ECE2018 Guided Posters Cardiovascular (8 abstracts)
Turner syndrome and cardiovascular risk
Bernardo Marques 1 , Margarida Bastos 2 , Diana Oliveira 2 , Diana Martins 2 , Adriana Lages 2 , Mara Ventura 2 , Nelson Cunha 2 , Lúcia Fadiga 2 , Diana Catarino 2 & Francisco Carrilho 2
1Deparment of Endocrinology, Instituto Português de Oncologia de Coimbra Francisco Gentil, EPE, Coimbra, Portugal; 2Department of Endocrinoloy, Diabetes and Metabolism, Centro Hospitalar e Universitário de Coimbra, EPE, Coimbra, Portugal.
Introduction: Turner Syndrome (TS) is associated with cardiovascular anomalies and account for a threefold higher mortality in these women. The most common findings are congenital malformations of the heart (CMH), aortic dissection, valvular heart disease (VHD), hypertension and ischemic heart disease. It has been suggested that the ocurrence of cardiovascular disease in TS women is related to their karyotype and possibly to growth hormone (GH) treatment. Our study aimed to assess cardiovascular risks in patients with TS.
Methods/design: This was a retrospective study of 64 patients with TS identified from our institutional database. They were categorized in three groups, according to their karyotype: group 1 included 24 patients with monosomy X, group 2 comprised 21 patients with mosaicism, and group 3 comprised 19 patients with structural aberrations of X chromossome. We assessed age, treatment with GH, pubertal development, lipid profile, diabetes mellitus, body mass index, blood pressure and cardiac and valvular abnormalties. The association between variables was evaluated using Fisher’s exact test and paired samples t test.
Results: The patients evaluated were aged 23–69 years old (S.D. 36±10.1), with median follow-up time of 20±8.3 years. VHD was present in 19 patients (30%) and CMH were detected in 17 patients (27%), the most common being aortic coarctation (n=11). CMH were detected more frequently in group 1 patients (P=0.001), namely aortic coarctation (8 of the 11 cases detected, P=0.001). Group 2 patients presented a higher rate of spontaneous puberty than the others (P=0.029). There were no differences regarding other cardiovascular risk factors and anomalies among the 3 groups, as well as association between GH treatment and the development of CMH or VHD.
Conclusion: The pathophysiology of the cardiovascular anomalies in TS is still unclear. In our study, monossomy X was associated with CMH and spontaneous pubertal development was associated with VHD. Life-long surveillance is recommended, namely evaluation of cardiac function, aortic diameter and blood pressure, in order to provide early identification and management of potentially serious cardiovascular conditions.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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