Speckle-tracking echocardiography correctly identifies segmental left ventricular dysfunction induced by scarring in a rat model of myocardial infarction

1 Imaging Section, Department of Cardiovascular Medicine, and 2 Lerner Research Institute, Departments of Cardiovascular Medicine and Stem Cell Biology, Cleveland Clinic Foundation, Cleveland, Ohio Submitted 26 October 2006 ; accepted in final form 23 January 2007 Speckle-tracking echocardiography (...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2007-06, Vol.292 (6), p.H2809-H2816
Hauptverfasser: Popovic, Zoran B, Benejam, Carlos, Bian, Jing, Mal, Niladri, Drinko, Jeannie, Lee, Kwangdeok, Forudi, Farhad, Reeg, Rachel, Greenberg, Neil L, Thomas, James D, Penn, Marc S
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Sprache:eng
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Zusammenfassung:1 Imaging Section, Department of Cardiovascular Medicine, and 2 Lerner Research Institute, Departments of Cardiovascular Medicine and Stem Cell Biology, Cleveland Clinic Foundation, Cleveland, Ohio Submitted 26 October 2006 ; accepted in final form 23 January 2007 Speckle-tracking echocardiography (STE) uses a two-dimensional echocardiographic image to estimate two orthogonal strain components. The aim of this study was to assess sensitivity of circumferential (S circ ) and radial (S rad ) strains to infarct-induced left ventricular (LV) remodeling and scarring of the LV in a rat. To assess the relationship among S circ , S rad , and scar size, two-dimensional echocardiographic LV short-axis images (12 MHz transducer, Vivid 7 echo machine) were collected in 34 Lewis rats 4 to 10 wk after ligation of the left anterior descending artery. Percent segmental fibrosis was assessed from histological LV cross sections stained by Masson trichrome. Ten normal rats served as echocardiographic controls. S circ and S rad were assessed by STE. Histological data showed consistent scarring of anterior and lateral segments with variable extension to posterior and inferior segments. Both S circ and S rad significantly decreased after myocardial infarction ( P < 0.0001 for both). As anticipated, S circ and S rad were lowest in the infarcted segments. Multiple linear regression showed that segmental S circ were similarly dependent on segmental fibrosis and end-systolic diameter ( P < 0.0001 for both), whereas segmental S rad measurements were more dependent on end-systolic diameter ( P < 0.0001) than on percent fibrosis ( P < 0.002). STE correctly identifies segmental LV dysfunction induced by scarring that follows myocardial infarction in rats. infarction; collagen; contractility Address for reprint requests and other correspondence: M. S. Penn, Bakken Heart-Brain Institute, Depts. of Cardiovascular Medicine and Stem Cell Biology, Cleveland Clinic Foundation, 9500 Euclid Ave., NE3, Cleveland, OH 44195 (e-mail: pennm{at}ccf.org )
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.01176.2006