Key result
Systemic hypertension linked to a ~50% higher rate of LVH during growth hormone replacement.
Why the study?
Scanty data are available on left ventricular geometric remodeling in hypertensive patients with adult-onset growth hormone deficiency undergoing growth hormone replacement therapy.
Does systemic hypertension counteract the benefits of growth hormone replacement therapy on left ventricular remodeling in adults with growth hormone deficiency?
Cohort (n=51)
Does systemic hypertension counteract the benefits of growth hormone replacement therapy on left ventricular remodeling in adults with growth hormone deficiency?
Systemic hypertension counteracts the potential benefits of growth hormone replacement therapy on left ventricular remodeling in adults with growth hormone deficiency, highlighting the need for strict blood pressure management.
Answers are grounded in this paper and cite their sources.
Hypertension may offset LV remodeling benefits of GH replacement in GHD; leaves open whether BP control modifies this association.
BACKGROUND: Systemic Hypertension (SH) is the main cause of left ventricular (LV) hypertrophy in the general population, but only scanty data are available on LV geometric remodeling (LVGR) in hypertensive patients with GH deficiency (GHD). AIM: We investigated hypertensive LVGR in adult-onset GHD patients, before (T0) and after 55±16 months (T1) of individualized GH replacement therapy (GHRT). SUBJECTS: Fifty-one patients, aged 45±15 yr, 29 women, were enrolled. Fifteen patients met criteria for SH (group A) whereas 36 were normotensive (group B). METHODS: An echocardiogram was performed on all patients, at least twice (at T0 and T1). LV geometric remodeling as a relationship between LV mass (LVM) index and relative wall thickness (RWT), LV volumes, and ejection fraction were measured. RESULTS: At T0, group A showed higher LV mass and LVM index values than group B; LV hypertrophy was found in 40% and 22% of patients, respectively (p=0.06). At T1, IGF-I levels had increased significantly in both groups. LV hypertrophy rate consistently increased in group A (from 40 to 60%, p<0.05), whereas slightly decreased in group B (from 22 to 19%, ns). Body surface area (p<0.001), age (p<0.05), and systolic blood pressure (p<0.05) were main determinants of LVM at multivariate analysis. CONCLUSIONS: Along with body surface area and age, SH was significantly related to abnormal LVGR (LV hypertrophy) in GHD patients. As a result, blood pressure management and caloric intake restrictions are deemed necessary for this subset of patients.
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Gregorio et al. (2013) conducted a cohort in Adult-onset growth hormone deficiency (n=51). Systemic hypertension vs. Normotension was evaluated on Left ventricular hypertrophy rate at follow-up (p=<0.05). In adults with growth hormone deficiency receiving replacement therapy, systemic hypertension was associated with an increase in left ventricular hypertrophy from 40% to 60% (p<0.05) over 55 months.
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