OBJECTIVES: This study delineates between infarcts varying in transmurality by using endocardial electrophysiologic information obtained during catheter-based mapping. BACKGROUND: The degree of infarct transmurality extent has previously been linked to patient prognosis and may have significant impact on therapeutic strategies. Catheter-based endocardial mapping may accurately delineate between infarcts differing in the transmural extent of necrotic tissue. METHODS: Electromechanical mapping was performed in 13 dogs four weeks after left anterior descending coronary artery ligation, enabling three-dimensional reconstruction of the left ventricular chamber. A concomitant reduction in bipolar electrogram amplitude (BEA) and local shortening indicated the infarcted region. In addition, impedance, unipolar electrogram amplitude (UEA) and slew rate (SR) were quantified. Subsequently, the hearts were excised, stained with 2,3,5-triphenyltetrazolium chloride and sliced transversely. The mean transmurality of the necrotic tissue in each slice was determined, and infarcts were divided into <30%, 31% to 60% and 61% to 100% transmurality subtypes to be correlated with the corresponding electrical data. RESULTS: From the three-dimensional reconstructions, a total of 263 endocardial points were entered for correlation with the degree of transmurality (4.6 +/- 2.4 points from each section). All four indices delineated infarcted tissue. However, BEA (1.9 +/- 0.7 mV, 1.4 +/- 0.7 mV, 0.8 +/- 0.4 mV in the three groups respectively, p < 0.05 between each group) proved superior to SR, which could not differentiate between the second (31% to 60%) and third (61% to 100%) transmurality subgroups, and to UEA and impedance, which could not differentiate between the first (<30%) and second transmurality subgroups. CONCLUSIONS: The degree of infarct transmurality extent can be derived from the electrical properties of the endocardium obtained via detailed catheter-based mapping in this animal model.
OBJECTIVES: This study delineates between infarcts varying in transmurality by using endocardial electrophysiologic information obtained during catheter-based mapping. BACKGROUND: The degree of infarct transmurality extent has previously been linked to patient prognosis and may have significant impact on therapeutic strategies. Catheter-based endocardial mapping may accurately delineate between infarcts differing in the transmural extent of necrotic tissue. METHODS: Electromechanical mapping was performed in 13 dogs four weeks after left anterior descending coronary artery ligation, enabling three-dimensional reconstruction of the left ventricular chamber. A concomitant reduction in bipolar electrogram amplitude (BEA) and local shortening indicated the infarcted region. In addition, impedance, unipolar electrogram amplitude (UEA) and slew rate (SR) were quantified. Subsequently, the hearts were excised, stained with 2,3,5-triphenyltetrazolium chloride and sliced transversely. The mean transmurality of the necrotic tissue in each slice was determined, and infarcts were divided into <30%, 31% to 60% and 61% to 100% transmurality subtypes to be correlated with the corresponding electrical data. RESULTS: From the three-dimensional reconstructions, a total of 263 endocardial points were entered for correlation with the degree of transmurality (4.6 +/- 2.4 points from each section). All four indices delineated infarcted tissue. However, BEA (1.9 +/- 0.7 mV, 1.4 +/- 0.7 mV, 0.8 +/- 0.4 mV in the three groups respectively, p < 0.05 between each group) proved superior to SR, which could not differentiate between the second (31% to 60%) and third (61% to 100%) transmurality subgroups, and to UEA and impedance, which could not differentiate between the first (<30%) and second transmurality subgroups. CONCLUSIONS: The degree of infarct transmurality extent can be derived from the electrical properties of the endocardium obtained via detailed catheter-based mapping in this animal model.
Authors: Peter J Psaltis; Andrew C W Zannettino; Stan Gronthos; Stephen G Worthley Journal: J Cardiovasc Transl Res Date: 2009-10-23 Impact factor: 4.132
Authors: Takeshi Sasaki; Christopher F Miller; Rozann Hansford; Juemin Yang; Brian S Caffo; Menekhem M Zviman; Charles A Henrikson; Joseph E Marine; David Spragg; Alan Cheng; Harikrishna Tandri; Sunil Sinha; Aravindan Kolandaivelu; Stefan L Zimmerman; David A Bluemke; Gordon F Tomaselli; Ronald D Berger; Hugh Calkins; Henry R Halperin; Saman Nazarian Journal: Circ Arrhythm Electrophysiol Date: 2012-11-13
Authors: Peter J Psaltis; Angelo Carbone; Darryl P Leong; Dennis H Lau; Adam J Nelson; Tim Kuchel; Troy Jantzen; Jim Manavis; Kerry Williams; Prashanthan Sanders; Stan Gronthos; Andrew C W Zannettino; Stephen G Worthley Journal: Int J Cardiovasc Imaging Date: 2010-06-29 Impact factor: 2.357
Authors: Mathew D Hutchinson; Edward P Gerstenfeld; Benoit Desjardins; Rupa Bala; Michael P Riley; Fermin C Garcia; Sanjay Dixit; David Lin; Wendy S Tzou; Joshua M Cooper; Ralph J Verdino; David J Callans; Francis E Marchlinski Journal: Circ Arrhythm Electrophysiol Date: 2010-12-03
Authors: Yi Zheng; Marlos R Fernandes; Guilherme V Silva; Cristiano O Cardoso; John Canales; Amir Gahramenpour; Fred Baimbridge; Maria da Graça Cabreira-Hansen; Emerson C Perin Journal: Exp Clin Cardiol Date: 2008
Authors: Noemi Pavo; Andras Jakab; Maximilian Y Emmert; Georg Strebinger; Petra Wolint; Matthias Zimmermann; Hendrik Jan Ankersmit; Simon P Hoerstrup; Gerald Maurer; Mariann Gyöngyösi Journal: PLoS One Date: 2014-11-19 Impact factor: 3.240
Authors: F J van Slochteren; R van Es; M Gyöngyösi; T I G van der Spoel; S Koudstaal; T Leiner; P A Doevendans; S A J Chamuleau Journal: Int J Cardiovasc Imaging Date: 2016-02-16 Impact factor: 2.357