Atrial Fibrillation and the NOAC s. John Raymond MS, PA-C, MHP February 10, 2018

Transcription

1 Atrial Fibrillation and the NOAC s John Raymond MS, PA-C, MHP February 10, 2018

2 Pathogenesis

3 EPIDEMIOLOGY Arrhythmia-related hospitalisations in the US Ventricular fibrillation 2% Atrial fibrillation 34% Ventricular tachycardia 10% Atrial flutter 4% Paroxysmal supraventricular tachycardia 6% Miscellaneous 21% Premature beats 6% Conduction abnormalities 8% Sick sinus syndrome 9% The most prevalent sustained rhythm disorder Accounts for 1/3 of hospitalisations due to cardiac rhythm disturbances Estimated prevalence in USA 2.2 and worldwide 5.5 million

4 PREVALENCE Prevalence % Age (years)

5 Predisposing Conditions Proportion of patients % Hypertension CHF CAD Hyper thyroidism Cardiomyopathy Depression / Anxiety Angina Diabetes PVD Idiopathic

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9 EKG Heart rate Heart rate Rhythm P-Wave QRS Complex A:>350bpm V:slow to rapid Irregularly irregular Fibrillatory (fine to course) <0.12 seconds

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12 Screening Procedures All patients o History o Physical examination o ECG o Echocardiogram: Identify structural heart disease Identify Left Ventricular Hypertrophy Identify increased LA Size Detect Clot in LA o Thyroid Function Selected patients Holter Monitor Invasive procedures

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14 Treatment Plan Unstable VS Stable <48 hrs >48hrs

15 Unstable pt-treatment Options Metal paddle ECG Heart rhythm in atrial fibrillation Cardioversion shock Normal heart rhythm SHOCK SHOCK SHOCK

16 Atrial Fibrillation > 48 Hours Control ventricular rate 3 weeks therapeutic oral anticoagulation TEE Strategy I.V Heparin DCC or Pharmacologic Cardioversion No LAA Thrombus LAA Thrombus Therapeutic Oral Anticoagulation -3wks Opt for Rate Control If LAA Thrombus still present Consider Antithrombotic Therapy

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18 Priorities in the Management of A FIB The Patient Care Pathway Rhythm Control Prevention of Thromboembolism Rate Control

19 RATE CONTROL VS RHYTHM CONTROL TRIALS AFFIRM(2002) RACE(2002) PAF(2000) STAF(2003) HOT CAFÉ(2004) RACE II ( 2010 )

20 AFFIRM Trial : Rate vs Rhythm Control Rate Rhythm Mortality, % 10 p=0.068 adjusted 5 0 Rhythm N: Time (years) Rate N:

21 APPROACH TO AFIB THERAPY Rate control plus anticoagulation preferred No or lesser AF symptoms Longer AF Hx More SHD Toxicity Risk Elderly Greater risk of proarrhythmia Rhythm control preferred Greater AF symptoms Symptoms despite rate control Younger age No or lesser SHD In anticoagulation candidates, continue anticoagulation indefinitely

22 Approach to Selecting Drug Therapy for Ventricular Rate Control* Atrial Fibrillation No Other CV Disease Hypertension or HFpEF LV Dysfunction or HF COPD Beta blocker Diltiazem Verapamil Beta blocker Diltiazem Verapamil Beta blocker Digoxin Beta blocker Diltiazem Verapamil Amiodarone

23 Strategies for Rhythm Control in Patients with Paroxysmal* and persistent AF

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25 Risk Factor Stroke Risk Stratification in AF CHADS 2 Score Cardiac failure 1 HTN 1 Age 75 y 1 Diabetes 1 Stroke 2 Total Score Annual Risk of Stroke (%) Lip GY, Halperin JL. Am J Med. 2010;123(6): Risk Factor CHA 2 DS 2 -VASc Score Cardiac failure 1 HTN 1 Age 75 y 2 Diabetes 1 Stroke 2 Vasc dz (MI, PAD, aortic ath) 1 Age y 1 Sex category (female) Stroke Rate, % 20 Relationship between CHA 2 DS 2 -VASc score and annual risk of stroke CHA 2 DS 2 -VASc Score

26 Antithrombotic Therapy ACC/AHA/ESC Guidelines 2006 Risk Factor Recommended Therapy No risk factors CHADS 2 = 0 One moderate risk factor CHADS 2 = 1 Any high risk factor or >1 moderate risk factor CHADS 2 >2 or Mitral stenosis Prosthetic valve Aspirin, mg qd Aspirin, mg/d or Warfarin (INR , target 2.5) Warfarin (INR , target 2.5) Warfarin (INR , target 3.0)

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32 NOAC s Compared to Warfarin ISCHEMIC STROKES: Similar HEMORRHAGIC STROKES: 50% Less BLEEDING: SERIOUS BLEEDS: 14% Less GI BLEEDS: 25% More MORTALITY: 10% Less

33 Characteristics of New Oral Anticoagulants 1,2 Drug Dabigatran Rivaroxaban Apixaban Betrixaban Edoxaban Mechanism of action Thrombin inhibitor FXa inhibitor FXa inhibitor FXa inhibitor FXa inhibitor Half-life h 5-9 h 12 h h 6-12 h Regimen BID QD, BID BID QD QD Peak to trough ~7x 12x (QD) 3-5x ~3x ~3x Renal excretion of absorbed drug ~80% 36-45% 25-30% ~15% 35% Potential for drug interactions P-glycoprotein inhibitor CYP3A4 substrate and P-glycoprotein inhibitor CYP3A4 substrate and P-glycoprotein inhibitor Not substrate for major CYPs CYP3A4 substrate and P-glycoprotein inhibitor 1. Usman MH, et al. Curr Treat Cardiovasc Med. 2008;10(5): Piccini JP, et al. Curr Opin Cardiol. 2010;25(4):

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35 Summary AF is a common disease that is increasing in prevalence For any patient with AF, decisions need to be made regarding antithrombotic therapy, rate control, and/or rhythm control Guidelines provide recommendations for the management of patients with AF Anticoagulation is essential in AF patients with risk markers, regardless of any restoration of SR New agents and procedures may provide antiarrhythmic and antithrombotic options with improved outcomes for managing AF

36 A-Fib vs. EP Labs

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