TITLE:
Regional Heterogeneity in 3D Myocardial Shortening in Hypertensive Left Ventricular Hypertrophy: A Cardiovascular CMR Tagging Substudy to the Life Study
AUTHORS:
Robert W. W. Biederman, Alistair A. Young, Mark Doyle, Richard B. Devereux, Eduardo Kortright, Gilbert Perry, Jonathan N. Bella, Suzanne Oparil, David Calhoun, Gerald M. Pohost, Louis J. Dell’Italia
KEYWORDS:
Hypertension, Left Ventricular Hypertrophy, Magnetic Resonance Imaging, Cardiac Mechanics, Heart Wall Motion, 3D
JOURNAL NAME:
Journal of Biomedical Science and Engineering,
Vol.8 No.3,
March
26,
2015
ABSTRACT: Background: Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumferential shortening (MWCS). Depressed MWCS is an adverse prognostic indicator, but whether this finding reflects reduced global or regional LV myocardial function, as assessed by three-dimensional (3D) myocardial strain, is unknown. Methods and Results: Cardiac Magnetic Resonance (CMR) tissue tagging permits direct evaluation of regional 3D intramyocardial strain, independent of LV geometry. We evaluated 21 hypertensive patients with electrocardiographic LVH in the LIFE study and 8 normal controls using 3D MR tagging and echocardiography. Patients had higher MR LV mass than normals (116 ± 40 versus 63 ± 6 g/m2, P = 0.002). Neither echocardiographic fractional shortening (32 ± 6 versus 33% ± 3%), LVEF (63% versus 64%) or mean end-systolic stress (175 ± 27 versus 146 ± 28 g/cm2) were significantly different, yet global MWCS was decreased by both echocardiography (13.4 ± 2.8 versus 18.2% ± 1.5%, P P P = 0.002) in LVH and greater in lateral and anterior regions versus septal and posterior regions ( P P P 0.60, P = 0.001 for both). Conclusions: In patients with hypertensive LVH, despite normal LV function via echocardiography or CMR, CMR intramyocardial tagging show depressed global MWCS while 3D MR strain revealed marked underlying regional heterogeneity of LV dysfunction.