Transmural Compensation of Myocardial Deformation to Preserve Left Ventricular Ejection Performance in Chronic Aortic Regurgitation Noriko Iida, RDCS, Yoshihiro Seo, MD, Tomoko Ishizu, MD, Hideki Nakajima, RDCS, PhD, Akiko Atsumi, MD, Masayoshi Yamamoto, MD, Tomoko Machino-Ohtsuka, MD, Ryo Kawamura, MD, Mami Enomoto, MD, Yasushi Kawakami, MD, and Kazutaka Aonuma, MD, Tsukuba, Japan Background: In patients with chronic aortic regurgitation (AR), systolic wall stress and volume overload affects left ventricular (LV) systolic function and remodeling. The aim of this study was to assess transmural rearrange- ments of myocardial deformation to preserve LV ejection performances using speckle-tracking echocardiog- raphy in patients with chronic AR. Methods: Ninety patients with AR were enrolled. On LV short-axis images, total, inner, and outer radial strain and circumferential strain at the inner, mid, and outer layers were calculated. On apical four-chamber images, endocardial longitudinal strain was calculated. End-systolic wall stresses were calculated using previous methods. Results: AR severities were classified as moderate in 31 patients, severe and preserved LV ejection fraction (LVEF) ($50%) in 42 patients, and severe and reduced LVEF (<50%) in 17 patients. Longitudinal strain was decreased even in the moderate AR group, despite normal end-systolic wall stress. Inner radial strain progres- sively decreased with increasing end-systolic wall stress, whereas outer radial strain in the moderate and severe AR and preserved LVEF groups was higher than in the control group. Consequently, total radial strain was preserved even in the severe AR and preserved LVEF groups with increased end-systolic wall stress. Similarly, despite reduced inner circumferential strain, outer circumferential strain was higher in the severe AR and preserved LVEF group than in the control group. All strain parameters were lower in the severe AR and reduced LVEF group with dramatically increased end-systolic wall stress than in other groups. Conclusions: Transmural strain analysis revealed that subendocardial dysfunction accompanied by increased wall thickening at the subepicardium may be a compensatory mechanism of wall thickening to preserve LVEF in patients with chronic AR. (J Am Soc Echocardiogr 2012;25:620-8.) Keywords: Aortic regurgitation, Strain, Wall stress, Speckle tracking echocardiography In chronic aortic regurgitation (AR), adaptation to increased preload and afterload results in left ventricular (LV) enlargement and increased myocardial mass. 1 LV eccentric hypertrophy inhibits the increase of wall stress, and patients with chronic AR remain asymptom- atic with preserved LVejection fractions (LVEFs) for a considerable pe- riod. 2-4 The development of afterload mismatch eventually causes LV dysfunction. 5,6 Therefore, previous studies have focused on the relation between LV ejection performance and LV wall stress. 6-10 As pathologic findings in the course of adaptation and failure to increased wall stress, rearrangement and slippage of myocardial fibers, the addition of new sarcomeres, hypertrophy, and interstitial fibrosis have been observed in chronic AR. 11-13 These myocardial structural changes affect myocardial function. However, how myocardial changes preserve global LV ejection performance has not yet been identified. Previous experimental studies have shown different changes between endocardial and epicardial deformation. 14-16 Recent clinical studies have demonstrated changes in myocardial function in patients with AR through regional myocardial deformation imaging, including speckle-tracking echocardiography (STE). 17-22 Software developed for STE allows the assessment of intramural myocardial strain measurements with an intramural speckle-tracking system in addition to the widely used standard strain analysis consist- ing of circumferential strain (CS), radial strain (RS), and longitudinal strain (LS). 23-26 The advantage of the system is the ability to separately measure endocardial, mid, and epicardial wall strain. In the present study, we aimed to assess whether rearrangements of myocardial deformation occurred as an adaptation and failure of From the Department of Clinical Laboratory, Tsukuba University Hospital, Tsukuba, Japan (N.I., H.N., Y.K.); and the Cardiovascular Division, Graduate School of Comprehensive Human Science (Y.S., T.I., A.A., M.Y., T.M.-O., R.K., M.E., K.A.), and Clinical Pathology Division, Graduate School of Comprehensive Human Science (T.I., Y.K.), University of Tsukuba, Tsukuba, Japan. Reprint requests: Yoshihiro Seo, MD, Cardiovascular Division, Institute of Clinical Medicine, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba 305-8575, Japan (E-mail: yo-seo@md. tsukuba.ac.jp). 0894-7317/$36.00 Copyright 2012 by the American Society of Echocardiography. doi:10.1016/j.echo.2012.02.005 620