Growth parameters and endocrine function in relation to echocardiographic parameters in children and adolescents with compensated rheumatic heart disease.

Abstract

To determine the effect of left ventricular and endocrine functions on linear growth in children with rheumatic heart disease (RHD) we studied 100 children and adolescents with RHD over a period of 1 year. The mean +/- SD for age of onset and duration of RHD were 7.3 +/- 3.8 years and 4.4 +/- 2.8, respectively. The cardiac lesions were mitral incompetence (n = 31), combined mitral and aortic incompetence (n = 64), and mitral stenosis (n = 5). Growth was assessed by determining both height standard deviation scores (HtSDS) and growth velocity standard deviation score (GVSDS) every 4 months, and sexual maturity was assessed according to Tanner's criteria. Two-hundred age-matched normal children served as controls for the growth data. Endocrine evaluation was performed in the 30 children with RHD who had age above 14 years (mean age 15.4 +/- 1.5 years), 20 age- and sex-matched normal children, and 20 age-matched children with constitutional delay of growth (normal variant short stature) (NVSS). Circulating concentrations of estradiol (E2) in girls, testosterone (T) in boys, and free T4 (FT4) were measured. Growth hormone (GH) response to clonidine provocation, LH and FSH response to LHRH stimulation, and in boys testosterone (T) response to HCG were evaluated. Echocardiographic evaluation of the left ventricular parameters was performed using a colour-coded echodoppler. The HtSDS and GVSDS of children with RHD were significantly lower than those for the normal control group. Delayed onset of puberty was evident in 16/30 of the children with RHD, and 6/ 30 more had sexual maturity score below 10th percentile for age and gender. In comparison with the age-matched normal group, those with RHD had significantly lower sexual maturity score (1.8 +/- 0.4 v. 3.25 +/- 0.8). All the children had normal GH response to clonidine provocation and normal FT4 concentrations. Basal and HCG stimulated T concentrations were significantly low in adolescents with RHD and E2 levels were non-significantly lower in girls with RHD compared to normal controls. LH response to LHRH was significantly decreased in RHD patients v. controls denoting delayed maturation of the hypothalamic-pituitary gonadal axis. HtSDS and GVSDS were correlated significantly with the left ventricular echocardiographic parameters, including left ventricular end diastolic diameter (LVEDD) (r = 0.57, and 0.617, respectively; P < 0.01), left ventricular end systolic diameter (LVESD) (r = 0.49, and 0.546, respectively; P < 0.01), left ventricular end diastolic volume (LVEDV) (r = 0.33 and 0.31, respectively; P < 0.05), left ventricular end systolic volume (LVESV) (r = 0.325 and 0.33, respectively; P < 0.05), peak velocity of circumferential fibres (Vcf) (r = 0.25 and 0.38, respectively; P < 0.05), and with pre-ejection period/ejection time (PEP/ET) (r = 0.14 and 0.47, respectively; P < 0.05). It appears that linear growth of children with RHD, without heart failure, depends on the left ventricular function. In addition, they have high incidence of delayed sexual development secondary to delayed maturation of their hypothalamic-pituitary gonadal axis.