Annibale Sandro Montenero,
Anselma Intini, Maria Grazia Bendini, Gemma Pelargonio, Katia Martini, Paolo Zecchi.
Istituto di Cardiologia, Universita Cattolica del Sacro Cuore, Rome, Italy
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The advent of catheter ablation using radiofrequency
current has revolutionized treatment for patients suffering from supraventricular
tachyarrhythmias involving either dual AV nodal pathways or an accessory atrioventricular
connection. The high success rate and the low incidence of complications reported from
well trained centers resulted in a large amount of patients that electively received this
interventional therapy. More recently curative catheter ablation has been used with
increasing success for patients with other atrial arrhythmias as ectopic atrial
tachycardia, incisional reentry tachycardia and atrial flutter5.
Our understanding of the electrophysiologic and anatomical substrate of atrial arrhythmias
has grown considerably, in large part as a result of the detailed mapping required for
successful ablation making even the acute pharmacological approach more feasible.
Therefore despite the successful results from catheter ablation, pharmacological therapy
is still used in the setting of the acute treatment of regular supraventricular
arrhythmias as first line of therapy. Documentation of the arrhythmia using a 12-lead ECG
is an important step in the management of the patient and make diagnosis and treatment of
the arrhythmia more appropriate. To identify the mechanism of the tachycardia may help to
define the critical components of the arrhythmias and the vulnerable parameter as proposed
by the Sicilian Gambit that introduced a rationale in the choice of the antiarrhythmic
agent. Despite the fact that the use of a bolus of iv adenosine triphosphate, which causes
transient and selective block of conduction through the fast pathway6,
may represent the drug of choice in the acute termination of AV nodal reciprocating
tachycardia, because of its effectiveness and short life7,
the vulnerable parameter, which is the most likely to be affected, would be the slow
pathway. Therefore, drugs with a specific effect on the antegrade slow pathway such as
calcium channels blockers (verapamil) or beta-blockers are effective in preventing
recurrences as well as slow pathway radiofrequency catheter ablation.
The arrhythmias associated with the Wolff-Parkinson-White syndrome include ortodromic
and antidromic reciprocating supraventricular tachycardia, being atrial fibrillation
rarely as a primary arrhythmias. The vulnerable parameter is the accessory pathway, which
has a Na+ dependent kinetic, and that, even in case of atrial fibrillation,
should be target. The acute interruption of an episode of reciprocating tachycardia may be
achieved by using sodium channels blockers such as propafenone or flecainide that, even in
the case of a preexcited atrial fibrillation can be safely used. These agents, in fact,
selectively affect antegrade and retrograde conduction through fast-conducting accessory
pathways.
To prevent recurrences, radiofrequency catheter ablation of the accessory pathway is
the more appropriate therapy with a very high success rate (98%) and low rate of
complications (1%).
The permanent form of junctional reciprocating tachycardia has been first described by
Coumel8 as a sort of tachycardia related to an
accessory pathway with decremental conduction that use the AV node as the antegrade limb.
The vulnerable parameter, even in this case, would be the accessory pathway which can be
affected by sodium channels blockers (flecainide or propafenone) or catheter ablation,
which is extremely recommended being the tachycardia incessant (permanent).
Atrial tachycardia may be due to reentry, abnormal automaticity or both mechanisms. In
the majority of these patients, the true mechanism can be correctly investigated only at
the time of the electrophysiologic study, making more difficult the definition of the
vulnerable parameter. Some of these tachycardias are catecolamine-sensitive and for them
the use of beta-blockers is appropriate, some can be controlled by using sodium-channel
blockers.
To identify the vulnerable parameter, either reentry or abnormal automaticity, is of
great importance in order to target radiofrequency catheter ablation which is the only
curative approach. In fact, in most of the istances, these tachycardias are resistant to
the pharmacological therapy that can only control the ventricular response.
Atrial flutter is due to reentry with the reentrant circuit confined to the right
atrium9 that travels cranially up the intraatrial
septum on the right side, goes up the truncus intercavarum, then turns caudally in the
crista terminalis, and then travels around the inferior vena cava to turn back up
(cranially) the interatrial septum. In this circuit, the central area of block in part
consists of the orifice of the inferior vena cava and an area of functional block between
the inferior vena cava caval orifice and the truncus intercavarum.
An area of slow conduction, which has a variable extension, exists inferiorly and
posteriorly in this circuit at the isthmus between the inferior vena cava and the
tricuspid annulus10 which probably is a combination of
anatomical and functional area of block. This area of slow condution would be the
vulnerable parameters even if several other factors should be took into account as a
wavelength, a pathlength and an excitable gap which can be fully or partial excitable.
Therefore, based on the fact that the onset of atrial flutter has not been completely
investigated, to block the area of slow conduction would be the more appropriate approach
either with drugs or with catheter ablation11.
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