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Atrial flutter is a supraventricular tachycardia that
is notorious disabling and antiarrhythmic drugs resistant, particularly with respect to
prevention of recurrences. Atrial flutter occurs more often in patients with structural
heart disease, may be paroxysmal or, less frequently, chronic. It is defined by the ECG
appearance of discrete and regular "flutter waves" with a "sawtooth"
appearance. The classification of atrial flutter proposed by Puech in 19701 and Waldo in 19772
which divided the atrial flutter in type I and type II is still valid. Type I (or typical)
atrial flutter is defined as a tachycardia with a flutter rate of 250 to 320 beats/minute;
it is easily influenced by programmed pacing, which can stop or induce the arrhythmia. The
type II is infrequently seen; it is faster (> 300 beats per minute) and is not
influenced by rapid atrial pacing. The authors identified in the type I two types of
atrial flutter, the "common type" where the flutter waves are inverted in leads
II, III and aVF and upright in V1 and the "uncommon type or reverse"
with a notched upright pattern in the inferior leads.
Some studies with mapping of the right atrium have established that the mechanism of
type I atrial flutter is a large reentrant circuit in the right atrium. The circuit
usually proceeds with counterclockwise sequence from the coronary sinus ostium region up
the atrial septum, crosses the roof of the right atrium and returns via the crista
terminalis to the coronary sinus orifice region2,3. The
region between the tricuspid anulus and inferior vena cava appears to be the zone of
critical slow conduction. While common type I atrial flutter rotates in a counterclockwise
sequence, atrial flutter with clockwise direction (uncommon or reverse) can be observed
and induced in patients with common type I atrial flutter. In the majority of patients
with clockwise atrial flutter, V1 is inverted and V6 upright.
The introduction of an effective nonpharmacologic technique, as catheter ablation,
opened new therapeutic prospectives for the management of this arrhythmia. Until the end
of the eighties, the most radical treatment of refractory atrial flutter was the delivery
of a unipolar direct current shock between the tip of a catheter posizioned against the
A-V node and cutaneous back patch4. The technique later
evolved to the use of radiofrequency (RF) energy to achieve intentional complete A-V
block. The most important disadvantage of catheter ablation of the A-V junction was
related to the fact that the patient should be made pacemaker-dependent.
Recent studies5-7 proposed RF ablation of AF with
anatomical approach between the tricuspid anulus and the inferior vena cava orifice.
Another approach based on electrophysiological criteria has been reported by Feld et al8. They suggested that a critical area of slow conduction
can be identified and ablated in the low posteroseptal right atrium with RF to terminate
and prevent recurrences of atrial flutter. This area is located near the coronary sinus
ostium and can be identified by the presence of prolonged low-amplitude fragmented
electrical activity.
Nevertheless the limit of the RF procedure is in all the reports the hight number of
recurrences of AF requiring new ablation procedure and sometimes antiarrhythmic drugs. RF
ablation in common AF has high acute success, but the recurrences are common (20-30%) and
may limit its usefulness5-8.
The challenge is to find an index of successful ablation after the abrupt termination
of atrial flutter during RF application9-10. The
reinduction attempt of AF with atrial bursts pacing at decreasing cycle lengths (350-150
ms) is not always sure and predictive parameter of success in the follow-up. Also the
number of RF pulses in our experience is not a predictive parameter of long-term outcome11.
In recent studies different authors12-15 provided
evidence that the mechanism of successful AF ablation targeting the inferior vena
cava-tricuspid anulus (IVC-TA) isthmus is local bidirectional conduction block. These
changes can be used as new and complementary electrophysiological end points for the
procedure.
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