Knowing Where to Look

Catheter ablation of monomorphic ventricular tachycardia (VT) late after myocardial infarction remains challenging. The reentrant circuits are located in large areas of infarction. Multiple morphologies of VT are commonly induced. Mapping often is difŽ cult when VT is unstable due to hemodynamic intolerance, lack of reproducible initiation with programmed stimulation, or frequent morphologic changes from one VT to another. When patients with a stable VT are selected for mapping and ablation, the targeted VT is successfully ablated in over approximately 70% of cases.1 ,2 Location of the reentrant circuit deep to the endocardium is a major reason for ablation failure. Although most infarct-related circuits are subendocardial, at least in part, some do not have an endocardial isthmus where the circuit can be interrupted. The circuit isthmus or even the entire circuit is in the subepicardium or deep within the interventricular septum.3 Epicardial circuits may be more common after inferior wall infarctions as compared with anterior wall infarctions. In some cases, an apparent isthmus is identiŽ ed on the endocardium, but the reentrant path appears to be relatively broad, or deep such that achieving interruption is difŽ cult. These concerns have stimulated the development of cooled radiofrequency (RF) ablation techniques to attempt to create deep ablation lesions. In a multicenter trial, an internally irrigated RF catheter abolished the targeted inducible VT in 75% of patients.2 Thus, many reentrant circuits remain out of reach or cannot be adequately located. Epicardial reentrant circuits can be approached directly by inserting a catheter into the pericardial space using the technique described by Sosa et al.4 Initial reports demonstrate feasibility, but many patients with postinfarct VT had prior cardiac surgery that renders the pericardial space inaccessible. Epicardial reentrant circuits potentially can be targeted by cannulating the epicardial veins, but only if a vein happens to traverse the circuit. Methods for ablating from small veins and assessment of the risk of injury to adjacent arteries remain to be deŽ ned.5 Catheter mapping and ablation are facilitated by knowledge of the likely location of the reentrant circuit, which can be predicted to a limited extent by the infarct location and QRS morphology of the VT. VT circuits after inferior wall infarction often involve the base of the ventricle, using a surviving isthmus of tissue beneath the mitral valve.6 -8 When this isthmus is used in the posterolateral to septal direction, the circuit exit often is at the septum and VT has a left bundle branch block-like conŽ guration in V1. Most of these VTs can be interrupted by ablation at the septal aspect of the mitral valve annulus. That some postinfarction VTs require ablation from the right heart perhaps is underappreciated.9 ,1 0 When a VT has a left bundle branch block-like conŽ guration in lead V1, assessment for possible bundle branch reentry is our Ž rst step. Limited mapping in the right ventricle then is performed. Entrainment usually shows long postpacing intervals indicating that the circuit is in the left ventricle. Lacroix et al.1 1 recently reported seven patients with VTs that displayed presystolic activation, indicating the likely circuit exit region, located in the epicardium at the crux of the heart. These VTs had a left bundle branch block-like conŽ guration in V1 and R waves across the precordium, similar to the QRS morphology produced by ventricular activation from a posteroseptal accessory pathway. One of these tachycardias was ablated by RF applications on both sides of the septum; the others were approached surgically. In this issue of the Journal, Kautzner et al.1 2 describe successful interruption of a similar VT by RF application from within the proximal coronary sinus. Their Figure 3 illustrates the proximity of the proximal coronary sinus to the posteroseptal aspect of the left ventricle. Awareness of this entity is important for electrophysiologists attempting VT ablation. Caution is, however, warranted. The distal right coronary artery often is closely adjacent to the insertion of the middle cardiac vein into the coronary sinus. Although accessory pathways often are safely ablated in this area, occlusion of the right coronary artery can occur. Such a complication might be more likely with cooled RF ablation or large-tip electrode catheters, which were not required in this case. On the other hand, if the adjacent coronary artery is occluded and not supplied by collateral  ow, there may be little consequence of arterial injury. Second, AV block occasionally occurs with ablation in the proximal coronary sinus, possibly related to damage to the AV nodal artery or the node itself. In the patient described, ablation in the coronary sinus was successful after ablation from the left ventricle failed. It is possible that the reentrant path was so broad that the left ventricular ablation lesions interrupted part of the path and the coronary sinus RF application completed the transecJ Cardiovasc Electrophysiol, Vol. 12, pp. 367-368, March 2001.