2014 aha af guideline
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- Atrial fibrillation (AF) prevalence increases with age, with over 1/3 of patients over 80 years old. It is associated with a higher risk of stroke, heart failure, and mortality. - Common risk factors for AF include hypertension, diabetes, heart disease, obesity, sleep apnea, smoking, and excessive alcohol use. - The CHA2DS2-VASc score is used to stratify stroke risk and determine need for anticoagulation in patients with non-valvular AF. Warfarin, dabigatran, rivaroxaban, and apixaban are recommended for stroke prevention depending on stroke risk and renal function. - Rate
![nonvalvular AF and a CHA2DS2-
VASc score of 0
have endstage CKD
(creatinine clearance [CrCl] <15 mL/min) or are on
hemodialysis, warfarin (INR
2.0 to 3.0)](https://image.slidesharecdn.com/2014ahaafguideline-140610115038-phpapp02/85/2014-aha-af-guideline-16-320.jpg)
2014 aha af guideline
- 2. increases in prevalence with advancing age. • 1% 12% • More than one third of patients with AF are ≥80 years of age 26% for men and 23% for women a 5-fold increased risk of stroke ; 3 fold increase of heart failure ; 2 fold increase in mortality • 3 times
- 3. DEFINITIONS
- 4. Term Definition Paroxysmal AF AF that terminates spontaneously or with intervention within 7 d of onset. Episodes may recur with variable frequency. Persistent AF Continuous AF that is sustained >7 d. Longstanding persistent AF Continuous AF of >12 mo duration. Permanent AF Permanent AF is used when there has been a joint decision by the patient and clinician to cease further attempts to restore and/or maintain sinus rhythm. Acceptance of AF represents a therapeutic attitude on the part of the patient and clinician rather than an inherent pathophysiological attribute of the AF. Acceptance of AF may change as symptoms, the efficacy of therapeutic interventions, and patient and clinician preferences evolve Nonvalvular AF AF in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.
- 5. the term “lone AF’” is potentially confusing and should not be used to guide therapeutic decisions.
- 8. • Increasing age • Hypertension • Diabetes mellitus • MI • VHD • HF • Obesity • Obstructive sleep apnea • Cardiothoracic surgery • Smoking • Exercise • Alcohol use • Hyperthyroidism • Increased pulse pressure • European ancestry • Family history • Genetic variants • Electrocardiographic LVH • Echocardiographic LA enlargement Decreased LV fractional shortening Increased LV wall thickness • Biomarkers Increased CRP Increased BNP
- 10. • In 5% to 15% of patients with AF, a TEE before planned cardioversion revealed a LA or LAA thrombus. • TEE can identify features associated with an increased risk of LA thrombus formation, including reduced LAA flow velocity, spontaneous LA contrast, and aortic atheroma
- 11. should be individualized should be based on the risk of thromboembolism irrespective of
- 12. nonvalvular AF, the CHA2DS2-VASc score mechanical heart valves, warfarin is recommended and the target (INR) intensity (2.0 to 3.0 or 2.5 to 3.5) nonvalvular AF warfarin (INR 2.0 to 3.0) (Level of Evidence: A), dabigatran (Level of Evidence: B), rivaroxaban (Level of Evidence: B), or apixaban . (Level of Evidence: B)
- 13. weekly during initiation and at least monthly unable to maintain a therapeutic INR level with warfarin Re-evaluation
- 14. • 9. Bridging therapy with UFH or LMWH mechanical heart valve AF without mechanical heart valves
- 15. Renal function prior to initiation at least annually with atrial flutter same risk profile
- 16. nonvalvular AF and a CHA2DS2- VASc score of 0 have endstage CKD (creatinine clearance [CrCl] <15 mL/min) or are on hemodialysis, warfarin (INR 2.0 to 3.0)
- 17. nonvalvular AF and a CHA2DS2- VASc score of 1 moderate-to- severe CKD reduced doses of direct thrombin or factor Xa inhibitors
- 18. AF undergoing PCI bare-metal stents may be considered Anticoagulation may be interrupted at the time of the procedure clopidogrel (75 mg once daily) concurrently with oral anticoagulants but without aspirin
- 19. not recommended in patients with AF and end-stage CKD or on hemodialysis
- 20. should not AF and a mechanical heart valve
- 21. AF in the setting of mitral stenosis increases the risk of stroke 20 •Silent AF
- 22. Risk Stratification Schemes (CHADS2, CHA2DS2-VASc, and HAS-BLED)
- 25. lowest risk may not be well identified. 2 due to prior stroke • women cannot achieve a CHA2DS2-VASc score of 0.
- 26. • CHA2DS2-VASc improved predictive ability women younger than 65 years of age anticoagulant treatment was not required.
- 27. • HAS-BLED • RIETE • HEMORRHAGES • ATRIA • HAS-BLED better discriminates risk • A score of ≥3 indicates potentially “high risk” for bleeding
- 28. •Aspirin was ineffective in preventing strokes in those >75 years of age and did not prevent severe strokes. •Moreover, aspirin has not been studied in a low-risk AF population
- 29. •ACTIVE-ATRIAL-
- 30. ECOSPIRIN+CLOPIDOGREL VS WARFARIN • ACTIVE-WTRIAL- • AVERROES (APIXABAN Versus ASPIRIN to Prevent Strokes)
- 31. The BAFTA compare warfarin with aspirin • Warfarin was superior in preventing stroke or systemic embolism without a significant increase in bleeding risk. 64% , the time in therapeutic range (TTR) of those taking warfarin were reported as 55% to 66%
- 32. 75 MG (crCL- 15-30 ml) but not 110 mg bleeding rates do not appear to be higher for dabigatran. proton pump inhibitors may reduce absorption of dabigatran.
- 33. risk of MI and ACSs in patients randomized to dabigatran multiple limitations of this type of analysis , this is not in a linear fashion
- 34. •OD With large meal fatal bleed and ICH lesser •safer in elderly •20 mg OD. 15 mg if crCL 30-49 ml/min.
- 35. hepatically eliminated >80 yrs ; weight <60 kg ; creatinine> 1.5 mg/ml 2.5 mg bd. • No datas to use in ESRD; pt on dialysis.
- 36. • More predictable pharmacological profiles, Fewer drug–drug interactions, • An absence of major dietary effects, and • Less risk of intracranial bleeding than warfarin rapid onset and offset of action bridging with parenteral anticoagulant therapy is not needed during initiation bridging may not be needed brief interruption of anticoagulation invasive procedures.
- 37. • Missing even 1 dose could result in a period without protection from thromboembolism black box warnings
- 39. Renal Function Dabigatran† Rivaroxaban† Apixaban† Normal/Mild Impairment 150 mg BID (CrCl >30 mL/min 20 mg HS (CrCl >50 mL/min) 5.0 or 2.5 mg BID Moderate Impairment 150 mg BID or 75 mg BID§ (CrCl >30 mL/min) 15 mg HS (CrCl 30–50 mL/min) 5.0 or 2.5 mg BID Severe Impairment 75 mg BID§ (CrCl 15–30 mL/min) 15 mg HS (CrCl 15–30 mL/min) No recommendation End-Stage CKD Not on Dialysis Not recommended¶ (CrCl <15 mL/min) Not recommended¶ (CrCl <15 mL/min) No recommendation End-Stage CKD on Dialysis Not recommended¶ (CrCl <15 mL/min) Not recommended¶ (CrCl <15 mL/min) No recommendation WARFARIN CAN BE USED IN ANY STAGE / ON DIALYSIS- WITH ADJUSTED DOSAGETO KEEP INR 2-3
- 40. Hemoclot thrombin clotting time • The use of activated charcoal • Dabigatran is dialyzable
- 41. Increased concentration if taken along with these drugs (P –glyco protein Inhibitors) • ketoconazole, • verapamil, • amiodarone, • dronedarone, • quinidine, and • clarithromycin Decreased efficacy if taken with these drugs- (P-glyco protein inducers) • phenytoin, • carbamazepine, • rifampin, and • St. John’s wort
- 43. stopping warfarin for up to 1 week and allowing the INR to normalize without substituting UFH is a recognized approach
- 44. • for pacemaker or implantable cardioverterdefibrillator implantation, catheter ablation, coronary angiography, and other vascular interventions, is to perform the procedure without interrupting warfarin.
- 45. • Pacemaker or defibrillator implantation with a therapeutic INR
- 46. • For elective surgery for 1 day for spinal puncture, spinal/epidural catheter, or major surgery) ≥48 hours
- 47. activated partial thromboplastin time for dabigatran prothrombin time for apixaban and rivaroxaban activated prothrombin complex concentrate recombinant factorVIIa
- 48. (“triple therapy”) in post PCI
- 49. • WATCHMAN DEVICE- • AMPLATZER CARDIAC PLUG • LARIAT SNARE
- 50. WATCH MAN DEVICE AMPLATZER DEVICE
- 51. LARIAT DEVICE
- 52. Class IIb • Epicardial techniques
- 53. • Endocardial techniques incomplete occlusion in ≥50% of subjects. • The LAAOS (Left Atrial Appendage Occlusion Study) :
- 54. Gillinov- Cosgrove clip LAA excluder system
- 58. RATE CONTROL IN AF
- 59. CLASS I 1. Control of the ventricular rate using a beta blocker or nondihydropyridine calcium channel antagonist is recommended for patients with paroxysmal, persistent, or permanent AF . (Level of Evidence: B) 2. Intravenous administration of a beta blocker or nondihydropyridine calcium channel blocker is recommended to slow the ventricular heart rate in the acute setting in patients without preexcitation. In hemodynamically unstable patients, electrical cardioversion is indicated . (Level of Evidence: B)
- 60. CLASS I 3. In patients who experience AF-related symptoms during activity, the adequacy of heart rate control should be assessed during exertion, adjusting pharmacological treatment as necessary to keep the ventricular rate within the physiological range. (Level of Evidence: C)
- 61. CLASS IIA 1. A heart rate control (resting heart rate <80 bpm) strategy is reasonable for symptomatic management of AF . (Level of Evidence: B) 2. Intravenous amiodarone can be useful for rate control in critically ill patients without preexcitation . (Level of Evidence: B) 3. AV nodal ablation with permanent ventricular pacing is reasonable to control the heart rate when pharmacological therapy is inadequate and rhythm control is not achievable . (Level of Evidence: B)
- 62. Class IIb 1. A lenient rate-control strategy (resting heart rate <110 bpm) may be reasonable as long as patients remain asymptomatic and LV systolic function is preserved (267). (Level of Evidence: B) 2. Oral amiodarone may be useful for ventricular rate control when other measures are unsuccessful or contraindicated. (Level of Evidence: C)
- 63. Class III: Harm 1. AV nodal ablation with permanent ventricular pacing should not be performed to improve rate control without prior attempts to achieve rate control with medications. (Level of Evidence: C) 2. Nondihydropyridine calcium channel antagonists should not be used in patients with decompensated HF as these may lead to further hemodynamic compromise. (Level of Evidence: C)
- 64. CLASS III Harm 3. In patients with pre-excitation and AF, digoxin, nondihydropyridine calcium channel antagonists, or intravenous amiodarone should not be administered as they may increase the ventricular response and may result in ventricular fibrillation . (Level of Evidence: B) 4. Dronedarone should not be used to control the ventricular rate in patients with permanent AF as it increases the risk of the combined endpoint of stroke, MI, systemic embolism, or cardiovascular death . (Level of Evidence: B)
- 65. Rate control in AF is an important strategy. It impacts quality of life, reduces morbidity, and decreases the potential for developing tachycardia-induced cardiomyopathy. In general, beta blockers are the most common agents utilized for rate control, followed by nondihydropyridine calcium channel blockers, digoxin, and amiodarone.
- 66. When rapid control of ventricular rate during AF is required, intravenous medications or electrical cardioversion may be used. Electrical cardioversion is preferred in patients with decompensated HF, ongoing myocardial ischemia, or hypotension. In hemodynamically stable patients with a rapid ventricular response, oral medications may be administered
- 67. Intravenous Administration Usual Oral Maintenance Dose Metoprolol tartrate 2.5–5.0 mg IV bolus over 2 min; up to 3 doses 25–100 mg BID Metoprolol XL (succinate) N/A 50–400 mg QD Atenolol N/A 25–100 mg QD Esmolol 500 mcg/kg IV bolus over 1 min, then 50–300 mcg/kg/min IV N/A Propranolol 1 mg IV over 1 min, up to 3 doses at 2 min intervals 10–40 mg TID or QID Nadolol N/A 10–240 mg QD Carvedilol Bisoprolol N/A N/A 3.125–25 mg BID 2.5–10 mg QD
- 68. DRUG IV ORAL Verapamil (0.075-0.15 mg/kg) IV bolus over 2 min, may give an additional 10.0 mg after 30 min if no response, then 0.005 mg/kg/min infusion 180–480 mg QD (ER) Diltiazem 0.25 mg/kg IV bolus over 2 min, then 5-15 mg/h 120–360 mg QD (ER) Digoxin 0.25 mg IV with repeat dosing to a maximum of 1.5 mg over 24 h 0.125–0.25 mg QD Amiodarone 300 mg IV over 1 h, then 10– 50 mg/h over 24 h 100–200 mg QD
- 69. BETA BLOCKERS AFFIRM study, beta blockers were the most effective and commonly used drug class for rate control . In patients with HF, carvedilol had efficacy for heart rate control and, in combination with digoxin, resulted in improved LV function . Combination therapy of beta blockers with other agents, including digoxin, is effective in ventricular rate control
- 70. Nondihydropyridine Calcium Channel Blockers Have direct AV nodal effects, used for ventricular rate control in both acute and chronic AF. Unless immediate rate control is required or an enteral route of administration is not available, oral administration is appropriate. Can improve exercise tolerance They may be used in patients with HF with preserved LV systolic function. These agents should not be used in patients with pre-excitation and AF due to the potential for shortening bypass tract refractoriness which may accelerate the ventricular rate to precipitate hypotension or ventricular fibrillation
- 71. Digoxin not usually first-line therapy Although intravenous digoxin does slow the ventricular response, onset of action requires >1 hour and the effect does not peak until approximately 6 hours after initial administration. Therefore, it is not an optimal agent In acute settings. it is ineffective at controlling the ventricular response during exercise. Digoxin may be combined with beta blockers or nondihydropyridine calcium channel blockers to improve ventricular rate control during exercise.
- 72. DIGOXIN…. Dose adjustment is required in patients with renal dysfunction, the elderly, and in the presence of drugs that reduce its excretion such as amiodarone, propafenone, or nondihydropyridine calcium channel blockers. in the DIG (Digitalis Investigation Group) trial, serum levels >0.9 ng/mL were associated with increased mortality. Because it can shorten cardiac action potential duration, should not be used in pre excitations.
- 73. AMIODARONE IN rate control Exerts sympatholytic and calcium antagonistic properties that can depress AV nodal conduction. Although intravenous amiodarone can be used in critically ill patients without pre-excitation to attain ventricular rate control, it is less effective than calcium channel blockers and requires a longer time to achieve rate control (7 hours versus 3 hours for diltiazem). There are limited data on the efficacy of chronic oral therapy with amiodarone for rate control during persistent AF, but in 1 small trial it had similar efficacy to digoxin.
- 74. Intravenous amiodarone does not have the same electrophysiologic effects as oral amiodarone. Its onset of action can be accelerated by a highdose amiodarone- loading regimen, but there is the potential for worsening hemodynamics in patients with recent decompensated HF or hypotension. It causes fatal arrhythmias in pre excitation with AF. Amiodarone has many potential toxicities and drug interactions that limit its long-term use for control of ventricular rate.
- 75. Dronedarone lacks iodine moieties of amiodarone. it should not be used for rate control in permanent AF should not be used for ventricular rate control in patients with HF and LV systolic dysfunction As it increases the likelihood of the combined endpoint of stroke, MI, systemic embolism, or cardiovascular death.
- 76. AV Nodal Ablation Patients most likely to benefit include those with tachycardiainduced cardiomyopathy with ventricular rate control refractory to medical therapy. usually reserved for elderly patients as it leads to pacemaker dependency No rate control medications are necessary, but anticoagulation to prevent thromboembolism is required based on the patient’s stroke risk. pacemaker implantation may be performed 4 to 6 weeks prior to the AV node ablation to ensure proper pacemaker function as malfunction due to lead dislodgement can be catastrophic.
- 77. Sudden death secondary to torsades de pointes or ventricular fibrillation has been reported after AV junction ablation- related to increased dispersion of ventricular refractoriness produced by sudden heart rate slowing and ventricular pacing . Postablation, the ventricular pacing rate is usually set between 90 bpm and 100 bpm and then gradually tapered over several months
- 78. lenient (<110) versus strict rate control (<80) RACE II TRIAL- At 3 years the primary composite endpoint of cardiovascular death, hospitalization for HF, stroke, embolism, bleeding, or life-threatening arrhythmic events was similar between the 2 groups ; thus, a strict rate control strategy did not improve outcomes. BUT due to many limitations, This single RCT does not provide sufficient evidence to assess definitive results of the impact- The degree of rate control, however, remains an area of uncertainty
- 79. AF NO OTHER CV DISEASE HTN OR HFpEF LV DYSFUNCTION OR HF COPD BB DILTIAZEM VERAPAMIL BB DILTIAZEM VERAPAMIL BB + DIGOXIN BB DILTIAZEM VERAPAMIL AMIODARONE
- 80. Rhythm Control
- 81. CURRENT STATUS RCTs comparing outcomes of a rhythm-control strategy with a rate- control strategy in patients with AF failed to show a superiority of rhythm control for either strategy on mortality . Furthermore, when applied in patients who are candidates for both treatment strategies (rhythm or rate control), a rhythm-control strategy results in more hospitalizations. Therefore, the routine use of a rhythm-control strategy is not warranted for some patients. But Catheter ablation has not been studied in this context.
- 82. Favour rhythm control….. Persistent symptoms associated with AF **** (MOST) Difficulty in achieving adequate rate control, Younger patient age, Tachycardia-mediated cardiomyopathy, First episode of AF, AF that is precipitated by an acute illness, and Patient preference Accepting AF as permanent in a patient may render future rhythm-control therapies less effective. So in young pts Early intervention with a rhythm-control strategy to prevent the progression of AF may be beneficial.
- 83. Thromboembolism Prevention: Recommendations Electrical and Pharmacological Cardioversion of AF and Atrial Flutter
- 84. …….?? Thromboembolic risk after cardioversion is highest in the first 72 hours and that the majority of events occur within 10 days. Due to migration of thrombi present at the time of cardioversion or to the formation and subsequent migration of de novo thrombi that form while atrial function is still depressed in the postcardioversion period.
- 85. Class I 1. For patients with AF or atrial flutter of 48-hour duration or longer, or when the duration of AF is unknown, anticoagulation with warfarin (INR 2.0 to 3.0) is recommended for at least 3 weeks prior to and 4 weeks after cardioversion, regardless of the CHA2DS2-VASc score and the method (electrical or pharmacological) used to restore sinus rhythm . (Level of Evidence: B) 2. For patients with AF or atrial flutter of more than 48 hours or unknown duration that requires immediate cardioversion for hemodynamic instability, anticoagulation should be initiated as soon as possible and continued for at least 4 weeks after cardioversion unless contraindicated. (Level of Evidence: C)
- 86. CLASS I 3. For patients with AF or atrial flutter of less than 48-hour duration and with high risk of stroke, intravenous heparin or LMWH, or administration of a factor Xa or direct thrombin inhibitor, is recommended as soon as possible before or immediately after cardioversion, followed by longterm anticoagulation therapy. (Level of Evidence: C) 4. Following cardioversion for AF of any duration, the decision regarding long-term anticoagulation therapy should be based on the thromboembolic risk profile (Section 4). (Level of Evidence: C)
- 87. CLASS IIA 1. For patients with AF or atrial flutter of 48-hour duration or longer or of unknown duration who have not been anticoagulated for the preceding 3 weeks, it is reasonable to perform a TEE prior to cardioversion and proceed with cardioversion if no LA thrombus is identified, including in the LAA, provided that anticoagulation is achieved before TEE and maintained after cardioversion for at least 4 weeks . (Level of Evidence: B) 2. For patients with AF or atrial flutter of 48-hour duration or longer, or when the duration of AF is unknown, anticoagulation with dabigatran, rivaroxaban, or apixaban is reasonable for at least 3 weeks prior to and 4 weeks after cardioversion . (Level of Evidence: C)
- 88. Class IIb 1. For patients with AF or atrial flutter of less than 48- hour duration who are at low thromboembolic risk, anticoagulation (intravenous heparin, LMWH, or a new oral anticoagulant) or no antithrombotic therapy may be considered for cardioversion, without the need for postcardioversion oral anticoagulation . (Level of Evidence: C)
- 89. TEE… The absence of left atrial thrombus on TEE does not preclude the need for anticoagulation during and after cardioversion. If thrombus is identified on TEE, the cardioversion should be postponed followed by ≥3 to 4 weeks of anticoagulation. If thrombus remains on repeat TEE, an alternative strategy such as rate control in conjunction with appropriate anticoagulation may be considered
- 91. A biphasic waveform is more effective than a monophasic waveform . Anteroposterior electrode placement is superior to anterolateral placement in some but not all studies . If an attempt at cardioversion using 1 electrode placement fails, another attempt using the alternative placement is recommended. The initial use of a higher-energy shock is more effective and may minimize the number of shocks required as well as the duration of sedation. Elective cardioversion should not be performed in patients with evidence of digoxin toxicity, severe hypokalemia, or other electrolyte imbalances until these factors are corrected
- 92. cardioversion in which sinus rhythm was not restored…. approaches that improve energy delivery and may allow for successful cardioversion include Increasing shock strength, Delivering a biphasic rather than monophasic waveform, Changing the shock vector by altering the electrode pad position, Improving energy transfer via pressure on the anterior electrode pad, or Using a drug such as ibutilide to lower defibrillation threshold
- 93. cardioversion in which sinus rhythm was restored but AF recurs…… Pretreatment with selected antiarrhythmic drugs may increase the likelihood of maintenance of sinus rhythm.
- 94. Class I 1. In pursuing a rhythm-control strategy, cardioversion is recommended for patients with AF or atrial flutter as a method to restore sinus rhythm. If cardioversion is unsuccessful, repeated direct-current cardioversion attempts may be made after adjusting the location of the electrodes or applying pressure over the electrodes, or following administration of an antiarrhythmic medication . (Level of Evidence: B) 2. Cardioversion is recommended when a rapid ventricular response to AF or atrial flutter does not respond promptly to pharmacological therapies and contributes to ongoing myocardial ischemia, hypotension, or HF. (Level of Evidence: C)
- 95. CLASS I 3. Cardioversion is recommended for patients with AF or atrial flutter and pre-excitation when tachycardia is associated with hemodynamic instability. (Level of Evidence: C)
- 96. Class IIa 1. It is reasonable to perform repeated cardioversions in patients with persistent AF provided that sinus rhythm can be maintained for a clinically meaningful period between cardioversion procedures. Severity of AF symptoms and patient preference should be considered when embarking on a strategy requiring serial cardioversion procedures. (Level of Evidence: C)
- 98. Class I 1. Flecainide, dofetilide, propafenone, and intravenous ibutilide are useful for pharmacological cardioversion of AF or atrial flutter provided contraindications to the selected drug are absent. (Level of Evidence: A)
- 99. Class IIa 1. Administration of oral amiodarone is a reasonable option for pharmacological cardioversion of AF . (Level of Evidence: A) 2. Propafenone or flecainide (“pill-in-the-pocket”) in addition to a beta blocker or nondihydropyridine calcium channel antagonist is reasonable to terminate AF outside the hospital once this treatment has been observed to be safe in a monitored setting for selected patients . (Level of Evidence: B)
- 100. Class III: Harm 1. Dofetilide therapy should not be initiated out of hospital owing to the risk of excessive QT prolongation that can cause torsades de pointes . (Level of Evidence: B)
- 101. IBUTELIDE Pharmacological cardioversion is most likely effective when initiated within 7 days after the onset of an episode of AF. In patients with recent onset AF, intravenous administration of ibutilide restored sinus rhythm in about 50% of patients with an average conversion time of <30 minutes. Ibutilide pretreatment also improves the efficacy of transthoracic electrical cardioversion of AF. The major risk is excessive QT prolongation, which can cause polymorphic ventricular tachycardia/torsades de pointes. occurs in up to 3% to 4% of patients.
- 102. IBUTELIDE…… ECG monitoring should be continued for ≥4 hours after administration and resuscitation equipment must be immediately available. Ibutilide should be avoided in patients with base line QT prolongation, Marked hypokalemia, or a very low ejection fraction (EF) (<30%) - because of the risk of ventricular proarrhythmia. Some experts administer magnesium sulfate intravenously prior to administering ibutilide in an attempt to lower this risk
- 103. AMIODARONE Intravenous amiodarone may facilitate slowing of the ventricular rate in AF, but the effect to restore sinus rhythm is often delayed. In 1 study, oral amiodarone loaded over the course of several weeks resulted in conversion of persistent AF to sinus rhythm in about 25% of patients
- 104. A beta blocker or non dihydropyridine calcium channel antagonist should be administered ≥30 minutes before administering the Vaughan Williams Class IC (FLECAINIDE AND PROPAFENONE) agent to prevent a rapid ventricular response due to 1:1 AV conduction during atrial flutter. Flecainide and Propafenone should be avoided in patients with CAD and significant structural heart disease (Increases mortality)
- 105. Amiodarone 600–800 mg daily in divided doses to a total load of up to 10 g, then 200 mg QD as maintenance 150 mg over 10 min, then 1 mg/min for 6 h, then 0.5 mg/min for 18 h or change to oral dosing Flecainide 200–300 mg x 1* Propafenone 450–600 mg x 1* Ibutilide 1 mg over 10 min; may repeat 1 mg once if necessary (weight <60 kg use 0.01 mg/kg) Dofetilide 125-500 ,based on cr.clearance
- 107. Class I 1. Before initiating antiarrhythmic drug therapy, treatment of precipitating or reversible causes of AF is recommended. (Level of Evidence: C) 2. The following antiarrhythmic drugs are recommended in patients with AF to maintain sinus rhythm, depending on underlying heart disease and comorbidities (Level of Evidence: A): a. Amiodarone b. Dofetilide c. Dronedarone d. Flecainide e. Propafenone f. Sotalol
- 108. CLASS I 3. The risks of the antiarrhythmic drug, including proarrhythmia, should be considered before initiating therapy with each drug. (Level of Evidence: C) 4. Owing to its potential toxicities, amiodarone should only be used after consideration of risks and when other agents have failed or are contraindicated. . (Level of Evidence: C)
- 109. Class IIa 1. A rhythm-control strategy with pharmacological therapy can be useful in patients with AF for the treatment of tachycardia-induced cardiomyopathy. (Level of Evidence: C)
- 110. Class IIb 1. 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. (Level of Evidence: C)
- 111. Class III: Harm 1. Antiarrhythmic drugs for rhythm control should not be continued when AF becomes permanent including dronedarone . (Level of Evidence: B) 2. Dronedarone should not be used for treatment of AF in patients with New York Heart Association (NYHA) class III and IV HF or patients who have had an episode of decompensated HF in the past 4 weeks . (Level of Evidence: B)
- 112. Factors influencing the type of drug… Structural heart diseases (CAD,LVH,HF etc) Baseline QT prolongation, History of torsades de pointes during therapy with a QT interval prolonging drug, Potassium wasting syndromes, Patient age, Renal or hepatic dysfunction Because of its toxicity profile, amiodarone should only be used after consideration of risks and when other agents have failed or are contraindicated.
- 113. !! Decisions regarding anticoagulation should be based on the patient’s individual stroke risk profile and not on the response to antiarrhythmic drug therapy. Antiarrhythmic drug efficacy is modest and asymptomatic AF recurrences are common. A rhythm-control strategy should not result in cessation of antithrombotic therapy, rate control therapy, or treatment of underlying heart disease
- 114. In selecting a strategy of rhythm control with an antiarrhythmic drug, providing for adequate rate control in the event of AF recurrence should also be considered. Once antiarrhythmic drug therapy The transition from frequent AF to infrequent, well-tolerated recurrence of AF is a reasonable outcome and does not necessarily indicate that the therapy should be discontinued. However, if attempts at rhythm control are abandoned (e.g., after AF has been declared permanent), the antiarrhythmic drug should be discontinued.
- 115. In general, antiarrhythmic drugs have the potential to precipitate or worsen bradycardia due to sinus node dysfunction or abnormal AV conduction. A history of syncope, sinus bradycardia, PR interval prolongation, and bundle-branch block - raise concerns for a risk of bradyarrhythmia during antiarrhythmic drug therapy.
- 116. Class IA drugs (quinidine and disopyramide, pooled data) were associated with increased mortality compared with controls. Antiarrhythmic drugs that prolong the QT interval, notably Sotalol, dofetilide, and disopyramide have a risk of causing torsades de pointes and should be avoided in patients at increased risk of this form of proarrhythmia. Bradycardia, Advanced age, Hypokalemia, hypomagnesemia, Female sex, Baseline prolonged QT interval, congenital long-QT syndrome, Concomitant use of other QT-prolonging therapies, HF, and possibly LV hypertrophy.
- 117. Amiodarone and dronedarone have very rarely been associated with prolongation of the QT interval and torsades de pointes.
- 118. DRUG DOSAGE TO MAINTAIN SINUS RHYTHM USE WITH CAUTION Amiodarone Oral: 400–600 mg daily in divided doses for 2-4 wk; maintenance typically 100- 200 mg QD IV: 150 mg over 10 min; then 1 mg/min for 6 h; then 0.5 mg/min for 18 h or change to oral dosing; after 24 h, consider decreasing dose to 0.25 mg/min · Infranodal conduction Disease. Lung disease Quinidine 324–648 mg every 8 h Prolonged QT interval, Diarrhea Flecainide 50–200 mg once every 12 H · Infranodal conduction disease • HF,CAD,Atrial flutter · Brugada syndrome · Renal or liver disease Propafenone Immediate release: 150–300 mg once every 8 h · Extended release: 225–425 mg once every 12 h SAME AS FLECAINIDE Sotalol 40–160 mg once every 12 h Prolonged QT interval · Renal disease,Hypokalemia · Diuretic therapy · HF,Asthma
- 119. AMIODARONE Has a long half-life of weeks Large volume of distribution into adipose tissue Suppression of sinus and AV nodal function can occur early within the first few days of oral therapy, the antiarrhythmic effect and QT prolongation can be delayed for days or weeks- HENCE NEED LOADONG LOAD. Loading dose with FOOD – to increase absorption
- 120. CAUTION AND PRECAUTION! Warfarin, newer anti coagulants, digoxin- toxicity if taken along with amiodarone. In SCD-HeFT (Sudden Cardiac Death in Heart Failure Trial) Amiodarone therapy was associated with an increase in noncardiac mortality in patients with NYHA class III HF. A mixed treatment comparison of amiodarone, dronedarone, flecainide, propafenone, and sotalol for the treatment of AF or atrial flutter found that amiodarone had the largest reduction of AF recurrence but was associated with the highest rate of patients experiencing ≥1 serious adverse event and treatment withdrawals due to adverse events.
- 121. CAUTION… The risk of many toxicities, including pulmonary toxicity, is dose-related and can be fatal so it not a first-choice agent (especially in younger patients) when other antiarrhythmic drugs are an option
- 122. BUT…. In maintaining sinus rhythm, among all the drugs amiodarone is most effective. Lesser QT alteration. In patients with left ventricular hypertrophy, HF, CAD, and/or previous MI, - amiodarone is associated with a low risk of pro arrhythmia, making it an appropriate initial choice to prevent recurrent AF in these clinical settings
- 123. Chronic oral doses of ≤200 mg daily may be effective and result in fewer side effects than higher-dose regimens. Doses of other medications for rate control should be reduced when the rate slows after initiation of amiodarone and stopped if the rate slows excessively.
- 124. FLECAINIDE AND PROPAFENONE Only in a structuraly normal heart. Both are negative ionotropes. Use dependent increase in the PR and QRS of up to 25% may occur- Giant U waves and >25% increase in QRS- reduce the dose. Propafenone can cause metallic taste. Dizziness and visual disturbances very rarely. Caution in the presence of other conduction system diseases- BBB.
- 125. SOTALOL Not effective for conversion of AF to sinus rhythm, but it may be used to prevent recurrent AF. Initiate sotalol in hospital with electrocardiographic monitoring to observe for QT prolongation and proarrhythmia in the absence of an implanted cardioverter defibrillator. During follow-up, serum potassium and magnesium levels and renal function should be checked periodically
- 126. DISOPYRAMIDE Because of its prominent vagolytic pharmacological effects, disopyramide is useful in AF that occurs in the setting of high vagal tone (“vagally mediated AF”), such as sleep. Its negative inotropic effects may be desirable in patients with HCM associated with dynamic outflow tract obstruction . Otherwise, it is avoided in all other structural heart disease.
- 127. QUINIDINE NO negative inotropic effects Can be used when there is advanced renal dysfunction. Quinidine requires close ECG monitoring at initiation. Use only when all others fail- increases mortality.
- 128. Upstream Therapy: Recommendations Class IIa 1. An ACE inhibitor or angiotensin-receptor blocker (ARB) is reasonable for primary prevention of new- onset AF in patients with HF with reduced LVEF . (Level of Evidence: B)
- 129. Class IIb 1. Therapy with an ACE inhibitor or ARB may be considered for primary prevention of new-onset AF in the setting of hypertension . (Level of Evidence: B) 2. Statin therapy may be reasonable for primary prevention of new-onset AF after coronary artery surgery . (Level of Evidence: A)
- 130. Class III: No Benefit 1. Therapy with an ACE inhibitor, ARB, or statin is not beneficial for primary prevention of AF in patients without cardiovascular disease . (Level of Evidence: B)
- 131. AF Catheter Ablation to Maintain Sinus Rhythm: Recommendations
- 132. Class I 1. AF catheter ablation is useful for symptomatic paroxysmal AF refractory or intolerant to at least 1 class I or III antiarrhythmic medication when a rhythm control strategy is desired . (Level of Evidence: A) 2. Prior to consideration of AF catheter ablation, assessment of the procedural risks and outcomes relevant to the individual patient is recommended. (Level of Evidence: C)
- 133. Class IIa 1. AF catheter ablation is reasonable for selected patients with symptomatic persistent AF refractory or intolerant to at least 1 class I or III antiarrhythmic medication . (Level of Evidence: A) 2. In patients with recurrent symptomatic paroxysmal AF, catheter ablation is a reasonable initial rhythm control strategy prior to therapeutic trials of antiarrhythmic drug therapy, after weighing risks and outcomes of drug and ablation therapy . (Level of Evidence: B)
- 134. CLASS IIB 1. AF catheter ablation may be considered for symptomatic long-standing (>12 months) persistent AF refractory or intolerant to at least 1 class I or III antiarrhythmic medication, when a rhythm control strategy is desired . (Level of Evidence: B). 2. AF catheter ablation may be considered prior to initiation of antiarrhythmic drug therapy with a class I or III antiarrhythmic medication for symptomatic persistent AF, when a rhythm control strategy is desired. (Level of Evidence: C)
- 135. The efficacy of radiofrequency catheter ablation for maintaining sinus rhythm is superior to current antiarrhythmic drug therapy for maintenance of sinus rhythm in selected patient populations. Especially for paroxysmal AF in younger patients with little to no structural heart disease. Evidence is insufficient to determine whether AF catheter ablation reduces all-cause mortality, stroke, and HF.
- 136. most patients enrolled in trials of AF catheter ablation have generally been younger, healthy individuals ; The safety and efficacy of catheter ablation are less well established for other populations of patients, especially patients with longstanding persistent AF, very elderly patients, and patients with significant HF including tachycardia- induced cardiomyopathy. The RAAFT II & The MANTRA-PAF TRIAL- At the 24-month follow-up, more patients in the ablation group were free from any AF or symptomatic AF and quality of life was significantly better. However, total AF burden was not significantly different between the 2 groups and major complications requiring intervention were more common in the ablation group
- 137. Recurrence After Catheter Ablation Recurrences of AF after catheter ablation are common during the first 3 months and do not preclude long-term success. when AF occurs early after catheter ablation, a pharmacologic rhythm control approach rather than early repeat ablation should be considered. Patients who develop persistent AF within the 3 months following ablation may require cardioversion .
- 138. Recurrent AF after 3 months is usually an indication of recovery of pulmonary vein conduction and may respond to repeat ablation or initiation of an antiarrhythmic drug. Recurrence of AF following ablation is 3- to 7-fold more likely to be asymptomatic compared with prior to ablation
- 139. Anticoagulation Therapy Periablation There is well-established risk of peri procedure stroke or TIA associated with AF catheter ablation. Both intraprocedural heparin and oral anticoagulation for ≥2 months postprocedure are recommended. AF catheter ablation should not be performed in patients who cannot be treated with anticoagulant therapy during and following the procedure. Continuation of anticoagulation >2 months following AF catheter ablation, if the procedure is perceived successful, should be based on consideration of the patient's thromboembolic risk profile , bleeding risk, and patient choice
- 140. Several reports indicate that AF catheter ablation may be performed with fewer complications when oral warfarin anticoagulation is continued as an alternative to a bridging approach with UFH or LMWH. Reports with dabigatran- where dabigatran 1 or 2 doses are stopped prior to procedure - reports suggest that the use of dabigatran is associated with a similar risk of bleeding and thromboembolic complications compared with uninterrupted warfarin.
- 141. Catheter Ablation in HF catheter ablation may be reasonable to treat symptomatic AF in selected patients with significant LV dysfunction and HF ,especially where the LV dysfunction is thought to be due to AF itself.
- 142. Complications Following AF Catheter Ablation - 4-5% older age, females, CHADS score>2 – more risk Cardiac tamponade/perforation Phrenic nerve injury Atrial-esophageal fistula Air embolism Iatrogenic atrial flutter Mitral valve injury requiring surgery Pericarditis MI Pulmonary vein stenosis Radiation injury Stroke or TIA Femoral pseudo aneurysm Arteriovenous fistula Hematoma
- 143. Pacemakers and Implantable Cardioverter- Defibrillators for the Prevention of AF Attempts to prevent AF episodes by proprietary overdrive atrial pacing algorithms that react to premature atrial complexes are inconsistent. Therefore, permanent pacing is not indicated for the prevention of AF in patients without other indications for pacemaker implantation. Atrial defibrillators to automatically cardiovert AF do not have clinical value. ICDs are not indicated for rhythm control of AF.
- 144. NO STRUCTURAL HEART DISEASE DOFETILIDE DRONADARONE SOTALOL CATHETER ABLATION CATHETER ABLATION HF STRUCTURAL HEART DISEASE FLECAINIDE PROPAFENONE SOTALOL DOFETILIDE DRONEDARONE AMIODARONE AMIODARONE AMIODARONE DOFETILIDE CAD
- 146. Class IIa 1. An AF surgical ablation procedure is reasonable for selected patients with AF undergoing cardiac surgery for other indications. (Level of Evidence: C) CLASS IIB 1. A stand-alone AF surgical ablation procedure may be reasonable for selected patients with highly symptomatic AF not well managed with other approaches . (Level of Evidence: B)
- 147. CATHETER VS SURGICAL ABLATION The FAST (Atrial Fibrillation Catheter Ablation Versus Surgical Ablation Treatment) trial Patients either had left atrial dilation and hypertension or failed prior catheter ablation . Freedom from atrial arrhythmias was greater after surgical ablation compared with catheter ablation, but the complication rate after surgical ablation was higher. Decisions must be made on the basis of patient preference, and institutional experience and outcomes with each therapy
- 148. Specific Patient Groups and AF
- 149. Athletes Paroxysmal or persistent AF is common in athletes. May require ambulatory ECG monitoring and/or exercise testing to a level of exertion similar to that of the intended sport . Radiofrequency catheter ablation or a “pill-in-the-pocket” approach can be considered in athletes
- 150. ELDERLY Rate control strategy is often preferred Direct-current cardioversion is less often warranted Beta blockers or nondihydropyridine calcium channel antagonists are preferred. Digoxin can be useful for rate control in the relatively sedentary individual
- 151. HOCM Class I 1. Anticoagulation is indicated in patients with HCM with AF independent of the CHA2DS2-VASc score . (Level of Evidence: B).
- 152. Class IIa 1. Antiarrhythmic medications can be useful to prevent recurrent AF in patients with HCM. Amiodarone, or disopyramide combined with a beta blocker or nondihydropyridine calcium channel antagonists are reasonable therapies. (Level of Evidence: C) 2. AF catheter ablation can be beneficial in patients with HCM in whom a rhythm-control strategy is desired when antiarrhythmic drugs fail or are not tolerated . (Level of Evidence: B)
- 153. Class IIb 1. Sotalol, dofetilide, and dronedarone may be considered for a rhythm-control strategy in patients with HCM . (Level of Evidence: C)
- 154. HOCM…. AF poorly tolerated symptomatically. Hence, a rhythm-control strategy is preferred AF is associated with increased mortality in patients with HCM and is primarily due to HF. The HF risk associated with AF in patients with HCM is worse in patients with outflow obstruction and those who develop AF before 50 years of age. Digoxin, a positive inotrope, may increase the outflow gradient in HCM patients and should be avoided. An ICD may provide added safety with QT interval-prolonging drugs.
- 155. AF IN ACS
- 156. Class I 1. Urgent direct-current cardioversion of new-onset AF in the setting of ACS is recommended for patients with hemodynamic compromise, ongoing ischemia, or inadequate rate control. (Level of Evidence: C) 2. Intravenous beta blockers are recommended to slow a rapid ventricular response to AF in patients with ACS who do not display HF, hemodynamic instability, or bronchospasm. (Level of Evidence: C) 3. For patients with ACS and AF with CHA2DS2-VASc score of 2 or greater, anticoagulation with warfarin is recommended unless contraindicated. (Level of Evidence: C)
- 157. Class IIb 1. Administration of amiodarone or digoxin may be considered to slow a rapid ventricular response in patients with ACS and AF associated with severe LV dysfunction and HF or hemodynamic instability. (Level of Evidence: C) 2. Administration of nondihydropyridine calcium antagonists might be considered to slow a rapid ventricular response in patients with ACS and AF only in the absence of significant HF or hemodynamic instability. (Level of Evidence: C)
- 158. ACS… The incidence of AF in patients with ACS ranges from 10% to 21% independent predictor of in-hospital mortality & long-term outcome For patients who develop transient AF as a complication of ACS and who do not have a prior history of AF, the need for anticoagulation and the duration of oral anticoagulation should be based on the patient’s CHA2DS2-VASc score. The novel oral anticoagulants have not been evaluated in the context of AF and ACS. ACEI reduces the incidence of AF.
- 159. Hyperthyroidism: Recommendations Class I 1. Beta blockers are recommended to control ventricular rate in patients with AF complicating thyrotoxicosis unless contraindicated. (Level of Evidence: C) 2. In circumstances in which a beta blocker cannot be used, a nondihydropyridine calcium channel antagonist is recommended to control the ventricular rate. (Level of Evidence: C)
- 160. Hyperthyroidism….. Incidence- 5% to 15% Treatment is directed primarily toward restoring an euthyroid state Efforts to restore normal sinus rhythm may be deferred until the patient is euthyroid. The risks and benefits of treating patients with AF with a known history of thyroid disease with amiodarone should be carefully weighed prior to initiation of therapy and patients should be monitored closely.
- 161. Acute Noncardiac Illness Management of the underlying condition is the first line. Rate control preferred. unless contraindicated, a beta blocker is the preferred initial drug. The role of anticoagulation is less clear and likely disease-specific, and needs to be addressed on the basis of risk profile and duration of AF.
- 162. Pulmonary Disease: Recommendations Class I 1. A nondihydropyridine calcium channel antagonist is recommended to control the ventricular rate in patients with AF and chronic obstructive pulmonary disease. (Level of Evidence: C) 2. Direct-current cardioversion should be attempted in patients with pulmonary disease who become hemodynamically unstable as a consequence of new onset AF. (Level of Evidence: C)
- 163. Correction of hypoxia and acid-base imbalance are of primary importance. Non–beta-1 selective blockers, sotalol, propafenone, and adenosine are contraindicated in patients with bronchospasm. BB may be given if no bronchospasm. Digoxin and amiodarone may also be considered.
- 164. WPW and Pre- Excitation Syndromes: Recommendations
- 165. CLASS I 1. Prompt direct-current cardioversion is recommended for patients with AF, WPW, and rapid ventricular response who are hemodynamically compromised . (Level of Evidence: C) 2. Intravenous procainamide or ibutilide to restore sinus rhythm or slow the ventricular rate is recommended for patients with pre-excited AF and rapid ventricular response who are not hemodynamically compromised . (Level of Evidence: C) 3. Catheter ablation of the accessory pathway is recommended in symptomatic patients with preexcited AF, especially if the accessory pathway has a short refractory period that allows rapid antegrade conduction . (Level of Evidence: C)
- 166. Class III: Harm 1. Administration of intravenous amiodarone, adenosine, digoxin (oral or intravenous), or nondihydropyridine calcium channel antagonists (oral or intravenous) in patients with WPW syndrome who have pre-excited AF is potentially harmful as they accelerate the ventricular rate . (Level of Evidence: B)
- 167. WPW…. Ablation of the accessory pathway does not always prevent AF, especially in older patients, and additional pharmacological or ablative therapy may be required. Once the accessory pathway has been eliminated, the process of selecting pharmacological therapy is the same as for patients without pre-excitation. Oral amiodarone can slow or block accessory pathway conduction during chronic oral therapy. BB should be used with caution.
- 169. CLASS I 1. Control of resting heart rate using either a beta blocker or a nondihydropyridine calcium channel antagonist is recommended for patients with persistent or permanent AF and compensated HF with preserved EF (HFpEF) . (Level of Evidence: B) 2. In the absence of pre-excitation, intravenous beta blocker administration (or a nondihydropyridine calcium channel antagonist in patients with HFpEF) is recommended to slow the ventricular response to AF in the acute setting, with caution needed in patients with overt congestion, hypotension, or HF with reduced LVEF (Level of Evidence: B)
- 170. CLASS I 3. In the absence of pre-excitation, intravenous digoxin or amiodarone is recommended to control heart rate acutely in patients with HF . (Level of Evidence: B) 4. Assessment of heart rate control during exercise and adjustment of pharmacological treatment to keep the rate in the physiological range is useful in symptomatic patients during activity. (Level of Evidence: C) 5. Digoxin is effective to control resting heart rate in patients with HF with reduced EF. (Level of Evidence: C)
- 171. CLASS IIB 1.A combination of digoxin and a beta blocker (or a nondihydropyridine calcium channel antagonist for patients with HFpEF), is reasonable to control resting and exercise heart rate in patients with AF . (Level of Evidence: B) 2. It is reasonable to perform AV node ablation with ventricular pacing to control heart rate when pharmacological therapy is insufficient or not tolerated . (Level of Evidence: B) 3. Intravenous amiodarone can be useful to control the heart rate in patients with AF when other measures are unsuccessful or contraindicated. (Level of Evidence: C)
- 172. CLASS IIA 4. For patients with AF and rapid ventricular response causing or suspected of causing tachycardia induced cardiomyopathy, it is reasonable to achieve rate control by either AV nodal blockade or a rhythm-control strategy . (Level of Evidence: B) 5. For patients with chronic HF who remain symptomatic from AF despite a rate-control strategy, it is reasonable to use a rhythm-control strategy. (Level of Evidence: C)
- 173. Class IIb 1. Oral amiodarone may be considered when resting and exercise heart rate cannot be adequately controlled using a beta blocker (or a nondihydropyridine calcium channel antagonist in patients with HFpEF) or digoxin, alone or in combination. (Level of Evidence: C) 2. AV node ablation may be considered when the rate cannot be controlled and tachycardia mediated cardiomyopathy is suspected. (Level of Evidence: C)
- 174. Class III: Harm 1. AV node ablation should not be performed without a pharmacological trial to achieve ventricular rate control. (Level of Evidence: C) 2. For rate control, intravenous nondihydropyridine calcium channel antagonists, intravenous beta blockers, and dronedarone should not be administered to patients with decompensated HF. (Level of Evidence: C)
- 175. A patient who presents with newly detected HF in the presence of AF with a rapid ventricular response should be presumed to have a rate- related cardiomyopathy until proved otherwise. In this situation, it is common practice to initiate amiodarone and then arrange for cardioversion a month later. Amiodarone has the advantage of being both an effective rate-control medication and the most effective antiarrhythmic medication with a low risk of proarrhythmia.
- 176. Postoperative Cardiac and Thoracic Surgery: Recommendations
- 177. Class I 1. Treating patients who develop AF after cardiac surgery with a beta blocker is recommended unless contraindicated . (Level of Evidence: A) 2. A nondihydropyridine calcium channel blocker is recommended when a beta blocker is inadequate to achieve rate control in patients with postoperative AF . (Level of Evidence: B)
- 178. Class IIa 1. Preoperative administration of amiodarone reduces the incidence of AF in patients undergoing cardiac surgery and is reasonable as prophylactic therapy for patients at high risk for postoperative AF . (Level of Evidence: A) 2. It is reasonable to restore sinus rhythm pharmacologically with ibutilide or direct-current cardioversion in patients who develop postoperative AF, as advised for nonsurgical patients . (Level of Evidence: B)
- 179. 3. It is reasonable to administer antiarrhythmic medications in an attempt to maintain sinus rhythm in patients with recurrent or refractory postoperative AF, as advised for other patients who develop AF . (Level of Evidence: B) 4. It is reasonable to administer antithrombotic medication in patients who develop postoperative AF, as advised for nonsurgical patients . (Level of Evidence: B) 5. It is reasonable to manage well-tolerated, new-onset postoperative AF with rate control and anticoagulation ,with cardioversion if AF does not revert spontaneously to sinus rhythm during follow-up. (Level of Evidence: C)
- 180. Class IIb 1. Prophylactic administration of sotalol may be considered for patients at risk of developing AF following cardiac surgery . (Level of Evidence: B) 2. Administration of colchicine may be considered for patients post operatively to reduce AF following cardiac surgery . ( Level of Evidence: B)
- 181. Familial (Genetic) AF: Recommendation Class IIb 1. For patients with AF and multigenerational family members with AF, referral to a tertiary care center for genetic counseling and testing may be considered. (Level of Evidence: C)
- 183. AF WITH UNSTABLE HEMODYNAMICS, CHEST PAIN CARDIOVERSION NEW AF OR UNKNOWN / NO BASELINE ECG ANTI COAGULA TE BB (IV OR ORAL) KNOWN AF/ ELDERLY
- 184. NON CARDIAC ILLNESS POST CT SURGERY BB / CCB STRUCTURAL HRT DISEASE WITH LV DYSFUNCTION AMIODARONE IF FIRT LINE DRUGS FAILS OR NOT SUITABLE