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Endocrine Abstracts (2013) 32 P184 | DOI: 10.1530/endoabs.32.P184

ECE2013 Poster Presentations Cardiovascular Endocrinology & Lipid Metabolism (41 abstracts)

Adults with GH deficiency have subclinical longitudinal left ventricular dysfunction, without significant vascular function impairment, suggesting intrinsic myocardial disease

Corin Badiu 1, , Sorina Mihaila 2 , Raluca Mincu 2 , Ruxandra Dobrescu 1 & Dragos Vinereanu 2,

1National Institute of Endocrinology, Bucharest, Romania; 2University Hospital, Bucharest, Romania; 3C. Davila University of Medicine and Pharmacy, Bucharest, Romania.

Aims: GH deficiency (GHD) is associated with increased cardiovascular events. We aimed to evaluate cardiac, arterial, and endothelial function, by conventional and 2D speckle tracking echocardiography (STE), and biomarkers (proBNP and troponin I), in GHD patients by comparison with normal individuals with similar cardiovascular risk profile.

The study included 52 GHD patients (46.9±15.6, 36 males), free of cardiovascular disease, severe hypertension or diabetes and 50 normals (N). Global LV systolic function was assessed from LV fractional shortening (FS), LV ejection fraction (LVEF), MAPSE, and cardiac index (CI). By STE, longitudinal LV function was assessed from: global longitudinal systolic strain (GLS), global longitudinal systolic, early and late diastolic strain rate (SRs, Sre, SRl); radial function from global radial strain (GRS); circumferential function from global circumferential strain (GCS); and LV torsion from basal (RotB) and apical rotation (RotA), LV torsion (LVtor), twist rate (TR) and untwist rate (UTR). Arterial function was assessed from intima-media thickening (IMT), local wave speed (LWS), Peterson elasticus modulus, and stiffness index (β); endothelial function from flow mediated dilation (FMD).

Results: In GHD patients, conventional systolic LV parameters were significantly decreased compared to N (FS: 28±8.5 vs 38.6±7.3; LVEF: 54±8 vs 66±8; MAPSE: 12±2 vs 16±2; CI: 2.1±0.75 vs 2.7±0.77, all P<0.001), but did not always exceed the normal range. 2D STE revealed significantly decreased GLS (−17.15±2.7 vs −19.3±3.3, P<0.001), and GCS (51.2±17 vs -18.8±3.24, P=0.002), with similar GRS. In addition, GHD had decreased values for systolic, early and late diastolic SR (SRs, SRe, and SRl), when compared to normal subjects (−0.9±0.4 vs −1.1±0.2, P=0.016; 1.15±0.4 vs 1.31±0.3, P=0.027; 0.71±0.19 vs 0.96±0.21, P<0.001). They also had lower RotB (−4.78±2.6 vs −6.2±2.1, P=0.003), LV torsion (1.8±0.6 vs 2.3±1.1, P=0.011), TR (92.8±30 vs 121±52, P=0.002), and UTR (99±36 vs −132±47, P<0.001), but similar apical rotation. Arterial and endothelial function parameters were similar between groups. While troponin I was normal in all patients, proBNP levels were significantly increased in the GHD group.

Conclusion: GHD patients have subclinical LV systolic and diastolic dysfunction, best revealed by STE, associated with increased proBNP levels and correlates to the level of GH deficiency (r=0.614, P<0.001). Our findings suggest that patients with GHD have intrinsic myocardial disease, probably due to insufficient contractile function of the myocardial fibres.

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