Speckle tracking imaging (STI) was employed to investigate the effect of right ventricular (RV) volume and pressure overload on left ventricular (LV) rotation and twist in 35 patients with atrial septal defect (ASD), 18 of which with pulmonary hypertension, and 21 healthy subjects serving as controls. The peak rotations of 6 segments at the basal and apical short-axises and the average peak rotation and interval time of the 6 segments in the opposite direction during early systolic phase were measured respectively. LV twist versus time profile was drawn and the peak twist and time to peak twist were calculated. LV ejection fraction (EF) was measured by Biplane Simpson. Compared to ASD patients without pulmonary hypertension and healthy subjects, the peak rotations of posterior, inferior and postsept walls at the basal level were lower (P<0.05), and the average counterclockwise peak rotation of 6 segments at the basal level during early systolic phase was higher (P<0.05), and the average interval time was delayed (P<0.05). LV peak twist was also lower (P<0.05), and had a significant negative correlation with pulmonary arterial systolic pressure (r=-0.57, P=0.001). No significant differences were found in LVEF among the three groups. It was suggested that although RV volume overload due to ASD has no significant effects on LV rotation and twist, LV peak twist is lower in ASD patients with pulmonary hypertension. Thus LV twist may serve as a new indicator of the presence of pulmonary hypertension in ASD patients.
Cardiology/methods ; Echocardiography/methods ; Echocardiography, Doppler/methods ; Heart Septal Defects, Atrial/metabolism ; Heart Septal Defects, Atrial/*pathology ; Heart Ventricles/pathology ; Hypertension ; Nuclear Proteins/*metabolism ; Systole ; Twist Transcription Factor/*metabolism ; Ventricular Function, Left

The changes of adrenomedullin (ADM), endothelin-1 (ET-1) and nitric oxide (NO) levels before and after operation in congenital heart disease (CHD) associated with pulmonary hypertension (PH) were observed in order to investigate their role in CHD with PH and their clinical significance. The CHD patients were divided into 3 groups according to pulmonary artery systolic pressure (PASP): Non-PH group: PASP < or = 30 mmHg (n = 11); mild-PH group: PASP 31-49 mmHg (n = 10); moderate or severe-PH group: PASP > or = 50 mmHg (n = 12). The control group consisted of 15 health children. Plasma ADM, ET-1 and NO levels were determined by radioimmunoassay and colorimetry methods. The correlation between ADM and ET-1, NO, PASP was analyzed. The changes in plasma ADM, ET-1 and plasma NO on the 7th day after operation among the groups were compared. The results showed that plasma ADM levels in non-PH group were significantly higher than that in control group (P < 0.05), but there was no significant difference in ET-1 and NO levels between the two groups (P > 0.05). ADM and ET-1 levels in mild-PH group were significantly elevated as compared with those in non-PH group (both P < 0.05), but NO levels were decreased (P < 0.05). ADM and ET-1 levels in moderate or severe-PH groups were increased as compared with those in mild-PH group (both P < 0.01), but NO level significantly declined (P < 0.05). On the 7th day after operation, plasma ADM and ET-1 levels in PH group were significantly decreased (P < 0.05, P < 0.01) as compared with those before operation, but there was no significant difference in NO levels (P > 0.05). But NO levels in non-PH group were significantly increased (P < 0.05). Plasma ADM levels in CHD were positively correlated with PASP and ET-1 (r = 0.77, P < 0.01; r = 0.82, P < 0.01), negatively correlated with NO (r = -0.56, P < 0.05). It was concluded that during the progression of PH in the cases of CHD, plasma ADM, ET-1 and NO might play an important role in the development of PH. The increased ADM may represent a compensatory mechanism. It can interact with NO and ET-1 to regulate pulmonary circulation in the pathophysiology of PH with CHD. ADM may be involved in the defence mechanism against further increase of pulmonary arterial pressure. ADM could be used as a reliable indicator of the severity of CHD associated PH.
Adolescent ; Adrenomedullin ; Child ; Child, Preschool ; Endothelin-1 ; metabolism ; Female ; Heart Septal Defects, Atrial ; complications ; metabolism ; surgery ; Heart Septal Defects, Ventricular ; complications ; metabolism ; surgery ; Humans ; Hypertension, Pulmonary ; etiology ; metabolism ; Infant ; Male ; Nitric Oxide ; metabolism ; Peptides ; metabolism ; Postoperative Period

BACKGROUND AND OBJECTIVES: The purpose of this study was to investigate whether a brief cardiopulmonary by-pass, with mild hypothermia and normal flow, would have any deleterious effects on brain metabolism in children. This is the first study using localized in vivo proton magnetic resonance spectroscopy (1H-MRS) in brains of children with ASD undergoing open-heart surgery (OHS). SUBJECTS AND METHODS: Seven children undergoing surgical closure of ASD, with mild hypothermia and normal flow cardiopulmonary by-pass, were studied. Their ages ranged from 18 to 47 months, and body weights ranged from 11 to 17 kg. We performed 1H-MRS before OHS, and 1-3 months after, then compared the values of brain metabolite ratios before and after surgery. The values from our patients were compared to those from 12, age-matched, normal children. All MR imaging, and localized 1H-MRS, were performed using a GE 1.5T SIGNA system (General Electric Medical System, Milwaukee, USA). Image guided STEAM-spectra were obtained from, the parietal white matter (PWM), and occipital gray matter (OGM), with TE of 30 msec, and TR of 3 sec, using a PROton Brain Exam (PROBE) (General Electric Medical System, Milwaukee, USA). RESULTS: All metabolite ratios, measured by 1H-MRS, from patients before surgery showed no significantly difference from postoperative values. However, [choline/creatine] ratios, obtained from PWM, were higher in both pre- and postoperative ASD patients, as compared to those of normal children. CONCLUSION: We concluded, that brain metabolism, measured by 1H-MRS, does not change significantly after OHS, for children with ASD, with mild hypothermia and normal flow.
Body Weight ; Brain ; Cardiopulmonary Bypass ; Child* ; Heart Septal Defects, Atrial* ; Heart* ; Humans ; Hypothermia ; Magnetic Resonance Imaging ; Magnetic Resonance Spectroscopy* ; Metabolism* ; Protons* ; Rabeprazole ; Thoracic Surgery*

PURPOSE: Long-term administration of anticonvulsants in children with epilepsy may cause short stature, hypocalcemia and low bone mineral density. This study was performed for the early detection of abnormal bone metabolism in children with epilepsy on taking anticonvulsants. METHODS: Thirty children aged 5 to 16 years who were diagnosed with epilepsy were enrolled in this study. All had taken anticonvulsants for more than one year. Bone mineral density of lumbar vertebra was measured by dual-energy X-ray absorptiometry. Serum calcium, phosphorous, alkaline phosphatase, 25-hydroxycholecalciferol[25(OH)D3], parathyroid hormone, and urine deoxypyridinoline were measured as biochemical bone markers. Bone age and body mass index were also calculated. RESULTS: Bone minreal density, body mass index, bone age, and height were significantly decreased in two female patients who had taken two antiepileptic drugs for more than four years and they also had chronic diseases such as cerebral palsy with microcephaly, encephalomalacia, and microcephaly with atrial septal defect. Bone mineral density had significant positive correlations with body mass index(P<0.01) and bone age(P<0.01). CONCLUSION: This study showed chronic medication of anticonvulsants in children may cause low bone mineral density and short stature. Bone age and body mass index could be the important surrogate markers to find the population at risk. More studies, including a large study population and long term cohort study, will be required.
Absorptiometry, Photon ; Alkaline Phosphatase ; Anticonvulsants* ; Biomarkers ; Body Mass Index ; Bone Density* ; Calcium ; Cerebral Palsy ; Child* ; Chronic Disease ; Cohort Studies ; Encephalomalacia ; Epilepsy* ; Female ; Heart Septal Defects, Atrial ; Humans ; Hypocalcemia ; Metabolism ; Microcephaly ; Parathyroid Hormone ; Population Characteristics ; Spine