Cardiovascular impairment in children, adolescents, and young adults with type 1 diabetes mellitus (T1DM).

Left ventricular (LV) function was assessed in 42 patients (mean age +/- SD, 18.45 +/- 3.76 years; 17 males) with type I diabetes mellitus (T1DM; mean duration 9.89 years) and in 43 healthy controls (mean age +/- SD, 18.27 +/- 3.36 years; 18 males). Systolic, diastolic cardiac function and LV dimensions were assessed using M-mode and Doppler echocardiography. Neural autonomic function was assessed by measuring RR variation during deep breathing, Valsava maneuver, 30/15 ratio, and blood pressure response to standing. Fractional shortening, peak velocity of early ventricular filling (E wave), peak velocity of LV filling (A wave), E/A ratio, deceleration time, isovolumic relaxation time, LV dimensions (interventricular septum, posterior wall thickness, end diastolic diameter [EDD] and systolic diameter [ESD]) were all comparable between patients with T1DM and controls. However, in 11 T1DM patients with microalbuminuria and/or retinopathy, EDD, ESD, E/A ratio, and E wave were all lower (p = 0.0011, p = 0.019, p = 0.0011, and p = 0.030, respectively) while, A wave, heart rate, and diastolic blood pressure were all higher (p = 0.008, p = 0.0024 and p = 0.004, respectively) compared to matched for age and sex controls. Furthermore, in six of the 11 T1DM patients with microangiopathy who had E/A <1.12 (<2 SD of the control mean), significant and marginally significant correlations were found between E/A ratio and the duration of the disease as well as the mean HbA1c of the last year (r = -0.38, p = 0.011 and r = -0.287, p = 0.064, respectively). In conclusion, it has been found that impairment of diastolic, but not systolic, LV function can be detected early in young patients with T1DM and microangiopathy.

M-mode echocardiographic evaluation of systolic function, LV volume and mass in children on growth hormone therapy.

Since abnormal endogenous growth hormone (GH) secretion in adults is associated with cardiac dysfunction, it is important to ensure that GH therapy in children and adolescents does not cause similar effects. Forty-two growth hormone-deficient children (Group 1) (19 girls, 23 boys) were evaluated. Six girls and seven boys were prepubertal with a mean age of 6.65 yr (range 4.37-9.73 yr). Twenty-nine were pubertal (13 girls, 16 boys), mean age 13.57 yr (range 10.08-16.76 yr). The patients had been on long-term GH therapy for 34.97 +/- 18.78 months with an average weekly dose of 17.61 IU/m2/wk. The mean height SDS was -2.85 +/- 1.22 for boys and -2.5 +/- 0.64 for girls at the onset of therapy, and at the time of examination -1.8 +/- 1.32 for the boys and 1.87 +/- 0.94 for the girls. Thirty-four normal control subjects (Group 2) matched for age, sex and body size were also studied. Left ventricular volume (LV), mass and systolic function [shortening fraction (FS)] were evaluated by two-dimensional guided M-mode echocardiography. Blood pressure was also measured. No differences in blood pressure were observed between patients and controls. There was no correlation of GH dose and duration of therapy with LV measurements. No significant differences were found between Group 1 and Group 2. These observations suggest that long term administration of GH does not produce adverse cardiac effects in GH deficient children. Nevertheless, longer follow-up studies are still needed to confirm the safety of long-term rhGH treatment.