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Myocardial function in aortic stenosis--insights from radial multilayer Doppler strain

Left ventricular (LV) radial tissue Doppler imaging (TDI) strain increases gradually from the subepicardial to the subendocardial layer in healthy individuals. A speckle tracking echocardiography study suggested this gradient to be reduced in parallel with increasing aortic stenosis (AS) severity. W...

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Published in:Cardiovascular ultrasound 2015-02, Vol.13 (1), p.8-8, Article 8
Main Authors: Cramariuc, Dana, Gerdts, Eva, Hjertaas, Johannes Just, Cramariuc, Alexandru, Davidsen, Einar Skulstad, Matre, Knut
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description Left ventricular (LV) radial tissue Doppler imaging (TDI) strain increases gradually from the subepicardial to the subendocardial layer in healthy individuals. A speckle tracking echocardiography study suggested this gradient to be reduced in parallel with increasing aortic stenosis (AS) severity. We used TDI strain in 84 patients with AS (mean age 73 ± 10 years, 56% hypertensive) for superior assessment of layer strain. 38 patients had non-severe and 46 severe AS by aortic valve area corrected for pressure recovery. Peak systolic radial TDI strain was measured in the subendocardial, mid-myocardial and subepicardial layers of the basal inferior LV wall, each within a region of interest of 2 × 6 mm (strain length 2 mm). Radial strain was lower in the subepicardial layer (33.4 ± 38.6%) compared to the mid-myocardial and subendocardial layers (50.3 ± 37.3% and 53.0 ± 40.0%, respectively, both p 
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A speckle tracking echocardiography study suggested this gradient to be reduced in parallel with increasing aortic stenosis (AS) severity. We used TDI strain in 84 patients with AS (mean age 73 ± 10 years, 56% hypertensive) for superior assessment of layer strain. 38 patients had non-severe and 46 severe AS by aortic valve area corrected for pressure recovery. Peak systolic radial TDI strain was measured in the subendocardial, mid-myocardial and subepicardial layers of the basal inferior LV wall, each within a region of interest of 2 × 6 mm (strain length 2 mm). Radial strain was lower in the subepicardial layer (33.4 ± 38.6%) compared to the mid-myocardial and subendocardial layers (50.3 ± 37.3% and 53.0 ± 40.0%, respectively, both p &lt; 0.001 vs. subepicardial). In the subendo- and midmyocardium, radial strain was lower in patients with severe AS compared to those with non-severe AS (p &lt; 0.05). In multivariate regression analyses including age, heart rate, inferior wall thickness, hypertension, and AS severity, radial strain in the mid-myocardium was primarily attenuated by presence of hypertension (β = -0.23) and AS severity (β = -0.26, both p &lt; 0.05), while radial strain in the subendocardium was significantly influenced by AS severity only (β = -0.35, p &lt; 0.01). In AS, both the AS severity and concomitant hypertension attenuate radial TDI strain in the inferior LV wall. 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In multivariate regression analyses including age, heart rate, inferior wall thickness, hypertension, and AS severity, radial strain in the mid-myocardium was primarily attenuated by presence of hypertension (β = -0.23) and AS severity (β = -0.26, both p &lt; 0.05), while radial strain in the subendocardium was significantly influenced by AS severity only (β = -0.35, p &lt; 0.01). In AS, both the AS severity and concomitant hypertension attenuate radial TDI strain in the inferior LV wall. 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A speckle tracking echocardiography study suggested this gradient to be reduced in parallel with increasing aortic stenosis (AS) severity. We used TDI strain in 84 patients with AS (mean age 73 ± 10 years, 56% hypertensive) for superior assessment of layer strain. 38 patients had non-severe and 46 severe AS by aortic valve area corrected for pressure recovery. Peak systolic radial TDI strain was measured in the subendocardial, mid-myocardial and subepicardial layers of the basal inferior LV wall, each within a region of interest of 2 × 6 mm (strain length 2 mm). Radial strain was lower in the subepicardial layer (33.4 ± 38.6%) compared to the mid-myocardial and subendocardial layers (50.3 ± 37.3% and 53.0 ± 40.0%, respectively, both p &lt; 0.001 vs. subepicardial). In the subendo- and midmyocardium, radial strain was lower in patients with severe AS compared to those with non-severe AS (p &lt; 0.05). In multivariate regression analyses including age, heart rate, inferior wall thickness, hypertension, and AS severity, radial strain in the mid-myocardium was primarily attenuated by presence of hypertension (β = -0.23) and AS severity (β = -0.26, both p &lt; 0.05), while radial strain in the subendocardium was significantly influenced by AS severity only (β = -0.35, p &lt; 0.01). In AS, both the AS severity and concomitant hypertension attenuate radial TDI strain in the inferior LV wall. The subendocardial radial strain is mainly influenced by AS severity, while midmyocardial radial strain is attenuated by both hypertension and AS severity.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>25890306</pmid><doi>10.1186/s12947-015-0001-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged
Anisotropy
Aortic Valve Stenosis - complications
Aortic Valve Stenosis - diagnostic imaging
Aortic Valve Stenosis - physiopathology
Compressive Strength
Echocardiography, Doppler - methods
Elastic Modulus
Female
Humans
Male
Reproducibility of Results
Sensitivity and Specificity
Shear Strength
Stress, Mechanical
Tensile Strength
Ventricular Dysfunction, Left - diagnostic imaging
Ventricular Dysfunction, Left - etiology
Ventricular Dysfunction, Left - physiopathology
title Myocardial function in aortic stenosis--insights from radial multilayer Doppler strain
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