Catheter ablation remains a good first line choice for the palliative treatment of symptomatic typical atrial flutter
- AF, atrial fibrillation
- AV, atrioventricular
- RF, radiofrequency
- supraventricular arrhythmias
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Radiofrequency (RF) catheter ablation was first used in the 1990s and completely changed the management of supraventricular tachycardias. After about 20 years of development, clinical electrophysiological methods provided accurate knowledge of tachycardia mechanisms that led first to successful surgical treatment, then to exquisite anatomical localisation, allowing endocardial catheter ablation. Clear separation of the mechanisms into focal discharge, accessory pathway dependent or intranodal re-entry was an essential step and, during this process, the general term “supraventricular”, encompassing multiple mechanisms, started to lose some of its meaning.
Perhaps the paradigm of catheter ablation effectiveness is Wolff-Parkinson-White syndrome, where a congenital structural abnormality,1 the accessory atrioventricular (AV) pathway, is fully responsible for the disease mechanisms. Once the anomaly is identified, intracardiac mapping can locate the anomaly with great precision; then RF ablation can induce a localised necrosis that affects the accessory pathway, eliminating its functional consequences2–4 with very low morbidity and mortality.5–7 Not only does RF ablation produce a complete cure, but it also provides experimental proof of the pathogenic working diagnosis, as it completely prevents recurrence of AV re-entrant tachycardias. Nevertheless, atrial fibrillation (AF) can recur in some patients, particularly in older individuals,8,9 when the accessory pathway is not the only cause of AF.
NODAL RE-ENTRANT TACHYCARDIA
This clear cut view cannot be wholly applied to all supraventricular tachycardias. In nodal re-entrant tachycardia, despite a very high rate of success and an important research effort, it is not completely clear if it is ablation of the AV node extensions,10 or the intermediate AV nodal tissue, or even the myocardium around the tricuspid ring showing nodal-like electrophysiological properties that interrupts the circuit.11 In focal atrial tachycardia a lower efficacy rate and a higher recurrence rate7 probably reflects our incomplete knowledge of the mechanism and the anatomic bases. Recent work by the Taipei group has disclosed some unique features, such as channelling of conduction for some distance from the focus to the point where activation spreads throughout the atria, and the anatomic and functional bases for this peculiar path of activation are unknown.12 Even so, in atrial tachycardia ablation can eliminate the focus of origin of the abnormal activation and prevent tachycardia recurrence.
ABLATION OF ATRIAL FLUTTER
Ablation of typical atrial flutter is quite a different proposition in several aspects. We are very successful at interrupting the arrhythmia and preventing its recurrence, but we do not know what its cause is. Practically all epidemiological data have lumped flutter and fibrillation together and we are ignorant of what may make some 10% of these mixed populations have atrial flutter and the others AF, nor do we have any anatomic or functional data that let us separate both populations or clarify why flutter occurs more in men than women by a ratio of 3:1. The inferior vena cava–tricuspid isthmus has become the universally accepted target for ablation of the typical flutter circuit, due to its accessibility and because it is located far from the AV node, even though we have no evidence that this site is the cause of atrial flutter. The relatively slower conduction described through this isthmus13 in relation to the anterior right atrial wall is also found in a control population without flutter and probably depends on fibre architecture and anisotropic conduction.14,15 Ablation and interruption of isthmus conduction does nothing to the disease mechanisms that cause flutter in the first place and, if indeed the causes of flutter and fibrillation are the same, basic progression to later development of atrial fibrillation should be expected.16
However, clinically atrial flutter can be difficult to manage. If it is the initial presenting sign or the result of drug treatment for AF, flutter is a troublesome arrhythmia, often poorly tolerated because of a rapid, difficult to control, AV conduction rate. The efficacy of isthmus ablation is well established and its safety record outstanding.17–20 The procedure is therefore applicable in almost any clinical circumstance, which by itself would make catheter ablation a good choice as first line treatment. If AF occurs later, it can be controlled more easily in most cases.
The report in this issue of Heart by Da Costa and colleagues21 agrees with previous experience in regard to a low rate of flutter recurrence and other atrial tachycardia recurrences—it is the new atrial fibrillation occurrence rate around 15% that could not be affected by flutter ablation. Flutter could be an inducer of fibrillation through shortening and dispersion of refractory periods by the fast atrial rate, an effect described by Wijffels and others as electrical remodelling,22,23 and a potential cause for perpetuation of atrial fibrillation. But even though this may play a role in some patients in whom flutter ablation prevents further episodes of fibrillation,24 the data presented by Da Costa and colleagues21 suggest that this may not be so important, as delaying ablation by an average of two years did not have a detrimental effect. Nevertheless, the patients undergoing earlier ablation probably were more likely to not need antiarrhythmic drugs or anticoagulants, and suffer less tachycardia episodes during that time, which could have been a worthwhile benefit by itself.
LACK OF PREVENTIVE STRATEGY
The problem with our present management of atrial flutter and AF is the lack of a clear, long term primary and secondary preventive strategy. Both isolated drug treatment or catheter ablation of atrial flutter may be the equivalent of administering nitrates and β blockers to a patient with effort angina, without paying any attention to his hypertension, high cholesterol, or smoking 40 cigarettes per day. In contrast with accessory pathways, and probably also with nodal re-entrant tachycardia, even though flutter ablation terminates the arrhythmia and prevents its recurrence, it does not stop progression of whatever basic atrial disease caused it. Prevention of AF will depend more on identifying these pathogenic mechanisms and learning to contain or revert atrial myocardial damage. In the meantime, given its efficacy and safety, catheter ablation remains a good first line choice for the palliative treatment of symptomatic typical atrial flutter.
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