Abstract 12094: Adults with Growth Hormone Deficiency Have Intrinsic Myocardial Disease with Decreased Longitudinal Left Ventricular Function and Torsion
Growth hormone deficiency (GHD) is associated with increased cardiovascular events, however, the detailed mechanisms were not assessed extensively. We set up this study in order to evaluate cardiac, arterial, and endothelial function, by conventional and speckle tracking echo, in GHD patients by comparison with normal individuals (N).
Methods. 30 GHD patients (46±14 years, 18 males) with low cardiovascular risk factors were compared with 30 matched N. Global LV systolic and diastolic functions were assessed from ejection fraction (EF), indexed cardiac output (COi), E/Vp and E/Ea ratios; longitudinal function from global longitudinal strain (GLS), and the sum of all times from the AVC to peak strain (SumTAVC); radial function from global radial strain (GRS); circumferential function from global circumferential strain (GCS); and LV torsion from peak basal (RotB) and apical rotation (RotA), and derived times (time to RotB/RotA), LV torsion (LVtor), twist rate (TR), untwist rate (UTR), time-to-peak twist (TT), and time from the AVC to UTR (AVC-UTR). Arterial function was assessed from intima-media thickening (IMT), local wave speed (LWS), and stiffness index (β); endothelial function from flow mediated dilation (FMD).
Results. GHD patients had all global, longitudinal, and circumferential systolic parameters significantly decreased, but with similar GRS (52±16 vs 52±15%) (table). They had also higher dyssynchrony, end-diastolic LV pressure, and lower torsion with prolonged AVC-UTR. RotB correlated with GLS (r=0.4, p<0.05). Arterial and endothelial functions were similar to N.
Conclusions. GHD patients have subclinical longitudinal and circumferential LV dysfunction, with maintained radial function; these were correlated with impaired LV torsion. Since arterial and endothelial functions were not affected, our findings suggest that patients with GHD have intrinsic myocardial disease, due probably to insufficient development of the myocardial fibers.
- © 2011 by American Heart Association, Inc.