TY - JOUR
T1 - Value of layer-specific strain distribution patterns in hypertrophied myocardium from different etiologies
AU - Huang, Mu shiang
AU - Lee, Wen Huang
AU - Tsai, Huey Ru
AU - Liu, Yen Wen
AU - Liu, Ping Yen
AU - Tsai, Wei Chuan
N1 - Funding Information:
This study was supported by grant MOST 104-2314-B-006-086 and MOST 106-2314-B-006-043 from the Ministry of Science and Technology, Taiwan, Executive Yuan.
Funding Information:
This study was supported by grant MOST 104-2314-B-006-086 and MOST 106-2314-B-006-043 from the Ministry of Science and Technology, Taiwan , Executive Yuan.
Publisher Copyright:
© 2019 Elsevier B.V.
PY - 2019/4/15
Y1 - 2019/4/15
N2 - Background: Intrinsic myocardial mechanics might have different patterns because of the different etiologies of myocardial hypertrophy. We used layer-specific strain to compare those with aortic stenosis (AS) and hypertrophic cardiomyopathy (HCM) and examined the differences in strain distribution pattern and for their clinical implications. Methods: Comprehensive echocardiography was done in 3 groups: 129 with moderate-to-severe AS, 172 consecutive patients with HCM, and 58 healthy controls. Left ventricle (LV) layer-specific deformation parameters were obtained using two-dimensional speckle tracking echocardiography. The transmural strain gradient was defined as the strain difference between subendocardial and subepicardial myocardium. Both diseased groups were further divided based on the median value of transmural strain gradient for the hemodynamics correlation. Results: Compared with the HCM group, the AS group had more preserved transmural longitudinal strain gradient (4.49 ± 1.3% vs. 3.61 ± 1.2%, p < 0.001), which was not significantly different from that of the healthy controls (4.49 ± 1.3% vs. 4.54 ± 1.0%, p = 0.975). And only in AS group the transmural circumferential strain correlated with myocardium mass index (r = −0.237, p = 0.008), and the hemodynamic profiles (LV ejection fraction and LA pressure) were correlated well with transmural strain gradient, in that the lower subgroup had a significantly lower LV ejection fraction and higher average E/E′. Conclusions: Myocardium hypertrophy from different etiology resulted in different layer-specific strain distribution pattern. The loss of an adequate transmural strain gradient correlated with hemodynamics and might reflect intrinsic myocardial dysfunction.
AB - Background: Intrinsic myocardial mechanics might have different patterns because of the different etiologies of myocardial hypertrophy. We used layer-specific strain to compare those with aortic stenosis (AS) and hypertrophic cardiomyopathy (HCM) and examined the differences in strain distribution pattern and for their clinical implications. Methods: Comprehensive echocardiography was done in 3 groups: 129 with moderate-to-severe AS, 172 consecutive patients with HCM, and 58 healthy controls. Left ventricle (LV) layer-specific deformation parameters were obtained using two-dimensional speckle tracking echocardiography. The transmural strain gradient was defined as the strain difference between subendocardial and subepicardial myocardium. Both diseased groups were further divided based on the median value of transmural strain gradient for the hemodynamics correlation. Results: Compared with the HCM group, the AS group had more preserved transmural longitudinal strain gradient (4.49 ± 1.3% vs. 3.61 ± 1.2%, p < 0.001), which was not significantly different from that of the healthy controls (4.49 ± 1.3% vs. 4.54 ± 1.0%, p = 0.975). And only in AS group the transmural circumferential strain correlated with myocardium mass index (r = −0.237, p = 0.008), and the hemodynamic profiles (LV ejection fraction and LA pressure) were correlated well with transmural strain gradient, in that the lower subgroup had a significantly lower LV ejection fraction and higher average E/E′. Conclusions: Myocardium hypertrophy from different etiology resulted in different layer-specific strain distribution pattern. The loss of an adequate transmural strain gradient correlated with hemodynamics and might reflect intrinsic myocardial dysfunction.
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U2 - 10.1016/j.ijcard.2019.01.044
DO - 10.1016/j.ijcard.2019.01.044
M3 - Article
C2 - 30711265
AN - SCOPUS:85060755037
SN - 0167-5273
VL - 281
SP - 69
EP - 75
JO - International Journal of Cardiology
JF - International Journal of Cardiology
ER -