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What is Atrial Fibrillation

January C.T, et al. J. Am Coll Cardio. 2014:21

What is Atrial Fibrillation?

  • Supraventricular arrhythmia:
    • Supraventricular—originate above bundle of His, char by abnormal P waves w/ normal QRS and QTc intervals
  • Uncoordinated atrial activation and ineffective atrial contraction
  • Irregularly, irregular pulse

Atrial Fibrillation (or A. Fib)

  • Most common cardiac arrhythmia
  • EKG: irregular R-R intervals, no distinct repeating p waves, and irregular atrial activity
  • Worldwide: 33.5 million, ~3-6 million in US
  • Prevalence increases with age (>65), 3% of men and 2% of women
  • Contributes to >99,000 deaths per year
  • 20% of patients who have a stroke associated with AF receive an AF diagnosis at the time of stroke or shortly thereafter

Annual Death Rates from AF (2015)

•AF was the underlying cause of death in ~24,000 people and listed on ~150,000 US death certificates

•In adjusted analyses from the Framingham Heart Study, AF was associated with an increased risk of death in both males (OR, 1.5; 95% CI, 1.2-1.8) and females (OR, 1.9; 95% CI, 1.5-2.2)

–AF diminishes the survival advantage typically observed in females

Classification

  • Paroxysmal (occasional)
    • Terminates spontaneously or with intervention within 7 days
  • Persistent
    • Continuous—sustained > 7 days
  • Longstanding persistent
    • Continuous— > 12 months in duration
  • Permanent
    • Acceptance of AF: Permanent: when patient and doctor make joint decision to stop further attempts to restore and/or maintain sinus rhythm
    • Represents a therapeutic attitude vs. an inherent pathophysiologic attribute of AF
  • Attitudes and acceptance of AF may change as symptoms, efficacy of therapies, and patient/clinician preferences evolve

Nonvalvular

  • In absence of rheumatic mitral stenosis, mechanical/bioprosthetic heart valve, or mitral valve repair
  • Important because it guides therapy

January CT, et al. J Am Coll Cardiol. 2014;64:21

Strokes in AF Lead to More Disability

Lin HJ, et al. Stroke 1996;27(10):1760-1764. Tu HT, et al. Cerebrovasc Dis. 2010;30(4):389-395.

  • Larger infarcts (52 vs. 15 ml, P=0.05)
  • Higher mortality (HR= 1.84)
  • More severe hemorrhagic transformation (29% vs. 5%, P=0.002)

Risk Factors and Underlying Comorbidities to Address in Chronic AF Management

Major risk factors

  • Older age
  • Obesity
  • (Borderline) hypertension

Other risk factors

•(Pre) diabetes

•Heart failure

•Prior cardiothoracic surgery

•Smoking

•Prior stroke

•Obstructive sleep apnea

•Drug use Alcohol consumption

•Vascular disease

•Hyperthyroidism

•Lipid profile

•Coronary artery disease

•Physical inactivity

•Chronic kidney disease

•COPD

•Valve disease

•Inflammatory diseases

Brandes A, et al. Arrhythm Electrophysiol Rev.2018;7(2):118-127.Steinhubl S, et al. JAMA. 2018;320(2):146-155.

Pathophysiology

AF occurs when structural and/or electrophysiological abnormalities alter atrial tissue to promote abnormal impulse formation and/or propagation.

Heart has Purkinje fibers (specialized cardiac muscle fibers that rapidly transmit impulses from the atrioventricular node to the ventricles)

  • Fibers are split into 2 branches

Normal

  • Electrical impulse (action potential) travels down both branches
  • Meet in the connecting p/w and cancel each other out

Reentry

  • When there is a block in one of the branches, the AP only travels down one branch leads to No longer canceled out
  • Travels retrograde through the block and can then travel down the 1st branch again
  • leads to indefinite propagation leads to abnormal impulses in AF

These abnormalities are caused by diverse pathophysiological mechanisms

A.Fib Normal vs re-entry

AF begets AF

Atrial structural abnormal

  • Any disturbance in atrial structure that increases susceptibility to AF
  • Most commonly d/t extracardiac factors that increases left atrium pressure, cause atrial dilation and alter wall stress
  • Structural abnormal à alter impulse conduction/refractoriness

Mechanisms of AF

Mechanism of A. Fib

Electrophysiological mech

  • Triggers of AF
    • Abnormal focal discharges initiate AF
    • Rapidly firing foci most commonly from left atrium
    • Conduction abnormal that promote reentry d/t depolarized resting potentials that promote sodium channel inactivation
    • Abnormal intracellular calcium handling d/t diastolic calcium leak from sarcoplasmic reticulum, which can trigger delayed after-depolarization
  • ANS
    • Activation of para and/or sympathetic NS can provoke atrial arrhythmias
    • Sympathetic: activates beta-1 adrenergic R
      • Cardiac excitatory effects: increased conduction, contraction, irritability of foci
    • Parasympathetic: activates cholinergic R
      • Cardiac inhibitory effects:

Pathophysiological mechanisms

  • Atrial tachycardia remodeling: AF begets AF
  • Inflammation and ox stress
    • Inflammationà increased concentration of C-reactive protein (marker of inflammation, high-sensitivity C-rp assay can determine risk for CAD)
  • RAAS
    • Angiotensin II, ACE and aldosterone are synthesized locally in atrial myocardium and are increased during AF

Automaticity: ability of cardiac muscle to spontaneously depolarize in a reg constant manner

Key Points

•AF is common

•Prevalence increases with age

•Proper diagnosis and classification are key to properly manage arrhythmia and minimize stroke risk

Symptoms

  • Fluttering in the chest
  • Feeling faint, weakness, syncope

A.Fib increases your risk of thromboembolic stroke

Treatment

  • Rate Control
    • Control ventricular rate with beta blockers or non-DHP calcium channel blockers and AV nodal ablation
      • Medications
      • Arteriovenous (AV) junction ablation + pacemaker (PPM)
  • No attempt made to restore SR
  • Rhythm Control
    • Long-term management with cardioversion, antiarrhythmics, and radiofrequency catheter ablation
    • Attempt made to restore SR
  • Anticoagulation
    • Prevention of thromboembolism

BB: block sympathetic tone (atenolol, metoprolol, nadolol, propranolol, carvedilol)

CCB: direct AV nodal effects, block L-type Ca channels (diltiazem, verapamil)

January CT, et al. J Am Coll Cardiol. 2014;64:21

What Is AF Ablation?

•Cardiac ablation: Procedure using energy to create lesions (resulting in scarring) in the atria with the goal of stopping abnormal electrical conduction

•Pulmonary vein (PV) isolation: Electrical isolation of the PVs, which are well-known triggers for AF and are the key lesion set for an AF ablation

•Cavo-tricuspid isthmus ablation: Done in patients with concomitant atrial flutter

•Types of ablation:

–Catheter-based: Minimally invasive

–Surgical: Maze, minimally invasive, usually concomitant with open-heart surgeries (e.g., CABG)

–Hybrid approach: Catheter-based + minimally invasive surgery

Calkins H, et al. Heart Rhythm. 2017;14(10);e275-e444.

AADs

•Recurrence rates

–Amiodarone: 35%

–Sotalol: 63%

–Propafenone: 63%

•Adverse events

–Amiodarone: 18%

–Sotalol/propafenone: 11%

 Singh BN, et al. N Engl J Med. 2005;352:1861-1872.Pedersen OD, et al. Circulation. 2001;104:292-296.Freemantle N, et al. Europace. 2011;13:329-345.Piccini JP, et al. J Am Coll Cardiol. 2009;54:1089-1095.The AFFIRM First Antiarrhythmic Drug Substudy Investigators.J Am Coll Cardiol. 2003;42:20-29.Lafuente-Lafuente C, et al.Cochrane Database Syst Rev. 2007;(4):CD005049.

Key Points

•Rate control is an option for patients with few symptoms and in whom maintaining SR will be risky, challenging, or unsuccessful

–Can be achieved with medications or AV junction ablation and pacing

•Rhythm control is an option for symptomatic patients, or those who develop a cardiomyopathy–Better option for younger patients with less advanced heart disease

–Can be achieved with AADs or catheter ablation