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Ventricular Enlargement (ventricular + enlargement)
Selected AbstractsMyocardial growth before and after birth: clinical implications,ACTA PAEDIATRICA, Issue 2 2000AM Rudolph Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally. [source] Pulmonary Regurgitation after Tetralogy of Fallot Repair: Clinical Features, Sequelae, and Timing of Pulmonary Valve ReplacementCONGENITAL HEART DISEASE, Issue 6 2007Naser M. Ammash MD ABSTRACT Pulmonary regurgitation following repair of tetralogy of Fallot is a common postoperative sequela associated with progressive right ventricular enlargement, dysfunction, and is an important determinant of late morbidity and mortality. Although pulmonary regurgitation may be well tolerated for many years following surgery, it can be associated with progressive exercise intolerance, heart failure, tachyarrhythmia, and late sudden death. It also often necessitates re-intervention. Identifying the appropriate timing of such intervention could be very challenging given the risk of prosthetic valve degeneration and the increased risk of reoperation. Comprehensive informed and regular assessment of the postoperative patient with tetralogy of Fallot, including evaluation of pulmonary regurgitation, right heart structure and function, is crucial to the optimal care of these patients. Pulmonary valve replacement performed in an experienced tertiary referral center is associated with low operative morbidity and mortality and very good long-term results. Early results of percutaneous pulmonary valve replacement are also promising. [source] Asymmetrical lateral ventricular enlargement in Parkinson's diseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2009M. M. Lewis Background:, A recent case report suggested the presence of asymmetrical lateral ventricular enlargement associated with motor asymmetry in Parkinson's disease (PD). The current study explored these associations further. Methods:, Magnetic resonance imaging (3T) scans were obtained on 17 PD and 15 healthy control subjects at baseline and 12,43 months later. Baseline and longitudinal lateral ventricular volumetric changes were compared between contralateral and ipsilateral ventricles in PD subjects relative to symptom onset side and in controls relative to their dominant hand. Correlations between changes in ventricular volume and United Parkinson's disease rating scale motor scores (UPDRS-III) whilst on medication were determined. Results:, The lateral ventricle contralateral to symptom onset side displayed a faster rate of enlargement compared to the ipsilateral (P = 0.004) in PD subjects, with no such asymmetry detected (P = 0.312) in controls. There was a positive correlation between ventricular enlargement and worsening motor function assessed by UPDRS-III scores (r = 0.96, P < 0.001). Discussion:, There is asymmetrical lateral ventricular enlargement that is associated with PD motor asymmetry and progression. Further studies are warranted to investigate the underlying mechanism(s), as well as the potential of using volumetric measurements as a marker for PD progression. [source] Cerebral blood flow in patients with diffuse axonal injury , examination of the easy Z -score imaging system utilityEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2007T. Okamoto To evaluate the utility of easy Z -score imaging system (eZIS) in 27 diffuse axonal injury (DAI) cases. Twenty-seven DAI patients were examined with an magnetic resonance imaging (MRI) T2* sequence and with eZIS (seven women, 20 men; age range, 19,35 years; median age: 26.6 years). In this investigation, we excluded patients who exhibited complications such as acute subdural hematoma, acute epidural hematoma, intracerebral hematoma, or brain contusion. We examined the neuropsychological tests and correlated with findings from MRI/eZIS. Furthermore, we evaluated the degree of ventricular enlargement in the bifrontal cerebroventricular index (CVI). Patients were divided into two groups: the enlargement group (bifrontal CVI > 35%, 12 patients) and the non-enlargement group (bifrontal CVI < 35%, 15 patients). All of the patients showed cognitive deficits as observed from the neuropsycological test results. Fifteen out of 27 patients by MRI T1/T2 weighted images and fluid attenuated inversion recovery (FLAIR), 22 out of 27 patients by MRI T2* weighted images and 24 out of 27 patients by eZIS showed abnormal findings. In MRI T2* weighted imaging, the white matter from the frontal lobe, corpus callosum, and brainstem showed abnormal findings. With eZIS, 22 patients (81.5%) showed blood flow degradation in the frontal lobe, and 12 patients (44.4%) in cingulate gyrus. In the enlargement group, Functional Independence Measure, Mini-Mental State Examination, Verbal IQ (VIQ)/Full Scale IQ (FIQ), Trail Making Test-B (TMT-B), and Non-paired of Miyake Paired Test were significantly lower. Amongst 12 patients without ventricular enlargement who had no abnormal findings in MRI T1/T2 weighted images and FLAIR, abnormal findings were detectable in seven patients with MRI T2* weighted imaging and to 10 patients with eZIS. Results of the MRI examination alone cannot fully explain DAI frontal lobe dysfunction. However, addition of the eZIS-assisted analysis derived from the single photon emission computed tomography (SPECT) data enabled us to understand regions where blood flow was decreased, i.e., where neuronal functions conceivably might be reduced. [source] Reader variability in the use of diagnostic terms to describe white matter lesions seen on cranial scans of severely premature infants: The ELGAN studyJOURNAL OF CLINICAL ULTRASOUND, Issue 8 2010Sjirk Westra MD Abstract Purpose To evaluate reader variability of white matter lesions seen on cranial sonographic scans of extreme low gestational age neonates (ELGANs). Methods In 1,452 ELGANs, cranial sonographic scans were obtained in the first and second postnatal weeks, and between the third postnatal week and term. All sets of scans were read independently by two sonologists. We reviewed the use of four diagnostic labels: early periventricular leucomalacia, cystic periventricular leucomalacia, periventricular hemorrhagic infarction (PVHI), and other white matter diagnosis, by 16 sonologists at 14 institutions. We evaluated the association of these labels with location and laterality of hyperechoic and hypoechoic lesions, location of intraventricular hemorrhage, and characteristics of ventricular enlargement. Results Experienced sonologists differed substantially in their application of the diagnostic labels. Three readers applied early periventricular leucomalacia to more than one fourth of all the scans they read, whereas eight applied this label to ,5% of scans. Five applied PVHI to ,10% of scans, while three applied this label to ,5% of scans. More than one third of scans labeled cystic periventricular leucomalacia had unilateral hypoechoic lesions. White matter abnormalities in PVHI were more extensive than in periventricular leucomalacia and were more anteriorly located. Hypoechoic lesions on late scans tended to be in the same locations, regardless of the diagnostic label applied. Conclusions Experienced sonologists differ considerably in their tendency to apply diagnostic labels for white matter lesions. This is due to lack of universally agreed-upon definitions. We recommend reducing this variability to improve the validity of large multicenter studies. © 2010 Wiley Periodicals, Inc. J Clin Ultrasound 38:409,419, 2010 [source] R6/2 neurons with intranuclear inclusions survive for prolonged periods in the brains of chimeric miceTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2007Anton Reiner Abstract The R6/2 mouse possesses mutant exon 1 of human Hdh, and R6/2 mice with 150 CAG repeats show neurological abnormalities by 10 weeks and die by 15 weeks. Few brain abnormalities, however, are evident at death, other than widespread ubiquitinated neuronal intranuclear inclusions (NIIs). We constructed R6/2t+/t, , wildtype (WT) chimeric mice to prolong survival of R6/2 cells and determine if neuronal death and/or neuronal injury become evident with longer survival. ROSA26 mice (which bear a lacZ transgene) were used as WT to distinguish between R6/2 and WT neurons. Chimeric mice consisting partly of R6/2 cells lived longer than pure R6/2 mice (up to 10 months), with the survival proportional to the R6/2 contribution. Genotypically R6/2 cells formed NIIs in the chimeras, and these NIIs grew only slightly larger than in 12-week pure R6/2 mice, even after 10 months. Additionally, neuropil aggregates formed near R6/2 neurons in chimeric mice older than 15 weeks. Thus, R6/2 neurons could survive well beyond 15 weeks in chimeras. Moreover, little neuronal degeneration was evident in either cortex or striatum by routine histological stains. Nonetheless, striatal shrinkage and ventricular enlargement occurred, and striatal projection neuron markers characteristically reduced in Huntington's disease were diminished. Consistent with such abnormalities, cortex and striatum in chimeras showed increased astrocytic glial fibrillary acidic protein. These results suggest that while cortical and striatal neurons can survive nearly a year with nuclear and extranuclear aggregates of mutant huntingtin, such lengthy survival does reveal cortical and striatal abnormality brought on by the truncated mutant protein. J. Comp. Neurol. 505:603,629, 2007. © 2007 Wiley-Liss, Inc. [source] Chronic Hydrocephalus in AdultsBRAIN PATHOLOGY, Issue 3 2004Richard J Edwards Chronic hydrocephalus is a complex condition, the incidence of which increases with increasing age. It is characterised by the presence of ventricular enlargement in the absence of significant elevations of intracranial pressure. The clinical syndrome may develop either as a result of decompensation of a "compensated" congenital hydrocephalus, or it may arise de novo in adult life secondary to a known acquired disturbance of normal CSF dynamics. The latter may be due to late onset acqueductal stenosis or disruption of normal CSF absorptive pathways following subarachnoid hemorrhage or meningitis ("secondary" normal pressure hydrocephalus (NPH)). In some cases the cause of the hydrocephalus remains obscure ("idiopathic" NPH). In all forms of chronic hydrocephalus the clinical course of the disease is heavily influenced by changes in the brain associated with aging, in particular cerebrovascular disease. Recent research has challenged previously held tenets regarding the CSF circulatory system and this in turn has led to a radical rethinking of the pathophysiological basis of chronic hydrocephalus. [source] Transcatheter closure of coronary artery fistulae using the Amplatzer duct occluderCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2006Sarina K. Behera MD Abstract Objective: The aim of this study is to report our experience using the Amplatzer Duct Occluder (ADO) for occlusion of significant coronary artery fistulae (CAF). Background: Transcatheter closure of CAF with coils is well described. Use of newer devices may offer advantages such as improved control of device placement, use of a single instead of multiple devices, and high rates of occlusion. Methods: A retrospective review of all patients catheterized for CAF from July 2002 through August 2005 was performed. Results: Thirteen patients with CAF underwent cardiac catheterization, of which a total of 6 patients had ADO placement in CAF (age, 21 days to 56 years; median age, 4.3 years and weight, 3.8 kg to 74.6 kg; median weight, 13.3 kg). An arteriovenous wire loop was used to advance a long sheath antegrade to deploy the ADO in the CAF. Immediate and short-term outcomes (follow-up, 3 months to 14 months; median follow-up, 8.5 months) demonstrated complete CAF occlusion in 5 patients and minimal residual shunt in 1 patient (who had resolution of right atrial and right ventricular enlargement). On follow-up clinical evaluation, all 6 patients had absence of fistula-related murmurs, and 2 previously symptomatic patients had resolution of congestive heart failure symptoms. Early complications included transient palpitations and atrial arrhythmia in the 2 oldest patients (52 and 56 years old). Conclusions: Use of the ADO is applicable for transcatheter closure of significant CAF. Advantages of using the ADO include the antegrade approach, use of a single device, and effective CAF occlusion. © 2006 Wiley-Liss, Inc. [source] | ||||||||||