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Ventricular tachycardia (VT) can occur in hearts that appear upon conventional imaging to be structurally normal. In structurally normal hearts, VT commonly arises from the outflow tracts. Outflow tract ectopy can manifest itself as frequent premature ventricular complexes (PVCs), salvos of VT, and sustained VT. Exercise or emotional stress can trigger outflow tract VT. The prognosis for outflow tract VT is generally favorable, but there is potential for developing PVC-related cardiomyopathy and, rarely, for sudden cardiac death. Therapy is directed by the calcium-dependent delayed after-depolarizations that can lead to an underlying automatic focus. Calcium channel blockade by means of verapamil can be an effective therapy. The automatic focus can also be targeted for ablation by identifying the site of ventricular tissue that is activated earliest by a PVC. Catheter ablation of the automatic focus is an effective therapeutic option.1
A detailed understanding of the anatomy of the outflow tracts and their relation to the surface electrocardiographic (ECG) leads and neighboring cardiac structures is crucial to the understanding of outflow-tract VT electrocardiographic nuances and to the safe performance of catheter ablation. Despite their names, the right ventricular outflow tract (RVOT) is farther left in the body than is the left ventricular outflow tract (LVOT) (Fig. 1 2), and the RVOT is anterior to the LVOT (Fig. 2).
This anatomic framework aids in understanding the electrocardiographic manifestation of outflow tract VT. First, the outflow tracts are superior structures, and activation originating from these sites is directed inferiorly, thereby producing a QRS appearance that is strongly positive in the inferior leads (II, III, and aVF) and negative in aVL and aVR. Additional leads (particularly leads V1 and I) can further refine the ECG localization within the outflow tracts.3
Lead V1 is both a right-sided and anterior lead. Since the RVOT is anterior and leftward within the body, when the impulse begins in the RVOT and spreads away posteriorly and leftward, V1 should manifest a predominately negative complex. In the evaluation of outflow tract ectopy, the presence of an R wave in V1 should trigger consideration of a more posterior origin, which could create an anteriorly directed vector (toward VJ. The more posterior structures to consider include the posterior RVOT, the anterior LVOT, and the posterior LVOT. A point of origin from the posterior RVOT might have a small amount of anterior myocardial tissue to activate, leading to a tiny R wave in V however, most myocardial activation is still at a distance from lead Vr Since the posterior RVOT is adjacent to the anterior LVOT, consideration should be given to mapping the neighboring LVOT to an earlier site of activation, should the automatic focus be mapped to the posterior RVOT. The aorta is a central structure within the heart, and the LVOT lies posterior to the RVOT. Consequently, the LVOT is farther from lead V1, and an LVOT origin can propagate toward V1, thereby producing an R wave.3
Lead I is a left-sided lead, and an RVOT origin near the pulmonary valve would manifest itself with a negative complex, as the impulse spreads from the left side of the body to the right. An RVOT origin can have a biphasic appearance if the origin is on the anterior or posterior aspect of the RVOT. Lead I can also be positive when activation originates from the right margin of the RVOT. Accordingly, the activation patterns of leads I and V1 can conceptually be synthesized to anticipate the site of outflow tract origin. Figure 3 shows an example of an RVOT VT.
A thorough understanding of the anatomy of the outflow tracts is crucial not only to mapping outflow tract ectopy but to anticipating and avoiding potential ablation complications, such as damage to the conduction system or the coronary arterial system. One can easily be misled by mapping to ablate at a distance from the true automatic focus. The bundle of His is located in the membranous septum, which is at risk of collateral damage due to its location relative to the outflow tracts.2 The bundle of His lies between the juncture of the right and noncoronary cusps and the juncture of the tricuspid valve's anterior and septal leaflets. Outflow tract morphologic ectopy can have supra-valvular automatic foci as a consequence of muscular sleeves that cross the pulmonary valve and the right and left coronary cusps of the aortic valve.4,5 The left main coronary artery is directly posterior to the distal RVOT and is at risk of injury due to ablation in the distal posterior RVOT. Another important consideration in ablation is correct identification of the source of the RVOT ectopy. Outflow tract ectopy is most commonly due to an automatic focus, so mapping and then ablating the earliest site of activation is vital.3 Remnants of the conduction system near the right ventricle can present a mapping challenge.
In summary, the outflow tracts have a complex anatomy that is important to consider in the evaluation and treatment of outflow tract ectopy. The electrocardio-graphic patterns that the various outflow tract activations exhibit are better understood within the anatomic framework. An understanding of the anatomic relationships between the targets and the potential sites of complications improves the safety of ablation of outflow tract ectopy.
Address for reprints: Samuel J. Asirvatham, MD, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55905
Presented at the Thirteenth Symposium on Cardiac Arrhythmias: Practical Approach to Heart Rhythm Disorders; Houston, 18 February 2012.