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How to Treat .

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NEED TO KNOW
Atrial fibrillation is one of the causes of an irregularly irregular pulse .
Atrial fibrillation ( AF ) is diagnosed based on an ECG revealing irregularly timed QRS complexes with no discernible P waves .
AF is either valvular , if it is accompanied by certain specific valvular pathologies ( mechanical aortic or mitral valve , any rheumatic mitral valve disease , or at least moderate mitral stenosis ) or non-valvular ( all other AF , including , confusingly , all cardiac valvular disease that does not come under the definition of valvular AF ).
The non-gender specific
CHA 2
DS 2
-VA score is used to calculate stroke risk , with a NOAC recommended for those with nonvalvular AF and a CHA 2
DS 2
-VA score of 2 or above , in the absence of contraindications .
Treat valvular AF with warfarin , regardless of CHA 2
DS 2
-VA score .
Document and regularly review a rate or rhythm control method .
While AF may be sporadic , it is often a sign of untreated underlying disease such as obesity , obstructive sleep apnoea , hypertension or excessive alcohol intake .

Atrial fibrillation

Dr Gregory Harvey ( left ) Basic physician trainee , Concord Repatriation General Hospital , Sydney , NSW .
Professor David Brieger ( right ) Head of the department of cardiology , Concord Repatriation General Hospital , Sydney , NSW .
First published online on 28 April 2023
INTRODUCTION
ATRIAL fibrillation is the most common
arrhythmia seen in clinical practice and is associated with significant mortality and morbidity ; this risk can be mitigated with good clinical management . 1
The presence of atrial fibrillation ( AF ) is associated with a 3.7-fold increased risk of death and a fivefold increased risk of cardiovascular death , most of which is attributed to stroke , coronary artery disease ( CAD ) and congestive cardiac failure . 2
This How to Treat provides GPs with an overview of AF and aims to update GPs on optimal AF management .
EPIDEMIOLOGY
THE estimated prevalence of AF is 2-4 % in the general population . 3 , 4 However , its distribution is heavily skewed with regard to age — the Framingham Heart Study noted that 37 % of those who had survived to the age of 55 subsequently developed AF . 5 The prevalence is likely underestimated because of the frequency of subclinical AF . 6 In addition to age , AF is associated with obesity , obstructive sleep apnoea ( OSA ), alcohol intake , smoking , diabetes mellitus , male
gender , hypertension , congestive cardiac failure , CAD and a first-degree relative with AF . 7
AF is more prevalent among Aboriginal and Torres Strait Islander peoples , with an associated increase in morbidity and mortality . 8 In Australia , the prevalence of AF is expected to double over the next 20 years . 9 This is in large part because of our ageing population and the increased prevalence of contributory diseases such as obesity , but also partly the result of better detection of AF . 9
About one fifth of those with a first presentation of AF have an identifiable precipitant , with surgery or pneumonia identified in three fifths of cases . 10 The cumulative incidence of AF recurrence over a five-year period in those with a first presentation of AF is about 50 %, and those without an identifiable precipitant have a 25 % increased risk of recurrence . 10
AETIOLOGY AND PATHOGENESIS
AF is characterised by a self-perpetuating
cycle of high frequency , chaotic electrical conduction in the atria . This results in irregular , and often very
frequent , electrical conduction to the ventricles . This manifests mechanically as quivering or ‘ fibrillation ’ of the atria , as opposed to synchronous contraction to fill the ventricles .
AF is thought to result from abnormal atrial substrate that is the result of injury and / or fibrosis in the atria , which can occur because of age , direct damage ( from cardiothoracic surgery or ischaemia ) or systemic disease . This abnormal atrial substrate interferes with normal electrical conduction . AF further damages the atria , leading to an increased risk of further and more persistent AF , summarised by the maxim : “ AF begets AF ”. 7
The stagnant blood flow that results from the absence of synchronised contraction predisposes the patient to the formation of clots . Most clots are thought to form in the left atrial appendage ( LAA ), a small earshaped outpouching of the left atrium ( see figure 1 ), because of the especially low-flow state of blood in this area . 7
CLINICAL MANIFESTATIONS AND DIAGNOSIS
AF has a very broad range of
presentations ranging from
asymptomatic to fatal . It may present with non-specific symptoms such as fatigue and decreased exercise tolerance , or more classically , with unpleasant palpitations .
The condition may also present with acute decompensated heart failure , which can be due to a combination of the loss of the contribution of atrial contraction to ventricular filling ( the ‘ atrial kick ’), impaired ventricular filling from high ventricular rates , and the decreased ventricular ejection fraction that is also seen with high ventricular rates . Devastating stroke or other signs of AF-related cardioembolism are not uncommon presentations .
The duration and frequency of AF also varies , from a few transient seconds on rare occasions , to being permanently present . AF is generally considered ‘ paroxysmal ’ if it reverts to sinus rhythm within seven days of onset , and ‘ persistent ’ or ‘ permanent ’ when it continues beyond this time frame . AF is designated as ‘ persistent ’ when there are ongoing attempts to restore and maintain sinus rhythm , and ‘ permanent ’ when a decision has been made by patient and physician to accept the presence of AF , and