SFEBES2012 Poster Presentations Pituitary (43 abstracts)
The characterisation of growth hormone-related cardiac disease with magnetic resonance imaging
Julia Thomas 1 , Abhishek Dattani 2 , Thomas Burchell 1, , Filip Zemrak 2 , Bernard Khoo 4 , Shern Chew 3 , Felicity Kaplan 5 , William Drake 3 , Simon Aylwin 6 , Mark Gurnell 7 , Scott Akker 3 , Steffen Petersen 2 , Ceri Davies 3 , Ashley Grossman 8 & Marta Korbonits 1
1Centre for Endocrinology, Barts & the London School of Medicine, QMUL, London, United Kingdom; 2NIHR Cardiovascular Biomedical Research Unit, Barts & the London School of Medicine, QMUL, London, United Kingdom; 3Endocrinology, St Bartholomew's Hospital, Barts & the London NHS Trust, London, United Kingdom; 4Endocrinology, University College London, London, United Kingdom; 5Endocrinology, Lister Hospital, East and North Hertfordshire NHS Trust, Stevenage, United Kingdom; 6Endocrinology, King's College Hospital, London, United Kingdom; 7Endocrinology, Addenbrooke's Hospital, Cambridge, United Kingdom; 8Oxford Centre for Diabetes & Metabolism, University of Oxford, Oxford, United Kingdom.
Acromegaly causes a distinct cardiomyopathy. Growth hormone deficiency (GHD) limits cardiac response to exercise and increases cardiac mortality. Cardiac magnetic resonance imaging (CMR) is considered the gold standard for assessment of cardiac mass and provides data on function, fibrosis, valves and ischaemia. Twenty-three patients with abnormal GH levels (acromegaly, n=13; adult-onset GHD, n=10) and 23 matched controls underwent CMR. Patients had repeat CMR at 6 and 12 months after treatment. Cardiac parameters were normalised to body surface area. Patients with acromegaly demonstrated increased left ventricular (LV) mass index (LVMi) in females (P=0.0019) and males (P=0.0055). Patients had increased LV end diastolic volume index (EDVi) (P=0.0055), stroke volume index (SVi) (P=0.048), cardiac output index (CI) (P=0.020), a trend towards increased end systolic volume index (ESVi) (P=0.062) and increased right ventricular (RV) SVi (P=0.031). Patients with GHD did not have significantly different LV mass than controls but LVMi was at (males) or below (females) the lower limit of published reference ranges. Patients had reduced LVEDVi (P=0.025), RVEDVi (P=0.034) and RVSVi (P=0.045). There were no differences in heart rate or ejection fraction and no correlation between LVMi and IGF-I. At one year, IGF-I SDS had fallen in patients with acromegaly (P=0.036). In males, there was no difference in LVMi between patients and controls; females continued to demonstrate increased LVMi. There was no difference in LVEDVi and CI between patients and controls but SVi was decreased (P=0.002). At one year, IGF-I SDS had risen in patients with GHD (P=0.0032). In males, LVMi had moved from the bottom to the centre of normal range (55.4 vs. 62.9 g/m2, normal range 55.4–74.0). Female LVMi also increased. Acromegaly is associated with cardiac hypertrophy, as demonstrated by increased LV mass and volume markers, which improves with treatment. GH replacement increases cardiac mass in patients with adult-onset GHD.
Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.
Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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