REVIEW Showing Up Channels for Postinfarct Ventricular Tachycardia Ablation CHRISTIAN DE CHILLOU, M.D., PH.D.,*,† ISABELLE MAGNIN-POULL, M.D.,* MARIUS ANDRONACHE, M.D., PH.D.,* FREDERIC SACHER, M.D.,‡ LAURENT GROBEN, M.D.,* AHMED ABDELAAL, M.D.,* LUCIAN MURESAN, M.D.,* SOUMAYA JARMOUNI, M.D.,* JEROME SCHWARTZ, M.D.,* PIERRE JA ¨ IS, M.D., PH.D.,‡ and ETIENNE ALIOT, M.D.* From the *D´ epartement de Cardiologie, Institut Lorrain du Cœur et des Vaisseaux & Universit´ e Henri Poincar´ e, Nancy, France; †IADI INSERM U947, Universit´ e Henri Poincar´ e, Nancy, France; and ‡D´ epartement de Cardiologie, Hˆ opital Cardiologique du Haut-L´ evˆ eque & Universit´ e Victor Segalen, Bordeaux, France The number of scar-related ventricular tachycardia (VT) ablation procedures is increasing worldwide. This is certainly due to the ever growing number of patients implanted with an implantable cardioverter defibrillator in whom an ablation procedure may be required to better control the ventricular arrhythmia burden, but is also likely related to our better understanding of the arrhythmias mechanisms as well as the improvement of the mapping techniques during the last 15 years. Most VTs, especially those arising after myocardial infarction, depend on a critical isthmus. Defining precisely the critical isthmus of postinfarct VT may be challenging, particularly when the arrhythmia is poorly tolerated. In the literature, there are extensive data concerning the value of conventional electrophysiological techniques, especially entrainment mapping in association with postpacing interval measurements, regarding the identification of postinfarct VT isthmuses. There are, however, other—sometimes emerging—approaches to image critical postinfarct VT channels. We have summarized these, reviewing data from the published literature as well as our own experience. (PACE 2012; 35:897–904) ventricular tachycardia, myocardial infarction, catheter ablation A reentrant mechanism 1–3 explains most postinfarct ventricular tachycardias (VTs). The presence of a so-called “protected isthmus” is critical for the maintenance of these VTs 4 and is therefore the target of the catheter ablation which aims to transect the isthmus perpendicularly to its activation wave front. Unmasking such a protected isthmus, or “channel,” is the critical part of any postinfarct VT ablation procedure and may be very challenging, especially in patients with multiple VT morphologies and/or poorly tolerated, unmappable VTs. From basic “low- tech” electrophysiological (EP) tools to more sophisticated “high-tech” systems with integrated data, this article will review how to unveil such channels in postinfarct VT patients. Address for reprints: Christian de Chillou, M.D., Ph.D., D´ epartement de Cardiologie, Institut Lorrain du Cœur et des Vaisseaux, 1, rue du Morvan, 54511 Vandoeuvre l` es Nancy, France. Fax: 33 3 83 15 38 56; e-Mail: c.dechillou@chu-nancy.fr Received October 11, 2011; revised February 24, 2012; accepted April 2, 2012. doi: 10.1111/j.1540-8159.2012.03429.x Postinfarct-Related VT Circuit: Histology and Pathophysiology A normal ventricular wall is formed of different layers of myocardial fibers packed together without interstitial fibrosis. After myocar- dial infarction, presence of connective tissue is found between bundles of surviving myocardial cells which may be tightly packed together or composed of cells separated by abundant fibrous tissue. 5 These surviving bundles of myocytes can form conduction channels within the infarct scar, with slow conduction which predisposes to unidirectional conduction block and reentry excitation. In 1993, de Bakker et al. 6 beautifully demon- strated that slow conduction within the infarct scar was related to the presence of fibrosis. Indeed, the authors showed that in cases of large time gaps over short distances, clusters of surviving muscle bundles separated by fibrous tissue were present. Importantly, they noticed that the conduction velocity was very inhomogenous within the infarct area, with a quite normal conduction time along the fiber direction, as opposed to a very slow conduction perpendicular to the fiber direction caused by a “zigzag” course of activation which has to proceed along pathways C 2012, The Authors. Journal compilation C 2012 Wiley Periodicals, Inc. PACE, Vol. 35 July 2012 897