Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Real time ultrasound scans using an ATL 300C sector scanner with 5-7.5 MHz transducer were performed on days 1, 4, 7 and thereafter as clinically necessary on 153 consecutively discharged very low birthweight (VLBW) infants. One hundred and forty-six long-term survivors were assessed fully at 2 years. The prevalence of cerebroventricular haemorrhage (CVH) in these survivors was 34.2% (grade 1-21.2%; grade 2-4.8%; grade 3-3.4%; grade 4-4.8%), ventricular dilatation 19.9% (including 4.1% with ventriculoperitoneal shunt), and ischaemia 9%. Impairments at 2 years were classified as nil, mild, moderate, severe or multiply severe, based on the criteria of Kitchen et al. Overall, 120 infants (82.2%) were unimpaired and 6.2% had mild, 3.4% had moderate, 4.1% had severe and 4.1% had multiply severe impairment. The major factors associated with impairment were gestational age less than 28 weeks, birthweight less than 1000 g, vaginal delivery, respiratory distress syndrome, mechanical ventilation, pulmonary air leaks and CVH. When these factors were reanalysed in a logistic regression model for odds ratios, only CVH (P less than 0.005) and birth by spontaneous vaginal delivery (P less than 0.05) were significant. The prevalence of impairment was 11.4% with no CVH, 6.5% grade 1, 71% grade 2, 20.0% grade 3 and 100.0% grade 4 CVH. The sensitivity of CVH of grade 2 or greater as a screening test was 64.7% for impairment, 78.6% for cerebral palsy and 70% for severe intellectual handicap. The mean general quotient (GQ) (Griffiths) at 2 years for infants with CVH was 89.1, and 97.5 for those without CVH (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neonatal cranial ultrasonography as predictor of 2 year outcome of very low birthweight infants. 247 34

A case study is presented of a premature infant delivered at 32 weeks' gestation by cesarean section. At birth the infant had massive cardiomegaly with extreme left ventricular dilatation as well as severe congestive heart failure and respiratory distress. The findings at autopsy suggest that the cardiac dysfunction was secondary to a myocardial infarct occurring in utero.
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PMID:Dilatation of the left ventricle in a newborn: probable in utero myocardial infarction. 294 55

Left ventricular dimensions and function were assessed by serial M mode and cross sectional echocardiography in ten infants and young children with heart muscle disease characterised by left ventricular dilatation and impaired systolic function presenting in congestive heart failure, severe respiratory distress, or both. The patients were followed for 8-60 months after their initial admission. The aetiology was probably viral in all cases. One patient died three weeks after diagnosis. Left ventricular size and function returned to normal in only one child; however, various degrees of improvement were found in seven others who were symptom free at follow up. This study demonstrates that serial echocardiography adequately defines this disease in infants and young children and that invasive evaluation is seldom required. Furthermore, it emphasises the fact that even in symptom free children an echocardiographic picture that is indistinguishable from dilated cardiomyopathy may persist; such patients required continued follow up.
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PMID:Viral myocarditis simulating dilated cardiomyopathy in early childhood: evaluation by serial echocardiography. 373 Feb 10

We studied 4 very low birth weight infants with secondary cystic lesions in the cerebellum by serial cranial ultrasound and computed tomography. These infants presented severe respiratory distress, asphyxia at birth and intraventricular hemorrhage. In the neonatal period, cranial ultrasound examination showed significant intraventricular hemorrhage and posthemorrhagic ventricular dilatation with intraparenchymal hemorrhage. However, a cerebellar cyst was not seen in any of the infants. We found evidence of cerebellar hemorrhage by ultrasound in only one patient. Follow-up ultrasound examinations and CT scans showed progressive posthemorrhagic ventriculomegaly in three of the infants and large cystic lesions in the infratentorial area from 3 to 6 months old in all 4 infants. We conclude that the cystic lesions were caused by hemorrhagic and hypoxic-ischemic insults which occurred in very low birth weight infant.
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PMID:Secondary cystic lesions in the cerebellum in very low birth weight infants. 390 33

The postnatal changes of cerebral blood flow velocity in 35 preterm neonates with or without complications were measured with a bidirectional Doppler flow meter. In the cases without complications, the pulsatility index for the anterior cerebral artery (ACA-PI) was high shortly after birth, and gradually decreased after 6 hrs as that in normal term neonates. However ACA-PI showed large variations in the cases with respiratory distress. On the other hand, ACA-PI in the cases with subependymal hemorrhage (SEH) was low during the first 6 hrs after birth, and thereafter showed no significant changes. ACA-PI in the cases with intraventricular hemorrhage (IVH) was high during the first 6 hrs after birth and then decreased when IVH was found on ultrasound scanning. ACA-PI increased gradually with progression of post-hemorrhagic ventricular dilatation. The difference of high PI in IVH and low PI in SEH during the first few hrs after birth suggests that the pathogenesis of SEH may be different from the mechanism of intraventricular rupture from SEH. Low PI values in the infants with SEH may be related to intrapartum events, while the changing patterns of high to low PI in the infants with IVH suggest postnatal hemodynamic changes.
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PMID:Cerebral blood flow velocity in preterm neonates. 406 74

Twelve newborn infants of poorly-controlled diabetic mothers were transferred from outlying maternity hospitals for neonatal intensive care. Respiratory distress and cardiomegaly were the presenting signs. Ten infants were large for dates (macrosomic) and had echocardiographic evidence of myocardial hypertrophy, reduced ejection time, and systolic anterior movement of the mitral valve (in 6 infants). These findings are similar to those of adults with idiopathic hypertrophic subaortic stenosis. Two infants died. In survivors the myocardial hypertrophy persisted for at least 2 weeks but the evidence of functional subaortic stenosis had disappeared by 4-7 days. The 2 infants who were appropriately grown had cardiomegaly as a result of ventricular dilatation. This was associated with hypoglycaemia and acidosis, and disappeared when these metabolic disturbances were corrected.
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PMID:Hypertrophic cardiomyopathy in infants of poorly-controlled diabetic mothers. 719 89

We present the clinical and neuroimaging findings of five patients (four males, one female; mean age 12 years) affected by congenital myotonic dystrophy and the correlation with their molecular genetic analysis. At birth all five presented severe muscular weakness and hypotonia, associated with feeding difficulties and respiratory distress. In the same patients, congenital clubfoot or more generalized arthrogryposis was also evident. Lymphocyte DNA was characterized in each by a CTG repeat longer than 1300 in the region of the myotonic dystrophy gene in chromosome 19. The patients' neurological condition was evaluated by clinical examination, intelligence tests, electroencephalography, and brain magnetic resonance imaging. All five suffered from some impairment of intellectual function (IQ ranged from 52 to 79). In three a longitudinal evaluation of the cognitive deficit detected no deterioration. In all patients magnetic resonance imaging showed some degree of ventricular dilatation, loosely correlated to the cognitive impairment; in three there was hypoplasia of the corpus callosum and in two mild abnormalities of supratentorial white matter. The relationship between the size of the CTG repeat expansion found in lymphocyte DNA and the cerebral abnormalities appeared inconsistent in this unusual myoencephalopathy of the newborn.
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PMID:Clinical and neuroimaging study of central nervous system in congenital myotonic dystrophy. 1032 16

There is some controversy regarding the indications for transesophageal echocardiography in patients with suspected systemic embolism. The present case report refers to a 65 year old male admitted to the hospital for ischemic acute cerebrovascular accident, which was confirmed by cerebral computerized tomography. A transthoracic echocardiogram was performed showing right atrial and ventricular dilatation. A transesophageal echocardiogram was also performed to exclude thromboembolism and clarify dilatation of the right cavities. Mild spontaneous echocontrast was present in the left atrium without images of thrombus; an interatrial septal aneurysm with patent foramen ovale was found with right to left flow; an image compatible with a very mobile, large, proximal thrombus in the main pulmonary artery was observed. A venous duplex scan was performed, demonstrating venous thrombosis in the right popliteal and femoral veins. Pulmonary arteriography showed a large thrombus in the right pulmonary branch extending to the median lobe and a smaller thrombus in the left pulmonary branch. Apparently, the patient had no predisposing factors for thromboembolism. Full-dose heparin was started followed by oral anticoagulation. An inferior vena cava filter was implanted. At hospital discharge the pulmonary thrombus had disappeared and the right cardiac cavities had returned to normal size. The interatrial aneurysm had disappeared and foramen ovale was no longer patent. After 36 months of clinical follow up on oral anticoagulation, the patient remains asymptomatic without neurological sequelae nor respiratory distress.
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PMID:[Diagnosis of paradoxal and concomitant pulmonary thromboembolism with transesophageal echocardiography: a clinical case]. 1101 85

A male fennec fox (Fennecus zerda) kit was examined for lethargy, inappetence, and weight loss. Clinical findings included respiratory distress, a gallop rhythm, and retinochoroiditis. Radiography indicated pleural effusion and cardiomegaly. Echocardiographic findings included left ventricular dilatation, low left ventricular ejection fraction, and atrioventricular valvular regurgitation. Necropsy findings were compatible with a diagnosis of congestive heart failure caused by myocarditis. Histopathology showed a disseminated infection with Toxoplasma gondii causing myocarditis, skeletal polymyositis, gastrointestinal myositis, and panuveitis. Toxoplasma-induced myocarditis should be included in the differential diagnosis of heart failure and retinochoroiditis in the fennec fox.
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PMID:Heart failure caused by toxoplasmosis in a fennec fox (Fennecus zerda). 1553 72

Pediatric cardiomyopathies are a heterogenous group of conditions of which dilated cardiomyopathies are the most common clinicomorphologic subtype. However, the etiology and pathogenesis of many cases of dilated cardiomyopathies remain unknown. We describe a series of 5 cases of a rare but clinically and histologically distinctive dilated cardiomyopathy that was uniformly lethal in early infancy. The 5 cases include 2 pairs of siblings. There was parental consanguinity in 1 of the 2 pairs of siblings. Death occurred in early infancy (range, 22-67 days; mean, 42 days) after a short history of general lethargy, decreased feeding, respiratory distress, or cyanosis. There was no specific birth or early neonatal problems. Autopsy revealed congestive cardiac failure and enlarged, dilated hearts with ventricular dilatation more pronounced than atrial dilatation, and endocardial fibroelastosis. Histology showed prominent hypertrophic nuclear changes of cardiac myofibers and markedly increased myocyte mitotic activity including occasional atypical mitoses. Immunohistochemical staining for Mib1 showed a markedly increased proliferative index of 10% to 20%. Ancillary investigations, including molecular studies, did not reveal a primary cause for the cardiomyopathies. This distinctive dilated cardiomyopathy characterized by unusual histologic features of myocyte nuclear hypertrophy and marked mitotic activity is lethal in early infancy. Its occurrence in 2 pairs of siblings suggests familial inheritance. Although the underlying molecular pathogenesis remains to be elucidated, it is important to recognize this distinctive entity for purposes of genetic counseling.
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PMID:Mitogenic cardiomyopathy: a lethal neonatal familial dilated cardiomyopathy characterized by myocyte hyperplasia and proliferation. 2030 41


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