Cardiac Functional Reserve is Diminished in Growth Hormone‐Deficient Adults

Abstract

Various studies have shown that patients with severe growth hormone deficiency (GHD) have diverse changes in left ventricular (LV) size or performance but so far there is no direct indication of cardiac reserve ability to maintain the circulation during peak exercise. We tested the hypothesis that patients with severe GHD have reduced cardiac reserve function compared with healthy controls. Eighteen patients with severe GHD were studied and compared with 18 age-, sex-, and body mass index (BMI)-matched healthy controls. Peak cardiac power and cardiorespiratory fitness were investigated using noninvasive hemodynamic measurements during maximal cardiopulmonary exercise testing. Compared with matched controls, the cardiac power of GHD patients during exercise to volitional exhaustion was significantly reduced by 15% (mean ± SD: 4.4 ± 1.0 watts (W) vs. 5.2 ± 1.0 W, P = 0.02), despite attaining similar aerobic exercise peaks (VO 2max , GHD: 2390 ± 822 mL/min vs. controls: 2461 ± 872 mL/min, P = 0.80) and similar peak respiratory exchange ratios. The lower peak cardiac power could not be accounted for by peripheral alterations because both groups reached similar peak exercise systemic vascular resistances. Patients with GHD also had lower cardiac chronotropic reserve (peak heart rate: 154 ± 21 bpm vs. 174 ± 11 bpm, P = 0.001) and a lower cardiac pressure-generating capacity (systolic blood pressure [SBP] 160 ± 25 mmHg vs. 200 ± 15 mmHg, P < 0.0001). Using this robust noninvasive method of assessing functional cardiac pumping capacity we have for the first time shown that patients with severe GHD have a significantly impaired cardiac functional reserve associated with chronotropic incompetence and impaired pressure-generating capacity.

Impaired aerobic exercise adaptation in children and adolescents with craniopharyngioma is associated with hypothalamic involvement

“…In studies on adults with combined pituitary hormone deficiency with and without GH replacement, cardiac output investigated at rest was not different from that of controls (38,39). In another study on 18 GHD adults with no rhGH treatment and appropriate replacement for other pituitary hormone deficiencies, cardiac output and peripheral vascular resistance at rest and during exercise were comparable to those of controls (40,41), whereas maximal systolic BP was lower, as in our study: the authors suggested that this was due to a lower pressure-generating capacity of the heart. We did not perform systematic cardiac and vascular evaluation in our study and we are not aware of such evaluation in previous studies on subjects with CP.…”

IGF-1 and atherothrombosis: relevance to pathophysiology and therapy

“…A deficient GH/IGF-1 axis, conversely, worsens cardiac contractility and the exerciseinduced increase in cardiac output [219], whereas the IGF-1/PI3K/Akt axis appears to be able to increase Ca 2+ channel activity, with an overall increase in the influx and re-uptake of Ca 2+ ions, which has a consequence of improving inotropism and lusitropism [220]. In a mouse model of diabetic cardiomyopathy, the induced expression of the IGF-1R gene prevented the onset of diastolic dysfunction, fibrosis and preserved cardiac function [221].…”