Jonathan C L Rodrigues1,2, Antonio Matteo Amadu3,4, Amardeep Ghosh Dastidar3, Neelam Hassan5, Stephen M Lyen3,6, Christopher B Lawton3, Laura E Ratcliffe7, Amy E Burchell7, Emma C Hart2,7, Mark C K Hamilton3,6, Julian F R Paton2,7, Angus K Nightingale7, Nathan E Manghat3,6. 1. NIHR Bristol Cardiovascular Biomedical Research Unit, Cardiac Magnetic Resonance Department, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Upper Maudlin Street, Bristol BS2 8HW, UK jonrodrigues@doctors.org.uk. 2. School of Physiology, Pharmacology and Neuroscience, Biomedical Sciences, University of Bristol, BS8 2TD, UK. 3. NIHR Bristol Cardiovascular Biomedical Research Unit, Cardiac Magnetic Resonance Department, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Upper Maudlin Street, Bristol BS2 8HW, UK. 4. Department of Radiology, University of Sassari, Sassari, Italy. 5. Severn Postgraduate Medical Education Foundation School, NHS Health Education South West, Bristol, UK. 6. Department of Radiology, Bristol Royal Infirmary, University Hospitals Bristol NHS Foundation Trust, Bristol, UK. 7. CardioNomics Research Group, Clinical Research and Imaging Centre, Bristol Heart Institute, University Hospitals Bristol NHS Foundation Trust, Bristol, UK.
Abstract
AIMS: We sought to determine the prevalence of asymmetric hypertensive heart disease (HHD) overlapping morphologically with hypertrophic cardiomyopathy (HCM) and to determine predictors of this pattern of hypertensive remodelling. METHODS AND RESULTS: One hundred and fifty hypertensive patients underwent 1.5 T cardiovascular magnetic resonance imaging. Twenty-one patients were excluded due to concomitant cardiac pathology that may confound the hypertrophic response, e.g. myocardial infarction, moderate-severe valvular disease, or other cardiomyopathy. Asymmetric HHD was defined as a segmental wall thickness of ≥15 mm and >1.5-fold the opposing wall in ≥1 myocardial segments, measured from short-axis cine stack at end-diastole. Ambulatory blood pressure, myocardial replacement fibrosis, aortic distensibility and aortoseptal angle were investigated as predictors of asymmetric HHD by multivariate logistic regression. Out of 129 hypertensive subjects (age: 51 ± 15 years, 50% male, systolic blood pressure: 170 ± 30 mmHg, diastolic blood pressure: 97 ± 16 mmHg), asymmetric HHD occurred in 21%. Where present, maximal end-diastolic wall thickness (EDWT) was 17.8 ± 1.9 mm and located exclusively in the basal or mid septum. In asymmetric HHD, aortoseptal angle (114 ± 10° vs. 125 ± 9° vs. 123 ± 12°, P < 0.05, respectively) was significantly reduced compared to concentric left ventricular hypertrophy (LVH) and compared to no LVH, respectively. Aortic distensibility in asymmetric HHD (1.01 ± 0.60 vs. 1.83 ± 1.65 mm2/mmHg × 103, P < 0.05, respectively) was significantly reduced compared to subjects with no LVH. Age (odds ratio [95th confidence interval]: 1.10 [1.02-1.18], P < 0.05) and indexed LV mass (1.09 [0.98-1.28], P < 0.0001) were significant, independent predictors of asymmetric HDD. CONCLUSIONS: Asymmetric HHD morphologically overlapping with HCM, according to the current ESC guidelines, is common. Postulating a diagnosis of HCM on the basis of EDWT of ≥15 mm should be made with caution in the presence of arterial hypertension particular in male subjects with elevated LV mass. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: We sought to determine the prevalence of asymmetric hypertensive heart disease (HHD) overlapping morphologically with hypertrophic cardiomyopathy (HCM) and to determine predictors of this pattern of hypertensive remodelling. METHODS AND RESULTS: One hundred and fifty hypertensive patients underwent 1.5 T cardiovascular magnetic resonance imaging. Twenty-one patients were excluded due to concomitant cardiac pathology that may confound the hypertrophic response, e.g. myocardial infarction, moderate-severe valvular disease, or other cardiomyopathy. Asymmetric HHD was defined as a segmental wall thickness of ≥15 mm and >1.5-fold the opposing wall in ≥1 myocardial segments, measured from short-axis cine stack at end-diastole. Ambulatory blood pressure, myocardial replacement fibrosis, aortic distensibility and aortoseptal angle were investigated as predictors of asymmetric HHD by multivariate logistic regression. Out of 129 hypertensive subjects (age: 51 ± 15 years, 50% male, systolic blood pressure: 170 ± 30 mmHg, diastolic blood pressure: 97 ± 16 mmHg), asymmetric HHD occurred in 21%. Where present, maximal end-diastolic wall thickness (EDWT) was 17.8 ± 1.9 mm and located exclusively in the basal or mid septum. In asymmetric HHD, aortoseptal angle (114 ± 10° vs. 125 ± 9° vs. 123 ± 12°, P < 0.05, respectively) was significantly reduced compared to concentric left ventricular hypertrophy (LVH) and compared to no LVH, respectively. Aortic distensibility in asymmetric HHD (1.01 ± 0.60 vs. 1.83 ± 1.65 mm2/mmHg × 103, P < 0.05, respectively) was significantly reduced compared to subjects with no LVH. Age (odds ratio [95th confidence interval]: 1.10 [1.02-1.18], P < 0.05) and indexed LV mass (1.09 [0.98-1.28], P < 0.0001) were significant, independent predictors of asymmetric HDD. CONCLUSIONS: Asymmetric HHD morphologically overlapping with HCM, according to the current ESC guidelines, is common. Postulating a diagnosis of HCM on the basis of EDWT of ≥15 mm should be made with caution in the presence of arterial hypertension particular in male subjects with elevated LV mass. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Amy E Burchell; Jonathan C L Rodrigues; Max Charalambos; Laura E K Ratcliffe; Emma C Hart; Julian F R Paton; Andreas Baumbach; Nathan E Manghat; Angus K Nightingale Journal: J Clin Hypertens (Greenwich) Date: 2016-10-19 Impact factor: 3.738
Authors: J C L Rodrigues; T Erdei; A G Dastidar; B McIntyre; A E Burchell; L E K Ratcliffe; E C Hart; M C K Hamilton; J F R Paton; A K Nightingale; N E Manghat Journal: J Hum Hypertens Date: 2016-09-08 Impact factor: 3.012
Authors: Danny A J P van de Sande; Jan Hoogsteen; Pieter A Doevendans; Hareld M C Kemps Journal: BMC Cardiovasc Disord Date: 2019-01-06 Impact factor: 2.298
Authors: Jonathan C L Rodrigues; Antonio Matteo Amadu; Amardeep Ghosh Dastidar; Iwan Harries; Amy E Burchell; Laura E K Ratcliffe; Emma C Hart; Mark C K Hamilton; Julian F R Paton; Angus K Nightingale; Nathan E Manghat Journal: J Clin Hypertens (Greenwich) Date: 2018-03-08 Impact factor: 3.738
Authors: Jonathan C L Rodrigues; Stephen Rohan; Amardeep Ghosh Dastidar; Iwan Harries; Christopher B Lawton; Laura E Ratcliffe; Amy E Burchell; Emma C Hart; Mark C K Hamilton; Julian F R Paton; Angus K Nightingale; Nathan E Manghat Journal: Eur Radiol Date: 2016-07-01 Impact factor: 5.315