Key result
One year of growth hormone replacement therapy significantly increased left ventricular mass index from 53.8 to 57.3 g/m2 in patients with adult-onset growth hormone deficiency.
Why the study?
Does growth hormone replacement improve myocardial structure and function in adult-onset growth hormone deficiency?
Observational (n=20)
Single-blind
Yes
Does growth hormone replacement improve myocardial structure and function in adult-onset growth hormone deficiency?
CMR demonstrates that adult-onset growth hormone deficiency is associated with reduced aortic area and a trend toward reduced left ventricular mass index, which increases after 1 year of growth hormone replacement.
Answers are grounded in this paper and cite their sources.
GH replacement was associated with increased LVMI in adult-onset GHD; hypothesis-generating and should not yet change practice or monitoring.
Growth hormone (GH) can profoundly influence cardiac function. While GH excess causes well-defined cardiac pathology, fewer data are available regarding the more subtle cardiac changes seen in GH deficiency (GHD). This preliminary study uses cardiac magnetic resonance imaging (CMR) to assess myocardial structure and function in GHD. Ten adult-onset GHD patients underwent CMR, before and after 6 and 12 months of GH replacement. They were compared to 10 age-matched healthy controls and sex-matched healthy controls. Left ventricular (LV) mass index (LVMi) increased with 1 year of GH replacement (53.8 vs. 57.0 vs. 57.3 g/m 2 , analysis of variance p = 0.0229). Compared to controls, patients showed a trend towards reduced LVMi at baseline (51.4 vs . 60.0 g/m 2 , p = 0.0615); this difference was lost by 1 year of GH treatment (57.3 vs. 59.9 g/m 2 , p = 0.666). Significantly reduced aortic area was observed in GHD (13.2 vs. 19.0 cm 2 /m 2 , p = 0.001). This did not change with GH treatment. There were no differences in other LV parameters including end-diastolic volume index (EDVi), end-systolic volume index, stroke volume index (SVi), cardiac index and ejection fraction. There was a trend towards reduced baseline right ventricular (RV)SVi (44.1 vs. 49.1 ml/m 2 , p = 0.0793) and increased RVEDVi over 1 year (70.3 vs. 74.3 vs. 73.8 ml/m 2 , p = 0.062). Two patients demonstrated interstitial expansion, for example with fibrosis, and three myocardial ischaemia as assessed by late gadolinium enhancement and stress perfusion. The increased sensitivity of CMR to subtle cardiac changes demonstrates that adult-onset GHD patients have reduced aortic area and LVMi increases after 1 year of GH treatment. These early data should be studied in larger studies in the future.
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Thomas et al. (2016) conducted an observational in Adult-onset growth hormone deficiency (n=20). Growth hormone replacement vs. Baseline (pre-treatment) was evaluated on Left ventricular mass index (LVMi) (p=0.0229). One year of growth hormone replacement therapy significantly increased left ventricular mass index from 53.8 to 57.3 g/m2 in patients with adult-onset growth hormone deficiency.
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