bution of viable myocardium in the ischemic myocardium has not been quantified and fully elucidated. To address this issue, we evaluated transmural myocardial strain profile (TMSP) in dogs with myocardial infarction using a newly developed tissue strain imaging. TMSP was obtained from the posterior wall at the epicardial left ventricular short-axis view in 13 anesthetized open-chest dogs. After control measurements, the left circumflex coronary artery was occluded for 90 min to induce subendocardial infarction (SMI). Subsequently, latex microbeads (90 m) were injected in the same artery to create transmural infarction (TMI). In each stage, measurements were done before and after dobutamine challenge (10 g ⅐ kg Ϫ1 ⅐ min Ϫ1 for 10 min) to estimate transmural myocardial viability. Strain in the subendocardium in the control stage increased by dobutamine (from 53.6 Ϯ 17.1 to 73.3 Ϯ 21.8%, P Ͻ 0.001), whereas that in SMI and TMI stages was almost zero at baseline and did not increase significantly by dobutamine [from 0.8 Ϯ 8.8 to 1.3 Ϯ 7.0%, P ϭ not significant (NS) for SMI, from Ϫ3.9 Ϯ 5.6 to Ϫ1.9 Ϯ 6.0%, P ϭ NS for TMI]. Strain in the subepicardium increased by dobutamine in the control stage (from 23.9 Ϯ 6.1 to 26.3 Ϯ 6.4%, P Ͻ 0.05) and in the SMI stage (from 12.4 Ϯ 7.3 to 27.1 Ϯ 8.8%, P Ͻ 0.005), whereas that in the TMI stage did not change (from Ϫ1.0 Ϯ 7.8 to Ϫ0.7 Ϯ 8.3%, P ϭ NS). In SMI, the subendocardial contraction was lost, but the subepicardium showed a significant increase in contraction with dobutamine. However, in TMI, even the subepicardial increase was not seen. Assessment of transmural strain profile using tissue strain imaging was a new and useful method to estimate transmural distribution of the viable myocardium in myocardial infarction. myocardial infarction; strain; viability; echocardiography IT IS WELL KNOWN that myocardial contraction has transmural heterogeneity. Several experimental studies confirmed that the subendocardium contributes greater to overall myocardial thickening than the subepicardium (6, 25). On the other hand, when a reduction of coronary blood flow occurs, a severe reduction of perfusion and kinesis occurs in the subendocardium, but only a trivial reduction can be detected in the subepicardium (5, 31). After a long period of ischemia, myocardial necrosis progresses from the endocardium to the epicardium (8, 13).Myocardial strain reflects regional myocardial function. With the recent advancement of tissue Doppler echocardiography, myocardial strain can be obtained noninvasively (3, 33) and has been reported to be useful to quantify regional myocardial systolic function in ischemic heart disease (9, 11, 24, 29, 36). The recently developed myocardial strain imaging system provides us myocardial strain in each wall layer and shows its distribution in a form of transmural myocardial strain profile (TMSP; see Ref. 1). Thus combination of TMSP and dobutamine stress echocardiography (DSE), which has been used for the assessment of myocardial viability (18), is expected to demonstr...