AIM To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy(HCM).METHODS We prospectively assessed 20 patients(mean age 53 ± 16 years,range:18-81 years,10 were male),with apical HCM. We measured global longitudinal peak systolic strain(GLPSS) in the midwall and endocardium of the left ventricle. RESULTS The diastolic thickness of the 4 apical segments was 16.25 ± 2.75 mm. All patients had a normal global systolicfunction with a fractional shortening of 50% ± 8%. In spite of supernormal left ventricular(LV) systolic function,midwall GLPSS was decreased in all patients,more in the apical(-7.3% ±-8.8%) than in basal segments(-15.5% ±-6.93%),while endocardial GLPPS was significantly greater and reached normal values(apical:-22.8% ±-7.8%,basal:-17.9% ±-7.5%). CONCLUSION This study shows that two-dimensional strain was decreased mainly confined to the mesocardium,while endocardium myocardial deformation was preserved in HCM and allowed to identify subclinical LV dysfunction. This transmural heterogeneity in systolic strain had not been previously described in HCM and could be explained by the distribution of myofibrillar disarray in deep myocardial areas. The clinical application of this novel finding may help further understanding of the pathophysiology of HCM. AIM To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy (HCM). METHODS We prospectively assessed 20 patients (mean age 53 ± 16 years, range: 18-81 years, 10 were male) , with apical HCM. We measured global longitudinal peak systolic strain (GLPSS) in the midwall and endocardium of the left ventricle. RESULTS The diastolic thickness of the 4 apical segments was 16.25 ± 2.75 mm. All patients had a normal global systolic function with a fractional Shortening of 50% ± 8%. In spite of supernormal left ventricular (LV) systolic function, midwall GLPSS was decreased in all patients, more in the apical (-7.3% ± -8.8%) than in basal segments (-15.5% ± -6.93%) while the endocardial GLPPS was significantly greater and reached normal values ​​(apical: -22.8% ± -7.8%, basal: -17.9% ± -7.5%). CONCLUSION This study shows that two-dimensional strain was decreased mainly confined to the mesocardium, while endocardi um myocardial deformation was preserved in HCM and allowed to identify subclinical LV dysfunction. This clinical application of this novel finding was in HCM and could be explained by the distribution of myofibrillar disarray in deep myocardial areas. may help further understanding of the pathophysiology of HCM.