학술논문
Quinapril treatment curtails decline of global longitudinal strain and mechanical function in hypertensive rats.
Document Type
Academic Journal
Author
Wilson AJ; Department of Radiology, Stanford University, Stanford, California, USA.; Sands GB; Auckland Bioengineering Institute.; Wang VY; Department of Radiology, Stanford University, Stanford, California, USA.; Pontre B; Department of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.; Ennis DB; Department of Radiology, Stanford University, Stanford, California, USA.; Young AA; Department of Anatomy and Medical Imaging, University of Auckland, Auckland, New Zealand.; Department of Biomedical Engineering, King's College London, London, UK.; LeGrice IJ; Auckland Bioengineering Institute.; Nash MP; Auckland Bioengineering Institute.; Department of Engineering Science, University of Auckland, Auckland, New Zealand.
Source
Publisher: Wolters Kluwer Health, Inc Country of Publication: Netherlands NLM ID: 8306882 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1473-5598 (Electronic) Linking ISSN: 02636352 NLM ISO Abbreviation: J Hypertens Subsets: MEDLINE
Subject
Language
English
Abstract
Background: Left ventricular (LV) global longitudinal strain (GLS) has been proposed as an early imaging biomarker of cardiac mechanical dysfunction.
Objective: To assess the impact of angiotensin-converting enzyme (ACE) inhibitor treatment of hypertensive heart disease on LV GLS and mechanical function.
Methods: The spontaneously hypertensive rat (SHR) model of hypertensive heart disease ( n = 38) was studied. A subset of SHRs received quinapril (TSHR, n = 16) from 3 months (mo). Wistar Kyoto rats (WKY, n = 13) were used as controls. Tagged cardiac MRI was performed using a 4.7 T Varian preclinical scanner.
Results: The SHRs had significantly lower LV ejection fraction (EF) than the WKYs at 3 mo (53.0 ± 1.7% vs. 69.6 ± 2.1%, P < 0.05), 14 mo (57.0 ± 2.5% vs. 74.4 ± 2.9%, P < 0.05) and 24 mo (50.1 ± 2.4% vs. 67.0 ± 2.0%, P < 0.01). At 24 mo, ACE inhibitor treatment was associated with significantly greater LV EF in TSHRs compared to untreated SHRs (64.2 ± 3.4% vs. 50.1 ± 2.4%, P < 0.01). Peak GLS magnitude was significantly lower in SHRs compared with WKYs at 14 months (7.5% ± 0.4% vs. 9.9 ± 0.8%, P < 0.05). At 24 months, Peak GLS magnitude was significantly lower in SHRs compared with both WKYs (6.5 ± 0.4% vs. 9.7 ± 1.0%, P < 0.01) and TSHRs (6.5 ± 0.4% vs. 9.6 ± 0.6%, P < 0.05).
Conclusions: ACE inhibitor treatment curtails the decline in global longitudinal strain in hypertensive rats, with the treatment group exhibiting significantly greater LV EF and GLS magnitude at 24 mo compared with untreated SHRs.
(Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)
Objective: To assess the impact of angiotensin-converting enzyme (ACE) inhibitor treatment of hypertensive heart disease on LV GLS and mechanical function.
Methods: The spontaneously hypertensive rat (SHR) model of hypertensive heart disease ( n = 38) was studied. A subset of SHRs received quinapril (TSHR, n = 16) from 3 months (mo). Wistar Kyoto rats (WKY, n = 13) were used as controls. Tagged cardiac MRI was performed using a 4.7 T Varian preclinical scanner.
Results: The SHRs had significantly lower LV ejection fraction (EF) than the WKYs at 3 mo (53.0 ± 1.7% vs. 69.6 ± 2.1%, P < 0.05), 14 mo (57.0 ± 2.5% vs. 74.4 ± 2.9%, P < 0.05) and 24 mo (50.1 ± 2.4% vs. 67.0 ± 2.0%, P < 0.01). At 24 mo, ACE inhibitor treatment was associated with significantly greater LV EF in TSHRs compared to untreated SHRs (64.2 ± 3.4% vs. 50.1 ± 2.4%, P < 0.01). Peak GLS magnitude was significantly lower in SHRs compared with WKYs at 14 months (7.5% ± 0.4% vs. 9.9 ± 0.8%, P < 0.05). At 24 months, Peak GLS magnitude was significantly lower in SHRs compared with both WKYs (6.5 ± 0.4% vs. 9.7 ± 1.0%, P < 0.01) and TSHRs (6.5 ± 0.4% vs. 9.6 ± 0.6%, P < 0.05).
Conclusions: ACE inhibitor treatment curtails the decline in global longitudinal strain in hypertensive rats, with the treatment group exhibiting significantly greater LV EF and GLS magnitude at 24 mo compared with untreated SHRs.
(Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)