Published online Apr 26, 2017. doi: 10.4330/wjc.v9.i4.363
Peer-review started: September 27, 2016
First decision: October 20, 2016
Revised: December 30, 2016
Accepted: January 14, 2017
Article in press: January 14, 2017
Published online: April 26, 2017
Processing time: 214 Days and 2.7 Hours
To explore regional systolic strain of midwall and endocardial segments using speckle tracking echocardiography in patients with apical hypertrophic cardiomyopathy (HCM).
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.
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 endocardial GLPPS was significantly greater and reached normal values (apical: -22.8% ± -7.8%, basal: -17.9% ± -7.5%).
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.
Core tip: In this study we prospectively assessed 20 patients with apical hypertrophic cardiomyopathy (HCM) in which we used speckle tracking echocardiography for measuring global longitudinal peak systolic strain in the midwall and endocardium of the left ventricle. We showed that two-dimensional strain was decreased mainly confined to the mesocardium, while endocardial deformation was preserved. This finding allowed to identify subclinical left ventricular systolic 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.