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Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
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Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
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Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study

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Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study
Journal Article

Cardiac function in growth hormone deficient patients before and after 1 year with replacement therapy: a magnetic resonance imaging study

2011
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Overview
Assessed by conventional echocardiography the influence of growth hormone deficiency (GHD) and effects of replacement therapy on left ventricle (LV) function and mass (LVM) have shown inconsistent results. We aimed to evaluate cardiac function before and during replacement therapy employing the gold standard method cardiac magnetic resonance imaging (CMRI) and measurements of circulating levels of B-type natriuretic peptides. Sixteen patients (8 males and 8 females, mean age 49 years (range 18-75)) with severe GHD and 16 matched control subjects were included. CMRI was performed at baseline and after 1 year of GH replacement therapy. IGF-I, B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) were measured after 0, 1, 2, 3, 6 and 12 months of treatment. IGF-I Z-score increased from (median (IQR)) −2.3 (−3.8 to −1.4) to 0.5 (−0.3 to 1.7). LVM index (LVMI), ejection fraction (range 63-80%), cardiac output index and levels of BNP and NT-proBNP were similar at baseline in patients compared to controls (P-values from 0.09 to 0.37). The patients had significantly smaller LV end-diastolic volume index (P = 0.032) and end-systolic volume index (P = 0.038). No significant change in LV systolic function or LVM occurred during 1 year of GH treatment. BNP levels were unchanged (P = 0.88), whereas NT-proBNP tended to decrease (P = 0.052). Assessed by the highly sensitive and precise CMRI method, untreated GHD was not associated with impaired systolic function or reduced LVMI and 1 year of GH replacement using physiological doses did not influence cardiac mass or function.