- What is cardiac ablation?
- What is cardiac ablation used for?
- Other treatments for atrial fibrillation
- Who should have ablation?
- Ablation procedures
- What else can be done by ablation?
- Complications of ablation procedures
Cardiac ablation for the treatment of heart rhythm disorder is a procedure in which radiofrequency energy is used to carefully destroy (or ablate) abnormal tissue in the heart. In this operation, a thin tube (the catheter) is passed into the heart, carrying a small probe. This probe puts out the energy necessary to destroy cardiac tissue. Abnormal tissue in the heart can cause the heart to have an abnormal rhythm – the aim of this procedure is to eliminate the abnormal rhythm, often called an arrhythmia.
Atrial Fibrillation (AF) is one of the arrhythmias treatable by cardiac ablation. The atrium is the name for the two upper chambers of the heart. Blood collects here before passing to the lower chambers. AF results from disorganised conduction of electrical impulses through the atria of the heart causing chaotic contractions of the atria (or fibrillation). During AF the atria can be receiving 300 – 600 impulses a minute, which is why the atria contracts so erratically. As a result, the atria are generally much less effective at pumping blood. Additionally, the atria are responsible for the initiation of the heart beat. Without a steady impulse coming from the atria, the ventricles (or main pumping chambers) often beat irregularly and fast which can cause symptoms such as palpitations and breathlessness.
Evidence suggests that maintaining a normal rhythm (often called sinus rhythm) in patients with AF has significant benefits for health. It has been commonplace to use prescription drugs to maintain sinus rhythm in such patients. However, there is the potential for unpleasant and unwelcome side effects, as well as other more serious complications. Thus there is new interest in methods for maintaining sinus rhythm, ones that do not involve drugs. One such strategy is catheter ablation. Cardiac ablation for the treatment of AF is part of a range of treatments for arrhythmia. Many people with AF will take warfarin. This is not to treat the arrhythmia, but to treat one of the potential complications of AF; stroke.
With improving technology, ablation strategies have changed. More patients are considered for catheter ablation than previously. One such group is patients whose AF is proving difficult to control with medications. Also, more patients with a structural heart disease such as ischaemic or valvular disease are also being offered this therapy. Many cardiologists, particularly those experienced with using ablation, would now consider ablation ahead of drug therapy such as amiodarone, particularly in younger patients. A second group of patients that seem to benefit from ablation are those that have complications related to AF. An example is patients with tachycardia-bradycardia syndrome. In the past many of these individuals have received cardiac pacemakers in order to prevent symptoms such as fainting. In this situation, ablation, and stopping anti-arrhythmic drugs is associated with recovery the heart’s internal pacing, and an artificial pacemaker may no longer be required. Patients with heart failure, even in the absence of obvious symptoms, benefit from ablation.
The heart’s pumping ability (also known as the ejection fraction) may improve by about 20% with the maintenance of the heart’s proper rhythm, almost regardless of the extent of structural heart disease . Arrythmias may result in clots forming, and spreading to other parts of the body. Such patients are often treated with drugs that thin the blood and stop it from clotting (called anticoagulants). Patients who are unable to be maintained on long term anticoagulant medications (i.e. warfarin)) due to bleeding problems can instead be treated by ablation, removing the need for medication. For persistent or permanent AF, ablation currently is more challenging. Consequently, the arrhythmia must be associated with major symptoms and resistant to anti-arrhythmic drugs before the procedure can be justified. In this group, the ablation procedures are generally longer, often multiple procedures are required and the complication rate is higher than in patients with occasional (or paroxysmal) AF.
It is now recognized that Atrial Fibrillation results because of triggers that maintain the atria in fibrillation. While many areas are potential sources of initiating triggers, the pulmonary veins (PV) are recognized as the dominant source, causing up to 94% of AF symptoms. Thus, pulmonary vein ablation has emerged as a dominant strategy for AF. Remember that by ablation we can “cut out” these triggers and slow the number of electrical impulses that reach the atria. This procedure may be referred to as ‘pulmonary vein isolation.’ Therefore, ablation can terminate AF in up to 75% of cases. In addition, 40-60% of these patients cannot be artificially stimulated to AF after ablation.
The image above demonstrates the posterior view of a left atrium, reconstructed from a CT scan and used to guide ablation (lesions marked in orange) The two right sided veins have been isolated with two circles. The left sided veins share a common trunk and a larger circle has been used for isolation.
Despite ablation of the triggers initiating AF, most patients with persistent or permanent AF, and approximately 20-40% of patients with paroxysmal AF, have further episodes of fibrillation. In these patients improved ablation outcomes rely on an additional procedure on top of normal ablation, called substrate modification. In patients with persistent or permanent AF this is invariably required. This substrate modification works on the idea that atrial ablation can compartmentalize the muscle mass of the atria, containing the fibrillation and preventing its spread. Alternatively, atrial ablation can reduce the muscle mass to prevent its ability to sustain a fibrillation. When performed with pulmonary vein isolation, these extra ablations improve the success rate by 10-20% in paroxysmal AF, and by 30-50% in persistent or permanent AF.
Although complications from atrial fibrillation (AF) ablation procedures are not common they can be significant. The most concerning of these is the potential for stroke from a blood clot (thromboembolism) during the procedure. Minimizing this devastating complication requires meticulous planning. Doctors use anti-clotting drugs known as anticoagulants (i.e. warfarin) for at least four (4) weeks before the procedure, an echocardiogram evaluation (an ultrasound scan of the heart) immediately before the procedure, specific care during the procedure (minimizing the use of the catheter within the left atrium, care of the probe’s sheath, and use of anticoagulant medications) and specific care after the procedure (anticoagulation until the absence of AF is proven).
Another complication is pulmonary vein stenosis. This is where the pulmonary vein reduces in diameter. Changes in ablation technique, improved catheter technology and increased operator experience have greatly reduced the risk. The current risk of pulmonary vein stenosis (of more than 50% reduction in PV diameter) is less than 2%, with most patients being asymptomatic. In a leading centre for AF ablation, out of 2000 patients having PV ablation, severe symptomatic PV stenosis (>70%) was observed in four (4) patients. Nevertheless, a screening regime is used in patients having ablation with the use of CT or MRI scans, looking for stenosis, immediately after the procedure. Any ablation procedure can result in the creation of new conduction abnormalities. These new abnormalities may be able to support a flutter circuit – i.e., new fibrillation. After pulmonary vein isolation alone, approximately 5% present with spontaneous atrial flutter. The risk of such new arrhythmias is greater following substrate modification and accounts partly for the need for multiple procedures.
Four to six (4-6) weeks following an ablation procedure, an increasing arrhythmic effect may be observed. These arrhythmias appear to be different in nature to more common arrhythmias – they rarely continue long term, and the symptoms they produce can usually be easily managed. During the procedure, the heart itself may be pierced by the equipment – this is called a cardiac perforation. Cardiac perforation can result in cardiac tamponade, where blood accumulates around the heart and compresses it. This complication is, in general, uncommon with pulmonary vein isolation alone. However; it may be as high as 4-6% with substrate modification. In general, there are no long-term consequences if prompt drainage can be performed. Appropriate treatment centres have available facilities for such a prompt drainage available. More recently, an accumulating number of cases have been reported of injuries outside the heart, as a result of ablation. Structures injured include the phrenic nerve, and damage to the gastric nerves resulting in digestive problems and atria-oesophageal fistula. The latter complication has resulted in a fatal outcome in some patients.
The last decade has seen significant developments in our understanding of atrial fibrillation (AF), and has led to the development of catheter ablation and surgical techniques that have demonstrated the real possibility of achieving a cure of AF. Ablation limited to the pulmonary veins and nearby areas provides a success rate of approximately 70% in paroxysmal AF and 20-30% in persistent or permanent AF. These results are further improved by additional substrate modification. For patients with persistent or permanent AF, PV isolation and substrate modification can still result in long-term freedom from AF, but generally multiple procedures are required and the complications rates are increased. Emerging evidence and technological improvements will broaden the use of these techniques in patients with AF in the future.
Article kindly contributed by:
Martin K. Stiles, MBChB, FRACP (Electrophysiology Fellow), Glenn D. Young, MBBS, FRACP (Electrophysiologist) and Prashanthan Sanders, MBBS, PhD, FRACP (Electrophysiologist) from The Cardiovascular Research Centre, Department of Cardiology, Royal Adelaide Hospital and the Department of Medicine, University of Adelaide, Adelaide, South Australia.
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