Value of layer-specific strain distribution patterns in hypertrophied myocardium from different etiologies

Mu shiang Huang, Wen-Huang Li, Huey Ru Tsai, Yen-Wen Liu, Ping-Yen Liu, Wei-Chuan Tsai

Research output: Contribution to journalArticle

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 languageEnglish
Pages (from-to)69-75
Number of pages7
JournalInternational Journal of Cardiology
Volume281
DOIs
Publication statusPublished - 2019 Apr 15

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Aortic Valve Stenosis
Hypertrophic Cardiomyopathy
Myocardium
Heart Ventricles
Hemodynamics
Hypertrophy
Echocardiography
Mechanics
Pressure

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

@article{dedae33f7fed44e2b10f4e9d8a6709a1,
title = "Value of layer-specific strain distribution patterns in hypertrophied myocardium from different etiologies",
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.",
author = "Huang, {Mu shiang} and Wen-Huang Li and Tsai, {Huey Ru} and Yen-Wen Liu and Ping-Yen Liu and Wei-Chuan Tsai",
year = "2019",
month = "4",
day = "15",
doi = "10.1016/j.ijcard.2019.01.044",
language = "English",
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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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