IN THE NAME OF GOD

Atrial Fibrillation

Dr.Sima Sayah

Spring 1394

ELECTROCARDIOGRAPHIC FEATURES

Atrial fibrillation (AF) is a supraventricular arrhythmia characterized electrocardiographically by:

low-amplitude baseline oscillations

(fibrillatory or f waves)

an irregularly irregular ventricular rhythm.

The f waves have a rate of 300 to 600 beats/min and are variable in amplitude, shape, and timing

In some patients, f waves are very small and not perceptible on the electrocardiogram.

The ventricular rate during AF in the absence of negative dromotropic agents is typically 100 to 160 beats/min.

AF +regular V.rate

The ventricular rhythm can be regular during AF in patients with a ventricular pacemaker who are fully paced and when a third-degree atrioventricular (AV) block with a regular escape rhythm is present

When there is a third-degree AV block with a junctional escape, a Wenckebach exit block in the AV junction (as can occur during digitalis toxicity) results in a regularly irregular ventricular rate

CLASSIFICATION OF ATRIAL FIBRILLATION

paroxysmal :AF that terminates spontaneously within 7 days ,

persistent: AF present continuously for more than 7 days

longstanding :AF that is persistent for longer than 1 year ,

permanent : longstanding AF refractory to cardioversion .

“permanent AF” is not necessarily permanent in the literal sense because it may be eliminated successfully by surgical or catheter ablation.

Some patients with paroxysmal AF can occasionally have episodes that are persistent, and vice versa

The predominant form of AF determines how it should be categorized.

Lone AF

AF that occurs in patients younger than 60 years who do not have hypertension or any evidence of structural heart disease.

at lower risk for thromboemboli complications

the absence of structural heart disease allows the safe use of rhythm-control drugs such as flecainide

Paroxysmal AF can also be classified clinically on the basis of the autonomic setting in which it most often occurs

Approximately 25%, vagotonic AF:

in which AF is initiated in the setting of high vagal tone, typically in the evening when the patient is relaxing or during sleep. Drugs that have a vagotonic effect (such as digitalis) can aggravate vagotonic AF, and drugs that have a vagolytic effect (such as disopyramide) may be particularly appropriate for prophylactic therapy.

Adrenergic AF, approximately 10% to 15%:

beta blockers not only provide rate control but can also prevent the onset of AF.

Most patients have a mixed or random form of paroxysmal AF, with no consistent pattern of onset.

Comparison between AF &AFL

AF

AF

AF with a rapid ventricular rate of 160 beats/min.

Atrial fibrillation with complete heart block and a regular junctional rhythm at a rate of 45 beats/min.

EPIDEMIOLOGY OF ATRIAL FIBRILLATION

AF is the most common arrhythmia treated in clinical practice

The most common arrhythmia for which patients are hospitalized;(33%)

AF is associated with : fivefold increase in the riskfor stroke

twofold increase in the risk for all-cause mortality.

AF is also associated with the development of heart failure.

Incidence

o AF is age and sex related:

o ranges from 0.1% per year before the age of 40 years to>>

o higher than 1.5% per year in women >>

o and higher than 2% per year in men older than 80 years.

o Heart failure, aortic and mitral valve disease, left atrial enlargement, hypertension, and advanced age are independent risk factors for the development of AF, as are obesity and obstructive sleep apnea

o Another risk factor is psoriasis, which when severe, triples the risk for AF in patients younger than 50 years.

MECHANISMS OF ATRIAL FIBRILLATION

The mechanisms responsible for AF are complex:

Triggering events may differ from maintenance mechanisms.

There are probably two electrophysiologic mechanisms of AF:

1. one or more automatic, triggered, or microreentrant foci, so-called drivers, which fire at rapid rates and cause fibrillation-like activity, and multiple reentrant circuits meandering throughout the atria that annihilate and reform wavelets, thereby perpetuating the fibrillation.

In many studies the left atrium contains the site of dominant frequency discharge, with a left-to-right gradient

Both mechanisms may be present simultaneously

Rapid discharges from the pulmonary veins are the most common triggers of AF and may also play a perpetuating role, more so in paroxysmal AF than in persistent AF.

This is why pulmonary vein isolation is particularly effective for elimination of paroxysmal AF

PVI?

In persistent AF, changes in the atrial substrate, including interstitial fibrosis, which contributes to slow, discontinuous, and anisotropic conduction, may give rise to complex fractionated atrial electrograms(CFAEs) and reentry. Therefore, pulmonary vein isolation is rarely sufficient to eliminate persistent AF, and additional ablation of the atrial substrate is usually necessary.

GENETIC FACTORS

Several mutations have been identified.

These mutations cause a gain of function of repolarization potassium currents that results in shortening of atrial refractoriness and facilitation of atrial reentry.

Multiple polymorphisms that are associated with AF that is idiopathic, are associated with structural heart disease, or occur postoperatively

have also been identified. The end results are changes in calcium handling, fibrosis, conduction, and inflammation that predispose to AF.

CAUSES OF ATRIAL FIBRILLATION

1. hypertension (usually with left ventricular hypertrophy;

2.Ischemic heart disease,

3. mitral valve disease,

4. hypertrophic cardiomyopathy,

5. dilated cardiomyopathy.

Less common causes of AF are

a.restrictive cardiomyopathies such as amyloidosis, constrictive pericarditis, and cardiac tumors.

b. Severe pulmonary hypertension is often

associated with AF.

Obesity and obstructive sleep apnea

Obesity: atrial dilation and an increase in systemic inflammatory factors are responsible for the relationship between obesity and AF.

sleep apnea : hypoxia, surges in autonomic

tone, and hypertension.

AF is sometimes induced by tachycardia

potentially correctible causes:

hyperthyroidism,

excessive alcohol intake

Clinical symptomes

range from none to severe and functionally disabling. The most common symptoms of AF are palpitations, fatigue, dyspnea, effort intolerance, and lightheadedness.

Polyuria can occur because of the release of atrial natriuretic peptide.

Syncope is an uncommon symptom of AF

irregularly irregular pulse

“pulse deficit,”

DIAGNOSTIC EVALUATION

history

24-hour Holter recording

event monitor

Laboratory testing:TFT,LFT, renal function tests

Echocardiography

Chest radiography

A stress test

PREVENTION OF THROMBOEMBOLICCOMPLICATIONS

Risk Stratification:

CHADS2

CHA2DS2-VASc score more accurately:

In this risk score system, cardiac failure, hypertension, diabetes,vascular disease, 65 to 74 years of age, and female sex are worth 1point each, whereas age 75 years or older and previous stroke or transient ischemic event are worth 2 points.

A large-scale study demonstrated that renal failure is also an independentrisk factor for stroke in patients with AF

The relative riskfor a thromboembolic event in the absence of anticoagulation was 1.4 in patients with an estimated glomerular filtration rate lower than 45 mL/min/1.73 m2.

In recent years, advanced mapping technologies, along with studies in animal

models, have suggested the potential for complex pathophysiological mechanisms

responsible for AF, including the following:

(1) continuous aging or degeneration of atrial tissue and the cardiac conduction system;

(2) progression of structural heart disease, such as valvular heart disease and cardiomyopathy;

(3) myocardial ischemia, local hypoxia, electrolyte derangement, and metabolic disorders (e.g., atherosclerotic heart disease, chronic lung disease,hypokalemia, and hyperthyroidism);

(4) inflammation related to pericarditis or myocarditis, with or without cardiac surgery;

(5) genetic predisposition; and

(6)spontaneous or drug-induced autonomic dysfunction.

Role of Autonomic Nervous System inAtrial Fibrillation

A number of studies have suggested that both divisions of the autonomic nervous system are involved in the initiation, maintenance, and termination of AF, with a predominant role of the parasympathetic system.

Parasympathetic stimulation shortens the atrial refractory period, increases its dispersion, and decreases the wavelength of reentrant circuits that facilitate initiation and perpetuation of AF.

the data available in fact indicate that the risk for thromboembolic complications is the same in patients with paroxysmal and persistent AF. Even 15 minutes of AF may be long enough to result in local cardiac platelet activation and endothelial dysfunction, which predispose to thrombus formation during an acute episode of AF.

Modern-day dual-chamber pacemakers and implantable cardioverter-defibrillators (ICDs) are capable of detecting short episodes of asymptomatic AF that would otherwise not have been detected clinically

Subclinical atrial tachyarrhythmias were independently associated with a 2.5-fold increase in the risk for stroke.

An important consideration in patients treated with an oral anticoagulant is the risk for bleeding. HAS-BLED score

- Hypertension,

- abnormal renal or liver function,

-stroke,

- bleeding history or predisposition,

-labile international normalized ratio (INR),

- older age (>75 years),

- concomitant drug (antiplatelet agent or nonsteroidal anti-inflammatory drug) or alcohol use.

As the score increases from 0 to the maximum of 9, there is a stepwise increase in the risk for bleeding in patients treated with warfarin.

For example, in one study the annual rate of major bleeding was 1.1% in patients with a HAS-BLED score of 0,

3.7% with a score of 3, and

12.5% with a score of 5

Aspirin and Other Antithrombotic Agents

Which of the following possible reasons explains the longH-A interval shown in Figure?A. Retrograde slow pathway activation B. Retrograde delay in the compact AV nodeC. Retrograde accessory pathway conduction D. Primary mechanism of tachycardia is atrial tachycardia with the V-A and H-A intervals not representing retrograde conduction (pseudointerval)E. All of the above