Ventricular Dilatation (ventricular + dilatation)

Distribution by Scientific Domains


Selected Abstracts


Magnetic Resonance Microscopy Defines Ethanol-Induced Brain Abnormalities in Prenatal Mice: Effects of Acute Insult on Gestational Day 7

ALCOHOLISM, Issue 1 2010
Elizabeth A. Godin
Background:, This magnetic resonance microscopy (MRM)-based report is the second in a series designed to illustrate the spectrum of craniofacial and central nervous system (CNS) dysmorphia resulting from single- and multiple-day maternal ethanol treatment. The study described in this report examined the consequences of ethanol exposure on gestational day (GD) 7 in mice, a time in development when gastrulation and neural plate development begins; corresponding to the mid- to late third week postfertilization in humans. Acute GD 7 ethanol exposure in mice has previously been shown to result in CNS defects consistent with holoprosencephaly (HPE) and craniofacial anomalies typical of those in Fetal Alcohol Syndrome (FAS). MRM has facilitated further definition of the range of GD 7 ethanol-induced defects. Methods:, C57Bl/6J female mice were intraperitoneally (i.p.) administered vehicle or 2 injections of 2.9 g/kg ethanol on day 7 of pregnancy. Stage-matched control and ethanol-exposed GD 17 fetuses selected for imaging were immersion fixed in a Bouins/Prohance solution. MRM was conducted at either 7.0 Tesla (T) or 9.4 T. Resulting 29 ,m isotropic spatial resolution scans were segmented and reconstructed to provide 3D images. Linear and volumetric brain measures, as well as morphological features, were compared for control and ethanol-exposed fetuses. Following MRM, selected specimens were processed for routine histology and light microscopic examination. Results:, Gestational day 7 ethanol exposure resulted in a spectrum of median facial and forebrain deficiencies, as expected. This range of abnormalities falls within the HPE spectrum; a spectrum for which facial dysmorphology is consistent with and typically is predictive of that of the forebrain. In addition, other defects including median facial cleft, cleft palate, micrognathia, pituitary agenesis, and third ventricular dilatation were identified. MRM analyses also revealed cerebral cortical dysplasia/heterotopias resulting from this acute, early insult and facilitated a subsequent focused histological investigation of these defects. Conclusions:, Individual MRM scans and 3D reconstructions of fetal mouse brains have facilitated demonstration of a broad range of GD 7 ethanol-induced morphological abnormality. These results, including the discovery of cerebral cortical heterotopias, elucidate the teratogenic potential of ethanol insult during the third week of human prenatal development. [source]


Original Article: Left ventricular geometry and cardiovascular mortality based on haemodialysis patient autopsy analyses

NEPHROLOGY, Issue 5 2010
IMARI MIMURA
ABSTRACT Aim: In end-stage renal disease (ESRD) patients, left ventricular hypertrophy (LVH) is common and a risk for cardiovascular events. LVH is geometrically classified into two major groups, concentric and eccentric, and accumulating evidence suggests eccentric LVH has a more negative effect than concentric LVH on ESRD outcome. However, there have been very few studies on the cardiac findings from ESRD patient autopsy in which the relationship between LVH geometry and mortality was analyzed. Methods: An observational study was performed with the autopsy findings in 30 haemodialysis patient cases between 2001 and 2006 at Mitsui Memorial Hospital, Tokyo. Between those who died of a cardiovascular cause and those who died of non-cardiovascular causes, we compared the heart/bodyweight ratio, left ventricular dilatation, and the extent of fibrosis of the left ventricle. Results: Heart/bodyweight ratio was significantly higher (P < 0.0001) in the cardiovascular mortality group (n = 11, 11.7 ± 2.5 g/kg) compared to the non-cardiac cause of death group (n = 19, 8.05 ± 0.7 g/kg). The dilatation of the left ventricle was significantly more frequent in the cardiovascular than the non-cardiac cause of death group (P = 0.016). Additionally, the fibrotic area of left ventricular cross-section was larger in the cardiovascular (1.63 ± 1.6%) than the non-cardiac group (0.83 ± 1.7%, P = 0.04). Conclusion: This autopsy study indicates that eccentric LVH in haemodialysis patients is closely associated with cardiovascular mortality. LVH geometry, as well as LVH severity, is worthy of consideration as a clinical predictor for cardiovascular mortality. [source]


Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2002
RAINER GRADAUS
GRADAUS, R., et al.: Effect of Ventricular Fibrillation Duration on the Defibrillation Threshold in Humans. Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 ± 11 years, 19 coronary artery disease, NYHA 2.2 ± 0.4, left ventricular ejection fraction 0.42 ± 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 ± 3.6 J after 10.3 ± 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with , 8 J. In these patients, the mean defibrillation threshold was 4.0 ± 2.1 J after 1.4 ± 0.3 seconds compared to 9.5 ± 3.1 J after 10.2 ± 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs. [source]


Late cardiotoxicity after bolus versus infusion anthracycline therapy for childhood cancers

PEDIATRIC BLOOD & CANCER, Issue 6 2003
Monesha Gupta MBBS
Abstract Objective To compare the long-term myocardial function of patients who had been treated with infusion anthracycline therapy (administered continuously over >24 hr, IG) versus bolus therapy (administered over <30 min, BG). Methods We selected 25 patients (BG) and 19 patients (IG) who had three or more years of disease free survival. We evaluated the echocardiograms for left ventricular shortening fraction (SF) obtained at baseline, within one year after the end of therapy (early follow-up), and on long-term follow-up. Results The mean anthracycline dose in the BG was 385 mg/m2 and in the IG was 345 mg/m2 (P,=,0.07). During therapy, one patient in BG and none in IG developed diminished SF. During early follow-up, five of the 22 patients in BG and one of the 17 patients in IG developed diminished SF (P,=,0.2). Of these five patients with diminished SF, three patients in BG and none in IG continued to have abnormally low SF long-term. At mean of 7 years, five of the 25 patients in BG and two of the 19 in IG had diminished SF on (P,=,0.7). Late left ventricular dilatation was seen in 8% in BG and 5% in IG (P,=,1.0). Conclusions At mean of 7 years after end of therapy, diminished cardiac function was seen in 20% of the patient who had received bolus anthracycline compared to 11% of patients who had received it via infusion. This difference did not prove to be statistically significant. Med Pediatr Oncol 2003;40:343,347. © 2003 Wiley-Liss, Inc. [source]


Echocardiographic changes and risk factors for left ventricular hypertrophy in children and adolescents after renal transplantation

PEDIATRIC TRANSPLANTATION, Issue 3 2004
Amr A. El-Husseini
Abstract:, Long-term consequences of cardiac alteration in children with chronic renal failure and after renal transplantation are largely unknown. In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular hypertrophy (LVH) or left ventricular dilatation. The correction of uremic state by renal transplantation leads to normalization of left ventricular contractility, regression of LVH and improvement of cavity volume and so dialysis patients with uremic cardiomyopathy would benefit from renal transplantation. We studied 73 patients, aged 17 yr or less, who underwent renal transplantation in our center. This cross-sectional study was performed 4.6 yr (median) after transplantation. Of the total, 48 were males and 25 were females. Transthoracic echocardiographic examination was performed for all cases. The effects of clinical, demographic, biochemical and therapeutic data on echocardiographic parameters were assessed. Multivariate analysis was used to assess the relation between the risk factors and the left ventricular muscle mass index. The most common echocardiographic abnormalities were the LVH (47.9%), left atrial enlargement (31.5%) and left ventricular dilatation and systolic dysfunction (13.7% for each). The pretransplant dialysis, arteriovenous fistula, acute rejection, cumulative steroid dose per square meter surface area, post-transplant hypertension, anemia and graft dysfunction were significant risk factors for LVH by univariate analysis. The significant factors by multivariate analysis were pretransplant dialysis, post-transplant hypertension and anemia. From this study we may conclude that LVH is a common problem among renal transplant children and adolescents. Early transplantation, control of hypertension and correction of anemia may be beneficial regarding left ventricular function and structure. [source]


Brain involvement in muscular dystrophies with defective dystroglycan glycosylation,

ANNALS OF NEUROLOGY, Issue 5 2008
Emma Clement MBChB
Objective To assess the range and severity of brain involvement, as assessed by magnetic resonance imaging, in 27 patients with mutations in POMT1 (4), POMT2 (9), POMGnT1 (7), Fukutin (4), or LARGE (3), responsible for muscular dystrophies with abnormal glycosylation of dystroglycan (dystroglycanopathies). Methods Blinded review of magnetic resonance imaging brain scans from 27 patients with mutations in 1 of these 5 genes. Results Brain magnetic resonance images were normal in 3 of 27 patients; in another 5, only nonspecific abnormalities (ventricular dilatation, periventricular white matter abnormalities, or both) were seen. The remaining 19 patients had a spectrum of structural defects, ranging from complete lissencephaly in patients with Walker,Warburg syndrome to isolated cerebellar involvement. Cerebellar cysts and/or dysplasia and hypoplasia were the predominant features in four patients. Polymicrogyria (11/27) was more severe in the frontoparietal regions in 6, and had an occipitofrontal gradient in 2. Pontine clefts, with an unusual appearance to the corticospinal tracts, were seen in five patients with a muscle-eye-brain,like phenotype, three patients with POMGnT1, one with LARGE, and one with POMT2 mutations. Prominent cerebellar cysts were always seen with POMGnT1 mutations, but rarely seen in POMT1 and POMT2. Brainstem and pontine abnormalities were common in patients with POMT2, POMGnT1, and LARGE mutations. Interpretation Our results expand the spectrum of brain involvement associated with mutations in LARGE, POMGnT1, POMT1, and POMT2. Pontine clefts were visible in some dystroglycanopathy patients. Infratentorial structures were often affected in isolation, highlighting their susceptibility to involvement in these conditions. Ann Neurol 2008;64:573,582 [source]


Ultrafiltration and Dry Weight,What Are the Cardiovascular Effects?

ARTIFICIAL ORGANS, Issue 3 2003
Article first published online: 2 APR 200, Bernd G. Stegmayr
Abstract: Long-term prognosis in dialysis is poor compared to that in healthy control persons. A worsening of the prognosis is noted especially for patients who at initiation of dialysis have congestive heart failure, ischemic heart disease, or left ventricular dysfunction or hypertrophy. This is the main reason that cardiovascular causes are the most common for morbidity in these patients. The weight obtained when normal urine output is present is the dry weight. With reduced ability to excrete the volume by the kidneys in end-stage renal disease (ESRD), the body will retain water and the patient will gain weight. This extra weight is due to volume overload. While volume overload may induce a rise in blood pressure, if the heart is in acceptable condition, a fast removal of fluid by ultrafiltration (UF) during dialysis may instead cause hypotension. Ultrafiltration failure in peritoneal dialysis (PD) patients may lead to successive water retention and overhydration with subsequent cardiac failure, while volume overload may occur over a few days in hemodialysis (HD) patients. Anemia or even too-high hematocrit may impair cardiac function further and worsen conditions caused by wrong dry weight. Thus, during long-term and sustained volume overload, left ventricular (LV) hypertrophy will occur in an eccentric manner. A sustained overload then may lead to cell death and LV dilatation and, eventually, systolic dysfunction. Once a severe left ventricular dilatation has developed, the blood pressure may decrease during volume overload. A worsened prognosis is seen if malnutrition and low albumin levels are present. Volume overload necessitates ultrafiltration to achieve dry weight. Thereby, volume contraction contributes to exaggerated stimulation of or response to activation of the RAS and alpha-adrenergic sympathetic systems. If ultrafiltration goes beyond these compensatory mechanisms, hypotension will occur and increase the risk for hypoperfusion of vital organs. Such episodes may cause cardiac morbidity, aspiration pneumonia, vascular access closure, or neurological complications (seizures, cerebral infarction), besides a more rapid lowering of residual renal function. Preventive measures are, first, finding the right dry weight; second, minimizing interdialytic weight gain; third, optimizing the target for hemoglobin (110,120 g/l); fourth, lowering dialysate calcium (1.25 mmol/l); and fifth, eventually using higher dialysate potassium if long dialyses are performed. [source]


Insights into the Pathogenesis of Hydrocephalus from Transgenic and Experimental Animal Models

BRAIN PATHOLOGY, Issue 3 2004
Leslie Crews
Hydrocephalus is a progressive brain disorder characterized by abnormalities in the flow of cerebrospinal fluid (CSF) and ventricular dilatation that leads to cerebral atrophy, and if left untreated, can be fatal. Genetic mutations, congenital malformations, infectious diseases, intracerebral hemorrhages and tumors are common conditions resulting in hydrocephalus. Although the causes of obstructive hydrocephalus are better understood, the mechanisms resulting in chronic, progressive communicating congenital and acquired hydrocephalus are less well understood. In this regard, recent studies in transgenic (tg) mice suggest that increased expression of cytokines such as TGF-,1 might play an important role by disrupting the vascular extracellular matrix (ECM) remodeling, promoting hemorrhages, and altering the reabsorption of CSF. In this context, the main objective of this manuscript is to provide an overview on the cellular and molecular mechanisms of hydrocephalus based on studies derived from tg and experimental animal models. [source]


Ultrasound measurements of the lateral ventricles in neonates: why, how and when?

ACTA PAEDIATRICA, Issue 9 2010
A systematic review
Abstract Germinal matrix-intraventricular haemorrhage and subsequent post-haemorrhagic ventricular dilatation (PHVD) are frequently encountered complications in preterm neonates. As progressive dilatation of the lateral ventricles may be associated with elevated intracranial pressure, ultrasound measurements of ventricular size play a major role in the evaluation of neonates at risk of ventricular dilatation as well as in assessing the effect of intervention for PHVD. A systematic search was carried out in Medline and Embase to identify neonatal and foetal ultrasound studies on lateral ventricular size. This review presents an overview of the available data concerning neonatal reference values for lateral ventricular size, the influence of gender, ventricular asymmetry and the effect of the mode of delivery on the phenomenon of ventricular reopening following birth. Conclusion:, Serial cranial ultrasound measurements of the lateral ventricles play a key role in the early recognition and therapeutic evaluation of post-haemorrhagic ventricular dilation and can be of prognostic value in neonates with ventricular dilatation. [source]


Cerebrospinal fluid drainage in posthaemorrhagic ventricular dilatation leads to improvement in amplitude-integrated electroencephalographic activity

ACTA PAEDIATRICA, Issue 6 2009
Monika Olischar
Abstract Aim: Progressive posthaemorrhagic ventricular dilatation (PHVD) may induce abnormal amplitude-integrated electroencephalographic (aEEG) activity prior to clinical deterioration or significant cerebral ultrasound changes. These abnormalities might be ameliorated with cerebrospinal fluid (CSF) drainage. The aims of this study were to investigate the occurrence of aEEG-abnormalities with progressive PHVD in relation to clinical and cerebral ultrasound changes and to evaluate whether CSF drainage results in aEEG improvement. Methods: aEEG and cerebral ultrasound scans were performed in 12 infants with PHVD, before and after CSF drainage, until normalization of aEEG occurred. Results: aEEG was abnormal with progressive PHVD in all patients. Concurrently, 60% of the patients were clinically stable without deterioration in ultrasonographic cerebral abnormalities. Post drainage, continuous pattern was restored in all but one patient, whereas the frequency of discontinuous pattern decreased in nine patients and burst-suppression pattern decreased in all but one patient. Low-voltage pattern was only observed in one patient who suffered severe grade IV IVH and died one week after EVD placement. Sleep-wake cycling matured in 75%. Conclusion: These findings demonstrate the impact of CSF drainage on compromised aEEG-activity associated with PHVD. aEEG changes indicative of impaired cerebral function were apparent before clinical deterioration or major ultrasound changes. These changes were reversible with CSF drainage. aEEG should therefore be used in addition to clinical observation and ultrasound when monitoring PHVD. [source]


Brain abnormalities in extremely low gestational age infants: a Swedish population based MRI study

ACTA PAEDIATRICA, Issue 7 2007
Sandra Horsch
Abstract Aims: Brain abnormalities are common in preterm infants and can be reliably detected by magnetic resonance (MR) imaging at term equivalent age. The aim of the present study was to acquire population based data on brain abnormalities in extremely low gestational age (ELGA) infants from the Stockholm region and to correlate the MR findings to perinatal data, in order to identify risk factors. Methods: All infants with gestational age <27 weeks, born in the Stockholm region between January 2004 and August 2005, were scanned on a 1.5 T MR system at term equivalent age. Images were analysed using a previously established scoring system for grey and white matter abnormalities. Results: No or only mild white matter abnormalities were observed in 82% and moderate to severe white matter abnormalities in 18% of infants. The Clinical Risk Index for Babies (CRIB II) score, use of inotropes, the presence of high-grade intraventricular haemorrhages and posthaemorrhagic ventricular dilatation were associated with white matter abnormalities. Conclusion: The incidence of moderate to severe white matter abnormalities in a population-based cohort of ELGA infants from the Stockholm region was 18%. To examine the clinical relevance of these promising results, neurodevelopmental follow up at 30 month corrected age, is ongoing. [source]


Amiodarone for Atrial Fibrillation Following Cardiac Surgery: Development of Clinical Practice Guidelines at a University Hospital

CLINICAL CARDIOLOGY, Issue 1 2008
Pharm D., Ujjaini Khanderia M.S.
Abstract Atrial fibrillation (AF) usually develops within the first 72 h following cardiac surgery, and is often self-limiting. Within 48 h of acute onset of symptoms, approximately 50% of patients spontaneously convert to normal sinus rhythm. Thus, the relative risks and benefits of therapy must be carefully considered. The etiology of AF following cardiac surgery is similar to that in non-surgical patients except that pericardial inflammation and increased adrenergic tone play an increasingly important role. Further, AF after surgery may be associated with transient risk factors that resolve as the patient moves out from surgery, and the condition is less likely to recur compared to AF arising in other circumstances. Immediate heart rate control is important in preventing ischemia, tachycardia-induced cardiomyopathy, and left ventricular dilatation. At our institution, amiodarone is frequently used as a first-line drug for treating AF after cardiac surgery. Inconsistent prescribing practices, variable dosage regimens, and a lack of consensus regarding the appropriate use of amiodarone prompted the need for developing practice guidelines. Multidisciplinary collaboration between the departments of cardiac surgery, pharmacy, and anesthesiology led to the development of a protocol for postoperative AF. We review the clinical evidence from published trials and discuss our guidelines, defining amiodarone use for AF in the cardiac surgery setting. Copyright © 2007 Wiley Periodicals, Inc. [source]


The Resting Electrocardiogram in the Management of Patients with Congestive Heart Failure: Established Applications and New Insights

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2007
JOHN E. MADIAS M.D.
The resting electrocardiogram (ECG) furnishes essential information for the diagnosis, management, and prognostic evaluation of patients with congestive heart failure (CHF). Almost any ECG diagnostic entity may turn out to be useful in the care of patients with CHF, revealing the non-specificity of the ECG in CHF. Nevertheless a number of CHF/ECG correlates have been proposed and found to be indispensable in clinical practice; they include, among others, the ECG diagnoses of myocardial ischemia and infarction, atrial fibrillation, left ventricular hypertrophy/dilatation, left bundle branch block and intraventricular conduction delays, left atrial abnormality, and QT-interval prolongation. In addition to the above well-known applications of the ECG for patients with CHF, a recently described association of peripheral edema (PERED), sometimes even imperceptible by physical examination, with attenuated ECG potentials, could extend further the diagnostic range of the clinician. These ECG voltage attenuations are of extracardiac mechanism, and impact the amplitude of QRS complexes, P-waves, and T-waves, occasionally resulting also in shortening of the QRS complex and QT interval duration. PERED alleviation, in response to therapy of CHF, reverses all above alterations. These fresh diagnostic insights have potential application in the follow-up of patients with CHF, and in their selection for implantation of cardioverter/defibrillator and/or cardiac resynchronization systems. If sought, PERED-induced ECG changes are abundantly present in the hospital and clinic environments; if their detection and monitoring are incorporated in the clinician's "routine," considerable improvements in the care of patients with CHF may be realized. [source]