A-Fib

Front 1

AF and CFAE's or complex fractionated atrial electrograms

Back 1

1. Role in A Fib has not been well clarified

2. Conclusion - CFAE plays an important role in the perpetuation of AF. Focal discharge and slow conduction, & pivoting action in CFAE region sustained wave propagation resulting in maintenance of AF

Front 2

SAFE-T

Back 2

Solatol Amiodarone AF Efficacy Trial -

Conclusion - restoration of Sinus Rhythm was associated with both long & short improvements in QOL, exercise performance and HR

Front 3

VALUE Trial

Back 3

Compared Valsataran & Amlodipine with new-onset AF and concluded that Valsataran reduced the development of new onset AF

Front 4

AF

Back 4

1. Most common form of arrhythmia
2. Affects over 5 million worldwide and 2.3 million in US
3. 43 % of all arrhythmias are AF

Front 5

What is AF

Back 5

1. Rapid arrhythmia caused when the upper chambers of the heart quiver and do not beat effectively.

2. AV synchrony is lost and this results in reduced atrial kick

Front 6

A Fib vs. A Flutter

Back 6

1. A Fib - > 300 bpm with irregular V response and is primarily a LA rhythm

2. A flutter >250-400 bpm with regular ventricular response and is primarily a RA response

You can be paced out of A Flutter but not out of A Fib

Front 7

Clincal Consequences of A-Fib

Back 7

1. Rapid V rates
2. Loss of atrial transport
3. Irregular rhythms
4. Stasis with Atrial Thrombi

Front 8

3 Classifications of A-Fib

Back 8

1. PAF or paroxysmal A - Fib -terminates spontaneously usually in 48 hours

2. Persistent A-Fib - will not terminate spontaneously but can be electrically cardioverted or converted with drugs

3. Permanent A-Fib - will not terminate spontaneously and is refractory to cardioversion

Front 9

Triggers vs Substrate

Back 9

Triggers responsible primarily for PAF and persistent AF but moves more toward substrate for Permanent AF

Front 10

Risk Factors for AF

Back 10

1. Aging
2. Male
3. Hypetension
4. Diabetes
5. Coronary Artery Disease - CAD
6. Diseases for heart valve or structures
7. Congestive Heart Failure

Front 11

Cardiac Etiologies of A-Fib (Causes

Back 11

1. Valvular Diseases
2. Vascular Diseases - Hypertension, CAD
3. Myocardial Diseases - HF, Cardiomyopathy, Acute MI, Hypertension

Front 12

Non-Cardiac Etiologies - Causes

Back 12

1. Pulmonary Pathologies - COPD, Embolism, Pneumonia
2. Diabetes
3. Alcohol Abuse
4. Hereditary but incidence is very rare

Front 13

Lone Atrial Fib:

Back 13

1. Absence of identifiable, cardiovascular, pulmonary or associated systemic disease

2. .8 to 2% of atrial fib patients

3. One study showed patients undergoing electrical cardioversion that 10% had lone AF

Front 14

Surgical Risk Factors for AF

Back 14

1. Age
2. Male
3. Hypertension
4. Intraaortic balloon pump
5. Pulmonary complications

Front 15

Echocardiographic Indicators for AF

Back 15

1. Left atrial dialation
2. P Wave duration - pts with SND & PAF - 56% AF free at 30 months with P waves <120 ms

3. P waves > 120 ms & notched is associated with high incidence of AF

Front 16

Reduce Risk for AF

Back 16

1. Alcohol
2. Beta Blockers
3. Higher cholesterol
4. Higher forced expiratory volume in 1 second

Front 17

A Fib

Back 17

1. Most common cardiac arrhythmia
2. Over the age of 60 - 4% or 1 / 25
3. Over the age of 80 10%

Front 18

A Fib Causes in 20th Century

Back 18

1. Hypertension
2. Rheumatic Heart Disease
3. CAD
4. Hyperthyroidism
5. Lone AF

Front 19

Who gets Atrial Tachyarrhthymias

Back 19

1. Bradycardia patients with a device
2. Over 50% have SND
3. Over 20% have AV Block

Front 20

AV Dissynchrony

Back 20

Typically not listed as a cause - AF causes loss of AV Synchrony but loss of AV Synchrony may cause AF

Front 21

Effects of A -Fib

Back 21

Hemodynamic

1. Loss of AV synchrony or atrial kick
2. Irregular V depolarization
3. Inappropriate increase in rate with exercise
4. Rate related cardiomyopathy

Hemostasiologic

Activation of platelets and blood coagulation system

Front 22

Studies

Back 22

1. Danish Study - looked at AAI vs VVI in patients with SND and development of A-Fib - .012

2. PASE (PAcing mode Selection in the Elderly) - compared VVIR to DDIR - QOL was superior in DDD vs VVI, Trend toward reduction in A-Fib in DDD vs. VVI but "ns"

3. CTOPP - Canadian Trial on Physiogic Pacing - compares VVIR and DDIR pacing. Factors favoring development of chronic A-Fib: age >74 years, SND, After 4 years --> 27.1% reduction in chronic A-Fib in DDDR vs VVIR

MOST Study - Pacing MOde Selection Trial

DDDR vs VVIR - ATI declined to participate in this study. 21% patients with preimplant PAF developed chronic A-Fib

Time to develop A Fib

VVIR pace 52 days
DDIR pace 124 days

Study favors DDIR

incidence of A Fib increased in all of these studies...

Front 23

AF Mechanisms

Back 23

a. 1896 Englemann proposed AF could result from a single atrial focus. Jais showed (1990s) AF cure by ablation of a single focus

b. Moe proposed multiple wavelet theory which was later confirmed by Allessie (1980s) by mapping experiments

Front 24

AF - Reentrant Mechanism

Back 24

general agreement that AF is a reentrant rhythm but precise mechanisms for its initiation and maintenance have not been resolved

Front 25

AF: initiation, perpetuation, & ablation

Back 25

1. 2 major factors for AF - focal drivers and wavelet reentry

2. Primary drivers are active in PAF and are often located in PV, SVC, vien of Marshall, and CS

3. Successful ablation requires elimination of drivers as well as breaking up the wavelets

Front 26

AF Structural Changes

Back 26

1. Structural changes with aging and fibrosis
2. Changes more extensive in AF patients
3. Lifetime risk of developing AF is 25%
4. Changes in the myocardial sleeves on the PVs.

Front 27

Structural Remodeling

Back 27

1. Chronic pressure overload can lead to structural changes resulting in interstitial fibrosis

2. Fibrosis leads to anistropy which leads to uncoupling of side to side connections of parallel fibers, slow conduction & conduction block

Front 28

Role of Angiotensin II in AF

Back 28

AF leads to fibrosis which increases with duration

Strongest triggers for fibrosis in dilation most often seen with:

1. CHF
2. CAD
3. Hypertension

ANG II may contribute to AF by:

1. Activation of intracellular pathways leading to hypertrophy & dilation

2. Aldosterone production enhancing fibrosis

Front 29

Focal AFib

Back 29

1. Initiation and maintenance of AF are due to rapidly discharging focal tachycardia

2. Mechanism is either abnormal automaticity or triggered activity because it's not inducible by NIPS

3. PV's are typically the source of ectopic foci and are an important source of ectopic beats initiating frequent PAF. These foci respond to treatment with RF ablation

Front 30

Focal Ablation

Back 30

1. Atrial foci can be identified in many patients with PAF

2. They may be amenable to ablation effectively curing or delaying development of chronic atrial fib

Front 31

Challenge of PV Ablation

Back 31

1. Difficult to map & time consuming - as each PV requires mapping
2. Pulmonary vein stenosis
3. Endothelial injury with thrombosis and embolism
4. Predisposition to other arrhythmias associated with ablation scars.

Hassaguerre (38%) recurrence rate after ablation

Front 32

AF Substrates

Back 32

not all patients show PV dilation or PV myocardial sleeves emphasizes the role of non-PV triggers for AF

Front 33

Other SVTs as AF Initiators

Back 33

SVTs can induce AF by means of mechanoelectrical feedback.

Increase in atrial pressure & stretch alters atrial refractoriness & increases dispersion of refractoriness. Helps to create substrate for reentry and Atrial Natural peptide release

Front 34

Conclusion:

Back 34

1. AF is heterogeneous disease with multiple etiologies and mechanisms

2. AF may arise from rapid discharging foci emanating from PVs or substrate abnormalities that promote multiple wavelets of reentry.

3. Electrophysiologic and structural remodeling form the substrate for reentry