Saturday, 18 July 2015

Atrial Fibrillation

Atrial fibrillation (AF) is the most common cardiac arrhythmia. It is rarely a one-time event. Patients who develop AF once tend to be predisposed to developing it again & again. Current research indicates that this is primarily due to a change in the expression of ion channels that is caused by fibrillation (which may be mediated by changes in intracellular calcium caused by rapid pacing). This electrical remodelling creates an electrical “substrate” that is conducive to producing reentry. Some of the characteristics associated with AF are:



  • Symptoms: palpitations, dyspnea, fatigue, decreased exercise tolerance, chest pain



  • ECG: lack of P waves, “irregularly irregular” timing between QRS complexes & pulse pressure. The QRS complex & T waves are typically normal in duration & shape



  • Risk factors: hypertension, age, CHF, previous AF



  • Associated Pathology: atrial dilation, fibrosis, myocyte apoptosis



  • Complications: thromboembolism (due to vascular stasis in left atrium) & stroke



  • Common Origin & Mechanism: in patients with heart failure, an electrical focus around a left pulmonary vein combined with an abnormal atria; ablation of tissue around the pulmonary vein is one form of current therapy for patients with combined AF & heart failure (Khan et al., 2008).


There are two approaches to the treatment of AF:


  • Rate control, allowing AF to persist but controlling the ventricular rate by drugs affecting the AV node ERP (Effective Refractory Period), and

  • Rhythm control – with cardioversion to normal sinus rhythm & chronic treatment with antiarrhythmic drugs to prevent the reoccurrence of AF.

Arguments in favour of rate control include:


  1. Its easily achievable in most patients

  2. Avoidance of use of antiarrhythmic agents with less desirable side effects/toxicity

  3. Risk of stroke can be reduced by anticoagulant therapy

Arguments in favour of rhythm control include:


  1. Rhythm control reduces the odds of thromboembolism

  2. It was thought that patients who remain in AF have a worse outcome than those treated with drugs that maintain a sinus rhythm.

What does the evidence say?
In 2008, the results of two studies, one in North America, and one in Europe were published in the New England Journal of Medicine. In both studies, rhythm control provided no advantage over ventricular rate control with respect to survival (Fig 15A). On the basis of these results, rate control is currently considered an equally “safe” approach for the treatment of AF, and rhythm control (if it is used) can be abandoned early if it is not fully satisfactory (e.g. the patient cannot tolerate the side effects of the drugs used to suppress AF). Surgical procedures (e.g. Mini Maze procedure) involving catheter ablation of ectopic foci around the pulmonary veins may also be successful in patients with otherwise relatively normal hearts.


Figure 15. Panel A: Kaplan-Meier Estimates of Death from Cardiovascular Causes (Primary Outcome). Among 1376 patients with atrial fibrillation and congestive heart failure who were followed for a mean of 37 months, 182 patients (27%) in the rhythm-control group died from cardiovascular causes, as compared with 175 patients (25%) in the rate-control group (hazard ratio, 1.06; 95% confidence interval, 0.86 to 1.30). (From Roy et al, 2008). Panel B: Kaplan-Meier Estimates of the Percentage of Patients Remaining Free of Recurrence of Atrial Fibrillation in the two treatment groups (hazard ratio for recurrence among patients in the amiodarone group, 0.43 [95 percent confidence interval, 0.32 to 0.57]). Follow-up began 21 days after randomization (designated day 0). (From: Roy et al, 2000).


Currently amiodarone appears to be superior to other antiarrhythmics in preventing the reoccurrence of AFib (Figure 15B).


Initial conversion from AF to sinus rhythm can be achieved by either DC defibrillation or by an i.v. bolus of Amiodarone or Flecainide. Patients who are placed on rate control treatment are typically given maintenance therapy with either verapamil, diltiazem, a beta blocker or digoxin (digoxin use is more common if the patient has systolic HF).


NICE Recommendation (2014)


Perform manual pulse palpation to assess for the presence of an irregular pulse that may indicate underlying atrial fibrillation in people presenting with any of the following:


  • Breathlessness/dyspnoea

  • Palpitations

  • Syncope/dizziness

  • Chest discomfort

  • Stroke/transient ischaemic attack. [2006]


Perform an electrocardiogram (ECG) in all people, whether symptomatic or not, in whom atrial fibrillation is suspected because an irregular pulse has been detected. [2006]


Assessment of stroke and bleeding risks

Use the CHA2DS2-VASc stroke risk score to assess stroke risk in people with any of the following:


  • Symptomatic or asymptomatic paroxysmal, persistent or permanent atrial fibrillation

  • Atrial flutter

  • A continuing risk of arrhythmia recurrence after cardioversion back to sinus rhythm. [new 2014]

Use the HAS-BLED score to assess the risk of bleeding in people who are starting or have started anticoagulation.


Stroke prevention


  • Do not offer stroke prevention therapy to people aged under 65 years with atrial fibrillation and no risk factors other than their sex (that is, very low risk of stroke equating to a CHA2DS2-VASc score of 0 for men or 1 for women). [new 2014]

  • Consider anticoagulation for men with a CHA2DS2-VASc score of 1

  • Offer anticoagulation to people with a CHA2DS2-VASc score of 2 or above, taking bleeding risk into account.

  • Anticoagulation may be with apixaban, dabigatran etexilate, rivaroxaban or a vitamin K antagonist.



When to offer rate or rhythm control

Offer rate control as the first‑line strategy to people with atrial fibrillation, except in people:


  • Whose atrial fibrillation has a reversible cause

  • Who have heart failure thought to be primarily caused by atrial fibrillation

  • With new‑onset atrial fibrillation

  • With atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm

  • For whom a rhythm control strategy would be more suitable based on clinical judgement.

Rate control


Offer either a standard beta‑blocker (that is, a beta‑blocker other than sotalol) or a rate‑limiting calcium‑channel blocker as initial monotherapy to people with atrial fibrillation who need drug treatment as part of a rate control strategy.


Consider digoxin monotherapy for people with non‑paroxysmal atrial fibrillation only if they are sedentary (do no or very little physical exercise).


If monotherapy does not control symptoms, and if continuing symptoms are thought to be due to poor ventricular rate control, consider combination therapy with any 2 of the following:


  • A beta‑blocker

  • Diltiazem

  • Digoxin.

Do not offer amiodarone for long‑term rate control.


Rhythm control


Consider pharmacological and/or electrical rhythm control for people with atrial fibrillation whose symptoms continue after heart rate has been controlled or for whom a rate‑control strategy has not been successful.


Cardioversion


For people having cardioversion for atrial fibrillation that has persisted for longer than 48 hours, offer electrical (rather than pharmacological) cardioversion.


Consider amiodarone therapy starting 4 weeks before and continuing for up to 12 months after electrical cardioversion to maintain sinus rhythm, and discuss the benefits and risks of amiodarone with the person.


For people with atrial fibrillation of greater than 48 hours" duration, in whom elective cardioversion is indicated:


Both transoesophageal echocardiography (TOE)‑guided cardioversion and conventional cardioversion should be considered equally effective.



Management for people presenting acutely with atrial fibrillation


Rate and rhythm control


  • Carry out emergency electrical cardioversion, without delaying to achieve anticoagulation, in people with life‑threatening haemodynamic instability caused by new‑onset atrial fibrillation.

  • In people with atrial fibrillation presenting acutely without life‑threatening haemodynamic instability, offer rate or rhythm control if the onset of the arrhythmia is less than 48 hours, and start rate control if it is more than 48 hours or is uncertain.

  • Consider either pharmacological or electrical cardioversion depending on clinical circumstances and resources in people with new‑onset atrial fibrillation who will be treated with a rhythm control strategy.

  • If pharmacological cardioversion has been agreed on clinical and resource grounds for new‑onset atrial fibrillation, offer:

  • Flecainide or amiodarone if there is no evidence of structural or ischaemic heart disease or

  • Amiodarone if there is evidence of structural heart disease.

  • In people with atrial fibrillation in whom the duration of the arrhythmia is greater than 48 hours or uncertain and considered for long‑term rhythm control, delay cardioversion until they have been maintained on therapeutic anticoagulation for a minimum of 3 weeks. During this period offer rate control as appropriate.

  • Do not offer magnesium or a calcium‑channel blocker for pharmacological cardioversion.

Anticoagulation


In people with new‑onset atrial fibrillation who are receiving no, or subtherapeutic, anticoagulation therapy:


  • In the absence of contraindications, offer heparin at initial presentation

  • Continue heparin until a full assessment has been made and appropriate antithrombotic therapy has been started

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Atrial Fibrillation

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