moves out of the cell the membrane potential stays positive and calcium will bind with actin
and myosin causing a contraction in the atrial or ventricular myocytes
• K+ out and Ca++ in
• Phase 3 – repolarization – K+ moves out making the cell more negative leading to a resting membrane
potential or phase 4
• K+ out
• Phase 4 – Resting membrane potential – is where the action potential starts. Na+ slowly leaks into
the cardiac myocyte and the K+ channels slowly close causing the membrane potential to become more
positive. Once the action potential reaches -70 mV a quick depolarization occurs which initiates phase 0
• K+ out and Na+ in
The action potential of the SA and AV nodes (less Na+ and more Ca++)
• Phase 0 – Slow depolarization
• Ca++ in
• Phase 3 – Repolarization
• K+ out (more negative)
• Phase 4 – Spontaneous depolarization – starts again in phase 4 with
the resting membrane potential. Cells within the SA /AV nodes have
automaticity which is spontaneous depolarization at a particular rate.
Without the SA node having a connection to the brain (sympathetic or
parasympathetic nervous system) there would be spontaneous depolarization of ~100 bpm. The
parasympathetic nervous system normally slows the heart rate down to a normal HR of 60 - 70 bpm.
Na+ slowly leaks into the cell, and T type Ca++ channels open making the cell more positive. As the
action potential approaches -50 mV the L type Ca++ channels open until a threshold of -30mV is
causing a spontaneous depolarization.
• Na+ in and Ca++ in
Depolarization = change in a cell's membrane potential, making it more positive, or less negative
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Normal Cardiac Conduction - 6
• Normal Cardiac conduction is transition from the sinus node to the Atrial muscle then to the AV node
then to the common bundle which splits into the right and left bundle branch leading to the Purkinje
fibers and out to the ventricular muscles.
Electrocardiogram (ECG) - 7
• P wave – atrial depolarization
• QRS complex – ventricular depolarization (atrial repolarization is
buried within the QRS complex and is unseen)
• T wave – ventricular repolarization
• PR interval – start of the P wave to the start of the Q wave
(prolongation here would result in a 1st degree heart block)
• QT interval – start of the Q wave to the end of the T wave which
represents ventricular contraction and relaxation. This varies based
on heart rate and must be corrected (QTc)
• Corrected QT (QTc) = QT Interval / √RR interval
- RR interval = 60/HR – this method helpful if patient is in irregular rhythm
12-Lead Electrocardiogram - 8
• The strip on the bottom (V5) is the best way to assess HR
• Each large block counted between each QRS complex assesses HR (e.g. 4 blocks btw QRS
300/4=75bpm OR count the number of QRS x 6 = 78
Arrhythmia Classification - 9
Normal sinus rhythm (NSR):
• HR between 60 and 100 bpm
• P waves are associated with each QRS
• Sinus bradycardia is < 60 bpm
• Sinus Tachycardia
• HR > 100 bpm (narrow QRS)
• P waves are associated at regular intervals with the QRS
• The narrow QRS is suggesting the electrical signal is coming from the atrial arrhythmias
• Paroxysmal Supraventricular Tachycardia (PSVT)
• HR > 100 bpm
• P waves are closer to the QRS interval which shows
origination other than the SA node
• Atrial fibrillation – also classified as:
• rapid ventricular rate (rvr) – HR > 100
• Controlled ventricular rate (cvr) – HR 60-100
• slow ventricular rate (svr) – HR < 60
★ This would be considered an irregularly irregular rhythm
• Atrial flutter
• Can also be classified as rvr, cvr and svr
★ Similar to A. Fib except for a sawtooth pattern associated
with the P waves
• The QRS complexes are fairly regular
Abnormal Cardiac Conduction (theories or functional models) - 11
• Increase Automaticity
• Remodeling (fibrosis) occurring within the atrial cardiac myocyte. This causes the slope of phase 4
to become more vertical increasing the depolarization rate possibly above the rate of the SA node.
Without this Parasympathetic inhibition heart rate can increase above 100 bpm
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Reentry
• A sinus impulse comes from the SA node through the atrium and continues to an area of fast
conduction OR slow conduction. This signal wants to go through the fast conduction pathway where
the refractory period is short. The signal could go through the slow pathway which has a longer
refractory period, but when it meets the slow conduction area it is blocked allowing delivery of the
signal only to the fast pathway. Premature electrical signals such as a PAC continue through this
dysfunctional fast pathway. If this pathway is refractory the signal will go through the slow pathway
meeting the fast pathway creating a reentry circuit sending fast signals down through the ventricles.
This creates a fast HR. This can occur anywhere within the heart that has remodeling (fibrosis)
Atrial Fibrillation (more theories)
• Focal activation with one area of increased automaticity sending inappropriate signals to the atria
creating atrial fibrillation. Catheter ablation could inhibit this activation.
• Remodeling of the atrium that allows for multiple foci are more difficult to treat with catheter
ablation. However, many of these inappropriate signals are sent from the pulmonary vein which may
be inhibited by catheter ablation.
Antiarrhythmic Agents 12
Vaughn-Williams classification
• Class I – block Na+ channels
• IA – moderate reduction in phase 0 slope; increase Action potential duration (APD), and increase
effective refractory Period (ERP)
- IA – Disopyramide, quinidine and procainamide (not commonly used anymore)
• IB – small reduction in phase 0 slope; reduce APD; decrease ERP
- IB – Lidocaine and mexiletine
• IC – pronounced reduction in phase 0 slope; no effect on APD or ERP
- IC – Flecainide and propafenone (most commonly used)
• Class II – β-blockers ( e.g. Metoprolol, atenolol, etc)
• Class III – (block K+ channels) Delay repolarization (phase 3) and thereby increase action potential
duration and effective refractory period.
• Dofetilide, amiodarone, dronedarone, sotalol, ibutilide (IV only for the electrical conversion only)
• Class IV – blocks calcium channels
• Verapamil and diltiazem (non-dihydropyridine CCBs)
• Miscellaneous
• Digoxin (used in combination e.g. Beta blockers or CCB to potentiate these agents), adenosine,
magnesium (adenosine and magnesium are IV only of treating arrhythmias)
Paroxysmal Supraventricular Tachycardia (PSVT) - 14
• Reentrant arrhythmia (creates a circuit that feeds on itself)
• Rhythm is regular, but p wave is often hidden in T wave
• Short, paroxysms are usually asymptomatic
• Symptoms associated with faster rates of longer duration
• Palpitations, dizziness, chest tightness or pain, SOB or anxiety (bolded items are most common)
PSVT - Management - 15
• Asymptomatic – Monitor
• Symptomatic - Treatment
• First-line treatments would include non-pharmacotherapy options of:
- Catheter Ablation of accessory pathway (cure in ~80% of patients)
- AV nodal ablation with pacemaker (this creates a third-degree heart block requiring a
pacemaker)
• Rate controlling anti-arrhythmics
• Beta-blockers or non-dihydropyridine CCBs
• Other anti-arrhythmics
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Class IC and Class III
Patient Case #1 (PSVT) - 16
• AA is a 68 yo male referred to cardiology for evaluation of recent episode of symptomatic PSVT
• Symptoms include: SOB, anxiety and palpitations. These episodes last approximately 60 minutes and
terminate spontaneously. Patient has tried both beta-blockers and nonDHP CCBs, but is intolerant due
to SOB, dizziness and hypotension.
• PMH: SVT, anxiety, insomnia, bronchiectasis (COPD), OSA and BPH
• Current medications
• ASA 81 mg daily, Digoxin 0.125 mg daily, Albuterol MDI 2 puffs prn, Symbicort 2 puffs bid,
Alprazolam 0.25 mg q6h prn, Citalopram 20 mg daily, Quetiapine 100 mg at bedtime for sleep,
Tamsulosin 0.4 mg at bedtime
• Bolded medications have associated with increasing QT interval, and albuterol could worsen
arrhythmia
Vitals: BP – 110/71 mm Hg, HR 72 bpm
Pertinent labs: SCr 2.0, K+ 4.8, CBC, thyroid and LFTs WNL
Diagnostic testing:
• EF greater than 55% and no valvular abnormalities or hypertrophy
• ECG (when symptomatic) – narrow complex tachycardia, long Refractory Period (RP), possible AV
nodal reentry tachycardia (AVNRT), AV reentry tachycardia (AVRT) or Atach
• ECG (now) – NSR, rare PACs, QRS 88 (narrow), QT/QTc 332 / 398 ms (normal)
Electrophysiology study (EP study):
• Inducible long RP tachycardia
• Unable to map tachycardia mechanism
• Suspect either atypical AVNRT versus Atach originating close to AV node
• Ablation not attempted due to proximity of slow pathway region to AV node.
Question 1: Based on past drug therapy history and EP study what would be a reasonable drug to treat
PSVT? Patient has failed beta blockers and NonDHP CCBs, and Catheter Ablation is also not indicated.
These are all class III or class IC antiarrhythmics and would be appropriate
• Sotalol (Class III), Dofetilide (Class III), Flecainide (Class IC), Amiodarone (Class III)
Question 2: What monitoring would be study, required for patient if he would be a reasonable drug to treat
PSVT?
• Sotalol – initiate within hospital, ECG after initiation, prolonged QTc, renal function, electrolytes, ECG
which monitors QT interval, changes in renal function.
• Dronedarone – potentially an option, not much strong randomize data in support use, and monitor
much like amiodarone.
Defining Atrial Fibrillation and Flutter - 19
Atrial fibrillation
• Loss of coordinated atrial activation (atria is quivering)
• Loss of atrial mechanical function
• ECG-replacement of P waves with fibrillatory waves
★ Considered Irregularly irregular
• Irregular and frequently rapid ventricular response
Atrial flutter
★ Saw-tooth pattern of regular atrial activation
• Reduced atrial function, but not entirely lost
• Commonly occurs with 2:1 AV block, resulting in a regular or irregular ventricular rate (most often 150
bpm)
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Causes of Atrial Fibrillation/Flutter - 20
Non-cardiovascular causes
• Acute/chronic alcohol ingestion
• Autonomic
• DM
• Genetic
• Obesity
• Pulmonary embolism
• Severe lung diseases
• Sleep apnea
• Thyroid disorders
• Others
Cardiovascular causes
• CAD
• HF
• HTN
• Valvular heart disease
• Others
Iatrogenic causes
• Beta-agonists
• Cardiac and non-cardiac surgery
• Others Intracardiac catheters
• Local anesthetics, caffeinated
beverages, other stimulants
• OTC cold remedies
Atrial fibrillation – consequences - 25
• Loss of atrial systolic function (atrial contribution to ventricular filling is lost)
• Irregular rapid ventricular contractions
• Cardiac output becomes reduced
• Abnormal blood flow and stasis in the atria which may cause the formation of intra-atrial
thrombus
STROKE Is the Most Common and Devastating Complication of Afib/flutter - 22
• All cause stroke rate with AF is 5% per year
• AF – is an independent risk factor for stroke
• ~5 fold increase in stroke risk
• ~15% of all strokes caused by AF
• Stroke risk increases with age
• Stroke risk persists whether systematic or asymptomatic AF
• A. Flutter stroke risk is not well characterized – risk likely between NSR and Afib
• These patients will be treated the same for stroke prevention
Clinical Presentation of Afib/flutter - 23
• AF presents with a wide range of symptoms which may include:
• Palpitations, dizziness, syncope, fatigue, dyspnea, chest pain, thromboembolism (STROKE), and
may result in death
• AF may also be asymptomatic
• Affect of asymptomatic AF has the potential for underlying electrical and structural damage to atrial
myocardium
• While AF symptoms alone may not always be severe, untreated disease can result in significant
morbidity and mortality
Stroke Risk in AF: CHADS2 Score - 24
• The easiest way to evaluated patient for treatment with aspirin OR oral anticoagulant is to use the
CHADS2 score.
• Each letter is associated with a point or points, and adding these gives the patient an estimated stroke
risk
• A patient with a score of 6 is at very high risk of stroke.
CHA2DS2-VASc - 26
Recommended Anticoagulation Therapy: CHADS2 or CHA2DS2-VASc
This newer scoring system is used in the lower risk population which allows for more appropriate risk
stratification
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0 Low Risk: Aspirin 81 to 325 mg daily
1 Moderate Risk: Aspirin or oral anticoagulant (OAC)
≥ 2 Moderate or High Risk: OAC unless contraindicated
Available oral anticoagulants (OACs)
• ASA 81 to 325 mg daily
• Warfarin with goal INR 2.5 (range 2.0 to 3.0)
• Dabigatran 150 mg bid
• Rivaroxaban 15 or 20 mg daily
• Apixaban…available soon!
★ Patients with any history of renal dysfunction or chronic
kidney disease (CKD) should stay away from newer agents,
and rely upon warfarin only.
The Chronic Progressive Nature of Untreated Afib/flutter May
Explain the Need for Early Intervention
The AF Continuum of Disease - 28
• Paroxysmal AF – is AF episodes ≤ 7 days and then spontaneously terminates
• Persistent AF – AF episodes > 7 days with no spontaneous termination
• Permanent AF – AF that cannot be converted to sinus rhythm (SR)
New Goals of AF Management - 29
• Comprehensive management of AF should address its
multiple impacts
• Along with stroke prevention and reduction of AF
burden successful management of AF should also aim at
further Reducing hospitalizations and Costs, as well as
CV morbidity and mortality
Case 2: New Onset Afib - 30
• AC is a 51 yo WF with a PMH of HTN, hypothyroidism,
s/p hysterectomy 5 years ago, and vasomotor symptoms
associated with menopause. She has been having mild
palpitations about once or twice a month for 3 months. On
PCP evaluation today, it is noted she is in afib with a cvr. BP 136/85 mm Hg, HR 78, weight 63 kg and
height 5’7”
• Medications: Chlorthalidone 25 mg daily, levothyroxine 0.88 mg qam, Cenestin 0.3 mg daily
• Labs: SCr 0.9 mg/dl, K+ 4.3 mmol/l, TSH 2.8, free T4 1.5, FBG 78 mg/dl, LFTs WNL, LDL 93 mg/dl,
HDL 52 mg/dl, TGs 112 mg/dl
Anticoagulation
CHADS2 = 1 – because of history of hypertension
CHA2DS2-VASc = 2 – because she also is a female, and treatment here would lean more to an oral
anticoagulant. The new agents can be considered in this patient because of her good renal function.
Options
ASA – 81 or 325 mg would be questionable because her CHA2DS2-VASc = 2
Warfarin, Dabigatran, Rivaroxaban, Apixiban
Rate versus Rhythm
• Patient mostly asymptomatic
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Unknown duration of afib
Consider echocardiogram to assess ejection fraction and to observe if patient has a thrombus formed
Could consider either rate or rhythm control
Patient preference?
In most patients rhythm control is not initiated at first, because an antiarrhythmic could dislodge an unseen
clot causing a stroke. Initially we would start this patient on rate control and anticoagulant
Rate options
• Metoprolol tartrate 25 mg bid
• Diltiazem ER 120 mg daily
Major Trials Comparing Rhythm Versus Rate Strategy - 32
Major trials include: such as
• AFFIRM, RACE, PIAF, STAF, HOT CAFE, AF-CHF
Major overall findings
★ Rhythm-control strategy not superior to rate-control strategy
• Rhythm control strategy has more adverse effects from the
medications and more hospitalizations due to cardioversion, etc.
• Therapy based on each patient’s symptoms and disease
• E.g. Patient has AFib and is symptomatic after control of the ventricular rate then rhythm control
strategy may be appropriate
• Management options for AF include rate control, stroke prevention, and maintenance of NSR
• Maintain good quality of life
Goals of Rate Control - 34
Outcomes
• Reduce symptomatic palpitations
• Improve ventricular performance, exercise capacity, hemodynamics
• Prevent (reverse) tachycardia-related cardiomyopathy
Ventricular rate goals
• 60-80 bpm at rest or > 20% decrease from baseline with symptom relief
• 90-115 bpm with exercise
Rate Control - 35
• HFrEF – avoid non-DHP CCBs; start low, go slow with β-blockers
• Digoxin does not prevent activity related increases HR, useful in sedentary patients and in HFrEF
• Digoxin + β-blocker is a useful combination IF additional HR control needed
RACE II: Rate Control Efficacy in Permanent Atrial Fibrillation - 36
• This study answer the question should we use strict rate control or lenient rate control
• With strict rate control there was an increase (though not significant) in the primary outcome
★ In a patient that is asymptomatic one may consider a lenient rate control strategy
Goals of Rhythm Control - 37
• Restore NSR – cardiovert patient either electrically or chemically
• Maintain NSR, prevent recurrence of AF – with antiarrhythmic therapy
• Reduce frequency of AF episodes, suppress symptoms, improve tolerability of recurrence, improve
exercise capacity, hemodynamics
• Prevent (reverse) tachycardia-related cardiomyopathy
• Limit drug toxicity
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Cardioversion - 38
Indications
• Hemodynamic compromise, HF, worsening angina → immediate cardioversion
• Symptomatic, persistent AF → elective cardioversion
Electrical versus chemical
• Electrical
• Pros – more effective than pharmacological
• Cons – requires conscious sedation/general anesthesia
• Chemical
• Pros – effective if conversion attempted within 7 days, more so if < 48 hours, convenient
• Cons – drug toxicity (e.g. Proarrhythmia with ibutilide), delayed onset
Do we need to anticoagulate with cardioversion? - 39
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YES, (due to stunning of the myocardium) if duration of AF unknown or > 48 hours and …
Hemodynamically stable – anticoagulate with warfarin (INR 2.0-3.0) for 3 weeks before and at least 4
weeks after cardioversion, control rate in the interim
• Transesophageal echocardiogram (TEE) guided approach
1. Perform TEE before cardioversion to detect thrombus – alternative to warfarin pretreatment
2. If no thrombus give heparin followed by warfarin, if thrombus present give warfarin as usual
Hemodynamically unstable – administer heparin bolus and infusion, proceed with cardioversion,
initiate oral anticoagulation (INR 2.0-3.0) and continue for at least 4 weeks after cardioversion
Typically, oral anticoagulation is continued for life after cardioversion unless contraindicated
2011 ACCF/AHA/HRS Guidelines - 40
Antiarrhythmic Approaches to Maintain SR in Patients with Recurrent PAF or Persistent AF
• No heart disease – most often used is flecainide or propafenone
• HTN – with LVH amiodarone is the best choice – without LVH flecainide or propafenone, then the
first-line therapy is not effective catheter ablation is most common
• CAD – sotalol / dronedarone is most commonly used if not effective use catheter ablation
• HF – amiodarone or dofetilide is he evidence-based choice, then if ineffective catheter ablation
Case 2: New Onset Afib - 41
• AC is a 51 yo WF with a PMH of HTN, hypothyroidism, s/p hysterectomy 5 years ago, and vasomotor
symptoms associated with menopause. She has been having mild palpitations about once or twice a
8
month for 3 months. On PCP evaluation today, it is noted she is in afib with a cvr. BP 136/85 mm Hg,
HR 78, weight 63 kg and height 5’7”
• Echocardiogram: EF > 55%, no valvular abnormalities, mild diastolic dysfunction, no LVH
• What would be the best AAD option for maintenance of NSR?
• Amiodarone or Dronedarone
• Propafenone
• Sotalol
Rhythm Control - 42
Flecainide (200-300 mg/d) and propafenone (450-900 mg/d)
• Well tolerated, low incidence of organ toxicity, and low incidence of proarrhythmia in ABSENCE of
structural heart disease
• AVOID in patients with LVH, CAD, or HFrEF
• Propafenone has β-blocking activity
• ADRs: 1:1 conduction in AFlutter (block AV-node with β-blocker or CCB), dizziness, headache, blurred
vision, worsen HF status)
• Flecainide – tremor
• Propafenone – bradycardia, heart block, taste disturbances
Amiodarone (dose titration may vary, e.g. LOAD because of long half-life 400 mg tid x 1 week 400 bid x 1
week 400 mg x 1 month, then 200 mg daily)
• Also controls rate
• Most effective AAD (however, only 30% effective)
• Effective maintenance agent but significant extracardiac toxicity, 1 in 6 patients discontinue
• Requires close monitoring because of many toxicities
• Many DIs (warfarin, digoxin, simvastatin, QT prolonging medications)
• Many AEs
Sotalol (80-320 mg/d)
• β-blocking properties
• AVOID in patients with HFrEF, severe renal dysfunction
• DIs: QT prolonging medications
• AEs: bradycardia, bronchospasm, worsening HF, hypotension
• Must be admitted to hospital to start this medication
Dofetilide (125 to 500 mcg bid)
• Less chronic organ toxicity than amiodarone
• AVOID in patients with severe renal dysfunction
• DIs: QT prolonging medications, inhibitors of renal cationic secretion
• Patients must be admitted to initiate
• MDs (and institution) must be certified to prescribe
Case 3: Rate versus Rhythm - 45
• AC is a 52 yo WF with a PMH of Afib, HTN, hypothyroidism, s/p hysterectomy 5 years ago, and
vasomotor symptoms associated with menopause. She has been on rate control and properly
anticoagulated for over 1 year. Over the last 2 months, she has had multiple admissions for SOB at rest
due to Afib. Rate are well controlled at rest and exercise. BP 112/62 mm Hg, HR 61, weight 66 kg and
height 5’7”
• Echocardiogram: EF < 20%, no valvular abnormalities, diastolic dysfunction cannot be evaluated, LA
4.3 cm, mild concentric LVH.
• Current medications: same as prior and metoprolol tartrate 50 mg bid and digoxin 0.125 mg daily
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Labs: SCr 1.1 mg/dl, K+ 4.1 mmol/l, TSH 3.9, free T4 1.45, FBG 96 mg/dl, LFTs WNL, LDL 86
mg/dl, HDL 51 mg/dl, TGs 128 mg/dl
What would be the best AAD option for maintenance of NSR?
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FIRST make sure patient is anticoagulated on warfarin or other oral anticoagulant
• Flecainide
• Dronedarone – NO because of worsening heart failure
• Amiodarone – now best option because HF with reduced ejection fraction
• Dofetilide – another good option because of HR with reduced ejection fraction. This drug is eliminated
through active secretion and may compete with a thiazide diuretic (may choose to eliminate
chlorthalidone)
Dronedarone - 46
• Multi-channel blocker
• Class I-IV Vaughan-Williams properties
• Dronedarone is an amiodarone analog
• Iodine removed to improve thyroid and possibly pulmonary safety
• Approved by the FDA in July 2009 to Reduce the risk of CV hospitalization in patients with
paroxysmal or persistent AF or AFL, with a recent episode of AF/AFL, and 1 or more associated CV
risk factors which include:
• Age >70, HTN, Diabetes, Prior CVA, LA diameter 50 mm or LVEF < 40%
• Treat patients who are in SR, or who will be cardioverted
• Contraindicated in class IV HF or lesser HF with recent decompensation
Dronedarone Safety - 48
• Safety profile of dronedarone has been established in > 6700 patients
• Low risk of extracardiac toxicities (<0.1%) (thyroid, pulmonary, dermatologic)
• Low risk of proarrhythmia (<0.1%)
• Most frequently reported adverse events
• Bradycardia, hypotension and worsening HF
• Serum creatinine increase without indications of renal toxicity (4% vs 1% for placebo)
• Rare cases of serious hepatotoxicity were reported in 2010 within 6 months of beginning therapy,
two required transplantation. MONITOR LFTs 1, 3, and q6 months with ECG
•
PALLAS study results showed a two-fold increase in death, and two-fold increases in stroke and
hospitalization for heart failure. These were patients with PERMANENT atrial fibrillation (i.e. Not
paroxysmal or persistent).
Dronedarone should not be prescribed for patients with permanent AF (atrial fibrillation). Healthcare
professionals are advised to monitor patients regularly (at least every six months) to ensure that they
remain within the approved indication and do not progress to permanent AF or new or worsening heart
failure.
Non-pharmacologic Therapy - 50
•
Catheter ablation
• RF is applied to isolate the PV (PVI)
• More successful than AADs
• Complications: catheter-site bleeding, CVA, MI, puncture, PV sclerosis
Maze procedure
• PVI and LAA removal
• Done in conjunction with CT surgery (e.g. Valve repair/replacement, CABG)
AV nodal ablation with pacemaker
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Induce complete heart block
Pace with a DC or BiVentricular PM
Key Points - 51
• EP study with catheter ablation is treatment of choice for symptomatic PSVT
• All patients with Afib/flutter need drugs to prevent stroke aspirin or OAC depending on estimated risk
• Rate and rhythm control strategies are both appropriate ways to manage Afib/flutter, the approach will
be patient-specific
• Selecting drug therapy in Afib/flutter depends patient characteristics and risk for toxicity
• Non-pharmacologic treatment options exist and are often considered when at least one drug therapy
option has failed.
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