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Background Professional athletes exhibit lower left ventricular wall thicknesses, diameters and mass (in females), with less frequent training-related electrocardiogram (ECG) changes, as compared with controls.Methods We studied the association of sex with left ventricular structure in trained early adolescents. Two hundred and six adolescent Caucasian athletes (mean age 13.8 ± 1.6, range 11.8–16.9 years, 158 males and 48 females), with similar degree of training underwent ECG and echocardiographic measurements of left ventricular diameters, thicknesses and mass, with relative wall thickness as the remodelling index.Results As compared with females, males exhibited greater maximal wall thickness (males = 8.7 ± 1.2 vs. females = 7.9 ± 0.8) and indexed left ventricular mass (100 ± 18 g/m2vs. 79 ± 12, p< 0.001), without differences in relative wall thickness (males = 0.35 ± 0.04 vs. females = 0.34 ± 0.04) and with higher prevalence of ECG-based left ventricular hypertrophy, sinus bradycardia and ST-elevation. An analysis of covariance, using age, body surface area, systolic blood pressure, heart rate and sex as the covariates, reported that sex is a strong predictor of left ventricular mass, maximal wall thickness, left ventricular diastolic diameter and ECG-based left ventricular hypertrophy. In a binary logistic regression model analysis sex, like left ventricular mass, predicted ST-trait elevation.Conclusions Our results suggest that, in early adolescence, female athletes have lower left ventricular mass and thicknesses compared with males, without geometrical differences. Therefore, sex, independent of age, is a strong determinant of structural parameters also in early adolescent athletes. These data indicate that sex-specific parameters are needed in the pre-participation cardiovascular screening of adolescent athletes.

Left ventricular hypertrophy in human and experimental hypertension is not always associated with pressure overload but seems to precede an increase in blood pressure. In this study, performed in male 5-week-old prehypertensive spontaneously hypertensive rats (SHR; n65) and age-matched Wistar–Kyoto rats (n56), the relationship between myocardial structure and activation of the adrenergic and nitric oxide systems was evaluated.

The iron chelation therapy in thalassemia major (TM) patients has been demonstrated to reduce cardiac morbidity and mortality. Deferoxamine (DFO) significantly improved survival but its use has several limitations due to reduced compliance. The once-daily oral chelator deferasirox (DFX) has been shown to remove iron from the liver and from the heart, with improved compliance. The efficacy of DFX in removing cardiac iron has been shown and significant improvements in myocardial T2* in patients with b-thalassemia with T2* levels < 20 ms have been demonstrated. The introduction in the clinical practice of the T2* Cardiac Magnetic Resonance (CMR) evaluation permitted a rapid, direct and highly reproducible method to assess myocardial and hepatic iron overload; moreover this technique allows to evaluate cardiac morphology and function. We evaluated the removal of cardiac iron and the cardiac function parameters in TM patients treated with DFX, undergoing CMR,followed at Hereditary Anemia Centre, Department of Internal Medicine in Milan.Forthy-one TM patients (22 females, 19 males, mean age 32 ± 6 yrs), treated with DFX, followed in a single centre, underwent a CMR, performed at baseline (T0), after a variable period of exposure to DFX (median: 12 months, range 4–48 months) and then after at least 6 months of treatment (T1) (median 12 months, range 6–19 months). CMR was performed at Cardiology and CMR Department “A. De Gasperis” at Niguarda Ca' Granda Hospital in Milan, using a 1.5 Tesla MR scanner (Avanto Siemens, Erlangen). The signal intensity of this region was measured for each image with the use of commercial software (CMRtools, Cardiovascular Imaging Solutions, London, UK). All T2* analyses were performed blinded to patient details. Ventricular volumes were analyzed with the same software and stroke volume and ejection fraction calculated from end diastolic and end systolic ventricular volumes. Patients were divided in two groups: group A (28 patients) with baseline T2* values > 20 ms and group B (12 patients) with baseline T2* between 10 and 20 ms.In the overall population, the mean deferasirox dose was 26±7 mg/kg/day; dose adjustment was based on iron intake and on liver and cardiac iron overload at CMR. Despite different durations of deferasirox exposure and different levels of myocardial iron overload, an average improvement of myocardial T2* from 27.4 ms to 29.8 ms was observed at T1 (P=0.004). A significant improvement in LVEF from 63.6 % to 66.5 % (P=0.013), indicative of improved cardiac function, was also observed. Similarly, both end-systolic and end-diastolic ventricular volume assessments (EDV, EDVI, ESV, ESVI) showed significant improvement at T1. No difference in median serum ferritin levels were found between group A and B. Myocardial T2* increased in both groups with DFX treatment, with a significant improvement observed in Group B patients (T2* at T0 was 15.7 ± 2.7 ms and at T1 19.6 ± 3.8 ms, P=0.003) (Table 1). LVEF significantly increased in both groups, from 65.7% to 68.0 % in Group A (P=0.01) and from 59.7% to 64.3% in Group B (P=0.04) (Table 1). In Group A, improvements in EDV, ESV and ESVI were also significant with deferasirox treatment; in Group B significant improvements were observed in ESV and ESVI (Table 1).These data confirm the effects of iron chelation with deferasirox in removing cardiac iron in beta TM patients with mild-to-moderate myocardial iron overload and preventing accumulation of myocardial iron in patients with normal baseline cardiac iron levels. Interestingly, improvements in cardiac function were observed both in patients with and without myocardial iron overload at baseline, however it was more significant in patients with normal T2* at baseline.No relevant conflicts of interest to declare.

Abstract 2159