Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 69-75 |
| Number of pages | 7 |
| Journal | International Journal of Cardiology |
| Volume | 281 |
| DOIs | |
| Publication status | Published - 2019 Apr 15 |
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
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Value of layer-specific strain distribution patterns in hypertrophied myocardium from different etiologies. / Huang, Mu shiang; Li, Wen-Huang; Tsai, Huey Ru; Liu, Yen-Wen; Liu, Ping-Yen; Tsai, Wei-Chuan.
In: International Journal of Cardiology, Vol. 281, 15.04.2019, p. 69-75.Research output: Contribution to journal › Article
TY - JOUR
T1 - Value of layer-specific strain distribution patterns in hypertrophied myocardium from different etiologies
AU - Huang, Mu shiang
AU - Li, Wen-Huang
AU - Tsai, Huey Ru
AU - Liu, Yen-Wen
AU - Liu, Ping-Yen
AU - Tsai, Wei-Chuan
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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UR - http://www.scopus.com/inward/citedby.url?scp=85060755037&partnerID=8YFLogxK
U2 - 10.1016/j.ijcard.2019.01.044
DO - 10.1016/j.ijcard.2019.01.044
M3 - Article
C2 - 30711265
AN - SCOPUS:85060755037
VL - 281
SP - 69
EP - 75
JO - International Journal of Cardiology
JF - International Journal of Cardiology
SN - 0167-5273
ER -