The derivative of tissue activation as a marker of arrhythmogenic myocardium

Published:October 18, 2022DOI:


      Mapping techniques to identify diseased myocardial substrate during ventricular tachycardia ablation procedures remain limited.


      We hypothesized that tissue derivative of the voltage with respect to time (dV/dt), the slope of the unipolar ventricular electrogram registered by local ventricular activation, represents a unique parameter for identifying potential arrhythmogenic tissue in the ischemic scar border zone.


      Using high-resolution electrical mapping, we examined dV/dt characteristics in the border zone of animals after chronic myocardial infarction (MI).


      Minimum dV/dt (dV/dtmin) in MI animals was less than that in control animals (−344.7 ± 68.7 in controls vs −174.2 ± 104.5 in MI; P < .001) and related to ventricular fibrosis. In MI animals, dV/dtmin values were divided into high (≤−200 μV/ms) and low (>−200 μV/ms) dV/dtmin. Low dV/dtmin regions harbored arrhythmogenic substrates that were characterized by (1) high responsiveness to sympathetic stimulation, (2) presence of late potentials, and (3) lower unipolar and bipolar voltage amplitudes.


      Our data indicate that dV/dtmin is a unique parameter for identifying arrhythmogenic myocardium and may add a useful metric to conventional mapping strategies.


      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to Heart Rhythm
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect


        • Horowitz L.N.
        • Harken A.H.
        • Kastor J.A.
        • Josephson M.E.
        Ventricular resection guided by epicardial and endocardial mapping for treatment of recurrent ventricular tachycardia.
        N Engl J Med. 1980; 302: 589-593
        • Schalij M.J.
        • van Rugge F.P.
        • Siezenga M.
        • van der Velde E.T.
        Endocardial activation mapping of ventricular tachycardia in patients: first application of a 32-site bipolar mapping electrode catheter.
        Circulation. 1998; 98: 2168-2179
        • Marchlinski F.E.
        • Callans D.J.
        • Gottlieb C.D.
        • Zado E.
        Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy.
        Circulation. 2000; 101: 1288-1296
        • Stevenson W.G.
        • Khan H.
        • Sager P.
        • et al.
        Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction.
        Circulation. 1993; 88: 1647-1670
        • Calkins H.
        • Epstein A.
        • Packer D.
        • et al.
        Catheter ablation of ventricular tachycardia in patients with structural heart disease using cooled radiofrequency energy: results of a prospective multicenter study.
        J Am Coll Cardiol. 2000; 35: 1905-1914
        • Tanner H.
        • Hindricks G.
        • Volkmer M.
        • et al.
        Catheter ablation of recurrent scar-related ventricular tachycardia using electroanatomical mapping and irrigated ablation technology: results of the prospective multicenter Euro-VT-study.
        J Cardiovasc Electrophysiol. 2010; 21: 47-53
        • Ajijola O.A.
        • Tung R.
        • Shivkumar K.
        Ventricular tachycardia in ischemic heart disease substrates.
        Indian Heart J. 2014; 66: S24-S34
        • Tung R.
        • Josephson M.E.
        • Bradfield J.S.
        • Shivkumar K.
        Directional influences of ventricular activation on myocardial scar characterization: voltage mapping with multiple wavefronts during ventricular tachycardia ablation.
        Circ Arrhythm Electrophysiol. 2016; 9e004155
        • Cohen C.J.
        • Bean B.P.
        • Tsien R.W.
        Maximal upstroke velocity as an index of available sodium conductance: comparison of maximal upstroke velocity and voltage clamp measurements of sodium current in rabbit Purkinje fibers.
        Circ Res. 1984; 54: 636-651
        • Cardinal R.
        • Rousseau G.
        • Bouchard C.
        • Vermeulen M.
        • Latour J.-G.
        • Pagé P.L.
        Myocardial electrical alteration in canine preparations with combined chronic rapid pacing and progressive coronary artery occlusion.
        Am J Physiol Heart Circ Physiol. 2004; 286: H1496-H1506
        • Ajijola O.A.
        • Lux R.L.
        • Khahera A.
        • et al.
        Sympathetic modulation of electrical activation in normal and infarcted myocardium: implications for arrhythmogenesis.
        Am J Physiol Heart Circ Physiol. 2017; 312: H608-H621
        • Yoshie K.
        • Rajendran P.S.
        • Massoud L.
        • et al.
        Cardiac TRPV1 afferent signaling promotes arrhythmogenic ventricular remodeling after myocardial infarction.
        JCI Insight. 2020; 5e124477
        • Bogun F.
        • Good E.
        • Reich S.
        • et al.
        Isolated potentials during sinus rhythm and pace-mapping within scars as guides for ablation of post-infarction ventricular tachycardia.
        J Am Coll Cardiol. 2006; 47: 2013-2019
        • Lue W.M.
        • Boyden P.A.
        Abnormal electrical properties of myocytes from chronically infarcted canine heart: alterations in Vmax and the transient outward current.
        Circulation. 1992; 85: 1175-1188
        • Pu J.
        • Boyden P.A.
        Alterations of Na+ currents in myocytes from epicardial border zone of the infarcted heart.
        Circ Res. 1997; 81: 110-119
        • Falcao S.
        • Rousseau G.
        • Baroudi G.
        • et al.
        Combined effects of reduced connexin 43, depressed active generator properties and energetic stress on conduction disturbances in canine failing myocardium.
        Pflugers Arch. 2007; 454: 999-1009
        • Severs N.J.
        • Bruce A.F.
        • Dupont E.
        • Rothery S.
        Remodelling of gap junctions and connexin expression in diseased myocardium.
        Cardiovasc Res. 2008; 80: 9-19
        • Zhou S.
        • Chen L.S.
        • Miyauchi Y.
        • et al.
        Mechanisms of cardiac nerve sprouting after myocardial infarction in dogs.
        Circ Res. 2004; 95: 76-83
        • Yokoyama T.
        • Lee J.-K.
        • Miwa K.
        • et al.
        Quantification of sympathetic hyperinnervation and denervation after myocardial infarction by three-dimensional assessment of the cardiac sympathetic network in cleared transparent murine hearts.
        PLoS One. 2017; 12e0182072
        • de Bakker J.M.T.
        • Wittkampf F.H.M.
        The pathophysiologic basis of fractionated and complex electrograms and the impact of recording techniques on their detection and interpretation.
        Circ Arrhythm Electrophysiol. 2010; 3: 204-213
        • Callans D.J.
        • Ren J.F.
        • Michele J.
        • Marchlinski F.E.
        • Dillon S.M.
        Electroanatomic left ventricular mapping in the porcine model of healed anterior myocardial infarction: correlation with intracardiac echocardiography and pathological analysis.
        Circulation. 1999; 100: 1744-1750
        • Wrobleski D.
        • Houghtaling C.
        • Josephson M.E.
        • Ruskin J.N.
        • Reddy V.Y.
        Use of electrogram characteristics during sinus rhythm to delineate the endocardial scar in a porcine model of healed myocardial infarction.
        J Cardiovasc Electrophysiol. 2003; 14: 524-529
        • Silberbauer J.
        • Oloriz T.
        • Maccabelli G.
        • et al.
        Noninducibility and late potential abolition: a novel combined prognostic procedural end point for catheter ablation of postinfarction ventricular tachycardia.
        Circ Arrhythm Electrophysiol. 2014; 7: 424-435
        • Jaïs P.
        • Maury P.
        • Khairy P.
        • et al.
        Elimination of local abnormal ventricular activities: a new end point for substrate modification in patients with scar-related ventricular tachycardia.
        Circulation. 2012; 125: 2184-2196

      Linked Article

      • Identifying the ventricular tachycardia arrhythmogenic substrate: The quest for the holy grail continues
        Heart Rhythm
        • Preview
          The development of electroanatomic mapping (EAM) technology during the 1990s transformed the field of cardiac electrophysiology.1 Substrate identification facilitated by EAM technologies has been the foundation of catheter ablation procedures for ventricular tachycardia (VT) in patients with structural heart disease. Because reentry typically is the mechanism of scar-related VT, substrate mapping techniques focus on (1) differentiating normal vs abnormal areas of myocardial tissue; and (2) identifying the underlying arrhythmogenic pathophysiological substrate, typically within areas of scar, that contribute to the formation of reentrant circuits.
        • Full-Text
        • PDF