Background: Growth hormone deficiency (GHD) is associated with increased cardiovascular events. Our preliminary data, on 20 patients, suggested the presence of subclinical longitudinal left ventricle (LV) dysfunction. Therefore, we performed detailed assessment of cardiac and arterial function in 50 patients with GHD, in order to assess the mechanisms of subclinical cardiac involvement. Methods: 50 patients with GHD (47±15 yrs, 34 males), free of any cardiovascular disease or diabetes, were compared with 50 normals (N) (age- and sex- matched). Global LV systolic function was assessed from fractional shortening (LVFS), ejection fraction (LVEF), MAPSE, and cardiac index (CI); regional LV systolic function, by speckle tracking echocardiography (STE), from global longitudinal strain (GLS), global radial strain (GRS), and global circumferential strain (GCS); torsion from basal and apical rotation (RotB, RotA), LV torsion (LVtor), twist and untwist rate (TR, UTR). Arterial function was assessed from intima-media thickening, local wave speed, elastic modul, and stiffness index (β); endothelial function from flow mediated dilation. ProBNP and stimulated seric growth hormone (GHs) were measured. Results: GHD patients had decreased parameters of global, longitudinal, and circumferential LV systolic functions (table), with similar GRS (51.6±18.2 vs 56±16.7); meanwhile, they had lower torsion and increased proBNP (61±50 vs 24±21, p=0.006). On contrary, they had normal arterial and endothelial functions. Levels of GHs correlated positively to LVtor and TR, and inversely to UTR (r=0.61, r=0.72, r=-0.63, all p<0.001). View this table: Table 1. Comparison between GHD patients and N Conclusion: Patients with GHD had subclinical LV systolic dysfunction. Since arterial and endothelial functions are not significantly affected, our findings suggest that GHD patients have intrinsic myocardial disease, probably due to insufficient development or contractile function of myocardial fibres.