Differentiation of hypertensive heart disease and hypertrophic cardiomyopathy with myocardial stiffness measurements: a shear wave imaging study using ultra-high frame rate echocardiography

Differentiation of hypertensive heart disease and hypertrophic cardiomyopathy with myocardial stiffness measurements: a shear wave imaging study using ultra-high frame rate echocardiography

Abstract Background Recently, cardiac shear wave (SW) elastography, based on high frame rate (HFR) echocardiography, has been proposed as new non-invasive technique for assessing myocardial stiffness. As myocardial stiffness increases with increasing wall stress, differences in measured operating my...

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Veröffentlicht in:European heart journal 2020-11, Vol.41 (Supplement_2)
Hauptverfasser: Cvijic, M, Bezy, S, Petrescu, A, Santos, P, Orlowska, M, Chakraborty, B, Duchenne, J, Pedrosa, J, Vanassche, T, Van Cleemput, J, Dhooge, J, Voigt, J.U
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container_issue Supplement_2
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container_title European heart journal
container_volume 41
creator Cvijic, M
Bezy, S
Petrescu, A
Santos, P
Orlowska, M
Chakraborty, B
Duchenne, J
Pedrosa, J
Vanassche, T
Van Cleemput, J
Dhooge, J
Voigt, J.U
description Abstract Background Recently, cardiac shear wave (SW) elastography, based on high frame rate (HFR) echocardiography, has been proposed as new non-invasive technique for assessing myocardial stiffness. As myocardial stiffness increases with increasing wall stress, differences in measured operating myocardial stiffness do not necessarily reflect differences in intrinsic myocardial properties, but can also be caused by mere changes in loading or chamber geometry. This complicates myocardial stiffness interpretation for different types of pathologic hypertrophy. Purpose To explore the relationship between myocardial stiffness and underlying pathological substrates for cardiac hypertrophy. Methods We included 20 patients with hypertension (HT) and myocardial remodelling (59±14 years, 75% male), 20 patients with hypertrophic cardiomyopathy (HCM) (59±16 years, 60% male) and 20 healthy controls (56±14 years, 75% male). Left ventricular (LV) parasternal long axis views were acquired with an experimental HFR scanner at 1293±362 frames per seconds. Propagation velocity of SW occurring after mitral valve closure in the interventricular septum (IVS) served as measure of operating myocardial stiffness (Figure A). To compare myocardial stiffness among hearts with differing loading conditions and chamber geometry, SW velocities were normalized to end-diastolic wall stress, estimated at IVS from regional wall thickness, longitudinal and circumferential regional radii of curvature, and non-invasively estimated LV end-diastolic pressure (EDP). Results SW velocities differed significantly between groups (p
doi_str_mv 10.1093/ehjci/ehaa946.0087
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As myocardial stiffness increases with increasing wall stress, differences in measured operating myocardial stiffness do not necessarily reflect differences in intrinsic myocardial properties, but can also be caused by mere changes in loading or chamber geometry. This complicates myocardial stiffness interpretation for different types of pathologic hypertrophy. Purpose To explore the relationship between myocardial stiffness and underlying pathological substrates for cardiac hypertrophy. Methods We included 20 patients with hypertension (HT) and myocardial remodelling (59±14 years, 75% male), 20 patients with hypertrophic cardiomyopathy (HCM) (59±16 years, 60% male) and 20 healthy controls (56±14 years, 75% male). Left ventricular (LV) parasternal long axis views were acquired with an experimental HFR scanner at 1293±362 frames per seconds. Propagation velocity of SW occurring after mitral valve closure in the interventricular septum (IVS) served as measure of operating myocardial stiffness (Figure A). To compare myocardial stiffness among hearts with differing loading conditions and chamber geometry, SW velocities were normalized to end-diastolic wall stress, estimated at IVS from regional wall thickness, longitudinal and circumferential regional radii of curvature, and non-invasively estimated LV end-diastolic pressure (EDP). Results SW velocities differed significantly between groups (p&lt;0.001). The controls had the lowest SW velocities (4.02±0.97 m/s), whereas values between HT and HCM group were comparable (6.46±0.99 m/s vs. 7.00±2.10 m/s; p=0.738). Considering end-diastolic wall stress, HCM patients had the same SW velocity at lower wall stress compared to HT (Figure B), indicating higher myocardial stiffness in the HCM group. SW velocities normalized for wall stress indicated significantly different myocardial stiffness among all groups (p&lt;0.001) (Figure C). In a multiple linear regression model, the underlying pathological substrate independently influenced SW velocity (beta 1.37, 95% CI (0.78–1.96); p&lt;0.001), while wall stress did not significantly affect its value (p=0.479). Conclusions Our study demonstrated that SW elastography can detect differences in myocardial stiffness in hypertensive heart and hypertrophic cardiomyopathy. Additionally, our results suggest that SW velocity is dominated by underlying myocardial tissue properties. We hypothesize that differential changes in cardiomyocytes and/or the extracellular matrix contribute to the differential myocardial stiffening in different pathologic entities of LV hypertrophy. Thus, SW elastography could provide useful novel diagnostic information in the evaluation of LV hypertrophy. Figure A, B, C Funding Acknowledgement Type of funding source: None</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/ehjci/ehaa946.0087</identifier><language>eng</language><publisher>Oxford University Press</publisher><ispartof>European heart journal, 2020-11, Vol.41 (Supplement_2)</ispartof><rights>Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com. 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids></links><search><creatorcontrib>Cvijic, M</creatorcontrib><creatorcontrib>Bezy, S</creatorcontrib><creatorcontrib>Petrescu, A</creatorcontrib><creatorcontrib>Santos, P</creatorcontrib><creatorcontrib>Orlowska, M</creatorcontrib><creatorcontrib>Chakraborty, B</creatorcontrib><creatorcontrib>Duchenne, J</creatorcontrib><creatorcontrib>Pedrosa, J</creatorcontrib><creatorcontrib>Vanassche, T</creatorcontrib><creatorcontrib>Van Cleemput, J</creatorcontrib><creatorcontrib>Dhooge, J</creatorcontrib><creatorcontrib>Voigt, J.U</creatorcontrib><title>Differentiation of hypertensive heart disease and hypertrophic cardiomyopathy with myocardial stiffness measurements: a shear wave imaging study using ultra-high frame rate echocardiography</title><title>European heart journal</title><description>Abstract Background Recently, cardiac shear wave (SW) elastography, based on high frame rate (HFR) echocardiography, has been proposed as new non-invasive technique for assessing myocardial stiffness. As myocardial stiffness increases with increasing wall stress, differences in measured operating myocardial stiffness do not necessarily reflect differences in intrinsic myocardial properties, but can also be caused by mere changes in loading or chamber geometry. This complicates myocardial stiffness interpretation for different types of pathologic hypertrophy. Purpose To explore the relationship between myocardial stiffness and underlying pathological substrates for cardiac hypertrophy. Methods We included 20 patients with hypertension (HT) and myocardial remodelling (59±14 years, 75% male), 20 patients with hypertrophic cardiomyopathy (HCM) (59±16 years, 60% male) and 20 healthy controls (56±14 years, 75% male). Left ventricular (LV) parasternal long axis views were acquired with an experimental HFR scanner at 1293±362 frames per seconds. Propagation velocity of SW occurring after mitral valve closure in the interventricular septum (IVS) served as measure of operating myocardial stiffness (Figure A). To compare myocardial stiffness among hearts with differing loading conditions and chamber geometry, SW velocities were normalized to end-diastolic wall stress, estimated at IVS from regional wall thickness, longitudinal and circumferential regional radii of curvature, and non-invasively estimated LV end-diastolic pressure (EDP). Results SW velocities differed significantly between groups (p&lt;0.001). The controls had the lowest SW velocities (4.02±0.97 m/s), whereas values between HT and HCM group were comparable (6.46±0.99 m/s vs. 7.00±2.10 m/s; p=0.738). Considering end-diastolic wall stress, HCM patients had the same SW velocity at lower wall stress compared to HT (Figure B), indicating higher myocardial stiffness in the HCM group. SW velocities normalized for wall stress indicated significantly different myocardial stiffness among all groups (p&lt;0.001) (Figure C). In a multiple linear regression model, the underlying pathological substrate independently influenced SW velocity (beta 1.37, 95% CI (0.78–1.96); p&lt;0.001), while wall stress did not significantly affect its value (p=0.479). Conclusions Our study demonstrated that SW elastography can detect differences in myocardial stiffness in hypertensive heart and hypertrophic cardiomyopathy. Additionally, our results suggest that SW velocity is dominated by underlying myocardial tissue properties. We hypothesize that differential changes in cardiomyocytes and/or the extracellular matrix contribute to the differential myocardial stiffening in different pathologic entities of LV hypertrophy. Thus, SW elastography could provide useful novel diagnostic information in the evaluation of LV hypertrophy. 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As myocardial stiffness increases with increasing wall stress, differences in measured operating myocardial stiffness do not necessarily reflect differences in intrinsic myocardial properties, but can also be caused by mere changes in loading or chamber geometry. This complicates myocardial stiffness interpretation for different types of pathologic hypertrophy. Purpose To explore the relationship between myocardial stiffness and underlying pathological substrates for cardiac hypertrophy. Methods We included 20 patients with hypertension (HT) and myocardial remodelling (59±14 years, 75% male), 20 patients with hypertrophic cardiomyopathy (HCM) (59±16 years, 60% male) and 20 healthy controls (56±14 years, 75% male). Left ventricular (LV) parasternal long axis views were acquired with an experimental HFR scanner at 1293±362 frames per seconds. Propagation velocity of SW occurring after mitral valve closure in the interventricular septum (IVS) served as measure of operating myocardial stiffness (Figure A). To compare myocardial stiffness among hearts with differing loading conditions and chamber geometry, SW velocities were normalized to end-diastolic wall stress, estimated at IVS from regional wall thickness, longitudinal and circumferential regional radii of curvature, and non-invasively estimated LV end-diastolic pressure (EDP). Results SW velocities differed significantly between groups (p&lt;0.001). The controls had the lowest SW velocities (4.02±0.97 m/s), whereas values between HT and HCM group were comparable (6.46±0.99 m/s vs. 7.00±2.10 m/s; p=0.738). Considering end-diastolic wall stress, HCM patients had the same SW velocity at lower wall stress compared to HT (Figure B), indicating higher myocardial stiffness in the HCM group. SW velocities normalized for wall stress indicated significantly different myocardial stiffness among all groups (p&lt;0.001) (Figure C). In a multiple linear regression model, the underlying pathological substrate independently influenced SW velocity (beta 1.37, 95% CI (0.78–1.96); p&lt;0.001), while wall stress did not significantly affect its value (p=0.479). Conclusions Our study demonstrated that SW elastography can detect differences in myocardial stiffness in hypertensive heart and hypertrophic cardiomyopathy. Additionally, our results suggest that SW velocity is dominated by underlying myocardial tissue properties. We hypothesize that differential changes in cardiomyocytes and/or the extracellular matrix contribute to the differential myocardial stiffening in different pathologic entities of LV hypertrophy. Thus, SW elastography could provide useful novel diagnostic information in the evaluation of LV hypertrophy. Figure A, B, C Funding Acknowledgement Type of funding source: None</abstract><pub>Oxford University Press</pub><doi>10.1093/ehjci/ehaa946.0087</doi></addata></record>
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title Differentiation of hypertensive heart disease and hypertrophic cardiomyopathy with myocardial stiffness measurements: a shear wave imaging study using ultra-high frame rate echocardiography
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