Abstract 14653: Patients with Growth Hormone Deficiency Have Global Atrial Dysfunction, Both Intrinsic, and Ventricular Dysfunction Related

Abstract

Purpose: Growth hormone deficiency in adults (GHD) is associated with increased cardiovascular events and we showed that GHD patients have subclinical bi-ventricular dysfunction. Our purpose was to further evaluate left atrial (LA) function and relation to LV dysfunction in these patients, by comparison with normal (N) individuals with similar cardiovascular risk profile.

Methods: 31 GHD patients (46±15yrs, 20 men) were compared to 31 age- and sex- matched N, using conventional and 2D strain echo. LA function was evaluated from 4C, 2C, and 3C views, using the P-wave onset as the reference point. We measured LA volumes at mitral valve closure and opening (MVCvol, MVOvol), at P-wave onset (Pvol), and global LA strain and strain rate. Active LA function was assessed by active EF (EFa=Pvol-MVCvol/Pvol), negative global atrial strain (GAS-) and late diastolic strain rate (GSRL); passive function from passive EF (EFp=MVOvol-Pvol/MVOvol), first/second positive global strain (GAS1+, GAS2+), and early negative diastolic global strain rate (GSRE); reservoir function from total atrial strain (TAS=GAS- plus GAS2+) and positive global SR at the begining of LV systole (GASR+); we also measured LA expansion index (EIx=MVOvol-MVCvol/MVCvol). Global LV systolic, early and late diastolic strain rate (GLSRs, GLSRe,GLSRl) were assessed from similar LV apical views.

Results: GHD patients had similar MVO- and P-vol, but increased MVCvol. They had significantly decreased LA active function (EFa, GAS- and GSRL). Passive LA function (GAS2+), and reservoir function (TAS, GSRL) were significantly decreased, with lower EIx. Active LA function (GAS-) correlated with LV GLSRl (r=410, p=0.03), passive and reservoir LA function (GAS1+, GAS2+, TAS) with GLSRe (r=0.58, r=0.65, respectivelly r=0.58, p<0.001).

Conclusions: GHD patients have global LA dysfunction with impairment of both intrinsic contraction, and passive relaxation induced by LV diastolic dysfunction.