ATRIAL FIBRILLATION - a patient's guide
Atrial fibrillation is an irregular heart beat which can lead to blood clots and strokes. This article looks the causes of the condition and what treatment is available.
What is it?
Atrial fibrillation (AF) is the most common rhythm irregularity of the heart. It occurs when the atria, the small chambers of the heart contract in an ineffective, haphazard fashion. This results in an irregular heart beat. Atrial fibrillation may be accompanied by a rapid heart rate, a reduction in blood pressure, and reduced filling of the main chambers (the ventricles), causing reduced pumping of the blood by the heart. Many patients are unaware that they have atrial fibrillation because it does not cause them any symptoms. AF is an important condition to manage because it significantly increases the likelihood of forming blood clots that can cause a stroke.
AF may be chronic (there all the time) or come and go (paroxysmal).
Important causes of Atrial Fibrillation:
- Ischaemic heart disease (coronary artery disease)
- Hypertension (high blood pressure)
- Rheumatic heart disease and valvular disease (e.g mitral stenosis)
- Cardiac electrical syndromes (e.g. Wolff-Parkinson-White)
- Pericardial diseases (diseases of the lining of the heart)
- Cardiomyopathy (diseases of the heart muscle)
- Overactive thyroid gland
- Acute infections such as pneumonia (usually the AF is transient)
- Alcohol (long and short-term use)
- Obstructive sleep apnoea
- Pulmonary embolism (blood clots in lung)
- Following cardiac/chest surgery
- Lung cancer
Ischaemic heart disease and hypertension are the most common causes, accounting for about 65% of cases. Some patients have no identifiable cause and are referred to as having "lone" AF.
The causes above lead to atrial fibrillation through a variety of different mechanisms. In many cases, increased pressure on the atria from a poorly functioning ventricle can disrupt the normal electrical activity of the atria. This disruption leads to haphazard contraction and subsequent atrial fibrillation.
Atrial fibrillation can be diagnosed by feeling the pulse and listening to the heart. An ECG (electrocardiograph) is needed to confirm the diagnosis and to make sure that the irregularity of the heart beat is not due to other rhythm disturbances.
There is growing evidence that prolonged cardiac monitoring in patients with suspected paroxysmal AF, using a portable cardiac rhythm monitor, or implantable monitor, increases the detection of patients. These patients are also at increased risk of strokes.
While many patients are asymptomatic, common symptoms of AF include fatigue, a reduced exercise ability and breathlessness. Palpitations and light-headedness may also occur. The symptoms of AF depend to a large extent on how rapid the heart rate is and the general fitness of the patient.
Other rarer symptoms of AF include those of a stroke, or pain and swelling in a limb as a result of a limb clot, or even abdominal pain, these symptoms result from clots travelling in the circulation and blocking blood supply to important organs.
Consequences of Atrial Fibrillation
Atrial fibrillation can cause blood pressure to drop and the heart to beat inappropriately fast. This reduces blood output from the heart, and can result in congestion in the legs and lungs, especially when pre-existing heart weakness is present. Poor contraction of the atria and enlargement of the atria can cause clots to form in the atria. These clots can travel in the circulation and cause strokes and blockages of other arteries.
What can be done about it?
When a doctor discovers that a patient has atrial fibrillation, either incidentally or because the patient is experiencing symptoms, there are four main treatment approaches. The most appropriate treatment depends on the individual and the type of AF they are experiencing. If the AF is in a young, healthy patient it is important to investigate and rule out reversible causes of AF such as hyperthyroidism or infection. Conversely, the management of AF in an older person with heart failure requires a different approach.
The four main treatment approaches are:
- Converting AF back to the normal cardiac rhythm (sinus rhythm).
- Preventing attacks of AF in cases where it comes and goes (paroxysmal AF).
- Controlling the rate of AF, particularly if the heart rate is rapid.
- Preventing clot formation and its consequences.
Converting AF back to the normal cardiac rhythm (sinus rhythm)
Some patients with AF should be considered for an attempt to convert the heart rhythm back into sinus (normal) rhythm. If reversible causes can be successfully treated first, this increases the success rate of conversion back to the normal rhythm (cardioversion).
Cardioversion can be accomplished by drugs, or by an electrical shock to the heart while under anaesthesia. Drugs that have been used include "class 1" antiarrhythmic drugs, such as flecainide, quinidine, and propafenone, and "class 3" agents such as amiodarone. All these drugs have potentially serious side-effects, and should be supervised by a specialist. Success rates vary from 20% to 80% depending on the underlying cause of the AF. Electrical cardioversion has similar success.
All patients who are being considered for cardioversion should be on anticoagulation therapy (thinning of the blood, usually achieved with a drug called warfarin) prior to the procedure unless the AF is of less than 2 days duration. Anticoagulation should be continued for at least 4 weeks after cardioversion, and in cases where a high risk of relapse exists, longer. This is to prevent a a pre-formed clot dislodging from the atria and being released into the circulation once the heart has started to beat normally again.
The use of transoesophageal ECHO, whereby ultrasound pictures of the chambers of the heart are viewed via a tube down the throat, is gaining use in assessing clearly whether any clot resides in the heart prior to cardioversion. In some cases this reduces the need for anticoagulation therapy. This is particularly helpful in symptomatic or compromised patients who require immediate cardioversion.
Cardioversion is less likely to be successful in older patients, those who have had AF for more than a year, those with hypertension, and those with structural heart disease. In these cases, we often accept that the patient’s heart will remain in atrial fibrillation and manage the rate of the heart beat and minimise the clot risk instead.
Preventing attacks of AF in cases where it comes and goes (paroxysmal AF)
The drugs mentioned above may be used to prevent attacks of AF, particularly after successful conversion into sinus rhythm. About 50% of patients remain in sinus rhythm one year after cardioversion, provided they remain on anti-arrhythmic drugs. A Cochrane review published in 2015 found that several antiarrhythmic drugs are moderately effective at maintaining a normal rhythm in the heart after conversion such as quinidine, flecainide, amiodarone and metoprolol. However these drugs are associated with increased side effects, and in particular, class IA drugs (quinidine, sotalol, dysopyramide) were associated with an increased risk of all-cause mortality. Studies have not yet been able to demonstrate a difference in stroke rates for those treated with anti-arrhythmic drugs and those without, so the possible clinically-relevant benefits are yet to to be established.
Controlling the rate of AF, particularly if the heart rate is rapid
In most cases, AF is permanent and cannot be converted to normal rhythm. Instead, the focus is on controlling the heart rate. Where the heart beat is rapid, the rate can be controlled with drugs that slow the electrical impulse from the atria to the ventricles. Useful drugs include beta-blockers, and calcium antagonists (such as diltiazem). Digoxin may also be used less commonly for this purpose.
In symptomatic patients or those with heart failure, a heart rate around 70-80 beats per minute is considered optimal. In asymptomatic patients and those without heart failure a heart rate to be lower than 100 beats per minute is a good rate to aim for.
Preventing clot formation and its consequences
While rate and rhythm control are important, the highest risk that untreated AF poses is the risk of a clot being sent off into the blood stream and causing a stroke or other blockage.
AF increases the risk of a clot forming in the heart because the uncoordinated contraction of the atria slows the blood down and creates the perfect environment for clots to form. To minimise this risk, anticoagulants are given to patients to thin their blood and prevent the formation of a blood clot.
The most commonly used anticoagulant in the treatment of both chronic and paroxysmal AF is warfarin. Warfarin thins the blood by preventing the formation of four clotting factors that help blood to clot. Its action inevitably increases the risk of bleeding. In most cases, the risk of a clot outweighs the risk of bleeding and so people decide to take warfarin. It is important to be aware that this may not be the case in every scenario.
In the right context, warfarin is a very effective drug. It is cheap and has been widely studied, however it does have its downsides. The action of warfarin in the blood stream is highly variable and is influenced by many different factors such as genetics, interactions with other drugs and the diet. The correct dose must be customised to each individual based on the results of a blood test that measures the time taken for blood to clot. This blood test is called an INR test and is measured frequently during the initial period of starting warfarin, following that it is usually tested on a weekly to monthly basis.
Not all patients are suitable candidates for treatment with warfarin. This is because the risk of bleeding will be higher than the risk of stroke or blood clot, either because patients have trouble remembering to take their medication, are unable to access regular monitoring, have a high risk of falls that cannot be minimised by other strategies, or have trouble with substance abuse and cannot reliably take medication.
The reversal agent for warfarin is vitamin K. Vitamin K quickly reverses the effects of warfarin and can be used when the INR is too high, or when significant bleeding takes place.
Novel Oral Anticoagulants (NOAC)
Alternative blood thinners to warfarin have recently been developed and become more popular among patients and doctors. These are dabigatran (Pradaxa), rivaroxaban (Xarelto) and apixaban (Eliquis). Dabigatran and rivaroxaban are funded in New Zealand. Dabigatran works by inhibiting thrombin - one of the main enzymes involved in the clotting pathway. Its effects are more direct than warfarin and its actions are therefore more predictable. It does not require regular blood tests, and has a lower risk of intracranial bleeding associated with it, although there may be a slightly increased risk of gastrointestinal bleeding. The issue in the past with this medication has been that there was no specific reversal agent for it, so in the case of life-threatening bleeding, there was no way of reversing it, putting people in potentially very dangerous situations.
The drug company that made dabigatran (Pradaxa) has recently developed an antibody that binds to it, preventing it from working. This direct reversal agent is still under clinical trials but is looking very promising. It is now available in many public hospitals in New Zealand if needed in the cases of severe bleeding, and should soon be available in most.
Rivaroxaban works through a slightly different pathway but has similar properties to dabigatran. A reversal agent has also been developed to specifically target this drug, and it is still in clinical trials but should be available in the future.
Neither of these drugs are safe to use in patients with a mechanical heart valve as they have been shown to increase the risk of clots in these cases. They are also not indicated for AF associated with some cases of Rheumatic valvular heart disease (for example mitral stenosis) .In these cases warfarin remains the anticoagulant drug of choice.
They can also be used to treat clots in the legs (deep vein thrombosis) or clots in the lungs (pulmonary emboli).
Who needs to be ‘anticoagulated’ and how do we make this decision?
Anticoagulation is not without its own risks. Being on warfarin increases the risk of bleeding by around 0.5% per year. In patients at a high risk of falls or other risks of bleeding, this can have a significant impact on the likelihood of patients having serious bleeding such as an intracranial haemorrhage (a stroke caused by bleeding rather than a clot) or gastric bleeding.
The yearly risk of stroke in patients with AF can be estimated using the CHA2DS2-VASc score. Each letter represents a risk factor for increasing the risk of ischaemic stroke. A patient with a score higher than 2 should be on anticoagulation.
Congestive heart failure, hypertension, diabetes, age >75, a previous stroke, vascular disease and being female, all contribute points to the calculation of this score. Any female over 75 with atrial fibrillation automatically has a score of 2.
The score that calculates the yearly risk of major bleeding from anticoagulation is the HAS-BLED score which takes into account blood pressure, abnormal kidney or liver function, bleeding predisposition, unstable INR measurements, taking drugs or alcohol. A score of 3 and above indicates a high risk of major bleeding and calls for alternatives to anticoagulation such as aspirin to be considered. Aspirin has only a very modest effect at reducing stroke rates in patients with atrial fibrillation.
These two risk scores need to be weighed up against each other and integrated into the clinical picture to form a decision that is best for the individual patient.
In younger patients, particularly those with "lone" AF (i.e. no identifiable cause and no cardiac abnormality), the risk of clot formation causing stroke is low, and clot prevention therefore may not be required.
Even if people experience ‘paroxysmal’ AF (AF that lasts less than 7 days and comes and goes), they do still require anticoagulation and are at just as high a risk of clot formation as people who are persistently in AF. Some may even argue that the risk of clots dislodging is higher in patients who go in and out of AF than those who are persistently in AF.
Strokes and AF
Research shows that the risk of a stroke for patients with AF on no clot prevention treatment, particularly if they are older or have had a previous stroke, is about 8-10% per year. This risk can be reduced with warfarin to about 2-4% per year. However, warfarin itself has a risk of causing bleeding of around 0.5% per year.
Other treatments for AF
Catheter ablation, a minimally invasive procedure in which the parts of the heart muscle are obliterated to prevent atrial fibrillation is also a treatment option for a select number of people. It is often considered in younger patients who are symptomatic and have failed cardioversion attempts with antiarrhythmic medication and electrical cardioversion.