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Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes
OBJECTIVE: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR). METHODS: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1....
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BMJ Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5099214/ https://www.ncbi.nlm.nih.gov/pubmed/27260191 http://dx.doi.org/10.1136/heartjnl-2016-309576 |
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author | Rodrigues, Jonathan C L Amadu, Antonio Matteo Dastidar, Amardeep Ghosh Szantho, Gergley V Lyen, Stephen M Godsave, Cattleya Ratcliffe, Laura E K Burchell, Amy E Hart, Emma C Hamilton, Mark C K Nightingale, Angus K Paton, Julian F R Manghat, Nathan E Bucciarelli-Ducci, Chiara |
author_facet | Rodrigues, Jonathan C L Amadu, Antonio Matteo Dastidar, Amardeep Ghosh Szantho, Gergley V Lyen, Stephen M Godsave, Cattleya Ratcliffe, Laura E K Burchell, Amy E Hart, Emma C Hamilton, Mark C K Nightingale, Angus K Paton, Julian F R Manghat, Nathan E Bucciarelli-Ducci, Chiara |
author_sort | Rodrigues, Jonathan C L |
collection | PubMed |
description | OBJECTIVE: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR). METHODS: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements. RESULTS: 88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m(2) vs concentric LVH: 73±15 mL/m(2) vs concentric remodelling: 55±9 mL/m(2), p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m(2) vs concentric LVH: 30±10 mL/m(2) vs concentricremodelling: 19±2 mL/m(2), p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: −12.8±4.6% vs concentric LVH: −15.5±3.1% vs concentric remodelling: –17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls. CONCLUSIONS: Myocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments. |
format | Online Article Text |
id | pubmed-5099214 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BMJ Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-50992142016-11-14 Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes Rodrigues, Jonathan C L Amadu, Antonio Matteo Dastidar, Amardeep Ghosh Szantho, Gergley V Lyen, Stephen M Godsave, Cattleya Ratcliffe, Laura E K Burchell, Amy E Hart, Emma C Hamilton, Mark C K Nightingale, Angus K Paton, Julian F R Manghat, Nathan E Bucciarelli-Ducci, Chiara Heart Aortic and Vascular Disease OBJECTIVE: Myocardial intracellular/extracellular structure and aortic function were assessed among hypertensive left ventricular (LV) phenotypes using cardiovascular magnetic resonance (CMR). METHODS: An observational study from consecutive tertiary hypertension clinic patients referred for CMR (1.5 T) was performed. Four LV phenotypes were defined: (1) normal with normal indexed LV mass (LVM) and LVM to volume ratio (M/V), (2) concentric remodelling with normal LVM but elevated M/V, (3) concentric LV hypertrophy (LVH) with elevated LVM but normal indexed end-diastolic volume (EDV) or (4) eccentric LVH with elevated LVM and EDV. Extracellular volume fraction was measured using T1-mapping. Circumferential strain was calculated by voxel-tracking. Aortic distensibility was derived from high-resolution aortic cines and contemporaneous blood pressure measurements. RESULTS: 88 hypertensive patients (49±14 years, 57% men, systolic blood pressure (SBP): 167±30 mm Hg, diastolic blood pressure (DBP): 96±14 mm Hg) were compared with 29 age-matched/sex-matched controls (47±14 years, 59% men, SBP: 128±12 mm Hg, DBP: 79±10 mm Hg). LVH resulted from increased myocardial cell volume (eccentric LVH: 78±19 mL/m(2) vs concentric LVH: 73±15 mL/m(2) vs concentric remodelling: 55±9 mL/m(2), p<0.05, respectively) and interstitial fibrosis (eccentric LVH: 33±10 mL/m(2) vs concentric LVH: 30±10 mL/m(2) vs concentricremodelling: 19±2 mL/m(2), p<0.05, respectively). LVH had worst circumferential impairment (eccentric LVH: −12.8±4.6% vs concentric LVH: −15.5±3.1% vs concentric remodelling: –17.1±3.2%, p<0.05, respectively). Concentric remodelling was associated with reduced aortic distensibility, but not with large intracellular/interstitial expansion or myocardial dysfunction versus controls. CONCLUSIONS: Myocardial interstitial fibrosis varies across hypertensive LV phenotypes with functional consequences. Eccentric LVH has the most fibrosis and systolic impairment. Concentric remodelling is only associated with abnormal aortic function. Understanding these differences may help tailor future antihypertensive treatments. BMJ Publishing Group 2016-10-15 2016-06-03 /pmc/articles/PMC5099214/ /pubmed/27260191 http://dx.doi.org/10.1136/heartjnl-2016-309576 Text en Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
spellingShingle | Aortic and Vascular Disease Rodrigues, Jonathan C L Amadu, Antonio Matteo Dastidar, Amardeep Ghosh Szantho, Gergley V Lyen, Stephen M Godsave, Cattleya Ratcliffe, Laura E K Burchell, Amy E Hart, Emma C Hamilton, Mark C K Nightingale, Angus K Paton, Julian F R Manghat, Nathan E Bucciarelli-Ducci, Chiara Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title | Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title_full | Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title_fullStr | Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title_full_unstemmed | Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title_short | Comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
title_sort | comprehensive characterisation of hypertensive heart disease left ventricular phenotypes |
topic | Aortic and Vascular Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5099214/ https://www.ncbi.nlm.nih.gov/pubmed/27260191 http://dx.doi.org/10.1136/heartjnl-2016-309576 |
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