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ATRIAL FIBRILLATION

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					ATRIAL FIBRILLATION

     Adeyeye V.O.
                   OUTLINE
•   Introduction
•   Epidemiology
•   Aetiology
•   Pathophysiology
•   Clinical features
•   Investigations
•   Clinical Classification
•   Management Strategies
               Introduction
• 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.
              Epidemiology
• 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.
               Epidemiology
• 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
  age group.
• 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.
                  Aetiology
• 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
  myocardium.
• More than 2/3rd of patients have other
  cardiovascular diseases.
              Cardiac causes
• Hypertension-commonest cause in Afro-
  Caribbeans.
• Ischaemic Heart Disease-commonest cause in
  Indo-Asians.
• Valvular heart disease
• Hypertrophic Cardiomyopathy
• Restrictive Cardiomyopathy
• Dilated Cardiomyopathy
• Congenital Heart Disease
• Constrictive Pericarditis
            Non-cardiac causes
•   High alcohol intake
•   Thyrotoxicosis
•   Diabetes
•   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
  stroke,thromboembolism,heart
  failure,prolonged hospital stay and greater
  health care costs.
              Pathophysiology
• 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.
             Clinical features
• Excessive ventricular
  rate:hypotension,pulmonary
  congestion,angina pectoris ,tachycardia-
  mediated cardiomyopathy.
• The pause following cessation of AF:syncope.
• Systemic
  embolisation:brain,extremities,renal,superior
  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
  patients.
              Investigations
• AF may often be a manifestation of underlying
  disorders; a careful clinical history must
  therefore be taken.
• Routine haematology
• Biochemistry
• 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
  electrical activity.
• 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
  diagnosis.
• 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.
          Clinical Classification
• AF may be classified as:
     acute < 48hrs
     chronic > 48hrs
Chronic AF may be :
     Paroxysmal
     Persistent
     Permanent
• Paroxysmal chronic AF is self terminating and
  has relapsing episodes.
• Persistent chronic AF has continuous episode
  but susceptible to pharmacological or
  electrical cardioversion.
• 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
  deemed inappropriate.
        Management Strategies
• 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
  antithrombotic therapy.
• 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
  cover.
• In permanent AF, the aim of management is
  heart rate control and appropriate
  antithrombotic therapy.
              Cardioversion
• 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
  conclusively proven.
• 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
  pharmacological cardioversion.
• 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
  anticoagulation.
• In some circumstances, TOE may be safely
  used to exclude thrombus and allow
  cardioversion without prior
  anticoagulation.
• This strategy can reduce the
  haemorrhagic complications of
  prolonged anticoagulation and waiting
  time, increasing the likelihood of
  successful cardioversion.
• 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
  cardioversion.
• 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
  of AF.
    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)
  alternatives.
• 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
  required.
• In most patients in whom rate control is
  needed, the best agents are β-blockers or
  rate-limiting calcium antagonists (diltiazem
  and verapamil).
            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
  disease
          Mgt of Refractory AF

• Occasionally, AF is refractory to
  pharmacological therapy and patients may
  have to be referred for electrophysiological
  interventions.
           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
  orifices.
• 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
  about 21%).
        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
  ischaemic attack.)
• When the thromboembolic risk is low or
  warfarin is contraindicated, aspirin, 75–300
  mg p.o. once daily, may be used as an
  alternative.
• Anticoagulation with warfarin is advised for
  certain patients:
• · 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
  anticoagulation.

				
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posted:8/26/2012
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