• Clinical features
• Clinical Classification
• Management Strategies
• Atrial fibrillation (AF) is the most common
sustained cardiac rhythm disorder .Although
many patients present with symptoms related
to the haemodynamic disturbances conferred
by the arrhythmia ,AF is also a major risk
factor for stroke and thromboembolism. In
patients aged 80-89yrs ,it is the single most
important independent risk factor for stroke.
• The epidemiology of AF has been based on
studies in mainly caucasian populations.The
prevalence appears to double with each
decade from 0.5% of the population aged 50-
59yrs to almost 9% at age 80-89yrs.
• Prevalence is slightly higher in men than
women.The overall prevalence of AF in the
general population of all ages is increasing at a
rate greater than any increase in the
recognised risk factors for AF.
• Atrial fibrillation is an independent risk factor
for increased mortality .The proportion of
strokes attributable to AF also increases
steeply with age. In the Framingham study,AF
accounted for 23.5% of strokes in individuals
aged 80-89yrs and was the strongest
independent causative factor in stroke in this
• Furthermore,AF is present in about 15-20% of
patients who suffer acute stroke,and stroke
associated with AF has higher morbidity and
mortality,greater disability,longer stays in the
hospital and lower rates of discharge home.
• AF is also associated with impaired cognitive
function and dementia.
• There are ethnic differences in the underlying
causes of AF in the UK.
• AF is usually associated with additional
underlying disorders that “stress” the atrial
• More than 2/3rd of patients have other
• Hypertension-commonest cause in Afro-
• Ischaemic Heart Disease-commonest cause in
• Valvular heart disease
• Hypertrophic Cardiomyopathy
• Restrictive Cardiomyopathy
• Dilated Cardiomyopathy
• Congenital Heart Disease
• Constrictive Pericarditis
• High alcohol intake
• Chronic Obstructive lung disease
• Pyrexial illnesses(esp. Pneumonia)
• Pulmonary embolism
• It should be appreciated that uncomplicated
coronary artery disease (CAD)per se is an
uncommon cause of AF ;often, myocardial
infarction or left ventricular dysfunction
associated with CAD is present.
• In young patients,alcohol should be
considered as a cause of AF, particularly after
a binge(so-called holiday heart syndrome)
AF in surgical patients
• Usually following most major surgical
procedures,particularly cardiothoracic surgery
(20-50% of patients)
• It is associated with
failure,prolonged hospital stay and greater
health care costs.
• AF is caused by multiple re-entrant electrical
wavefronts within the atria that replace
normal sinus rhythm,leading to asynchronous
electrical activity,loss of atrial systolic function
and an irregular,fast ventricular response.
• The loss of atrial systolic function results in
impaired haemodynamic function of the
heart,there is a decrease in stroke volume of
about 10% in normal individuals,and a greater
fall at fast ventricular rates because of the
reduction in diastolic filling time.
• Loss of atrial systolic function becomes more
important with age,coexisting impairment of
left ventricular systolic or diastolic
dysfunction and left ventricular
hypertrophy,because atrial systole usually
makes a greater contribution (≥30%) towards
the overall stroke volume in these situations.
• Loss of atrial systolic function also results in
increased stasis within the left atrium.This
promotes intra-atrial thrombus formation
,particularly in the left atrial appendage,which
leads to an increased risk of stroke and
systemic embolism .The left atrial
endocardium in AF has also been shown to
exhibit evidence of damage or dysfunction.
• With the combination of stasis ,atrial
endocardial damage and abnormal blood
constituents,AF can therefore be considered
to fulfill Virchow´s triad for thrombus
formation and to confer a truly prothrombotic
or hypercoagulable state.
• Excessive ventricular
congestion,angina pectoris ,tachycardia-
• The pause following cessation of AF:syncope.
mesenteric, coronary arteries, spleen.
• Loss of the contribution of atrial contraction
to cardiac output:fatigue
• Anxiety secondary to palpitations.
• Features of complications such as stroke or
pulmonary oedema may also be seen in the
• AF may often be a manifestation of underlying
disorders; a careful clinical history must
therefore be taken.
• Routine haematology
• Thyroid function tests
• AF may be suspected clinically by the presence
of irregularly irregular pulse, and loss of the
“a” wave from the jugular venous
waveform,but the diagnosis can be reliably
confirmed only by documentation of the
arrhythmia on ECG.
• Diagnostic 12-lead ECG features include:
*absence of detectable Pwaves
*presence of irregular ventricular response
*fine/coarse fluctuations in the baseline
throughout,representing asynchronous atrial
• Other causes of irregularly irregular pulse to
be excluded are:
• Multiple ventricular ectopics
• Atrial flutter with varying degree block
• Complete heart block,associated bradycardia.
• Patients with paroxysmal(intermittent) AF may
require ambulatory monitoring or(if the
paroxysms are infrequent) a cardiomemo
(patient-activated recorder) to “catch” an
episode of the arrhythmia and confirm the
• Exercise treadmill may be needed if the AF is
precipitated by exercise.
• Holter monitor:Useful in paroxysmal atrial
fibrillation to determine whether it was
triggered by another arrhythmia such as when
a premature atrial complex during a rapid
paroxysmal atrial tachycardia may cause the
immediate onset of atrial fibrillation.
• The role of echocardiography in the
assessment of patients with AF remains the
subject of debate. ECHO is not helpful in
making the diagnosis,but may provide useful
information on the aetiology of the
condition(e.g.mitral valve disease,LV
impairment),and can be a useful aid in refining
risk stratification for thromboprophylaxis.
• AF may be classified as:
acute < 48hrs
chronic > 48hrs
Chronic AF may be :
• Paroxysmal chronic AF is self terminating and
has relapsing episodes.
• Persistent chronic AF has continuous episode
but susceptible to pharmacological or
• Permanent chronic AF is continuous AF
despite attempts at cardioversion.
• A longer duration of arrhythmia and
concomitant heart disease increase the
likelihood that AF will remain permanent and
that cardioversion will be unsuccessful or
• This based on the clinical classification.For
example, the aim of management in
paroxysmal AF is prevention of paroxysms and
long term maintenance of sinus rhythm ; thus
drugs such as β-blockers and class 1 or 3 anti-
arrhythmic agents are required in addition to
• In persistent AF, the aim of management is
cardioversion back to sinus rhythm thus
electrical or pharmacological (class1 or 3
antiarrhythmic ) cardioversion can be
performed with adequate antithrombotic
• In permanent AF, the aim of management is
heart rate control and appropriate
• Restoration of sinus rhythm can improve
symptoms related to the abnormal
haemodynamics of AF. Cardioversion and
maintenance of sinus rhythm may potentially
reduce the long-term risk of stroke and
thromboembolism, though this has not been
• Paradoxically, the immediate risk of
thromboembolism is increased at the time of
cardioversion. Patients should therefore be
adequately anticoagulated for at least 3 weeks
before, and at least 4 weeks after, electrical or
• In urgent situations when prior
anticoagulation is not possible, heparin should
be administered, cardioversion performed and
oral anticoagulation continued for 4 weeks.
• Patients presenting with their first episode
of acute AF who have a clear history of
arrhythmia of duration less than 48 hours
may safely be cardioverted without prior
• In some circumstances, TOE may be safely
used to exclude thrombus and allow
cardioversion without prior
• This strategy can reduce the
haemorrhagic complications of
prolonged anticoagulation and waiting
time, increasing the likelihood of
• However, all patients still require a minimum
of 4 weeks’ anticoagulation after
cardioversion, regardless of TOE findings. This
is because of the delay in return of atrial
systolic function that may persist for several
weeks after cardioversion, during which time
thromboembolism may occur, even when no
thrombus was present at the time of
• Electrical DC cardioversion has a higher
success rate than any currently available
pharmacological agent. Class Ic drugs
(flecainide, propafenone) are probably more
effective than class III drugs (amiodarone).
• However, class Ic drugs are contraindicated in
the presence of ischaemic heart disease or LV
impairment. Importantly, digoxin is no more
effective than placebo in cardioversion of AF.
Maintenance of Sinus rhythm
• In patients with paroxysmal AF, or those with
persistent AF who are successfully
cardioverted, in whom the risk of relapse is
thought to be high, the priority is to maintain
sinus rhythm and minimize recurrent episodes
Maintenance of Sinus rhythm
• Amiodarone (oral maintenance dose 200 mg
once daily) is probably the most effective drug
currently available for this indication, but the
side-effects of long-term use may make it
unsuitable in many younger patients, in whom
β-blockers or class Ic agents are (less effective)
• The development of new oral class III drugs
(dofetilide, azimilide) may improve the current
limitations in choice of drugs for maintenance
of sinus rhythm.
• Digoxin has no role in the maintenance of
sinus rhythm, and may even exacerbate
paroxysms of AF
Heart rate control
• Occasionally, the ventricular rate is already
adequate and no rate-limiting drug is
• In most patients in whom rate control is
needed, the best agents are β-blockers or
rate-limiting calcium antagonists (diltiazem
Heart rate control
• Digoxin (oral maintenance dose 62.5–250 μg
once daily) is useful for controlling the heart
rate at rest, but not with exercise.
• The choice of drug is usually influenced by
the presence or absence of additional cardiac
Mgt of Refractory AF
• Occasionally, AF is refractory to
pharmacological therapy and patients may
have to be referred for electrophysiological
Mgt of Refractory AF
• These can include atrioventricular (AV) node
ablation and permanent pacemaker implantation,
focal AF ablation, and use of an atrial defibrillator
(atrioverter) for paroxysmal AF.
• Paroxysmal AF in association with sick sinus
syndrome may respond to atrial pacing, and
multi-site atrial pacing and new pacing algorithms
are showing potential as non-pharmacological
methods for managing AF.
• To date, the most successful
electrophysiological intervention in
paroxysmal AF resistant to drug therapy is the
so-called ‘ablate and pace’ procedure, in
which the AV node is identified and ablated
percutaneously (thereby inducing iatrogenic
complete heart block), and a permanent
pacemaker is simultaneously implanted to
prevent a reduction in ventricular rate.
• This procedure often improves the symptoms
of AF but does not reduce the
thromboembolic risk, and the abnormal
intracardiac haemodynamics remain.
• The field of electrophysiology is advancing
rapidly and it may become possible to ‘cure’
many cases of drug-resistant AF. Developing
techniques include localized ablation in early
‘focal’ AF originating from the pulmonary vein
• A percutaneous version of the MAZE
procedure (a surgical technique involving
multiple incisions in the atrial wall to block re-
entrant wavelets that is effective but is usually
limited to patients who are already
undergoing cardiothoracic surgery, particularly
involving the mitral valve).
• MAZE procedure is highly effective in
preventing atrial fibrillation: only one patient
out of 65 suffered a clinical recurrence of the
arrhythmia three or more months after the
procedure. Although the long-term outcome is
not known, it remains a promising procedure
when atrial fibrillation is not controlled by
medical therapy or in those cases complicated
by recurrent thromboembolism.
• · The ‘CORRIDOR' procedure effectively
isolates both the left and right atrium, leaving
a strip of myocardium connecting the sinus
node to the atrioventricular node. This
procedure does not prevent atrial fibrillation
but isolates the fibrillating atria. Although a
70% 'cure' rate is reported, sequential
atrioventricular contraction is not restored
(with the consequent haemodynamic effects
and the risk of thromboembolism).
Prevention of TE stroke
• Several clinical trials in the last decade
conclusively show that the risk of stroke from
AF can be reduced by warfarin therapy
(relative risk reduction about 68%) and, to a
lesser extent, aspirin (relative risk reduction
Prevention of TE stroke
• Warfarin is considered the treatment of choice
in prevention of stroke in non-valvular AF
(target INR 2.0–3.0), but such therapy carries a
potential risk of haemorrhagic complications
and regular INR checks are required to
maintain the intensity of anticoagulation.
• However, the risk of stroke and
thromboembolism in AF is not uniform and
risk stratification targets warfarin therapy at
the patients at highest risk of thromboembolic
stroke. (The risk of stroke in AF ranges from <
1% per year in individuals aged < 60 years with
‘lone AF’ to > 12% per year in those aged > 74
years with a history of stroke or transient
• When the thromboembolic risk is low or
warfarin is contraindicated, aspirin, 75–300
mg p.o. once daily, may be used as an
• Anticoagulation with warfarin is advised for
• · Undergoing cardioversion (electrical or drug).
• · With underlying mitral valve disease.
• · In left ventricular failure.
• · With cardiomyopathy.
• · Above the age of 60 years.
• Paroxysmal (intermittent) AF appears to carry
the same risk of stroke as persistent and
permanent AF, and thromboembolic
prophylaxis should be similar.
• Warfarin is often under-prescribed in elderly
patients, despite the high thromboembolic
risk in this age group. However, the risk:
benefit ratio of anticoagulation and bleeding
must be assessed carefully with regard to co-
morbidity, polypharmacy and impaired
cognitive function, which may hamper