TY - JOUR
T1 - Dissociation between wall thickening of normal myocardium and cyclic variation of backscatter during inotropic stimulation
AU - Feinberg, M. S.
AU - Gussak, H. M.
AU - Davila-Roman, V. G.
AU - Baumann, C. M.
AU - Miller, J. G.
AU - Perez, J. E.
N1 - Funding Information:
From the Cardiovascular Division and Department of Physics, Washington University, St. Louis, Missouri. This study was supported in art by an American Heart Association Minority Research Award, Da PIa s, Texas (Dr. D&ilaRom&), and by Grants ROl HL.53461 (Dr. Perez) and ROl Ht40320 [Dr. Miller) from the National Institutes of Health, Bethesda, Maryland. Manuscript received July 3 1, 1995; revised manuscript received October 18, 1995 and accepted October 20.
PY - 1996
Y1 - 1996
N2 - The purpose of this study was to determine the relation between increased myocardial wall thickening during inotropic stimulation and quantitative acoustic properties of normal myocardium in humans. We first validated a new 2-dimensional ultrasonic backscatter imaging approach for measurement of cyclic variation in the parasternal long-axis view against conventional M- mode integrated backscatter technique in 41 patients and controls (group. A). We then performed 2-dimensional ultrasonic integrated backscatter imaging in 18 patients (group B) with normal segmental function at baseline to determine the magnitude of the cyclic variation of the septum and the posterior wall before and during infusion of dobutamine (10 and 20 μg/kg/min). Group A patients showed a close correlation of the cyclic variation obtained by the new 2-dimensional ultrasonic integrated backscatter imaging approach and the conventional M-mode technique. Group B patients had mean values of cyclic variation that remained unchanged in the septum (4.4 ± 1.4, 4.3 ± 1.7, and 4.8 ± 1.6 dB at baseline and at each dobutamine stage, respectively, p = NS) and in the posterior wall (6.4 ± 1.7, 6.4 ± 1.8 and 6.1 ± 1.9 dB, respectively, p = NS) despite progressive dobutamine-induced increases in percent wall thickening (septum: 38 ± 10% to 57 ± 17% and 68 ± 19%, respectively, and posterior wall 42 ± 13% to 72 ± 20% and 77 ± 18%, respectively; both p <0.001 vs baseline for both walls). Thus, physical properties of normal myocardium remain unchanged during inotropic stimulation.
AB - The purpose of this study was to determine the relation between increased myocardial wall thickening during inotropic stimulation and quantitative acoustic properties of normal myocardium in humans. We first validated a new 2-dimensional ultrasonic backscatter imaging approach for measurement of cyclic variation in the parasternal long-axis view against conventional M- mode integrated backscatter technique in 41 patients and controls (group. A). We then performed 2-dimensional ultrasonic integrated backscatter imaging in 18 patients (group B) with normal segmental function at baseline to determine the magnitude of the cyclic variation of the septum and the posterior wall before and during infusion of dobutamine (10 and 20 μg/kg/min). Group A patients showed a close correlation of the cyclic variation obtained by the new 2-dimensional ultrasonic integrated backscatter imaging approach and the conventional M-mode technique. Group B patients had mean values of cyclic variation that remained unchanged in the septum (4.4 ± 1.4, 4.3 ± 1.7, and 4.8 ± 1.6 dB at baseline and at each dobutamine stage, respectively, p = NS) and in the posterior wall (6.4 ± 1.7, 6.4 ± 1.8 and 6.1 ± 1.9 dB, respectively, p = NS) despite progressive dobutamine-induced increases in percent wall thickening (septum: 38 ± 10% to 57 ± 17% and 68 ± 19%, respectively, and posterior wall 42 ± 13% to 72 ± 20% and 77 ± 18%, respectively; both p <0.001 vs baseline for both walls). Thus, physical properties of normal myocardium remain unchanged during inotropic stimulation.
UR - http://www.scopus.com/inward/record.url?scp=0029939355&partnerID=8YFLogxK
U2 - 10.1016/S0002-9149(97)89347-2
DO - 10.1016/S0002-9149(97)89347-2
M3 - Article
C2 - 8629594
AN - SCOPUS:0029939355
SN - 0002-9149
VL - 77
SP - 515
EP - 520
JO - American Journal of Cardiology
JF - American Journal of Cardiology
IS - 7
ER -