Publications by authors named "Christopher B Lawton"

5 Publications

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Cerebral Blood Flow Response to Simulated Hypovolemia in Essential Hypertension: A Magnetic Resonance Imaging Study.

Hypertension 2019 12 28;74(6):1391-1398. Epub 2019 Oct 28.

From the Faculty of Life Sciences, School of Physiology, Pharmacology and Neuroscience (S.N., Z.H.A., J.B., A.K.N., J.P., E.C.H.), University of Bristol, United Kingdom.

Hypertension is associated with raised cerebral vascular resistance and cerebrovascular remodeling. It is currently unclear whether the cerebral circulation can maintain cerebral blood flow (CBF) during reductions in cardiac output (CO) in hypertensive patients thereby avoiding hypoperfusion of the brain. We hypothesized that hypertension would impair the ability to effectively regulate CBF during simulated hypovolemia. In the present study, 39 participants (13 normotensive, 13 controlled, and 13 uncontrolled hypertensives; mean age±SD, 55±10 years) underwent lower body negative pressure (LBNP) at -20, -40, and -50 mmHg to decrease central blood volume. Phase-contrast MR angiography was used to measure flow in the basilar and internal carotid arteries, as well as the ascending aorta. CBF and CO decreased during LBNP (<0.0001). Heart rate increased during LBNP, reaching significance at -50 mmHg (<0.0001). There was no change in mean arterial pressure during LBNP (=0.3). All participants showed similar reductions in CBF (=0.3, between groups) and CO (=0.7, between groups) during LBNP. There was no difference in resting CBF between the groups (=0.36). In summary, during reductions in CO induced by hypovolemic stress, mean arterial pressure is maintained but CBF declines indicating that CBF is dependent on CO in middle-aged normotensive and hypertensive volunteers. Hypertension is not associated with impairments in the CBF response to reduced CO.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.119.13229DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7069391PMC
December 2019

Hypertensive heart disease versus hypertrophic cardiomyopathy: multi-parametric cardiovascular magnetic resonance discriminators when end-diastolic wall thickness ≥ 15 mm.

Eur Radiol 2017 Mar 1;27(3):1125-1135. Epub 2016 Jul 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.

Objectives: European guidelines state left ventricular (LV) end-diastolic wall thickness (EDWT) ≥15mm suggests hypertrophic cardiomyopathy (HCM), but distinguishing from hypertensive heart disease (HHD) is challenging. We identify cardiovascular magnetic resonance (CMR) predictors of HHD over HCM when EDWT ≥15mm.

Methods: 2481 consecutive clinical CMRs between 2014 and 2015 were reviewed. 464 segments from 29 HCM subjects with EDWT ≥15mm but without other cardiac abnormality, hypertension or renal impairment were analyzed. 432 segments from 27 HHD subjects with EDWT ≥15mm but without concomitant cardiac pathology were analyzed. Magnitude and location of maximal EDWT, presence of late gadolinium enhancement (LGE), LV asymmetry (>1.5-fold opposing segment) and systolic anterior motion of the mitral valve (SAM) were measured. Multivariate logistic regression was performed. Significance was defined as p<0.05.

Results: HHD and HCM cohorts were age-/gender-matched. HHD had significantly increased indexed LV mass (110±27g/m vs. 91±31g/m, p=0.016) but no difference in site or magnitude of maximal EDWT. Mid-wall LGE was significantly more prevalent in HCM. Elevated indexed LVM, mid-wall LGE and absence of SAM were significant multivariate predictors of HHD, but LV asymmetry was not.

Conclusions: Increased indexed LV mass, absence of mid-wall LGE and absence of SAM are better CMR discriminators of HHD from HCM than EDWT ≥15mm.

Key Points: • Hypertrophic cardiomyopathy (HCM) is often diagnosed with end-diastolic wall thickness ≥15mm. • Hypertensive heart disease (HHD) can be difficult to distinguish from HCM. • Retrospective case-control study showed that location and magnitude of EDWT are poor discriminators. • Increased left ventricular mass and midwall fibrosis are independent predictors of HHD. • Cardiovascular magnetic resonance parameters facilitate a better discrimination between HHD and HCM.
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http://dx.doi.org/10.1007/s00330-016-4468-2DOI Listing
March 2017

Prevalence and predictors of asymmetric hypertensive heart disease: insights from cardiac and aortic function with cardiovascular magnetic resonance.

Eur Heart J Cardiovasc Imaging 2016 Dec 24;17(12):1405-1413. Epub 2015 Dec 24.

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.

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 mm/mmHg × 10, 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.
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http://dx.doi.org/10.1093/ehjci/jev329DOI Listing
December 2016

Measurement of myocardium at risk with cardiovascular MR: comparison of techniques for edema imaging.

Radiology 2015 Apr 21;275(1):61-70. Epub 2014 Oct 21.

From the Bristol Heart Institute (E.J.M., C.B.L., N.M., M.C.K.H., C.B.) and Clinical Trial and Evaluation Unit (M.P., J.M.H.), University of Bristol, Bristol NIHR Cardiovascular Biomedical Research Unit, Level 7 Queens Bldg, Bristol Royal Infirmary, Bristol BS2 8HW, England; Heart Hospital, London, England (J.C.M.); and Siemens Healthcare, Frimley, England (P.J.W.).

Purpose: To determine variability and agreement for detecting myocardial edema with T2-weighted short-tau inversion recovery (STIR), acquisition for cardiac unified T2 edema (ACUT2E), T2 mapping, and early gadolinium enhancement (EGE) after successfully reperfused ST-segment-elevation myocardial infarction (STEMI) and diagnostic accuracy of each sequence to predict infarct-related artery (IRA).

Materials And Methods: Local ethics committee approved the study, with patient informed written consent. On day 2 after successful primary angioplasty for STEMI, 53 patients were prospectively enrolled; 40 patients (mean age, 60 years) completed study. Two sets of cardiac magnetic resonance (MR) images were obtained on same day 6 hours apart. Basal, midcavity, and apical sections were obtained with each sequence. Interobserver, intraobserver, and interimage variability (1 minus intraclass correlation coefficient) and agreement (Bland-Altman method) were assessed.

Results: Size of myocardial edema significantly differed. Mean size of myocardium at risk was similar between T2-weighted STIR (18.2 g) and T2 mapping (17.3 g) (P = .54). Mean size differed between T2-weighted STIR (18.2 g) and ACUT2E (14.0 g) (P = .01) and between T2-weighted STIR (18.2 g) and EGE (14.2 g) (P = .003). T2 mapping and EGE had best agreement (interobserver bias: T2-weighted STIR, -0.9 [mean difference] ± 9.6 [standard deviation]; ACUT2E, -2.5 ± 6.9; T2 mapping, -3.8 ± 4.7; EGE, -5.3 ± 5.9; interimage bias: T2-weighted STIR, 1.5 ± 5.8; ACUT2E, -0.8 ± 4.9; T2 mapping, 3.1 ± 4.0; EGE, 1.1 ± 4.9; intraobserver bias: T2-weighted STIR, 1.4 ± 5.8; ACUT2E, 0.6 ± 4.7; T2 mapping, 2.2 ± 3.1; EGE, 1.7 ± 2.9). Variability was lowest for T2 mapping (intraobserver, 0.05; interobserver, 0.09; interimage, 0.1) followed by EGE (intraobserver, 0.03; interobserver, 0.14; interimage, 0.14), with improved detection of territory of IRA versus ACUT2E (intraobserver, 0.11; interobserver, 0.22; interimage, 0.12) and T2-weighted STIR (intraobserver, 0.1; interobserver, 0.32; interimage, 0.1).

Conclusion: Cardiac MR methods to detect and quantify infarct myocardial edema are not interchangeable; T2 mapping is the most reproducible method, followed by EGE, ACUT2E, and T2-weighted STIR. Clinical trial registration no. NCT01468662
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http://dx.doi.org/10.1148/radiol.14131980DOI Listing
April 2015

Adaptations of aortic and pulmonary artery flow parameters measured by phase-contrast magnetic resonance angiography during supine aerobic exercise.

Eur J Appl Physiol 2014 May 7;114(5):1013-23. Epub 2014 Feb 7.

Congenital Heart Unit, Bristol Royal Hospital for Children/Bristol Heart Institute, Upper Maudlin Street, Bristol, BS2 8BJ, UK,

Purpose: Increased oxygen uptake and utilisation during exercise depend on adequate adaptations of systemic and pulmonary vasculature. Recent advances in magnetic resonance imaging techniques allow for direct quantification of aortic and pulmonary blood flow using phase-contrast magnetic resonance angiography (PCMRA). This pilot study tested quantification of aortic and pulmonary haemodynamic adaptations to moderate aerobic supine leg exercise using PCMRA.

Methods: Nine adult healthy volunteers underwent pulse gated free breathing PCMRA while performing heart rate targeted aerobic lower limb exercise. Flow was assessed in mid ascending and mid descending thoracic aorta (AO) and main pulmonary artery (MPA) during exercise at 180 % of individual resting heart rate. Flow sequence analysis was performed by experienced operators using commercial offline software (Argus, Siemens Medical Systems).

Results: Exercise related increase in HR (rest: 69 ± 10 b min(-1), exercise: 120 ± 13 b min(-1)) resulted in cardiac output increase (from 6.5 ± 1.4 to 12.5 ± 1.8 L min(-1)). At exercise, ascending aorta systolic peak velocity increased from 89 ± 14 to 122 ± 34 cm s(-1) (p = 0.016), descending thoracic aorta systolic peak velocity increased from 104 ± 14 to 144 ± 33 cm s(-1) (p = 0.004), MPA systolic peak velocity from 86 ± 18 to 140 ± 48 cm s(-1) (p = 0.007), ascending aorta systolic peak flow rate from 415 ± 83 to 550 ± 135 mL s(-1) (p = 0.002), descending thoracic aorta systolic peak flow rate from 264 ± 70 to 351 ± 82 mL s(-1) (p = 0.004) and MPA systolic peak flow rate from 410 ± 80 to 577 ± 180 mL s(-1) (p = 0.006).

Conclusion: Quantitative blood flow and velocity analysis during exercise using PCMRA is feasible and detected a steep exercise flow and velocity increase in the aorta and MPA. Exercise PCMRA can serve as a research and clinical tool to help quantify exercise blood flow adaptations in health and disease and investigate patho-physiological mechanisms in cardio-pulmonary disease.
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http://dx.doi.org/10.1007/s00421-014-2833-xDOI Listing
May 2014