Assessment of Myocardial Function and Injury by Echocardiography and Cardiac Biomarkers in African Children With Severe Plasmodium falciparum Malaria

Objectives: Perturbed hemodynamic function complicates severe malaria. The Fluid Expansion as Supportive Therapy trial demonstrated that fluid resuscitation, involving children with severe malaria, was associated with increased mortality, primarily due to cardiovascular collapse, suggesting that myocardial dysfunction may have a role. The aim of this study was to characterize cardiac function in children with severe malaria. Design: A prospective observational study with clinical, laboratory, and echocardiographic data collected at presentation (T0) and 24 hours (T1) in children with severe malaria. Cardiac index and ejection fraction were calculated at T0 and T1. Cardiac troponin I and brain natriuretic peptide were measured at T0. We compared clinical and echocardiographic variables in children with and without severe malarial anemia (hemoglobin 0.1 ng/mL) in n equals to 50, (48%), and median brain natriuretic peptide was within normal range (69.1 pg/mL; interquartile range, 48.4–90.8). At T0, median Cardiac index was significantly higher in the severe malarial anemia versus nonsevere malarial anemia group (6.89 vs 5.28 L/min/m2) (p = 0.001), which normalized in both groups at T1 (5.60 vs 5.13 L/min/m2) (p = 0.452). Cardiac index negatively correlated with hemoglobin, r equals to –0.380 (p 96%) of children with severe malaria have preserved myocardial systolic function. Although there is evidence for myocardial injury (elevated cardiac troponin I), this does not correlate with cardiac dysfunction. This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (http://ift.tt/2gIrZ5Y). The FEAST trial was supported by a grant (G0801439) from the Medical Research Council (MRC), United Kingdom provided through the (MRC) Department for International Development concordat, Centres for Global Health Research, Imperial College Wellcome Trust Center for Global Health, United Kingdom (100693/Z/12/Z). Dr. Kotlyar received funding from London School of Hygiene and Tropical Medicine (research support grant), and he received support for article research from Wellcome Trust/COAF. Dr. Maitland received support for article research from Wellcome Trust/COAF and Research Councils United Kingdom. Dr. Moore disclosed that this project was supported by a loan of ultrasound equipment from Philips Healthcare to Yale University for collection of echo data, and his institution received funding from Philips Healthcare. The remaining authors have disclosed that they do not have any potential conflicts of interest. For information regarding this article, E-mail: k.maitland@imperial.ac.uk ©2017The Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies

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