Background: In chronic aortic regurgitation (AR) patients, rearrangements of left ventricular (LV) wall deformation including contraction and thickening may occur to preserve LV ejection performance in the course of myocardial adaptation to increased systolic wall stress. We assessed transmural rearrangements of myocardial deformation by speckle tracking echocardiography in patients with chronic AR. Methods: We enrolled 90 patients with AR and 53 control subjects. On a LV short-axis B-mode image, total-, inner-half -, and outer-half radial strain (RS) and circumferential strain (CS) at inner, mid, and outer layers were calculated. Longitudinal strain (LS) was calculated on an apical 4-chamber image. Three components of end-systolic wall stress (ESS) were calculated: midwall circumferential (ESSc), meridional (ESSm), and inner radial (ESSr). AR severity was classified as moderate in 31 patients, severe with preserved LVEF ≥50% (severe ARpEF) in 42 patients, and severe with depressed LVEF <50% (severe ARdEF) in 17 patients. Results: LS was decreased even in the moderate AR group with normal ESSm. Inner-RS progressively decreased with increases of ESSr; however, outer-RS in the moderate and severe ARpEF groups was higher than that in the control group. Consequently, total-RS was preserved even in the severe ARpEF group with increased ESSr. Inner-CS was lower in the severe ARpEF group than in the control and moderate AR groups, however, outer-CS was higher in the severe ARpEF group than in the control group. All strain parameters were lower in the severe ARdEF group with dramatically increased ESS than in other groups. In 29 patients with aortic valve replacement (AVR), total-RS and outer-RS were significantly decreased after AVR. The ratio of inner-RS to outer-RS significantly increased after AVR and did not differ from that in the control group. Conclusions: Transmural strain analysis revealed rearrangements of wall deformation in the course of adaptation to increased ESS in patients with AR. As a distinctive rearrangement, subendocardial dysfunction accompanied by increased wall thickening in the subepicardium may indicate vertical compensation of wall thickening to preserve LVEF.