Entity

Time filter

Source Type

Toronto, Canada

Sivarajan V.B.,Labatt Family Heart Center | Sivarajan V.B.,University of Toronto | Bohn D.,University of Toronto
Pediatric Critical Care Medicine | Year: 2011

Background: Continuous monitoring of various clinical parameters of hemodynamic and respiratory status in pediatric critical care medicine has become routine. The evidence supporting these practices is examined in this review. Methodology: A search of MEDLINE, EMBASE, PubMed, and the Cochrane Database was conducted to find controlled trials of heart rate, electrocardiography, noninvasive and invasive blood pressure, atrial pressure, end-tidal carbon dioxide, and pulse oximetry monitoring. Adult and pediatric data were considered. Guidelines published by the Society for Critical Care Medicine, the American Heart Association, the American Academy of Pediatrics, and the International Liaison Committee on Resuscitation were reviewed, including further review of references cited. Results and Conclusions: Use of heart rate, electrocardiography, noninvasive and arterial blood pressure, atrial pressure, pulse oximetry, and end-tidal carbon dioxide monitoring in the pediatric critical care unit is commonplace; this practice, however, is not supported by well-controlled clinical trials. Despite the majority of literature being case series, expert opinion would suggest that use of routine pulse oximetry and end-tidal carbon dioxide is the current standard of care. In addition, literature would suggest that invasive arterial monitoring is the current standard for monitoring in the setting of shock. The use of heart rate, electrocardiography. and atrial pressure monitoring is advantageous in specific clinical scenarios (postoperative cardiac surgery); however, the evidence for this is based on numerous case series only. Copyright © 2011 by the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. Source


El-Khuffash A.F.,Rotunda Hospital | Jain A.,Mount Sinai Hospital | Jain A.,University of Toronto | Weisz D.,Sunnybrook Health science Center | And 2 more authors.
Journal of Pediatrics | Year: 2014

Objective To compare differences in tissue Doppler imaging, global longitudinal strain (GLS), and cardiac troponin T (cTnT) between infants with low (<200 mL/kg/min) and high (>200 mL/kg/min) left ventricular (LV) output 1 hour after duct ligation and assess the impact of milrinone treatment on cardiac output and myocardial performance. Study design LV function was assessed preoperatively and 1 and 18 hours postoperatively. Infants were categorized into a low-output or a normal-output group based on the echocardiographic assessment of LV output at 1 hour. Results Thirty infants with a mean gestation of 25.3 weeks were enrolled. LV basal lateral S′, basal septal S′, and basal right ventricular S′ were lower in the low-output group (n = 19) at 1 hour postoperatively, with no significant difference in GLS (low-output -10.3% vs high-output -14.4%, P >.05) or cTnT between the groups. Patients in the low-output group were treated with milrinone, and by 18 hours LV performance recovered to levels comparable with the high output group. cTnT values increased at 18 hours in the whole cohort with no significant difference between the groups. Conclusion Tissue Doppler imaging and GLS provide novel insights and further characterization of myocardial performance immediately after patent ductus arteriosus ligation. A reduction in tissue Doppler-derived LV systolic velocity may further help in monitoring cardiac performance after patent ductus arteriosus ligation and for monitoring the effects of treatment. © 2014 Elsevier Inc. All rights reserved. Source


James A.,Rotunda Hospital | Corcoran J.D.,Rotunda Hospital | Mertens L.,Labatt Family Heart Center | Franklin O.,Our Ladys Childrens Hospital | And 2 more authors.
Journal of the American Society of Echocardiography | Year: 2015

Background: There is a paucity of data on left ventricular (LV) rotational physiology, twist, and torsional mechanics in preterm infants. The principal aims of the present study were to assess the feasibility and reproducibility of measuring LV rotation, twist, and torsion in preterm infants (<29 weeks' gestation) using two-dimensional speckle-tracking echocardiography and to examine the changes in those parameters over the first week after birth. Methods: This was a prospective observational study involving preterm infants <29 weeks' gestation. Echocardiographic evaluations were performed on days 1, 2, and 5 to 7 after delivery. LV basal and apical rotation, LV twist, LV twist rate (LVTR), and LV untwist rate (LVUTR) were measured from the basal and apical short-axis parasternal views and calculated using two-dimensional speckle-tracking echocardiography. Torsion was also calculated by normalizing LV twist to LV end-diastolic length. One-way repeated-measures analysis of variance was used to compare values across the three time points. Intra- and interobserver reproducibility were assessed using Bland-Altman analysis and the intraclass correlation coefficient. Results: Fifty-one infants with a mean ± SD gestational age of 26.8 ± 1.5 weeks and a mean birth weight of 945 ± 233 g were included. There was high intra- and interobserver reproducibility for basal and apical rotation, LV twist, and LV torsion, with intraclass correlation coefficients ranging from 0.78 to 0.96 (P < .001 for all). Intra- and interobserver intraclass correlation coefficients for LVTR and LVUTR ranged from 0.70 to 0.88 (P < .001 for all). Apical rotation remained constant over the first week of age in a positive counterclockwise fashion (11.8 ± 5.0° vs 12.1 ± 6.1° vs 11.7 ± 8.3°, P = .92). Basal rotation changed from counterclockwise on day 1 to clockwise on day 7 (median, 5.5° [interquartile range, -0.3° to 8.3° ] vs 4.0 [interquartile range, -4.7° to 7.2°] vs -4.5° [interquartile range, -5.8° to -2.3°], P <. 001), with resultant net increases in twist and torsion (P < .05). There was no change in LVTR (P = .60), but LVUTR increased across the same time period (P = .01). Conclusions: Assessment of twist, LVTR, and LVUTR is feasible in preterm infants, with acceptable reproducibility. There are increases in LV twist and torsion in addition to LVUTR, suggesting changes in LV mechanics during the first week of age. © 2015 American Society of Echocardiography. Source


Chinnock R.,Loma Linda University | Webber S.A.,University of Pittsburgh | Dipchand A.I.,Labatt Family Heart Center | Brown R.N.,University of Alabama at Birmingham | George J.F.,University of Alabama at Birmingham
American Journal of Transplantation | Year: 2012

The objective was to determine the incidence and hazard for posttransplant lymphoproliferative disease (PTLD) in a study of 3170 pediatric primary heart transplants between 1993 and 2009 at 35 institutions in the Pediatric Heart Transplant Study. 147 of 151 reported malignancy events were classified as PTLD. Overall freedom from PTLD was 98.5% at 1 year, 94% at 5 years and 90% at 10 years. Freedom from PTLD was lowest in children (ages 1 to < 10 years) versus infants (<1 year) and adolescents (10 to < 18 years) with children at highest risk for PTLD with a relative risk of 2.4 compared to infants and 1.7 compared to adolescents. Positive donor EBV status was a strong risk factor for PTLD in the seronegative recipient, but risk magnitude was dependent on recipient age at the time of transplantation. Nearly 25% of EBV seronegative recipients of EBV+ donors at ages 4-7 at transplantation developed some form of PTLD. The overall risk for PTLD declined in the most recent transplant era (2001-2009, p = 0.003). These findings indicate that EBV status and the age of the recipient at the time of transplantation are important variables in the development of PTLD in the pediatric heart transplant recipient. © Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons. Source


Zaidi S.H.E.,A+ Network | Zaidi S.H.E.,University of Toronto | Zaidi S.H.E.,Toronto General Research Institute | Huang Q.,Toronto General Research Institute | And 4 more authors.
Journal of the American College of Cardiology | Year: 2010

Objectives: The aim of this study was to examine the function of the bone morphogenic protein growth differentiation factor 5 (Gdf5) in a mouse model of myocardial infarction (MI). Background: The Gdf5 has been implicated in skeletal development, but a potential role in the heart had not been studied. Methods: The Gdf5-knockout (KO) and wild-type (WT) mice were subjected to permanent left anterior descending coronary artery (LAD) ligation. Cardiac pathology, function, gene expression levels, and signaling pathways downstream of Gdf5 were examined. Effects of recombinant Gdf5 (rGdf5) were tested in primary cardiac cell cultures. Results: The WT mice showed increased cardiac Gdf5 levels after MI, with increased expression in peri-infarct cardiomyocytes and myofibroblasts. At 1 and 7 days after MI, no differences were observed in ischemic or infarct areas between WT and Gdf5-KO mice. However, by 28 days after MI, Gdf5-KO mice exhibited increased infarct scar expansion and thinning with decreased arteriolar density compared with WT. The Gdf5-KO hearts also displayed increased left ventricular dilation, with decreased contractility after MI. At 4 days after MI, Gdf5-KO mice exhibited increased cardiomyocyte apoptosis and decreased expression of anti-apoptotic genes Bcl2 and Bcl-xL compared with WT. Unexpectedly, Gdf5-KO hearts displayed increased Smad 1/5/8 phosphorylation but decreased p38-mitogen-activated protein kinase (MAPK) phosphorylation versus WT. The latter was associated with increased collagen gene (Col1a1, Col3a1) expression and fibrosis. In cultures, rGdf5 induced p38-MAPK phosphorylation in cardiac fibroblasts and Smad-dependent increases in Bcl2 and Bcl-xL in cardiomyocytes. Conclusions: Increased expression of Gdf5 after MI limits infarct scar expansion in vivo. These effects might be mediated by Gdf5-induced p38-MAPK signaling in fibroblasts and Gdf5-driven Smad-dependent pro-survival signaling in cardiomyocytes. © 2010 American College of Cardiology Foundation. Source

Discover hidden collaborations