[Nonketotic hyperglycemia--symptoms and etiology].
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Biomedical subjects
Publications and source records attributed to G Takada.
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To investigate the effects of dobutamine on the Doppler transmitral flow pattern in children with normal left ventricular function, Doppler echocardiography was used to measure the transmitral flow in 14 healthy children before and during infusion of dobutamine (5 micrograms/kg per minute). Cardiac output was measured by the thermodilution method, and stroke volume was calculated as the cardiac output divided by the heart rate. Dobutamine increased the peak velocity and flow velocity-time integral of early diastolic filling without changing those of atrial contraction and normalized peak velocity of early diastolic filling, suggesting an increase in left ventricular relaxation. Dobutamine increased the stroke volume and rate-corrected mean velocity of fiber shortening with reduced end-systolic wall stress, indicating an increase in left ventricular contractility. The percentage of increase in the flow velocity-time integral of early diastolic filling during dobutamine infusion tended to correlate with the increase in stroke volume (r = 0.67, p < 0.05) and with the decrease in end-systolic wall stress (r = -0.61, p < 0.05). Our results suggest that low-dose dobutamine increases left ventricular relaxation with enhanced systolic function. The observed decreased endsystolic wall stress might have caused enhanced relaxation characteristics with dobutamine.
Doppler transmitral flow velocity was measured in premature infants. The early diastolic peak velocity, the peak velocity of early diastole/peak velocity of atrial contraction ratio, and total flow velocity-time integral increased significantly with advancing gestational age and body weight. The peak filling rate normalized to stroke volume (NPFR) did not correlate with gestational age or body weight. Moreover, mean NPFR was not significantly different between premature and term infants. Thus NPFR demonstrates that changes in the left ventricular filling patterns with advancing gestational age and increasing body size are related to the progressive increase in loading conditions, rather than to sequential changes in myocardial properties.
We studied pulmonary venous (PV) flow patterns using Doppler echocardiography in 26 patients with ventricular septal defect less than 3 years of age. Fifteen patients had moderate or severe symptoms, and the remaining 11 had no significant symptoms. Peak velocity of PV diastolic flow and flow velocity integral of PV diastolic flow in the symptomatic patients were significantly larger than those in either asymptomatic patients or the normal controls. The ratio of PV diastolic flow velocity to PV systolic flow velocity and the ratio of flow velocity integral of PV diastolic flow to that of PV systolic flow in the symptomatic patients were significantly larger than those in either asymptomatic patients or the normal controls. The ratio of PV diastolic flow velocity to PV systolic flow velocity as well as the ratio of flow velocity integral of PV diastolic flow to that of PV systolic flow correlated with V wave in left atrial or pulmonary capillary wedge pressure and indexes of left ventricular mass and left atrial volume. We conclude that the abnormal pulmonary venous flow patterns in ventricular septal defect might be associated with large left-to-right shunting and left atrial pressure V wave.
To evaluate whether transthoracic Doppler echocardiography can reliably measure coronary flow velocity and coronary flow velocity reserve (CFVR) in the posterior descending coronary artery (PD) in children, we examined 32 patients who had congenital heart disease (ventricular septal defect in 10, tetralogy of Fallot in 6, tricuspid atresia in 3, double-outlet right ventricle in 2, patent ductus arteriosus in 2, and aortic valve stenosis in 2) and 7 patients who had a history of Kawasaki disease without stenosis or aneurysm formation of the coronary artery. Average peak flow velocity (APV) in the PD was measured by transthoracic Doppler echocardiography at the time of intracoronary Doppler study. CFVR was defined as the ratio of hyperemic to basal APV. Clear envelopes of basal and hyperemic APV in the PD were obtained in 23 of 32 patients by transthoracic Doppler echocardiography. APV obtained from transthoracic Doppler echocardiography correlated highly with that from the Doppler guidewire method (r=0.91). The mean difference between transthoracic Doppler echocardiography and the Doppler guidewire method was 0.1+/-2.9. There was an excellent correlation between transthoracic Doppler echocardiography and the Doppler guidewire method for the measurements of CFVR (r=0.84). The mean difference between transthoracic Doppler echocardiography and Doppler guidewire was -0.016+/-0.198. Noninvasive measurement of coronary flow velocity and CFVR in the PD using transthoracic Doppler echocardiography accurately reflects invasive measurement of coronary flow velocity and CFVR by the Doppler guidewire method in pediatric patients with various heart diseases.
We evaluated the effects of acute preload reduction with inferior vena cava (IVC) occlusion on myocardial velocities during systole (Sa), early (Ea) and late (Aa) diastole, isovolumic contraction (IVV), and myocardial acceleration (IVA) measured by tissue Doppler imaging (TDI) in pediatric patients. A total of 22 patients (5 +/- 3 years) were studied: 9 patients (4 +/- 3 years) with Kawasaki disease, 8 patients (6 +/- 3 years) with atrial septal defect and right ventricular (RV) volume overload, and 5 patients (5 +/- 4 years) with pulmonary stenosis and RV pressure overload. Using TDI, Sa, Ea, Aa, IVV were recorded at the base of the RV free wall from a four-chamber view. IVA was calculated by dividing IVV by the time interval from onset of IVV to the time at peak velocity of this wave. In each group, IVC occlusion caused significant decreases in peak Sa, peak Ea, and peak Aa (p < 0.05). However, IVV and IVA did not change during acute preload reduction. This study demonstrated the effects of acute preload reduction on TDI velocities. In contrast to peak Sa, peak Ea, and peak Aa, IVV and IVA were unaffected by preload within a physiological range.
To examine the effects of body mass index on left ventricular diastolic function, flow velocity patterns of the pulmonary vein and mitral valve were measured by pulse Doppler echocardiography in 21 asymptomatic obese children and were compared with those of an age-matched control population. The degree of obesity was calculated as (actual body mass index/ideal body mass index -1) x 100. The pulmonary venous flow indexes were peak systolic (S) and diastolic (D) velocities and peak D/S. The mitral inflow indexes were peak velocities of early diastole (E) and atrial contraction (A) and peak E/A. The pulmonary venous flow velocity pattern in obese patients was characterized by unchanged peak S, decreases in peak D (43 +/- 7 vs 51 +/- 8, p < 0.01) and peak D/S (0.98 +/- 0.19 vs 1.29 +/- 0.20, p < 0.01), suggesting the reduction in the early diastolic filling. The peak D/S decreased significantly with an increase in the percentage body mass index (r = -0.84, p < 0.01). In contrast to the pulmonary venous flow pattern (peak D > peak S) as seen in normal controls, all of the obese patients with > 70% over body mass index had abnormal pulmonary venous flow velocity patterns (peak D < peak S). The mitral flow velocity pattern in obese patients was also characterized by a decrease in early diastolic filling. However, these indices did not correlate with an increase in the percentage over body mass index. This study suggests that body mass index predicts the abnormality of left ventricular diastolic filling assessed by pulmonary venous flow patterns.
To evaluate how the size of the ductus arteriosus affects neonatal left ventricular (LV) volume and contractility, we serially obtained two-dimensional and Doppler echocardiograms at 2, 12, 24, and 120 hours after birth in 20 healthy infants. LV volume was calculated by the biplanar Simpson's rule, and ductus arteriosus size with left-to-right shunting was measured by two-dimensional and Doppler echocardiography. At 2 hours, the ductus arteriosus was at its maximal size, and the LV end-diastolic volume was 1.2-fold higher than at the subsequent hours after birth. Additionally, there was a significant linear correlation between the end-diastolic volume and the ductal diameter. In contrast, the peripheral vascular resistance, derived from blood pressure measurements and Doppler echocardiography, was lowest at 2 hours of age. The mean normalized systolic ejection rate, an index of contractility, remained constant throughout the study period. These results suggest that alterations in the LV end-diastolic volume soon after birth depend on changes in ductal flow, which in turn is affected by ductal diameter, and that the neonatal left ventricle operates at its maximal performance with limited contractility during ductal patency.
The objective of the study was to evaluate postnatal changes in left ventricular (LV) contractility in very low birth weight (VLBW) infants. An echocardiographic study comparing 18 VLBW infants without significant complications and 16 normal term infants was carried out at the Neonatal Intensive Care Unit in Akita University Medical Hospital, Japan. The echocardiographic examinations were performed within 6 hours of birth and on day 5. We obtained the relations between rate-corrected mean velocity of circumferential fiber shortening (mVcfc) and end-systolic wall stress (ESS), which were calculated from two-dimensional LV short-axis views to compensate for the distorted LV shape, and we compared these relations statistically. In both VLBW and term infants there were inverse linear correlations between mVcfc and ESS for each study period (p < 0.05). The regression line of VLBW infants had a lower y-intercept and a steeper slope than that of term infants at 6 hours of age but almost corresponded on day 5. It is concluded that the left ventricle of VLBW infants adapts to postnatal hemodynamic alterations with low contractility but operates with a contractile state similar to that of term infants on day 5.
We studied the change in pulmonary arterial diameter under prostaglandin E1 (PGE1) therapy in infants with ductus-dependent cyanotic heart disease (pulmonary atresia). Ten infants undergoing administration of PGE1 for more than 2 weeks were selected for this study. A classic Blalock-Taussig (BT) shunt was performed in seven patients and a modified BT shunt in three. The shunt was successful in all patients. The internal diameters of the right and left pulmonary arteries were measured before and after the start of PGE1 therapy using two-dimensional echocardiography. The pulmonary arterial index (PA index) was calculated to correct the diameters for body surface area. Both pulmonary arteries enlarged during the first week of PGE1 therapy in all 10 patients. Further increases in the two diameters were observed even after the first week of treatment in nine patients. Both the mean diameters at 2 weeks after the start of PGE1 were about 50% larger than the initial diameters (right; increased from 3.1 to 4.7 mm; left; increased from 3.0 to 4. 4 mm). Of the eight patients given PGE1 for more than 3 weeks, four showed no changes in pulmonary arterial diameters after the first 2 weeks and the remaining four showed a slight increase. PA indexes also showed a rapid increase during the first 2 weeks and no significant change thereafter. We suggest that, in infants with pulmonary atresia and small pulmonary arteries, the optimal pulmonary artery size for BT shunt insertion is achieved after 2 weeks of PGE1 infusion, with no further significant increase in size being observed after this time.
We measured changes in the regional cerebral metabolic rate of glucose (rCMRGlu) using 18F-fluorodeoxyglucose and positron emission tomography for the assessment of neurotoxicity in childhood acute lymphocytic leukemia treated with high-dose methotrexate (HD-MTX) therapy. We studied 8 children with acute lymphocytic leukemia (mean age: 9.6 years) treated with HD-MTX (200 mg/kg or 2,000 mg/M2) therapy. CMRGlu after HD-MTX therapy was most reduced (40%) in the patient who had central nervous system leukemia and was treated with the largest total doses of both intrathecal MTX (IT-MTX) and HD-MTX. CMRGlu in the whole brain after HD-MTX therapy was reduced by an average of 21% (P less than 0.05). The reductions of CMRGlu in 8 patients were correlated with total doses of both IT-MTX (r = 0.717; P less than 0.05) and systemic HD-MTX (r = 0.784; P less than 0.05). CMRGlu of the cerebral cortex, especially the frontal and occipital cortex, was reduced more noticeably than that of the basal ganglia and white matter. We suggest that the measurement of changes in rCMRGlu after HD-MTX therapy is useful for detecting accumulated MTX neurotoxicity.
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