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Objective: To analyse the structural and functional abnormalities in the large arteries in women with the Turner syndrome., Methods: Aortic stiffness (assessed by means of the carotid femoral pulse wave velocity), level of amplification of the carotid pressure wave (by applanation tonometry), and carotid remodelling (by high resolution ultrasound) were studied in women with the Turner syndrome. Clinical and ambulatory blood pressures were taken into account in the analysis. Thus, 24 patients with the Turner syndrome and 25 healthy female subjects matched for age were studied., Results: Women with the Turner syndrome had a higher augmentation index than the controls (Turner, mean (SD) 0.04 (0.14) v controls, -0.14 (0.13), p < 0.001) but a lower peripheral pulse pressure (39 (8) mm Hg v 47 (11) mm Hg, p = 0.010 in the clinic; 44 (5) mm Hg v 47 (6) mm Hg, p = 0.036 during the 24 hour ambulatory recording). The luminal diameter of the common carotid artery and the carotid-femoral pulse wave velocity were similar in the two groups, whereas carotid intima-media thickness tended to be higher in women with the Turner syndrome (0.53 (0.06) mm v 0.50 (0.05) mm, p = 0.06). After correction for body surface area, carotid intima-media thickness and pulse wave velocity were higher in women with the Turner syndrome., Conclusions: Vascular abnormalities observed in the Turner syndrome are implicated in the origin of the cardiovascular complications that occur in this syndrome. These abnormalities are morphological but also functional. An increase in the augmentation index can be explained in part by the short height of these patients.

Turner's syndrome is associated with congenital heart disease in a third of cases. Several reports of aortic dilatation and of death by dissection or rupture of the aorta have been published. The authors undertook a prospective study to assess the incidence of cardiac malformations and aortic dilatation in genetically confirmed Turner's syndrome. Twenty-six out of 34 patients recalled (76%), aged 7 to 30 years (average 17 +/- 6 years) accepted their inclusion in this study and underwent clinical examination, ECG, chest X-ray and echocardiography. Thirteen patients had a monosomy 45X and 13 a mosaic or structural abnormality. Six had a history of cardiovascular disease (operated coarctation: 2 cases, kinking: 2 cases, Hypertension: 2 cases). Eight patients (30%) had one or several anatomical cardiovascular abnormalities: bicuspid aortic valve (19.2%), abnormalities of the aortic isthmus (kinking or coarctation) (15.4%), aortic regurgitation (7.7%), mitral stenosis (3.8%), partial anomalous venous drainage (3.8%), patent ductus arteriosus (3.8%) and left superior vena cava (11.5%). Systematic evaluation of the aorta resulted in the diagnosis of dilatation of the ascending aorta in 1 case and dilatation of the sinus of Valsalva in 2 other cases. The authors conclude that echocardiographic evaluation is essential after the diagnosis of Turner's syndrome. It should be repeated regularly to detect dilatation of the aorta which carries the risk of serious complications, such as rupture or dissection of the aorta.

This paper reports the case of a patient with Turner's syndrome, who developed a myocardial infarction at the age of 36. Turner's syndrome, associated with gonadal insufficiency, increases atherosclerotic cardiovascular risks that must be assessed during the patient's follow-up.

The first treatment trials on patients presenting with Turner syndrome were successful in accelerating growth velocity. It is therefore essential to know the final height of the patients who were treated in order to ascertain whether or not growth hormone treatment increases final height. We are reporting on a group of 117 patients with Turner syndrome whose growth hormone treatment was initiated in 1986. The mean growth hormone dose was 0.74 IU/kg/week for an average period of 4 years. At the start of treatment, the patients' chronological age was 129/12 years, height -3.8 +/- 1.0 standard deviation scores (SDS) and bone age 10.5 +/- 2.1 years. Mean final height was 147.7 +/- 5.6 cm, i.e. a gain of 1.5 SDS. We noted no significant difference due to the type of chromosomal abnormality, nor to oxandrolone or estrogen-associated treatment. A significant correlation was found between final height, mean parental height, the duration of the treatment, height SDS at the start of treatment and growth hormone peak during pharmacological stimulation tests. However, there was no correlation between growth hormone dosage, chronological age and bone age at the start of treatment. These results show that the growth hormone treatment improves the final heights of patients with Turner syndrome.