Non-pharmacological Therapies in Atrial Flutter and Atrial Fibrillation

Atrial flutter and atrial fibrillation often co-exist, i.e. occur in the same patient at different times, but have different anatomical substrates in the heart. Atrial flutter is due to a macro-re-entrant circuit arising from the junction of the tricuspid valve annulus and inferior vena cava, while early atrial fibrillation is due to spontaneous depolarisation arising from around the pulmonary veins, most commonly from the ostium of the left superior pulmonary vein.

The commonest form of atrial flutter is due to a counter-clockwise macro-re-entrant current at the cavo-tricuspid isthmus. On the ECG, this is reflected in predominantly negative deflections in the inferior leads and in V5 & V6, and positive flutter waves in V1, as illustrated in the figure below.

Less common is clockwise atrial flutter, where the flutter waves have positive deflections in the inferior leads and lateral precordial leads, but are negative in V1, as shown below.

In practice, the management of anti-clockwise and clockwise flutter does not vary, as they both arise from the cavo-tricuspid junction. However, when flutter arises from other areas of the heart, it is called atypical flutter and the site of origin will have implications in terms of management, if radio-frequency ablation (RFA) is considered.

Atrial flutter differs in important ways from atrial fibrillation, apart from its site of origin. Flutter is a relatively unstable rhythm, and often reverts to sinus rhythm, particularly when the underlying contributing factors such as pulmonary embolism, hypoxia or ischaemia are addressed. It may also convert spontaneously into atrial fibrillation. Secondly, flutter waves are far more likely to be conducted across the AV junction compared with fibrillatory waves. Thus, the most common rate of atrial flutter is 300/minute, while the ventricular rate is 150/minute, i.e. 2:1 conduction. Flutter waves may also be conducted in a 3:1, 4:1 or 5:1 ratio, but higher ratios, in the absence of negatively chronotropic medications, indicates disease of the AV junction. Even ratios such as 2:1 or 4:1 are far more common than odd ratios such as 3:1 or 5:1. On the other hand, atrial fibrillatory waves occur at rates between 400-600, but the ventricular rate is usually between 90-170. Lesser ventricular rates usually connote AV junction disease, while higher rates may be seen in thyrotoxicosis, sympathetic overdrive, parasympathetic withdrawal or with bypass tracts.

Unlike atrial fibrillation, persistent atrial flutter is remarkably resistant to pharmacological manipulation. Most such cases should be considered for cardioversion following appropriate anti-coagulation, or if this is not possible or not acceptable, for RFA or overdrive atrial pacing. The cavo-tricuspid isthmus is relatively easy to access for RFA, and the procedure is usually safe, with very few complications.

In subjects who already have a pacemaker or a pacing line in situ, such as after cardiac surgery, overdrive atrial pacing is safe and offers a third non-pharmacological alternative.

Unlike with flutter, RFA in atrial fibrillation is technically much more difficult. This is because most fibrillatory waves arise from the ostia of the pulmonary veins, which must be included in any ablatory procedure (pulmonary vein isolation). RFA with atrial fibrillation commonly takes one of two forms- either segmental- limited to the pulmonary vein ostia with electrical mapping, or the technically easier circumferential RFA, which simply encircles the pulmonary veins. With the latter, special intra-procedure electrical mapping is not required. Atypical flutter, such as that arising from the left atrium, alluded to above, may be a complication of RFA for atrial fibrillation.

Access to the pulmonary veins requires septal puncture. There is a risk of causing a pericardial effusion and a small risk of causing an atrio-oesophageal fistula, which is often fatal. Thus, RFA in atrial fibrillation is often resorted to only after all pharmacological options have failed. Further, RFA only works for paroxysmal atrial fibrillation. Once fibrillation has become chronic, fibrillatory waves arise from all over the left atrium, and sometimes the right atrium, and is no longer amenable to RFA. Such cases can still be treated with a surgical procedure such as the Maze Procedure. The current version is Maze III. For obvious reasons, this is only practical when the patient is undergoing open heart surgery for another indication such as CABG or valve replacement. Subjects with paroxysmal atrial fibrillation who fail to respond to the Maze procedure may still respond to RFA.

When rhythm control is not possible or not practical, and drug therapy has failed, a non-pharmacological strategum for rate control in atrial fibrillation is to ablate the AV node and pace the ventricles. In most cases, this would comprise pacing the right ventricle alone. However, in subjects who otherwise fulfil the criteria for cardiac resynchronisation therapy, such as those with NYHA Class II, III or ambulatory IV heart failure, an ejection fraction <35% and QRS> 120 ms, a CRT or CRT-D device may be considered with good haemodynamic results.

It is worth mentioning that the risk of thrombo-embolism remains high soon after RFA in both flutter and fibrillation, and most experts would recommend continuing anticoagulation for at least 3-6 months. Apart from the fact that most recurrences occur during this period, it is cautionary that the period immediately following reversion to sinus rhythm, whether achieved through electrical or pharmacological means, is associated with a high risk of thrombo-embolism.