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Carole Moore, RN, MNSc, ACNP-BC Central Texas Veteran’s Health Care System Carole.Moore@va.gov

� d Decreased compliance of blood vessels through

arterial stiffening and thickening, d Mild left ventricular thickening, d A shift in the balance of early versus late

diastolic filling. d Changes result from:

�  cardiac cell enlargement �  apoptosis of neighboring cells �  subsequent fibrofatty infiltration of the

myocardium… this leads to conduction disorders

Effects of Aging on the Cardiovascular System

� d Aging is associated with

�  increased fat and collagen deposits surrounding the sinoatrial node which may result in �  delayed action potential propagation �  complete electrical separation of the node from

surrounding tissue � Decreased pacemaker cells in SA node by 90%

d Expected sinus bradycardia is muted by the reduction in parasympathetic activity

Sinoatrial node

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� d  Atrial fibrillation (AF) is the most common sustained dysrhythmia

�  Affects between 2.7 – 4.1 million Americans ATRIA Study �  1% total population; 9% for those >80 years �  More common in males than females (1.1 versus 0.8%) �  Expected to double in the next 25 years

�  Risk is progressive with age �  Life time risk over the age of 40 y/o is ~25% Framingham Heart Study �  AF is independently associated with a 50-90% increase in the risk of

death �  Treating AF adds an estimated $26 billion to healthcare costs in the

US annually �  Roughly $8700 per year per person with AF

d  Stroke risk �  15-20% of strokes are attributable to AF �  AF related strokes are more severe than non-AF related strokes

Epidemiology

� Prevalence of atrial fibrillation with age

In a cross-sectional study of almost 1.9 million men and women, the prevalence of atrial fibrillation increases with age, ranging from 0.1 for those <55 years of age to over 9 percent in those ≥85 years of age. At all ages, the prevalence is higher in men than women. Data from Go AS, Hylek EM, Phillips K, et al. Prevalence of diagnosed atrial fibrillation in adults: National implications for rhythm management and stroke prevention: The AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study. JAMA 2001; 285:2370.

� Normal anatomy & physiology

Washington Heart Rhythm Associates.

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� d Atrial fibrillation d Atrial flutter d Premature atrial contractions d Supraventricular tachycardia d Wolff-Parkinson-White syndrome d Multifocal atrial tachycardia d Sinus bradycardia d Sinus tachycardia d Sick sinus syndrome

Types of Atrial Arrhythmias

� d Common and benign d Originates away from the sinus node and sends

electrical signals through the upper chamber d Symptom: may feel skipped beat d Triggers include: caffeine, tobacco, alcohol, stress d No treatment

Premature atrial contractions

� d Rapid heart rate between 100-240 bmp d Begins and ends suddenly d Electrical impulse reenters the atrial muscle

(commonly due to variation in electrical system) d Symptoms: low blood pressure, lightheadedness,

presyncope, and sometimes syncope d Triggers include: caffeine, alcohol, exercise d Treat with ablation

Supraventricular tachycardia

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� d A form of SVT d Electrical signals fail to pause in the AV node due

to extra (accessory) connection between the top and bottom chambers of the heart

d Heart rates approach 240 bpm d Precursor to atrial fibrillation and dangerous

ventricular arrhythmias d Treat with ablation

Wolff-Parkinson-White (WPW) Syndrome

� d Characterized by variability in P wave morphology,

with three or more distinct P wave morphologies d Heart rates over 100 bpm d Associated with underlying pulmonary disease/

COPD (60%), heart disease (coronary, valve, LV diastolic dysfunction)

d Symptoms typically reflective of underlying disease

d Treat the underlying disease, consider CCB (verapamil) or BB (metoprolol); ablation

Multifocal atrial tachycardia

� d Heart rates over 100 bpm d Normal response to exercise, fever, dehydration,

pain, stress d May be triggered by adrenaline, caffeine,

nicotine, or alcohol d May reflect an underlying heart disease, lung

disease, thyroid disease, or endocrine disease d Treat underlying physiology d Consider use of negative chronotropic therapy

Sinus tachycardia

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� d Heart beats less than 60 bpm d Normal response in sleep and athletes d Associated with impaired impulse generation in

the SA node d May be triggered by negative chronotropic

medications (beta-blockers, nondihydropyridine calcium channel blockers)

d Symptoms may include lightheadedness, dizziness, hypotension, vertigo, syncope

Sinus bradycardia

� d Improper firing of electrical impulses caused by

disease or scarring of the sinus or sinoatrial node d Heart rates may fluctuate between bradycardia

and tachycardia d Symptoms may include palpitations, skipped-beats,

dizziness, lightheadedness, syncope, fatigue or weakness, confusion, and angina

d Treat with negative chronotropic medications (BB, CCB) to slow the heart rate and pacemaker implant to alleviate symptomatic bradycardia

Sick sinus syndrome

� Atrial flutter

Typical Cavotricuspid isthmus dependent Characteristics on ECG d  Negative sawtooth pattern

leads II, III, aVF d  Positive P wave in V1 d  Rate 240-300 bpm Ablation highly successful

Atypical Non-cavotricuspid isthmus dependent Characteristics on ECG d  Positive sawtooth pattern

leads II, III, aVF d  Negative P wave in V1 d  Rates may exceed 340 bpm Ablation more challenging

with less success

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�

Heart Rhythm Consult

� d  A supraventricular tachyarrhythmia with uncoordinated

atrial activation and consequently ineffective atrial contraction

d  Characteristics on an electrocardiogram (ECG) �  irregular R-R intervals (when atrioventricular [AV]

conduction is present) �  absence of distinct repeating P waves, and �  irregular atrial activity

d  Hemodynamic consequences include a variable combination of �  suboptimal ventricular rate control (too rapid or too slow), �  loss of coordinated atrial contraction (kick), �  beat-to-beat variability in ventricular filling, and �  sympathetic activation

Atrial fibrillation

�

Peninsula Heart Center

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�

Clinical Implications of Atrial Fibrillation

Gutierrez C & Blanchard DG. Atrial fibrillation: Diagnosis and treatment. Am Fam Physician. 2011 Jan 1;83(1):61-68

� d  Hypertensive heart disease - most common d  Coronary artery disease with MI or HF – atrial ischemia d  Valvular heart disease - increased LA dimension d  Cardiomyopathy/heart failure – atrial stretching d  Congenital heart disease – anomalies or defects d  Venous thromboembolic disease - ?atrial strain due to an increase

in pulmonary vascular resistance and cardiac afterload d  COPD d  Sleep apnea d  Diabetes mellitus – Possible increased left ventricular mass and

increased arterial stiffness d  Metabolic syndrome (esp. with BMI>30 d  Obesity - Increased LA pressure/volume and shortened effective

refractory period in LA and in proximal/distal pulmonary veins d  Chronic kidney disease

Risk Factors for Chronic Atrial Fibrillation

� d Cardiac surgery (30-60%) d Cardiac transplantation (10-24%) d Non-cardiac surgery (1-40%) d Hyperthyroidism (8-23%) d Inflammation/infection d Low magnesium d Alcohol/caffeine/medications d Family history/genetic d Autonomic dysfunction

Risk factors for Reversible Atrial Fibrillation

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� Term Definition

Paroxysmal AF 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.

Long-standing persistent AF

Continuous AF >12 mo in duration.

Permanent AF When the patient and clinician make a joint decision to stop 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 AF. * Acceptance of AF may change as symptoms, efficacy of therapeutic interventions, and patient and clinician preferences evolve.

Nonvalvular AF In the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair.

Atrial Fibrillation Terminology

� d Atrial arrhythmias are frequently found incidentally

during routine examinations d Symptoms may include: palpitations * dyspnea/dyspnea on exertion

reduced exercise capacity/stamina lightheadedness * chest discomfort * syncope d Urgent care (cardioversion) is indicated with:

�  Active ischemia (symptomatic with angina or electrocardiographic evidence).

�  Evidence of organ hypoperfusion (e.g., cold clammy skin, confusion, acute kidney injury).

�  Severe manifestations of heart failure (e.g., pulmonary edema).

Presentation

�

Algorithm: Acute Management of Atrial Fibrillation

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� d Rate Control versus Rhythm control

�  The AFFIRM, RACE, and AF-CHF trials demonstrated no mortality benefit between the 2 approaches

�  Restoring SR may decrease symptoms and risk of remodeling

�  Symptoms may not be recognized until SR restored �  Many will never experience a relapse to AF

d Reasons to avoid restoration of sinus rhythm �  Completely asymptomatic in the very elderly (>80 years)

or the patient with multiple comorbidities �  Asymptomatic with strong evidence of persistent AF for

more than three �  markedly dilated left atrium (>5.5 cm) �  review of prior EKGs demonstrate no evidence of sinus

Management Strategies

� d  Adequate rate control of the ventricular response

�  May decrease symptoms �  Critical in avoiding risk of tachycardia-mediated cardiomyopathy

d  Beta-blockers (Class II agents) �  IV or oral �  Metoprolol, esmolol �  Preferred after an acute myocardial infarction or exercise-induced angina

d  Calcium channel blockers (Class IV agents) �  IV or oral �  Diltiazem, verapamil �  Preferred with COPD/asthma

d  Digoxin �  Generally less effective and preferred in HF etiology �  Helpful when dealing with low normal blood pressures �  Does not convert atrial fibrillation to sinus rhythm

d  Amiodarone �  May be beneficial when other options fail to control rate

Rate Control

� d Methods:

� Electrical cardioversion � Chemical cardioversion/maintenance � EP study with ablation therapy

d Timing � Unless unstable, protect from stroke! �  Low stroke risk if arrhythmia began within 48-hours � Adequate anticoagulation for 3 weeks � Consider TEE

Rhythm Control

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� d  Preferred for initial onset

�  Duration of persistent AF inversely correlates to successful restoration of sinus rhythm

�  Most effective in converting arrhythmia to SR d Consider addition of antiarrhythmic drug (AAD);

�  Initial DCCV fails to achieve or maintain SR �  Evidence of prolonged AF (enlarged LA)

d Recommended energy: �  Atrial fibrillation: 120-200 joules �  Atrial flutter: 50-100 joules

d Not indicated in paroxysmal AF

Electrical Cardioversion

� d Antiarrhythmic drugs work by blocking:

� Na/K/Ca channels or adrenergic receptors d Many antiarrhythmic drugs have effects on

multiple ion channels and adrenergic receptors with varying cardiac and non-cardiac effects

Antiarrhythmic Drug Therapy

� Antiarrhythmic Drug Therapy

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� d  Class Ia

�  Procainamide, quinidine, disopyramide �  Main side effects: hypotension and QRS and QT prolongation in

patients with torsade de pointes �  Quinidine may increase diarrhea and thrombocytopenia �  Disopyramide helpful in hypertrophic cardiomyopathy due to

negative inotropic impact �  Not strong players in US

d  Class Ic �  Flecainide, propafenone �  Flecainide is use dependent

�  works best at high heart rates �  can also become toxic at the higher heart rates �  TST will demonstrate toxicity with QRS widening

�  Main side effects: proarrhythmia, QRS/QTc prolongation, dizziness, and visual disturbance

�  Requires addition of AV nodal blocking agents such as BB or CCB �  Contraindicated in structural heart disease

Pharmacologic Cardioversion

� d Class III

�  Amiodarone �  IV amiodarone has minimal effect in atrial tissue. �  Oral amiodarone prolongs atrial refractoriness

h  May be effective either alone or as an adjunct to DCCV to restore NSR

�  Extensive systemic side-effect profile h Thyroid toxicity: inhibits conversion of T4 to T3 h  Pulmonary toxicity: increased cough and/or dyspnea h Hepatic toxicity: low level transaminase elevationðcirrhosis

�  Significant drug interactions h Warfarin: potentiates anticoagulation effect of warfarin h Simvastatin (myositis) ; consider pravastatin

�  FDA has not labelled for use in atrial fibrillation

� d Class III (continued):

� Dronedarone � Mimics benefits of amiodarone with fewer

noncardiovascular side effects �  Contraindicated in:

h  CHF (increased mortality risk) h Permanent atrial fibrillation (increased risk for CV

death, stroke, increased rate of hospitalization) � Major side effects: GI distress � Monitor with EKGs at least quarterly and LFTs every

6 months

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� d Class III (continued):

� Sotalol & dofetilide �  Reverse use dependent

h works best on slow heart rates � Major side effects: �  Renal dose �  Strongly recommend 3 night hospitalization for

initiation of drug �  Ibutilide

� New IV AAD for acute termination of AF

� No Structural Heart Disease

Coronary Artery

Disease

Heart Failure

Severe Ventricular

Hypertrophy

First line Flecainide Propafenone Sotalol Dronedarone

Sotalol Amiodarone Dronedarone Dofetilide

Amiodarone Dofetilide

Amiodarone

Second line Amiodarone Dofetilide

Disopyramide (for Hypertrophic Cardiomyopathy)

Avoid Flecainide, Propafenone

Flecainide, Propafenone, Dronedarone

Flecainide, Propafenone

Recommendation for AAD Use

Zimetbaum P. Antiarrhythmic drug therapy for atrial fibrillation. Circulation. 2012 Jan 17; 125:381-389.

� d History lesson…

�  James Cox introduced an open heart surgical procedure that consisted of incisions and sutures that isolated compartments of the atria (a.k.a., Maze procedure, 1987)

�  Evolved into cryothermic and radiofrequency ablation �  Michael Haissaguerre and his team in Bordeaux, France

recognized that pulmonary vein foci played a key role in triggering atrial fibrillation (1990s)

�  Specialists in EP cardiology developed the method to accomplish the ablation using catheters through the groin or neck veins thereby avoiding incisions

d The goal is to create a barrier to the propagation of the atrial arrhythmia

EP Study with Ablation

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� d Minimally invasive d Relieves symptoms and improves quality of life d  Procedure is two part

�  Diagnostic: �  Maps electrical activity of the heart �  Identifies foci/ectopy

�  Interventional �  Pulmonary vein isolation �  AV node ablation (pacemaker dependent)

d Success rates: �  UNDER-ATP Trial identified 67-68% of patients (2113)

were AF free at 1 year

� d One of the most important management decisions

is whether oral anticoagulation should be prescribed to reduce the risk of stroke and embolization.

d The AFFIRM and RACE trials confirmed that stroke risk was similar despite rate versus rhythm control strategies.

d Strokes or similar thromboembolic event may be the first indication of an atrial arrhythmia

Stroke Risk

� d Consider both embolization risk and bleeding risk

(HAS-BLED score) d Discuss with patient and family d Consider bridging with LMWH when initiating heparin d Consider aspirin 81mg + clopidogrel 75mg for those

who are unable to tolerate stronger anticoagulation (fall risks, etc.)

d Timing after a stroke: �  After mild-moderate infarct: wait 24-48 hours �  After large infarct: wait for 2 weeks

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CHA2DS2-VASc ~or~ CHADS2

CHA2DS2-VASc CHADS2

CHF (LV dysfunction) 1 1

Hypertension 1 1

Age: 65+ or 75+

1 2

0 1

Diabetes mellitus 1 1

Stroke or other thromboembolic event 2 2

Vascular disease (CAD,MI,PAD, etc.) 1

Gender 1

Total possible points 9 6 Any score over 1 is suggestive for anticoagulation therapy

Risk Factors

Annual Stroke Risk

CH2ADS2-VASc CHADS2

0 0.2% 0.6%

1 0.6% 3.0%

2 2.2% 4.2%

3 3.2% 7.1%

4 4.8% 11.1%

5 7.2% 12.5%

6 9.7% 13.0%

7 11.2%

8 10.8%

9 12.2%

On the CHA2DS2-VASc score: Ø  8 points showed a lower risk than 7 points. Ø  These were the findings in the Swedish study. Ø  One should assume all scores ≥7 have a risk >10%.

0 is low risk * 1 is low-moderate risk * 2+ is moderate high risk

� Anticoagulation with Warfarin

d  Anticoagulation with warfarin or TSOA/NOAC �  Decreases stroke risk by up to 70% �  Associated with increased bleeding risk

d  Warfarin �  Requires regular lab monitoring of INR �  Therapeutic range: 2.0-3.0 �  Numerous dietary restrictions and potential drug interactions �  Preferred with patients

�  comfortable having periodic INR measurements and with relatively easy to control therapeutic range (therapeutic at least 70% of the time).

�  who are not likely to comply with the twice daily dosing of dabigatran and apixaban, and for whom once-a-day rivaroxaban or edoxaban is not available.

�  for whom the cost of the TSOA/NOACs is an important concern. �  with chronic severe kidney disease (estimated GFR less than 30 mL/min/

1.73m2). �  for whom TOAS/NOACs are contraindicated (due to comorbidities or

medications)

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�

Anticoagulation with TSOA/NOACs

d  All are now approved for use in PE/DVTs

d  Direct thrombin inhibitor �  Pradaxa (dabigatran)

�  Approved for use in PE/DVTs

�  Dosing:150mg twice daily �  Renal dose

h  SCr 30-50 and on dronedarone or ketoconazole: 75mg bid

h  SCr <30: contraindicated (not studied)

�  Geriatric (over 75): consider other agents

d  Factor Xa Inhibitors �  Eliquis (apixaban)

�  Dosing: 5mg twice daily h  Decrease to 2.5mg bid if

2 criteria are met: * age > 80 years

* weight < 60kg * SCr > 1.5

�  Xarelto (rivaroxaban) �  Dosing: 20mg daily �  Renal dose:

h  SCr 15-50: decrease to 15mg daily h  SCr <15: Contraindicated

� d Diagnosis of Atrial Fibrillation after stroke

d Cryptogenic stroke relation to atrial fibrillation d Secondhand smoke and atrial fibrillation

New Findings

� d Bridging Anticoagulation in Patients who Require

Temporary Interruption of Warfarin Therapy for an Elective Invasive Procedure or Surgery (BRIDGE) trial

d Botulinum toxin injections into epicardial fat pads

Emerging Therapies

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� d  CARDIO-FIT Study

�  Cardiorespiratory fitness was evaluated in 308 patients using exercise stress testing to determine METs prior to and after a tailored exercise program

�  Post intervention rhythm control evaluated with Holter monitor �  Atrial fibrillation burden and symptom severity decreased significantly in he group

with improved cardiorespiratory fitness (>2 METs verses <2 METs) �  No differences in baseline or follow-up characteristics �  METs gain >2resulted in a twofold greater probability of arrhythmia free survival

�  20% reduction in the risk of AF recurrence for each MET increase over baseline �  Pathak RK, Elliott A, Middeldorp ME, et al. Impact of CARDIOrespiratory

FITness on Arrhythmia Recurrence in Obese Individuals With Atrial Fibrillation: The CARDIO-FIT Study. J Am Coll Cardiol 2015:Jun 22.

d  Weight loss improves overall burden and symptom severity �  Patients who managed to lose >10% of their body weight had a 6-fold greater

chance of arrhythmia-free survival compared to patients in the other group. �  However, a weight fluctuation exceeding 5% was associated with a 2-fold

increased risk of a return of AF, even in the higher weight-loss group �  Pathak RK, et al. Long-Term Effect of Goal Directed Weight Management in an

Atrial Fibrillation Cohort: A Long-term Follow-Up Study (LEGACY Study). J Am Coll Cardiol. 2015 Mar 5. pii: S0735-1097(15)00761-5. doi: 10.1016/j.jacc.2015.03.002.

Therapies under investigation

� d  Buxton, A. Multifocal atrial tachycardia. UpToDate 2014, 9/30/2013.

d  Chen-Scarabelli, C. Supraventricular arrhythmias: An electrophysiology primer. Retrieved from the Internet on 5/10/2015 at http://www.medscape.com/viewarticle/502358_3

d  Chow GV, Marine JE, & Fleg JL. Epidemiology of arrhythmias and conduction disorders in older adults. Clin Geriatr. 2012 Nov; 28(4):539-553.

d  Dell’Orfano JT, Luck JC, Wolbrette DL, Patel H, & Naccarelli GV. Drugs for conversion of atrial fibrillation. Am Fam Physician. 1998 Aug 1;58(2):471-480. http://www.aafp.org/afp/1998/0801/p471.html

d  Dixit S, Pletcher MJ, Vittinghoff, et al. Secondhand smoke and atrial fibrillation: Data from the Health eHeart study. Published online: Sept 01, 2015 DOI: http://dx.doi.org/10.1016/j.hrthm.2015.08.004

d  Douketis, JD, Spyropoulos, AC, Kaatz, S, et al. Perioperative bridging anticoagulation in patients with atrial fibrillation. N Engl J Med. 2015; Jun 22. d  Favilla CG, et al. Predictors of finding occult atrial fibrillation after cryptogenic stroke. Stroke. 2015; Apr 7. d  January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG, Tchou PJ, Tracy CM, Yancy CW. 2014

AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2014;64:e1–76.

d  Lloyd-Jones, DM. Beyond the numbers: Epidemiology and treatment of atrial fibrillation. Medscape Cardiology, 2004;8(2). Retrieved from the Internet on 5/10/2015 at

http://www.medscape.org/viewarticle/494006

d  Pathak RK, Elliott A, Middeldorp ME, et al. Impact of CARDIOrespiratory FITness on Arrhythmia Recurrence in Obese Individuals With Atrial Fibrillation: The CARDIO-FIT Study. J Am Coll Cardiol 2015:Jun 22.

d  Pathak RK, et al. Long-Term Effect of Goal Directed Weight Management in an Atrial Fibrillation Cohort: A Long-term Follow-Up Study (LEGACY Study). J Am Coll Cardiol. 2015 Mar 5. pii: S0735-1097(15)00761-5. doi: 10.1016/j.jacc.2015.03.002.

d  Pokushalov E, Kozlov B, Romanov A, Strelnikov A, Bayramova S, Sergeevichev D, Bogachev-Prokophiev A, Zheleznev S, Shipulin V, Salakhutdinov N, Lomivorotov VV, Karaskov A, Po SS, Steinberg JS.

Botulinum toxin injection in epicardial fat pads can prevent recurrences of atrial fibrillation after cardiac surgery: results of a randomized pilot study. J Am Coll Cardiol. 2014 Aug 12;64(6):628-9. doi: 10.1016/j

d  Sposato LA, et al. Diagnosis of atrial fibrillation after stroke and transient ischaemic attack: a systematic review and meta-analysis. Lancet Neuro. 2015;14:377–387.

d  Wyndham CRC. Atrial fibrillation: The most common arrhythmia. Texas Heart Institute Journal. 200;27:257-67.

d  Zimetbaum P. Antiarrhythmic drug therapy for atrial fibrillation. Circulation. 2012 Jan 17; 125:381-389 d  Up-To-Date

�  Atrial fibrillation: Anticoagulant therapy to prevent embolization �  Epidemiology of and risk factors for atrial fibrillation �  Management of new onset atrial fibrillation �  Stroke in patients with atrial fibrillation

d  Images:

�  Gutierrez C & Blanchard DG. Atrial fibrillation: Diagnosis and treatment. Am Fam Physician. 2011 Jan 1;83(1):61-68 �  Heart Rhythm Consult. Retrieved from the Internet on 5/2015 at http://www.heartrhythmconsult.com/atrial-flutter �  Peninsula Heart Center. Retrieved from the Internet on 5/2015 at http://phc.org.au/information/diseases/arrhythmias/atrial-fibrillation �  Washington Heart Rhythm Associates LLC. Retrieved from the Internet on 5/2015 at http://www.washingtonhra.com/38.html

References

“You treat a disease, you win, you lose. You treat a person,

I guarantee you, you’ll win, no matter what the outcome.”

~ Robin Williams in Patch Adams