The heart has four chambers, and the top two are known as the atria (see figure below). Contraction of the heart is controlled by an electrical system with a pacemaker located at the top of the right atrium. As people age, and when other conditions such as high blood pressure develop, the ability to conduct electricity in the atria changes and can become chaotic, called fibrillation. When the atria fibrillate, the atria do not contract at all and blood inside can stagnate and form clots. Clots from the heart can break off and make their way to the brain resulting in a stroke. This is why atrial fibrillation is the leading cardiac cause of stroke in young people.
Normal electrical conduction and atrial fibrillation
AF usually first occurs intermittently, known in medical parlance as ‘paroxysmal’. Typically, the heart races very fast and irregularly and when this occurs it causes palpitations, breathlessness, lightheadedness, tiredness or even loss of consciousness. It can also occur without causing symptoms in up to 25% of people with AF.
Paroxysmal AF (or PAF) is usually triggered by an extra heartbeat, or ectopic, from just inside one of the pulmonary veins (see figure below). The pulmonary veins, of which there are usually four, carry blood back from the lungs to the left atrium. Episodes can last from seconds or minutes, to hours or days. The flipping in and out of rhythm when episodes occur can be very uncomfortable and sometime long pauses can occur after an episode of AF abruptly stops. Common precipitants include alcohol (sometimes even very small amounts), caffeine, tiredness and stress but AF can also occur for no obvious reason or even when asleep in some people.
If an AF episode lasts longer than 7 days it is called ‘persistent’. When AF lasts this long it means the electrical properties of the atria are sufficiently abnormal that they continue to fibrillate rather than spontaneously return to normal rhythm. This is more likely if a patient has a history of high blood pressure or has another cardiac disease. The typical natural history of AF is for it to start off as paroxysmal and with time become persistent. However, many patients present with persistent AF without a clear history of previous intermittent attacks.
If AF is persistent, treatments designed to convert and keep patients in normal rhythm are less effective than in paroxysmal AF and the longer AF has persisted, the less effective these treatment become. Although it can cause palpitations, persistent AF commonly causes tiredness, breathlessness and reduced exercise capacity. It also causes no symptoms in up to 25% of people.
Permanent AF is defined as AF that is present all the time (like persistent AF) but no efforts are made to try to restore normal rhythm, or efforts to do so have failed. Sometimes this strategy is chosen as the AF does not cause symptoms, sometimes because treatments to restore normal rhythm are deemed too risky or sometimes because the AF has been present for so long that it’s thought treatments are very unlikely to work.
The risk of stroke is the most important adverse effect of atrial fibrillation. The risk is not determined, as one might think, by the length of time you spend or have spent in AF. Rather it is one’s overall risk for stroke that is important. This risk is calculated by using a scoring system called the CHA2DS2-VASc score.
The CHA2DS2-VASc score is an acronym. It stands for:
If you have or have ever had one of these conditions you score one point for each, except age >75 or stroke/TIA which count as 2 points, hence CHA2DS2VASc score.
If you have a CHA2DS2VASc score or 1 or more, it is now recommended you take warfarin or a Novel Oral Anticoagulant for life to reduce your risk of stroke. So, if you are 65 or older and have AF, it is now recommended you are treated with an anticoagulant for the rest of your life (and not aspirin which is now known not to be beneficial). The only exception to this is if you are female and have no other risk factors. You still score 1 point on the CHA2DS2-VASc scoring system but you do not need to take warfarin or a Novel Oral Anticoagulant until or unless you score another point in the future.
AF is responsible for about 25% of all strokes. The rest are due to artery disease within the brain, most commonly seen in older people. Of patients who have a stroke due to AF, about 10% will die and a further 40% will have developed a permanent disability. This is why ensuring patients are appropriately anti-coagulated is so important.
In atrial fibrillation it is common for the heart to race uncontrollably, with heart rates as fast as 200/min. If the heart is left to race at these uncontrolled rates for long periods (weeks or months), some people will develop an enlarged heart and ultimately heart failure. One of the key aspects of treatment is to prevent the heart from beating rapidly when in AF, and different medications can be used to slow the heart. These drugs are especially useful for persistent and permanent AF and often work best in combination.
These drugs are also given in combination with a drug called Flecainide to treat paroxysmal AF, to prevent rapid heart rates.
In addition to the importance of reducing stroke and preventing heart failure, symptoms such as palpitations and breathlessness typically require treatment. There are broadly three treatment options for symptomatic AF. The first is medication, the second is a procedure called DC cardioversion (usually for persistent AF) and the third is a curative procedure called ablation (see below).
AF can be diagnosed on an ECG or on a cardiac monitor. It can also be detected by almost all implanted monitors (the Linq device), pacemakers and defibrillators.
There are numerous medications used to try and prevent AF episodes, most of which have been available for decades. These drugs are known as anti-arrhythmic drugs and include flecainide, propafenone, amiodarone and aotalol. Dronedarone is a new drug, which has now been limited in its prescription by the European Medicines Agency. It is only for use to prevent AF after a cardioversion and only in patients with normal hearts.
Medications are unfortunately not highly effective at maintaining normal rhythm for any length of time, the best being amiodarone with long term success achieved in about 30% of people. Sadly, amiodarone also has the highest number of unwanted and potentially dangerous side effects (including thyroid dysfunction, lung scarring, liver damage and excess skin sensitivity to sunlight). Flecainide, propafenone and sotalol have a very tiny risk of causing more serious heart rhythm disturbances and in rare cases dying, particularly if a patient develops heart failure or a heart attack, or exercises very strenuously. For these reasons, and to abolish symptoms, ablation is often considered to try and achieve a cure.
Cardioversion is a long-established technique that is designed to immediately restore normal rhythm when patients are in AF. If an electrical charge is applied across the chest when one is in AF, it resets all the cells of the atria allowing the heart’s own pacemaker to take over. This is performed under a light general anaesthetic with gel pads placed on the front and back of the chest and the ‘shock’ applied between the two. The shock only lasts a fraction of a second and is not always successful in restoring normal rhythm. If normal rhythm is restored, the shock has no further effect and the heart can flip back into AF at any time, even seconds later. The chance of remaining in normal rhythm one year after a cardioversion is only 50% and at 5 years is only 5%. Its use is therefore quite limited nowadays. It is usually offered to patients with persistent AF when they first present and it is also used in emergency situations when patients are unwell due to rapid AF. I use it as a tool to see if patients feel better in normal rhythm if they have mild symptoms, or the onset of AF was insidious. This is useful to see if ablation is likely to be beneficial.
Ablation is a technique of heating small areas of tissue within the heart to destroy that tissue to prevent abnormal heart rhythms from occurring. Although ablation for other arrhythmias was first performed in the early 1980’s, it was only developed for AF using ‘keyhole techniques’ in 1999 and only widespread around the world from the early 2000s. Since then there have been rapid and dramatic improvements in available technologies and the different techniques used with ever-increasing success rates. It is now by far the most commonly performed ablation procedure in the world. For more information please see the ‘AF ablation’ page.
AF Ablation in the left atrium
Unfortunately, AF almost always recurs once it has occurred once, although attacks can initially be separated by several years. Although drugs and cardioversion can keep it at bay temporarily, it is only ablation that can offer the chance of a permanent cure. Patients with AF are known to not live quite as long as those who do not have AF. It is not the AF itself that leads to death (although this can happen if stroke occurs) but it is believed to be a marker of general cardiovascular health. It is not known if successful ablation changes this prognosis but trials are underway to assess this (the CABANA and EAST trials). It is speculated by many electrophysiologists that successful ablation should have an impact on prognosis.
Unlike atrial fibrillation, atrial flutter is due to a single abnormal short circuit within either atrium. The commonest type is located in the right atrium and is known as typical atrial flutter (this is the heart rhythm disorder Tony Blair had, who went on to have successful ablation performed). Electricity rotates rapidly around the tricuspid valve, the valve between the right atrium and right ventricle. It can rotate in an anti-clockwise direction (known as typical flutter), or a clockwise direction (known as clockwise right atrial flutter).
There are several other types of ‘atypical’ flutter, which can occur in the left and right atrium. These are often seen after ablation within the left atrium for persistent AF, or in patients with congenital heart defects or those who have had surgery to either atrium. Like AF, flutter also leads to stagnation of blood within the atria and therefore there is a risk of forming clots leading to stroke. The CHA2DS2VASc scoring system is used in the same way as AF to determine which people need to take an anticoagulant. However, the threshold for performing curative ablation for flutter is lower than AF, as the success rates are higher, the risk often lower and drugs work particularly poorly for all types of flutter. The same CHA2DS2VASc score of 1 is used as the cut off for needing warfarin or an equivalent drug unless the point is for being female (see above).
In contrast to AF, first line treatment for typical atrial flutter is catheter ablation. This is because ablation for typical flutter is highly effective (90% cure with one attempt) and has a very low risk (1 in 500 – principally that of damage to the AV node requiring a pacemaker to be implanted, or making a tiny hole in the heart – requiring a drain to be inserted under the ribs, or very rarely surgery). It has been shown in randomized trials that ablation is significantly better than drugs or cardioversion as a first line treatment for typical flutter. The procedure is usually quick (30-60 minutes) and patients can return home the same day. Ablation in this part of the heart is often painful and for this reason may be performed under general anaesthetic.
It is also common for patients to have both AF and atrial flutter at the same or different times. Anti-arrhythmic drugs can help to control both, although atrial flutter is particularly resistant to medications, and some medications encourage AF to convert into flutter. A few people with both AF and flutter will be significantly improved if they have a flutter ablation on its own but most will need ablation of both arrhythmias to make a difference.