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010 Insights into hypertensive heart disease phenotypes: Spectrum of myocyte, interstitial and vascular changes by cardiovascular MRI
  1. Jonathan CL Rodrigues1,2,
  2. Antonio Matteo Amadu1,3,
  3. Amardeep Ghosh Dastidar1,4,
  4. Gergley Szantho1,
  5. Laura EK Ratcliffe5,
  6. Amy E Burchell4,5,
  7. Emma C Hart2,5,
  8. Mark CK Hamilton6,
  9. Angus K Nightingale4,5,
  10. Julian FR Paton2,5,
  11. Nathan E Manghat6,
  12. Chiara Bucciarelli-Ducci1,4
  1. 1NIHR Bristol Cardiovascular Biomedical Research Unit, Cardiac Magnetic Resonance Department, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol
  2. 2School of Physiology, Pharmacology and Neuroscience, Faculty of Biomedical Science, University of Bristol, Bristol
  3. 3Department of Surgical, Microsurgical and Medical Sciences, Institute of Radiology, University of Sassari, Italy
  4. 4Department of Cardiology, Bristol Royal Infirmary, University Hospitals Bristol NHS Foundation Trust, Bristol
  5. 5CardioNomics Research Group, Clinical Research and Imaging Centre, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol
  6. 6Department of Radiology, Bristol Royal Infirmary, University Hospitals Bristol NHS Foundation Trust, Bristol

Abstract

Introduction Hypertensive heart disease (HHD) can be classified into 4 left ventricular (LV) phenotypes: 1) normal, 2) concentric LV remodelling (LVr), 3) concentric LV hypertrophy (cLVH) and 4) eccentric LV hypertrophy (eLVH). The pathophysiology of the phenotypes is incompletely understood. We investigate extent of myocardial interstitial fibrosis and aortic impairment in HHD with cardiovascular magnetic resonance (CMR)

Methods 88 hypertensives (49 ± 14yrs, 57% male, SBP: 167 ± 30mmHg, DBP: 96 ± 14mmHg) underwent CMR (1.5T) and were compared with 29 age- and sex-matched normotensive controls (47 ± 14years, 59% male, SBP: 128 ± 12mmHg, DBP: 79 ± 10mmHg). Native T1 and extra-cellular volume fraction were measured. Circumferential myocardial strain was calculated by voxel-tracking. Aortic compliance was recorded.

Results At a structural level, increased LV mass in eccentric and concentric LVH resulted from: i) significantly increased myocardial cell volume (eLVH: 78 ± 19g/m2 vs cLVH: 73 ± 15g/m2 vs LVr: 55 ± 9g/m2 respectively, P < 0.05) and ii) significantly increased interstitial volume (eLVH: 33 ± 10g/m2 vs cLVH: 30 ± 10g/m2 vs LVr: 19 ± 2g/m2 respectively, P < 0.05). Functionally, eccentric and concentric LVH were associated with significantly impaired circumferential strain (eLVH: -12.8 ± 4.6% vs cLVH: -15.5 ± 3.1% vs LVr: -17.1 ± 3.2% vs controls: -17.4 ± 2.6% respectively, P < 0.05). Despite similar BP severity as LVH phenotypes, LV remodelling was associated with reduced aortic compliance but not associated with interstitial fibrosis or myocardial dysfunction relative to controls.

Conclusion Myocardial interstitial fibrosis is varies across HHD phenotypes with functional consequences. Eccentric LVH demonstrated the most interstitial fibrosis and systolic strain impairment. LV remodelling had normal myocardial, but abnormal aortic, function. Greater understanding of the pathophysiology of HHD phenotypes may help tailor future treatments.

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