Cardiac Structural Alterations of Acromegalic, Without Alteration in Cardiac Function, Evaluated by Doppler Echocardiography with Speckle Tracking
Marília Matos Oliveira,
Beatriz Hallal Jorge Lara,
Janaíne Machado Tomé,
Beatriz Pires Ferreira,
Maria Candida Calzada Borges,
Adriana Paula da Silva,
José de Oliveira Ferreira and
Maria de Fátima Borges
Global Journal of Health Science, 2021, vol. 13, issue 10, 32
BACKGROUND- Acromegaly is most commonly caused by growth hormone secreting pituitary (GH) macroadenoma. Cardiovascular events are the leading cause of death in this population. OBJECTIVE- To analyze the cardiac structural and functional changes in patients with acromegaly and to correlate the findings with the concentrations of GH and IGF-1 post treatment and with the presumed time of disease. METHOD- A quantitative study involving 19 individuals with acromegaly, 10 with inactive disease and 9 with active disease and 16 healthy individuals, matched by sex and age. Age ranged from 19 to 78 years. Two-dimensional echocardiogram and speckle tracking were performed. RESULTS- Mean left ventricular mass index (LVMI) were significantly higher in acromegalic patients (89.1 ± 27.9) compared to the control group (66.9 ± 15.7) (p = 0.015). There was a direct correlation between IGF-1 mean concentration and left ventricular systolic volume (LVSV) in acromegalic patients (r = 0.64; p = 0.004) even when the disease was inactive (n=10; r = 0.9; p = 0.002) and between IGF1 mean concentration and left ventricular diastolic volume (LVDV). The left ventricular ejection fraction (EF) and the global longitudinal strain (GLS) did not differ between groups (p> 0.05). CONCLUSION- Although patients with acromegaly had higher LVMI, they did not show difference in GLS indicating a small chance of progression to systolic disfunction. Direct correlation between IGF-1 and LDVD and LVSV demonstrates the relevance of a good hormonal control to reduce cardiac changes.
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Persistent link: https://EconPapers.repec.org/RePEc:ibn:gjhsjl:v:13:y:2021:i:10:p:32
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