Abstract

Sustained and nonsustained ventricular tachycardias originating from the right ventricular outflow tract have been always considered benign, and, in the vast majority of cases, they really are. Data from a decennial follow-up in 133 patients with sustained right ventricular outflow tract tachycardia and no major structural heart disease showed a favorable outcome with no death from cardiac cause. 1 Nevertheless, this arrhythmia may be responsible for disabling symptoms, such as syncope and presyncope, in roughly one-third of these otherwise healthy patients. 1 A repetitive nonsustained form of this arrhythmia may be responsible in some cases for dilated cardiomyopathy, which reverts within a few months after arrhythmia suppression by catheter ablation. 2 Moreover, in a multicenter report, four out of 27 patients with recurrent idiopathic ventricular fibrillation had this malignant arrhythmia triggered by ectopies that originated from the myocardium of the right ventricular outflow tract exhibiting the classic left bundle branch block morphology with an inferior axis deviation. 3 In these cases, a relatively shorter coupling interval of the ventricular ectopy (355 30 ms) seems to be useful in discriminating this minimal subset of patients who are at increased risk for sudden death. Based on all these data, the interest for mapping and ablation of right ventricular outflow tract tachycardia/ectopies seems justified. In this issue of Heart Rhythm, Bogun et al 4 investigate the spatial resolution of pace mapping in 16 consecutive patients affected by idiopathic ventricular tachycardia (n 3) or ectopies (n 13) originating in the right ventricular outflow tract. The authors use a sophisticated technology for a software-based objective quantification of the difference between the spontaneous ventricular tachycardia/ectopy QRS morphology and the paced one at each paced site. Moreover, they use a three-dimensional electroanatomic system for activation mapping during the spontaneous arrhythmia and to determine the distance between the arrhythmia site of origin (corresponding to the site of successful ablation) and the site at which stimulation obtained a QRS morphology with the higher combined sensitivity and specificity for good pace mapping (correlation coefficient 0.94). Not surprisingly, they found that the area identified by optimal pace mapping was wider than the one of earliest activation, as defined by the 10-ms isochrone at electroanatomic activation mapping during the spontaneous arrhythmia (1.8 0.6, range 1.0 ‐2.8 cm 2 , vs. 1.2 0.7, range 0.4 ‐3.5 cm 2 , respectively). Even more interesting, in three (19%) out of 16 cases, pace mapping at the site of successful ablation, all located in the “septal” aspect of the right ventricular outflow tract, resulted in inadequate QRS morphology, although it was the best pace-mapping site in these patients. The authors conclude that, when objectively evaluated, the spatial resolution of pace mapping is inferior to the one of activation mapping and that pace-mapping accuracy is not enough to localize the arrhythmia origin in approximately 20% of the cases. In fact, using the current mapping technology, why should pace mapping have equal or better accuracy compared with activation mapping, at least in the right ventricular outflow tract? Before proceeding deeper into this topic, it could be useful to consider some anatomy. The outflow tract is the tube-like portion of the right ventricular cavity, above the supraventricular crest. Its thickness is variable, ranging from approximately 3 to 6 mm, and it progressively decreases toward the plane of the pulmonary valve, with the thinnest part (1 mm or less) at the level at which the muscular infundibulum joins the wall of the pulmonary trunk. Although we usually refer to septal and free wall portions of the right ventricular outflow tract, it should be noted that the septal component is only in its most proximal part, at the branch point of the septomarginal trabeculation. Above this area, the right ventricular outlet curves to pass anterior and cephalad to the left ventricular outlet, and, therefore, any perforation in the septal part is more likely to go outside the heart than into the left ventricle (Figure 1). While coarse muscular trabeculations are characteristic of the right ventricular apex, other trabeculations are also present in the right ventricular outflow tract, although the region immediately beneath the pulmonary valve tends to be smooth. In normal hearts, the right ventricle is composed of

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