Cardiac performance and mass in adults with hypopituitarism: effects of one year of growth hormone treatment.

Abstract

We studied the effects of GH administration on myocardial structure and function in 20 patients with hypopituitarism (14 males and 6 females; mean +/- SE age, 47.2 +/- 2.6 yr; range, 31-59 yr) developed in adulthood because of pituitary or parapituitary tumors. All patients had GH deficiency (GHD), as assessed by a GH response of less than 4 micrograms/L to a standard insulin tolerance test (0.05 U kg, iv) and the combined pyridostigmine (120 mg, orally, at -60 min) plus GHRH (1 microgram/kg, iv, at 0 min) test. Patients received either placebo (n = 10) or GH substitution therapy (n = 10; 0.05 U/kg.day GH for 1 yr; 0.03 U/kg.day during the first month). M- and B-mode echocardiography and pulsed Doppler examination of transmitral flow were performed before treatment, 6 months and 1 yr after starting GH or placebo administration, and 15 days and 3 months after GH or placebo withdrawal. Twenty healthy subjects, matched for age, sex, body mass index, and physical activity, served as controls. Left ventricular dimensions, mass, and systolic function were normal in patients with adult-onset GHD; however, diastolic function, specifically E wave deceleration time, was altered. GH administration markedly increased left ventricular performance and reversed diastolic abnormalities at 6 and even more so at 12 months. On the other hand, a clear increase in left ventricular mass was seen after 12, but not after 6, months of GH administration (P < 0.01 vs. pretreatment values). In addition, although all changes induced by GH treatment disappeared within 3 months after GH withdrawal, at that time the increase in left ventricular mass was still detectable (P < 0.05 vs. pretreatment values). These data indicate that augmented left ventricular contractility is not strictly related to cardiac muscle growth, supporting the hypothesis that GH treatment increases the inotropic activity of myocardial fibers. In conclusion, GH treatment enhances cardiac function, increases cardiac mass, and reverses diastolic abnormalities in adults with hypopituitarism and GHD. However, long term studies are required to demonstrate that GH replacement therapy reduces cardiac death rate in these patients.

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

“…Our baseline observations, that GH-deficient patients have unchanged EF and LVMI compared to control subjects, are in accordance with some previous studies [10,11,26,54]. By contrast others have shown that untreated GHD seems associated with decreased LVM [7,13,17,[20][21][22]25] and reduced EF as assessed by echocardiography [7,22] as well as in two studies using radionuclide angiography [17,25].…”

Beginning to end: Cardiovascular implications of growth hormone (GH) deficiency and GH therapy

“…Echocardiography is not a very precise method for estimating ejection fraction because of the calculations that are required and also because of interobserver and intraobserver variability. Other studies in adult patients with either childhoodor adulthood-onset GHD have shown similar patterns of cardiac function and morphology in both patients and controls [48][49][50][51].…”

“…It should be noted that the dose of GH employed during the last decade has been substantially reduced compared with the initial experience in adults with GHD; currently, doses range from 4 to 6 lg/kg of body weight, compared with 20-26 lg/kg of body weight used in earlier studies. However, an increase in cardiac mass has been observed with both higher [65] and lower GH replacement doses [50]. ter Maaten et al [66] reported a significant increase in cardiac mass in adult men during the first year of GH replacement using supraphysiological doses.…”

Alteration of the growth hormone axis, visceral fat dysfunction, and early cardiometabolic risk in adults: the role of the visceral adiposity index

“…Growth hormone deficiency (GHD) in adult life is well known to be associated with increased fat and reduced lean mass, altered cardiac structure and function, adverse lipid profile, glucose intolerance and insulin resistance, and increased cardiovascular morbidity and mortality [1][2][3][4][5][6][7]. On the other hand, there is robust evidence that obesity results in a secondary reduction in GH secretion and that substantial weight loss may restore spontaneous and stimulated GH secretion [8][9][10][11][12][13].…”