Apart from the significant impact on quality of life caused by the symptoms in some patients, the two most important complications of atrial fibrillation are the increased potential for stroke and heart failure.
There is a greatly increased relative risk of stroke in patients who have AF. This risk is the same regardless as to whether the AF is permanently present (sustained AF) or intermittent (paroxysmal AF). AF increases the relative risk of stroke by 4 to 5 times that which it would have been in the same patient if they were in sinus rhythm. In those patients in whom the AF is secondary to a mitral valve damaged by rheumatic heart disease the increased relative risk is seventeen times greater than for those in a normal regular rhythm.
Clearly this represents a significant problem but the figure that really matters is what the absolute risk of stroke is in any given individual. Someone with an already high risk of stroke who has AF is much more disadvantaged than someone with a very low background risk.
The increased risk of stroke in AF is caused by small blood clots forming in the left atrium that then break away from the wall of the heart and travel in the circulation until they encounter a blood vessel the same size as themselves which they then block, cutting off the blood supply to the tissues past the blockage. If this happens in the circulation to the brain, which is very sensitive to oxygen starvation, the tissue dies causing the stroke.
The strategies for trying to reduce the risk are based on reducing the 'clotability' of the blood in the atrium. Two types or drugs can be used: anti-platelet medication or anti-coagulants.
The most commonly used drug is Aspirin. This makes the platelets in the bloodstream less 'sticky' and therefore less likely to clump together to form blood clots. For people who can't take Aspirin there is a newer drug called Clopidogrel that has similar effects.
The main drug used in this class is Warfarin which acts to reduce some of the proteins that the body makes that contribute to the formation of blood clots. When prescribed Warfarin to reduce the risk of stroke with AF the aim is to make the blood clot about 2 to 3.5 times slower than it would do normally. (The blood test used to measure this is called the INR - which stands for International Normalised Ratio).
Both groups of medications can cause problems in some people.
A very small number of people will find that Aspirin will trigger asthma. Rather more people find that regular aspirin causes significant upper gastro-intestinal problems including indigestion, inflammation of the gullet, stomach or small bowel, and in some cases even the development of ulcers. This may in some people lead to significant bleeding into the gut.
Warfarin actually has remarkably few true side effects but by making the blood less 'clotable' it makes people more likely to suffer prolonged bleeding or to have more extensive bruising if they injure themselves. Furthermore, different people may need very different doses of Warfarin to achieve the same effects on their blood clotting. For this reason there is no 'correct' dose of Warfarin but each person has to have the dose individually tailored to their needs. This means taking blood samples to check the effect that the drug is having on them at regular intervals.
Basically this is an exercise in calculating the absolute risk of stroke in an individual and the associated benefits and side effects of the two groups of the drugs. To assess the risk we use what is called the CHAD2 calculation. Here a patient scores a point for each of the following: heart failure, hypertension, age over 75 years, or diabetes. They score 2 points if they have had a previous transient ischaemic attack (TIA; mini-stroke) or stroke. The total score determines their absolute risk of developing a stroke each year and can be compared to the risk of a significant side effect from either of the drugs. This can be seen in the tables below.
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Patients scoring 0 or 1 would usually be treated with longterm Aspirin and those with higher scores offered Warfarin.
A new surgical intervention has recently become available which can be used to reduce stroke rates in patients that are at high risk of having strokes but cannot take Warfarin. It is called 'percutaneous occlusion of the left atrial appendage'. It has recently been widely reported in the the national press.
The left atrium has a side chamber called the left atrial appendage (LAA). This is a sausage-shaped cavity that is of varying size in different people. Most clots that form within the left atrium and give rise to strokes originate in this area and so it makes sense to try to close the cavity off. Devices have now been designed to do this.
The procedure is usually carried out under a general anaesthetic.
A catheter (long tube) is inserted into a vein in the leg and gently pushed up the vein until it reaches the right atrium in the heart. From here under X-ray control it is pushed through the wall between the right and left atria so that the tip of the tube wich contains the device is now in the left atrium. At the same time the heart is imaged using Transoesophageal Echocardiography (TOE) see Echocardiography which is used to measure the size of the left atrial appendage. The correct size of device in then placed in the mouth of the LAA and expanded to fill it and to fit snuggly and firmly.
The device is only of benefit in patients in whom their AF is not due to valvular heart disease as with valvular heart disease there remains a significant risk of clots forming outside of the LAA.
There is a small but significant risk of complications and these include:
In controlled trials comparing the effectiveness of device closure of the LAA to anticoagulation with Warfarin the stroke rate fell from 3.2% per year in the Warfarin treated population to 2.3% per year in the device treated population.
The National Institute for Health and Clinical Excellence (NICE) has issued an interventional procedure guidance (349) for this treatment. NICE
Whilst patients with poor left ventricular function or heart failure are much more likely to have rhythm disturbances in general (including atrial fibrillation) it is also true that occassionally atrial fibrillation can be the cause of heart failure.
Patients with already compromised heart function due to previous heart attack, cardiomyopathies or valvular heart disease may find that they experience a sudden and marked deterioration in their exercise capacity if their heart rhythm goes into atrial fibrillation. In some patients with normal pumping function of their hearts the change of rhythm to atrial fibrillation can produce a significant generalised weakness of the contractility of the muscle of the ventricles. This usually only occurs if the atrial fibrillation is sustained and at a persistently rapid rate. This is called a tachymyopathy. Controlling the heart rate and/or returning the heart to a normal regular (sinus) rhythm can restore the pumping function in these patients.
More information on the causes and treatments of heart failure can be found by following the link to Heart Failure. Heart Failure