NO SKIPPED BEATZ: A PRACTICAL REVIEW OF THE ANTI-ARRHYTHMIX. feat. Lance Ray, Pharm.D., BCPS
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1 NO SKIPPED BEATZ: A PRACTICAL REVIEW OF THE ANTI-ARRHYTHMIX feat. Lance Ray, Pharm.D., BCPS
2 Learning Objectives No Skipped Beatz: A Practical Review of Anti-arrhythmix Get Rhythm: The Anti-arrhythmic Remix (A Practical Review of Therapeutics) Get Rhythm: The Anti-arrhythmic Remix (A Practical Review of Therapeutics) Learning Objectives: (Pharmacists) 1. Summarize the pathophysiology of arrhythmias and describe how different antiarrythmic drug classes aim to control these rhythm disturbances 2. Describe various acute and long-term evidence-based approaches to therapy for atrial fibrillation 3. Identify various treatment strategies for other common supraventricular-, ventricular-, and brady-arrhythmias Learning Objectives: (Technicians) 1. Identify the common uses for anti-arrhythmic drugs while reviewing basic arrhythmia pathophysiology 2. Describe the concept of rate versus rhythm control in atrial fibrillation 3. Identify scenarios when electrical cardioversion are indicated for normal rhythm restoration ACPE description: We will briefly review the pathophysiology of common arrhythmias and how various agents aim to control them both in the acute and long-term setting. Landmark-trials and adverse effects will be profiled for common drugs. Bio: For the past nine years Lance has worked at Texas Health Harris Methodist Fort Worth as clinical-staff pharmacist then Emergency Department Pharmacist and Investigational Drug Pharmacist. He is adjunct assistant professor of pharmacotherapy at UNT College of Pharmacy and currently Treasurer for TSHP. He has just recently moved to Colorado and is at the moment missing out on skiing a fantastic powder day in the mountains to talk about anti-arrhythmics in Arlington.
3 Informal notes A practical approach to treatment of arrhythmia Learning arrhythmias and anti-arrhythmic drugs can suck Where the rubber meets the road So many slides - which slides are high-impact?
4 Review Nerve conduction SA node Atrial pacemaker AV node delay switch to allow ventricular filling. Speed bump Only [correct] pathway to conduct to ventricles Bundle of His and Purkinje system (branches) Muscle contraction unique cells (automaticity) Refractory period Important for impulse termination vicious loop if absent
5 Why do arrhythmias occur? Answer: Ion channel conduction disturbance Myocardial infarction (MI) Ischemia myocardial scarring Cardiovascular disease Ventricular hypertrophy Hypertension RAAS activation Genetic mutation/ polymorphism Increased sympathetic tone Hyperthyroidism Exercise Metabolic disturbances Diabetes Obesity Oxidative stress Age Smoking Alcohol use Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e. 2011
6 Case # 1 A 25 year-old male with no comorbidities presents to the ED with heart palpitations that began this morning and is determined to be in new onset atrial fibrillation. He has SOB. What is the preferred treatment strategy for this patient? Cardioversion Nothing Oral diltiazem Begin amiodarone for chemical cardioversion
7 Arrhythmias Asymptomatic Incidental finding Life-threatening Emergency Anti-arrhythmic drugs can be pro-arrhythmic
8 Concept of Re-entry Indefinite loop of impulse conduction Usually triggered by a critically timed premature beat (PAC or PVC) it s all about timing Can occur anywhere in the cardiac conduction system Atrium AF (multiple foci), Atrial flutter (one focus) Ventricle VT AV node AVNRT PSVT AF re-entry impulse excites surrounding tissue and AV node at a rate greater than the SA node VT re-entry impulse excites ventricle faster at greater rate than AV node dose So re-entrant arrhythmias are tachyarrhythmias
9 Re-entry Ventricular Re-entry We need to either - SLOW CONDUCTION Velocity (to a point that impulse dies out) or - PROLONG REFRACTORINESS (to block impulse) All anti-arrhythmic drugs do one or both of these Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
10 I Slows conduction II III Prolongs refractory period IV
11 I Slows conduction II III Prolongs refractory period IV Ca++
12 simplified Pacemaker action potential (SA, AV node) Slower conduction velocity Long refractory period Relies on Ca++ for initial depol. Ca++ All other cardiac cells His-purkinje nerves Myocardial cells Atria Ventricles Rely on Na+ for initial depol. Na+
13 Conduction abnormalities QRS complex Narrow (<120ms) Wide (>120ms) Tachyarrhythmias Supraventricular Sinus tachycardia enhanced automaticity of pacemakers and other cells. Re-entrant tachycardia Atrial fibrillation and Atrial flutter PSVT» AV nodal re-entrant tachycardia (AVNRT) (often referred to as SVT )» AV re-entrant tachycardia (AVRT) Wolff-Parkinson-White Syndrome (WPW) Ventricular VT VF Bradyarrhythmias Sinus bradycardia AV block
14 Clinical overview of ANTI-ARRHYTHMIC DRUGS (AADs)
15 Case #2 Which antiarrhythmic medication has the most systemic toxicities? Amiodarone Procainamide Sotalol Dofetilide
16 Clinical History 1950s lidocaine, quinidine 1980s surge of new anti-arrhythmic drugs (AAD) 1990s and on general decline in use Declined use for two reasons: 1. Toxicities with AADs (drug-interactions, proarrythmic!) 2. Technical advances in non-pharmacological therapy Catheter ablation of re-entry loops (Afib, Aflutter) Implantable cardioverter-defibrillators (ICD) for VT/VF
17 Classification of Antiarrhythmics Vaughn Williams Most frequently used classification system Limitations multiple mechanisms may exist for a drug/class Does not incorporate clinical indication (AF, VT) makes difficult to summarize classes Class Pharmacologic MOA Clinical MOA notes I Na + channel block Rhythm Class Ia, Ib, Ic II β-block Rate All B-blockers III K + channel block Rhythm Multiple MOAs IV Ca ++ channel block Rate Non-DHP CCB V Digoxin / adenosine ~rate / other Drugs not related
18 Rhythm vs. Rate Control Class I and III primarily rhythm control One of two mechanisms to overcome re-entry 1. prolong refractoriness (abolishing reentry possibility) 2. slow conduction (by the time re-entry is about to occur, new impulse has propagated from pacemaker (SA/AV node) Class II and IV primarily rate control Slow automaticity of pacemaker cells (SA, AV) blocks Calcium directly (CCB) or indirectly (β-blocker)
19 Class I AADs Ia Ib Ic Quinidine (PO) Disopryamide (PO) Procainamide (IV) Lidocaine (IV) Mexilitine (PO) Flecainide (PO) Propafenone (PO) CCV = chemical cardioversion SR = sinus rythm Clinical use/comments: - Supraventricular and ventricular arrhythmias - Little use of oral agents - Procainamide for immediate AF CCV - Limited to life-threatening ventricular arrhythmias - Mimics Ia agents in diseased tissue ( ph, hypoxia) - Most potent Na + blocking effects - First-line agents within Class I for Maintenance of SR for AF/AFlutter - Or life-threatening refractory ventricular arrhythmias AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
20 Class I ADRs Ia Ib Ic Quinidine (PO) Procainamide (IV) Disopryamide (PO) Lidocaine (IV) Mexilitine (PO) Flecainide (PO) Propafenone (PO) Major Individual ADRs Hemolytic anemia, GI upset Hypotension Anti-cholinergic symptoms (Vagolytic effect = HR) Acute liver injury, Bronchospasm, AV block Class effect QTc, TdP, Heart failure, ventricular arrhythmias Dizziness, sedation, confusion, blurred vision Dizziness, Heart failure, Ventricular arrhythmia Contraindicated in SHD CYP 2D6 substrates SDH = Structural Heart Disease AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
21 Summary of Class I AAD Use has greatly declined No new FDA approvals for class in 20 years Many patients do not tolerate and must discontinue therapy ( 20 30%) Most pro-arrhythmic of all Vaughan Williams Classes (limits use to younger/healthier patients) Class Ia additional K + -channel blocking TdP Class Ic potent conduction slowing
22 Class II Block B 1 -adrenergic receptors in heart decrease adrenergic tone primarily in SA/AV nodes conduction velocity, ERP, automaticity Clinical use: Most useful in slowing ventricular response AFib = RATE control Additional long-term anti-arrhythmic properties possible effects on electrical conduction use post-mi to prevent sudden cardiac death used in CHF to prevent cardiac remodeling
23 Acute rate control Which beta-blockers? virtually any Esmolol or Metoprolol available IV Chronic rate control (PO) Metoprolol Carvedilol (with HF) Atenolol Propranolol (non-selective and lipophilic) toxicity Most commonly used
24 Class III Amiodarone Sotalol Clinical use Most (?best) evidence in AF rhythm control IV is first line agent in acute VT/VF Supraventricular OR ventricular Dronedarone Ibutilide (IV) Dofetilide (PO) Only approved for supraventricular arrhythmias Used for acute chemical cardioversion AF/Atrial flutter sinus rhythm Dofetilide long term to maintain SR
25 Amiodarone is unique most commonly used AAD Displays actions of ALL Classes (I, II, III and IV) Predominantly class III Non-selective β-blocking, Ca ++ blocking effects Low-proarrhythmic effect IV therapy (acute indications for ACLS VT / VF) 150mg bolus IV, then 1mg/min x 6h, then 0.5mg/min x 18h slow onset with PO: loading regimen 400mg BID TID x 5 14 days, then mg daily Long half-life 60 days Adverse effects Drug interactions Inhibits MOST CYPs ACLS = Advanced Cardiac Life Support
26 Amiodarone - ADRs Associated with chronic therapy and cumulative doses Close monitoring Adverse Effect Monitoring Treatment Hyper/hypothyroidism (2 30%) Pulmonary fibrosis ( risk w/ cumulative dose) Routine thyroid function tests Annual CXR Thyroid/anti-thyroid supplement or DC DC therapy LFT abnormalities (15 25%) transient Routine LFTs Lower dose/dc Optic neuropathy (1 2%) Routine eye exams DC therapy Photosensitivity (25 75%) Use sun-block Preventative Blue-gray skin discoloration (1-3%) DC therapy TdP (<1%), bradycardia, hypotension Routine ECGs Dose adjustment Q J Med 2011; 104: Am J Med ;706 Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
27 Amiodarone Drug-Drug Interactions P-glycoprotein (P-gp) inhibitor Can increase digoxin levels by 2x Empirically reduce digoxin by 50% Inhibitor of CYP2C9, 2C19, 3A4, 2D6 warfarin (can elevate levels 0 200%) Empirically reduce warfarin dose by 30%
28 Dronedarone: Amiodarone without Iodine Dronedarone (Multaq ) (FDA approved in 2009) paroxysmal or persistent AF Similar properties (all 4 class effects) Non-iodinated Less organ toxicity than amiodarone Methylsulfonyl addition less lipophilic Only PO available Increased mortality in heart failure patients vs placebo Black Box Warning: NHYA Class IV or II-III w/ recent decompensation ANDROMEDA Study - NEJM 2008; 358: Dronedarone vs amiodarone Dronedarone less effective for rhythm control in AF than amiodarone Less adverse effects and less all-cause mortality than amiodarone $$$ J Am Coll Cardiol. 2009;54(12):
29 Dronedarone (Multaq ) CYP450 2D6 and 3A4 inhibitor Citalopram and TCAs are contraindicated Many other drugs: use caution P-gp inhibitor dronedarone increases levels of digoxin, rivaroxaban, dabigatran
30 Sotalol Non-selective B-Blocker with K + -blocking properties (Class II and III) Clinical use: Maintain sinus rhythm in AF As effective as Class I agents but less toxicity In general less effective than amiodarone but also less toxicity As effective as amiodarone in patients with ischemic heart disease/cad Avoid in HF Niche use long-term rhythm control pts w underlying CAD Clinical use: recurrent or sustained VT SAFE-T Investigators. N Engl J Med 2005;352: AFFIRM Investigators. N Eng J Med 2002;347: Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
31 Sotalol ADRs: Generally well-tolerated (<15% discontinue due to ADRs) Fatigue, bradycardia, dyspnea, dizziness, Possibility of TdP, initiation in-hospital preferred Renally eliminated Must be renally adjusted No CYP450-mediated drug interactions Black Box warning - QTc Betapace AF renal adjustments CrCl >60 ml/min: Give q12hr CrCl ml/min: Give once daily CrCl <40 ml/min: Contraindicated Formulations of sotalol Can be used for ventricular tachycardias Betapace AF (specifically indicated for AF) Same drug better labeling (?)
32 AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Pharmacotherapy: A Pathophysiologic Approach. 9 th ed. Less commonly used Class III Ibutilide (Corvert ) - IV One-time dose for immediate chemical cardioversion (CCV) When DCC not appropriate (C/I to anesthesia or refractory AF) acute onset AF, no comorbidities Dofetilide (Tikosyn ) - PO Oral CCV Must be initiated in hospital (minimum 3 days) Renally eliminated Highest risk of TdP since pure K+ channel blockade Eliminate other risk factors for TdP before therapy Correct low serum [Mg++] and [K+] ensure baseline QTc < 440 ms
33 Dofetilide (Tikosyn ) Black Box warning: To minimize the risk of induced arrhythmia, patients initiated or re-initiated on TIKOSYN should be placed for a minimum of 3 days in a facility that can provide calculations of creatinine clearance, continuous electrocardiographic monitoring, and cardiac resuscitation. TIKOSYN is available only to hospitals and prescribers who have received appropriate TIKOSYN dosing and treatment initiation education. Safe for patients with structural heart disease DIAMOND Study 59% conversion rate vs 34% in placebo 79% kept in SR at one year vs 42% placebo TdP occurrence of up to 3% (majority in first 3 days) 125mg 500mg PO q12h Titration algorithm Circulation. 2001; 104: Tikosyn package insert. 3/2015
34 Dofetilide initiation algorithm * Determine baseline QTc ( 440 ms) Eliminate drug interactions Replace K and Mg Estimate CrCl *Don t memorize rather know this exists and requires hospitalization
35 Class IV Verapamil and Diltiazem Specifically affect calcium channels in SA and AV node Decrease heart rate Most useful for rate control in AF and Atrial flutter
36 Class V - Digoxin Rate control via multiple mechanisms Narrow therapeutic index ( ng/ml) toxicity > 2.4 ng/ml Also used in CHF no increased survival data for either AF or CHF indication Clinical fit: little use for rate control More effective, more rapid and less toxic drugs available third line behind BB and CCB Use primarily when contraindications to other agents Can be useful in patients with AF and HF TREAT-AF Study (2014) Retrospective cohort of newly diagnosed AF patients in VA system (n = 122,465) After multivariate analysis (age, sex, renal function, HF, concomitant meds) Digoxin use associated with 26% higher mortality rate (p < 0.001) at ~ 5 years Unfavorable kinetics J Am Coll Cardiol. 2014;64: Pharmacotherapy: A Pathophysiologic Approach. 9 th ed. AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
37 Take away points I rhythm control - rarely used anymore II rate control in AF/Aflutter III rhythm control amiodarone most commonly used, beware of toxicities IV rate control in AF/Aflutter V dig and adenosine (AV node depression) No magic bullet Class I and III (rhythm control) falling out of fashion 1. Better therapies exist Conversion of rhythm with DCC Catheter ablation 2. Long term control of Rate > rhythm [AFFIRM Trial]
38 ATRIAL FIBRILLATION
39 Atrial Fibrillation (AF) Often grouped with atrial flutter: Less common than AF Same risks, prognosis and treatment modalities Common etiologies: Structural heart disease Myocardial ischemia / infarction Coronary artery disease (CAD) Valvular disorders Congenital defects CHF / hypertrophic cardiomyopathy Adrenergic stimulation: Thyrotoxosis, sepsis, physical exertion, illicit drug use Other Risk factors Diabetes mellitus Hypertension Smoking Medications (sympathomimetics) Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e. 2011
40 Atrial fibrillation Multiple re-entry loops Rapid atrial impulses ( /min) but no coordination to form atrial kick Irregular signal conduction through AV node = irregular ventricular beat Usually presents as AF with RVR Rapid Ventricular Response (RVR) ( slow ventricular response usually on rate-controlled drug or AV node block) ECG: Irregularly irregular ECG with multiple and no meaningful P wave (Many small P waves)
41 Atrial Flutter Rapid but regular atrial contraction Atrial rate 300 regularly irregular Usually 2:1 or 3:1 AV conduction Classic sawtooth pattern on ECG
42 Epidemiology of AF Prevalence: % of population ( million Americans) estimated million by 2050 Increases with age 4% over age 60 8% over age 80 Comorbidities: CHF (increases with severity) 4% AF in NYHA class I 50% AF in NYHA class IV A Go AS et al. Heart Disease and Stroke statistics 2013 update. Report from AHA. Circulation 2013;127:e6-e245 Lloyd-Jones DM, et al. Framingham Heart Study. Circulation. Aug ;110(9):1042-6
43 Projected AF incidence assuming no increase in age-adjusted AF incidence assuming continued increase in incidence rates Circulation vol. 114 no
44 AF begets AF Electrical remodeling Important to treat promptly
45 Afib Symptoms Symptoms Light-headedness Fatigue Breathlessness Palpitations Chest-tightness/pain Stroke in AF Atrial quivering Blood stasis coagulation thrombus forms in (left) atrium embolus travels to brain Ischemic stroke
46 Clinical Presentation of AF Symptoms: Common: Rapid heart rate / palpitations Shortness of breath Fatigue Severe: Hypotension, syncope Signs: (ECG findings) Irregularly irregular rhythym No discernable P-wave Ventricular rate of bpm (rapid ventricular response RVR ) Worse with pre-existing CHF Patient presents with stroke? Pharmacotherapy: A Pathophysiologic Approach. 9 th ed.
47 Treatment of Atrial Fibrillation
48 General Approach to AF Acute treatment - Symptom control - Decrease ventricular rate Consider restoring sinus rhythm - Risk vs benefit Prevent long-term complications - Thromboembolism - Recurrence of AF
49 Acute management Symptomatic AF Hemodynamically unstable Medical emergency electrical cardioversion (DCC) Stable Rate control Preferred in stable AF patients AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
50 Methods of Cardioversion Goal: to restore sinus rhythm Electrical shock Defibrillation Direct Current Cardioversion (DCC) Synchronized cardioversion Pharmacological (Chemical) Cardioversion Class I or Class III anti-arrhythmic adenosine New onset AF: spontaneous conversion rate ~60% at 24 hours) (still cardiovert if unstable) Musco, S et al. Med Clin N Am. 92 (2008)
51 acute management of AF Initial rate control IV Non-DHP CCB or Beta Blocker recommended Diltiazem IV bolus continuous infusion Not in decompensated HF metoprolol IV bolus (up to 3 doses) esmolol short t 1/2 = continuous infusion IV Digoxin (second-line) slow onset, full effect at hours Amiodarone if contraindications to above know that cardioversion can happen Initial Goal: HR < 100 January et al. AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
52 Rate vs Rhythm Overview Rate control Ventricular rate, leave in AF Symptom control Beta Blocker Calcium Channel Blocker Digoxin Rhythm control Restore and maintain sinus rhythm Restore Electrical cardioversion Direct current cardioversion (DCC) Pharmacological cardioversion Class I or III anti-arrhythmic maintain Pharmacologic Maintenance Class I or III anti-arrhythmic Catheter ablation
53 After initial rate / symptom control Cardioversion? DCC success rates (~80 90 %) Requires procedural sedation (anesthesia) Pharmacological Lower rates of cardioversion (~60 70% among most agents) Usually avoid cardioversion if: advanced age multiple comorbidities recurrent AF (risks/challenges of maintaining sinus rhythm outweigh benefit) 1. January et al. AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Musco, S et al. Med Clin N Am. 92 (2008)
54 Pharmacologic Cardioversion IV therapy agents Ibutilide Risk of TdP; pretreat with IV Magnesium sulfate Procainamide Hypotension, long infusion time Amiodarone Second line for pharmacologic conversion IV therapy usually converts within minutes to hours Oral therapy agents flecainide, propafenone, dofetilide Several contraindications AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
55 Cardioversion Carries Risk for Stroke AF for 48 hours, higher risk of stroke Anticoagulation 3 weeks prior to cardioversion or Trans-esophogeal echocardiogram (TEE) to rule our clot in atrium 4 weeks following cardioversion Most patients should be kept on long-term anticoagulation (CHEST 2012) AF < 48 hours Immediate cardioversion Anticoagulation at time of cardioversion Pharmacological cardioversion still carries risk of stroke Long-term anticoagulation based on long-term risk (will discuss later) AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
56 Proposed Initial Approach to AF Patient presents with Atrial Fibrillation no i.e. hypotension cardiac ischemia pulm edema Is patient stable? yes Rate control BB, CCB, or digoxin Immediate DCC + anticoaguation low < 48 hours Immediate Stroke risk High 48 hours or unknown duration Electrical or Pharmacological Cardioversion (Physician Preference) No Significant Cardiac History? yes Proceed w/ rate control Anticoagulation for 3 weeks or TEE to r/o clot cardioversion Anticoag for 4 weeks following/ or indefinite
57 So we ve successfully cardioverted DCC or CCV After one year, AF recurrence ~ 75 % if left untreated Even if treated, long-term rhythm control strategy reduces to 30 50% at 1 year Or we can forget about cardioversion and alleviate symptoms by slowing heart rate Either one is be acceptable depending on circumstance Lafuente-Lafuente C, et al. Arch Intern Med. 2006;166:
58 Rate vs Rhythm Overview Rate control Ventricular rate, leave in AF Symptom control Beta Blocker Calcium Channel Blocker Digoxin Rhythm control Restore and maintain sinus rhythm Restore Electrical cardioversion Direct current cardioversion (DCC) Pharmacological cardioversion Class I or III anti-arrhythmic maintain Pharmacologic Maintenance Class I or III anti-arrhythmic Catheter ablation
59 Long-term therapy RATE CONTROL OR RHYTHM CONTROL?
60 First, some background literature Landmark Trials CAST CAST II AFFIRM RACE RACE-II PIAF STAF HOT-CAFE AF-CHF
61 Cardiac Arrhythmia Suppression Trial [CAST] Fact: Patients post MI have arrhythmia/sudden death Hypothesis: treating patients post MI with Class I agent decreases arrhythmia/sudden death Study Protocol Flecainide vs. encainide vs placebo Patients 6 days 2 years post MI (n = 1498) Primary outcome: death or cardiac arrest due to arrhythmia Results: Trial stopped early at 10 months Mortality 5.7% (treatment group) vs 2.2% (placebo) (p = 0.004) NNH = 29 N Engl J Med 1991; 324:781 8
62 What is Structural Heart Disease?! Doesn t really mean much itself Broad term (perhaps overused) involving any: CAD Post MI Valve disease Ventricular dysfunction/hypertrophy (LV dysfunction/lvh)
63 Meta-analysis of quinidine therapy 6 randomized controlled trials reviewed (1980s) Quinidine vs c placebo after cardioversion At 12 months: 50 % quinidine groups in SR 25% of control groups in SR Total mortality rate: Quinidine 2.9 % vs Control 0.8% (p<0.05) Quinidine effective at rhythm control but 3x more lethal Coplen SE et al. Circulation Oct;82(4):
64
65 AFFIRM Trial Largest, most pivotal AF trial to date n = 4060 (at 213 clinical sites) Intention to treat (ITT design) Baseline characteristics of patients Age 65 years No contraindications to anticoagulation or a rate or rhythm drug Other risk factors for stroke/death New AF patients randomized to receive Long-term rate control CCB, BB, or digoxin (chosen by treating physician to control resting HR 80 or 110 after 6 min walk ) Long-term rhythm control Oral Class I/III drugs (chosen by treating physician) most common amiodarone > sotalol > propafenone, procainamide Warfarin mandated N Eng J Med 2002;347:
66 AFFIRM Results Cumulative Mortality from Any Cause No significant difference in mortality Rhythm group: Trend towards increased mortality N Eng J Med 2002;347:
67 AFFIRM Trial Considerations Rate control not worse that rhythm control overall Possibly superior in: Elderly CAD no CHF Rhythm group: Higher % of TdP, cardiac arrest, hospitalization (p = 0.01) Higher % of drug-related side effects ( p<0.05) 62% maintained in sinus rhythm at 5 years Stroke incidence similar in each group Limitations Multiple rate/rhythm drugs could be used in each group Selection bias Only applicable for age > 65 N Eng J Med 2002;347:
68 Other Landmark Trials RACE, PIAF, STAF, HOT-CAFE All consistent with results of AFFIRM Not applicable to HF patients AF-CHF trial (2008) AF patients with LVEF < 35% and HF symptoms Results: No advantage with rhythm control in HF AF-CHF: N Engl J Med 2008;358:
69 Where are we now? It is acceptable to leave patients in AF and only control rate Rate vs rhythm Comparable mortality and stroke [AFFIRM] Class I drugs used in extreme caution post-mi (i.e. any SHD) [CAST Study]
70 Long-term rate control strategy Goal: HR < 80 at rest (IIa LOE B) Lenient rate control is reasonable (HR <110 at rest) as long as pt remains asymptomatic and LV function preserved (Class 11b LOE B) Drug Therapy Oral therapy w βb or non-dhp CCB (I LOE B) Avoid DHP-CCB in HF (BB beneficial in HF) Avoid BB in pulmonary disease Amiodarone can be used if other measures unsuccessful (IIb LOE C) HF patients: Digoxin > Amiodarone (I LOE C)
71 When: Symptomatic patients despite rate control So when DO we pursue a long-term rhythm strategy? (convert & keep in SR) Unable to achieve HR 110 Rate OR Rhythm unnecessary when: New onset AF & likely to remain in SR after conversion Young patients, nocomorbitities, low risk factors, self-limiting AF Pill-in-the-Pocket Patients who have had a safety trial of propafenone or flecainide can utilize a single-dose approach outpatient upon AF onset (IIa LOE B) Recent-onset AF, no drugcontraindications AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76
72 Long-term Rhythm control Rhythm drugs that are still recommended: Flecainide Propafenone Amiodarone Dronedarone Sotalol Dofetilide Catheter Ablation increasingly used in AF Usually rhythm control is in addition to rate control
73 Rhythm control strategies vary specific population Structural Heart Disease [Class Ic (flecainide, propofenone) Contraindicated] CAD sotalol or dofetilide or dronedarone, HF amiodarone or dofetilide sotalol, and dronedarone should not be used in HF No structural Heart Disease (i.e. younger healthier patients) Class Ic (propofenone, flecainide) Hypertrophic cardiomyopathy Class Ia AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Lafuente-Lafuente C, Arch Intern Med 2006;166:
74 Another way to look at things. Most effective overall Amiodarone Most toxic (non-cardiac) ~ 50% effective at maintaining SR at 1 year sotalol flecainide propafenone dronedarone Rx based on niche indication Amiodarone vs Sotalol Two most prescribed anti-arrhythmics Amiodarone: better at maintaining SR, good in HF, more widely prescribed, but more toxic Sotalol: as effective in CAD, less side effects, but renally eliminated, (?advanced age) Both have AV nodal properties, limiting need for rate control (?) Class Ic very effective (and even preferred) given appropriateness Most oral agents require/recommend inpatient initiation of drug > 3 days Therapy Vole 7; 4 p. 391 AFFIRM Investigators. N Eng J Med 2002;347:
75 2014 AHA/ACC AF Guidelines (for rhythm control)
76 Another case More difficult.. But a more real-world case
77 55 yo M w presents with chest palpitations which began about one week prior. Has had sx off and on since and persistent since last night so came to ED. Nausea and mild SOB. Vital signs WNL upon exam except for HR. ECG shows Atrial fibrillation with RVR. HR = 140 PMHx: HTN, asthma Medications: valsartan 80mg daily Patient started on diltiazem IV for initial rate control and DCC planned. Immediate DCC indicated? A. Yes B. No 1. Pt is stable but AND 2. AF > 48 hours -- risk of clot high After DCC, patient reverts to SR but only lasts for 3 days until back in AF. Patient is also still symptomatic on rate control. Patient started on propafenone 150mg Q8H Prefer rhythm control in this patient. No structural heart disease A B C D E F One year later, patient sx have been well controlled. However, he has chest tightness and comes into the ED and diagnosed with a NSTEMI - Post PCI of the LCX - PAF in NSR (HR in 50s) Still prefer rhythm control still in this younger patient w recurrent AF Options for rhythm control at this point? Amiodarone Younger patient, caution with cumulative-dose toxicity Dofetilide Sotalol caution with asthma, bradycardia Propafenone Must stop any Class Ic agent since patient has CAD Flecainide contraindicated Dronedarone Per physician: long conversation had with patient on risks/benefits of sotalol vs dofetilide for rhythm control
78 Often not one perfect anti-arrhythmic drug
79 Maintenance of sinus rhythm Benefit of maintaining SR Side effects of anti-arrhythmic drug Balance varies based on Patient factors Drug
80 Cathater ablation What Radio-frequency ablation Cryo-ablation ( freezing ) How After reentry spot is located, high-frequency radiowaves burn a small area of tissue rendering it inactive. Difficult in AF because many re-entrant pathways exist Post-care and recurrence of AF 20-50% recurrence at one year(1) Majority within 3 months AAD added/continued for 3 months to reduce recurrence Higher success rate with multiple ablations Ganesan AN, J Am Heart Assoc Apr;2(2):e
81
82 Catheter ablation Atrial Flutter First line therapy 90% effective (because of one re-entrant focus) AF Class I recommendation: Symptomatic paroxysmal AF Class II recommendation Afib refractory to medication Not able to tolerate AAD non-compliant w/ AAD Can be chosen as first line rhythm control method over AAD Advantages: avoid long-term use of AAD Risks (4.5% of patients) thromboembolic events, cardiac tamponade, pulmonary vein stenosis AHA/ACC/HRS Atrial Fibrillation Guideline. JACC 2014;64(21):e1-e76 Spector P, et al. Am J Cardiol 2009;104:
83 Treating AF
84 QUESTIONS?
85 OTHER arrhythmias
86 The Pharm.D. ECG read 1. Rate? (tachy vs brady) 2. Regular R R intervals? 3. P waves?
87 What does a 12-lead ECG tell us? More than the pharmacist usually wants to know
88 Good review article(s) and videos Musco, S, et al. Drug Therapy for Atrial Fibrillation. Med Clin N Am. 92 (2008) WPW AVNRT tachycardia video on youtube WPW at 1:05 AVNRT at 6:15 The 6-second ECG
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