1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Atrial fibrillation

2. --Most common cardiac arrhythmia.
--Characteristics:
•The RR intervals “irregularly irregular.”
•There are no distinct P waves. Thus, even when P-P interval can be
defined, it is not regular and often less than 200 milliseconds =atrial
rate >300 beats/minute.
--The prevalence of paroxysmal AF, which is more likely to be detected
with ambulatory monitoring, is much higher
--ATRIA study in USA (1.9 million):
•The overall prevalence of AF was 1%; 70% were at least 65 years.
•The prevalence of AF ranged from 0.1% among adults less than 55
years of age to 9% in those ≥80 years of age.
•The prevalence was higher in men than women (1.1 versus 0.8 %)
--Incidence increases with age, IHD

3. RISK FACTORS AND DISEASE ASSOCIATIONS
-Hypertensive heart disease and coronary heart disease (CHD) are the
most common underlying disorders in developed countries
-In AMI, AF develops in 6-10% due to atrial ischaemia or atrial
stretching from HF
-Rheumatic heart disease is associated with a much higher incidence
of AF in developing countries
-HF
-HCM 10-28%, prognostic imp. unclear
-Congenital heart
ASD (20%, inc with age)
Ebstein's anomaly, PDA
After surgical correction of some other abnormalities, including
ventricular septal defect, tetralogy of Fallot, pulmonic stenosis, and
transposition of the great vessels

4. -10-14% documented PE
-COPD, peripartum cardiomyopathy, lupus myocarditis, and both
idiopathic and uremic pericarditis
-Possible causal relationship between obstructive sleep apnea (OSA)
and AF
-Obese individuals (BMI >30 kg/m2) are significantly more likely to
develop AF
-Metabolic syndrome
-Hyperthyroidism:
inc beta adrenergic tone, inc thyroid hormones (increased
automaticity and enhanced triggered activity of pulmonary vein
cardiomyocytes)
-Subclinical hyperthyroidism (dec TSH)
-Possible relationship between AF and hypothyroidism has been
suggested but not proven

5. Surgery
--The incidence is greatest in patients undergoing coronary artery
bypass graft (CABG) or cardiac valve surgery.
--Cardiac surgery :
30 to 40% early post CABG
37 to 50% after valve surgery
60% valve replacement plus CABG
10 to 24% of patients with a denervated transplanted heart, often in
the absence of significant rejection. Mostly within the first two weeks,
while AF developing after two weeks may be associated with an
increased risk of subsequent death
--Noncardiac surgery:
AF is less common after noncardiac compared to cardiac surgery.
Most episodes occurred within the first three days after surgery.
The risk was greatest with intrathoracic surgery (12%).

6. --Family history:
The presence of AF in a first-degree relative, particularly a
parent, has long been associated with an increase in risk
--Genetics:
-For the majority of patients, genetic susceptibility, if present, is
probably a polygenic phenomenon=combined effects of a
number of genes
-Some families have been identified in which AF inheritance
follows more typical Mendelian patterns, consistent with a
single disease-causing gene
-Mutations in SCN5A have also been identified in several other
cardiac disorders, including the long QT syndrome, the Brugada
syndrome, familial atrioventricular conduction block, and
familial sick sinus syndrome

7. --Birth weight:
A possible relationship between birth weight and the
development of AF
Incident AF increased significantly from the lowest to
the highest birth weight
--Inflammation and infection:
Inflammation, as determined by CRP, is not likely to be
causative of atrial fibrillation
--Pericardial fat is visceral adipose tissue with
inflammatory properties; both obesity and inflammation
are risk factors for AF

8. --Autonomic dysfunction:
The autonomic nervous system may be involved in the initiation
and maintenance of AF as both heightened vagal and
sympathetic tone can promote AF
--Other supraventricular tachyarrhythmias:
-Spontaneous transition between typical atrial flutter and AF
has been observed. In addition, AF is, in some patients,
associated with paroxysmal supraventricular tachycardia
(PSVT)
-Enhanced vagal tone, or atrial premature beat can cause stable
PSVT to degenerate into AF or retrograde conduction via the
accessory pathway of a premature beat, stimulating the atrial
myocardium during its vulnerable period

9. --Alchol:
AF occurs in up to 60% of binge drinkers with or without an
underlying alcoholic cardiomyopathy ="the holiday heart
syndrome.“ in most cases
--Caffeine:
Despite the theoretical relationship between caffeine and
arrhythmogenesis, there is no evidence in humans that
ingestion of caffeine in doses typically consumed can provoke
AF or any other spontaneous arrhythmia
--With regard to dietary fish intake and incident AF, three
cohort studies (approximately 45,000, 48,000, and 5000
individuals) found no relationship, while one (approximately
5000 individuals) suggested a reduction in AF burden

10. --Medications:
Certain medications can cause or contribute to the
development of AF =theophylline, adenosine (with the
WPW, due to conduction down the accessory
pathway), drugs that enhance vagal tone, such as
digitalis

11. Longterm outcome
1. Death : Death rate doubled (Only antithrombotic therapy has been
shown to reduce AF-related deaths).
2. Stroke (includes haemorrhagic stroke and cerebral bleeds):
Stroke risk increased; AF is associated with more severe stroke.
3. Hospitalizations:
Hospitalizations are frequent in AF patients and may contribute to
reduced quality of life.
4. Quality of life and exercise capacity:
Wide variation, from no effect to major reduction.
AF can cause marked distress through palpitations and other AF-
related symptoms.
5. Left ventricular function:
Wide variation, from no change to tachycardiomyopathy with acute
heart failure.

12. PATHOGENESIS
--Sustained AF seems to require the development of multiple wavelets
(rather than the single wavefront as seen in atrial flutter).
--Majority of episodes of paroxysmal AF (PAF) are triggered by atrial
premature beats, while a small number are preceded by typical atrial
flutter or atrial tachycardia
--Atrial premature beats appear to be most important as a trigger in
patients with PAF who have normal or near-normal hearts, much less
clear in patients with significant structural heart disease
--Ectopic foci are most often located near the pulmonary veins, in
patients with minimal or no structural heart disease
--Ablation of sites with a high dominant frequency, mostly located at
or close to the junction between the PVs and the left atrium, results in
progressive prolongation of the AF cycle length and conversion to
sinus rhythm in patients with paroxysmal AF, while in persistent AF,
sites with a high dominant frequency are spread throughout the entire
atria, and ablation or conversion to sinus rhythm is more difficult

13. --Other factors that may contribute to AF in near normal
patients include increased vagal tone and possible
subclinical myocarditis
--As AF becomes established, the refractory period of the
atrial muscle shortens (down-regulation of the L-type Ca2+
inward current, up-regulation of inward rectifier K+
currents) predisposes to further AF (ie, AF begets AF).
--Conversely, when sinus rhythm is sustained, these
electrophysiologic changes reverse (sinus rhythm begets
sinus rhythm).
--Echocardiographic risk factors: Left atrial enlargement,
increased left ventricular wall thickness and reduced left
ventricular fractional shortening.

14. Structural abnormalities associated with AF
Extracellular matrix alterations
Interstitial and replacement fibrosis
Inflammatory changes
Amyloid deposit
Myocyte alterations
Apoptosis
Necrosis
Hypertrophy
Dedifferentiation
Gap junction redistribution
Intracellular substrate accumulation (haemocromatosis, glycogen)
Microvascular changes
Endocardial remodelling (endomyocardial fibrosis)

15. Clinical correlates
1-Thrombo-embolism:
-LAA is the dominant source of embolism(90%) in non-valvular AF.
-‘Flow abnormalities’:
stasis within the left atrium,
reduced (LAA) flow velocities
spontaneous echo-contrast on(TOE).
-‘Endocardial abnormalities’:
Progressive atrial dilatation
endocardial denudation
oedematous/fibroelastic infiltration of the extracellular matrix.
-‘Abnormalities of blood constituents’:
haemostatic and platelet activation
Inflammation and growth factor abnormalities

16. 2-Haemodynamic changes:
Loss of coordinated atrial contraction (5-15% of COP)
High ventricular rates (dec filling as dec diastole)
Irregularity of the ventricular response
Decrease in myocardial blood flow
Long-term alterations such as atrial and ventricular
cardiomyopathy.

17. CLASSIFICATION (ACC/AHA/ESC)
applies to recurrent episodes of AF that last more than 30 seconds and that are unrelated to a reversible
cause
•First detected or diagnosed, irrespective of the duration or the presence or
absence of symptoms.
•Paroxysmal (ie, self-terminating or intermittent) AF:
Defined as recurrent AF (≥2 episodes) that terminate spontaneously in less
than seven days, usually less than 24 hours.
Progression to persistent and permanent AF occur in >50% beyond 10 years
despite antiarrhythmic therapy.
•Persistent AF:
Fails to self-terminate within seven days. Episodes often require
pharmacologic or electrical cardioversion to restore sinus rhythm.
The ESC recognizes a category called “long-standing persistent AF,” which
refers to AF that has lasted for one year or more when it has been decided to
adopt a rhythm control strategy.
•Permanent AF:
More than one year and cardioversion either has not been attempted or has
failed.

18. LONE AF
-Individuals with paroxysmal, persistent, or
permanent AF who have no structural heart disease.
-Less than 15 to 30% of cases of permanent AF and 25
to 45% of cases of paroxysmal AF
-Younger than those with structural heart disease and
are often male
-Often symptomatic and associate certain triggers with
episodes of AF: sleeping, exercise, alcohol, eating
-Family history of AF is present in up to 38%

19. RECURRENT AF
Continuous monitoring studies have shown that
approximately 90% of patients have recurrent episodes
of AF. However, up to 90% of episodes are not
recognized by the patient

21. History and physical examination
--Not all patients with AF are symptomatic.
--Description of the symptoms: onset or date of discovery,
the frequency and duration, severity, and qualitative
characteristics.
--Typical symptoms:
palpitations, tachycardia, fatigue, weakness, dizziness,
lightheadedness, reduced exercise capacity, increased
urination, or mild dyspnea.
More severe symptoms include dyspnea at rest, angina,
presyncope, or infrequently, syncope.
some patients present with an embolic event

22. --Precipitating causes: exercise, emotion, or alcohol.
--Disease associations:
cardiovascular or cerebrovascular disease, diabetes,
hypertension, chronic obstructive pulmonary disease,
or potentially reversible causes (eg, hyperthyroidism,
excessive alcohol ingestion).
--Examination: Abnormal findings may inform about
either contributing factors for (eg, murmur of mitral
stenosis) or the impact of (eg, evidence of heart failure)
AF or complications (eg, CVS)

23. Electrocardiogram
Essential………….
--The ECG should also be evaluated for the following
information:
•Markers of nonelectrical cardiac disease, such as left
ventricular hypertrophy (possible hypertension) or Q
waves (possible coronary artery disease)
•Markers of electrical heart disease, such as delta wave or
short PR interval (preexcitation) or bundle branch block
(conduction system disease)
•The QT interval (to identify the potential risk of
antiarrhythmic therapy).

24. Echocardiogram
--To evaluate the size of the right and left atria and the
size and function of the right and left ventricles
--To detect possible valvular heart disease, left
ventricular hypertrophy, and pericardial disease
--To assess peak right ventricular pressure.
--Transesophageal echocardiography is much more
sensitive for identifying thrombi in the left atrium or
left atrial appendage.

25. Additional testing
--Exercise testing :
-For patients with signs or symptoms of ischemic heart disease
(which is not a common cause of AF).
-Help guide pharmacotherapy for AF as some antiarrhythmic
medications are contraindicated in patients with coronary artery
disease
--Holter monitoring:
-To identify the arrhythmia if it is intermittent and not captured
on routine electrocardiography
-To assess overall ventricular response rates, especially in
individuals where a rate control strategy has been chosen
--TSH should be obtained in all patients with AF
--Complete blood count, a serum creatinine, an analysis for
proteinuria, and a test for diabetes mellitus

26. EHRA score (for symptoms severity)
Classification of AF-related symptoms:
EHRA I ‘No symptoms’
EHRA II ‘Mild symptoms’; normal daily activity not
affected
EHRA III ‘Severe symptoms’; normal daily activity
affected
EHRA IV‘Disabling symptoms’; normal daily activity
discontinued

27. CCS-SAF

29. Thank you