Assessment of myocardial function and injury by echocardiography and cardiac biomarkers in African children with severe Plasmodium falciparum malaria
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Author(s)
Type
Journal Article
Abstract
Objective: Perturbed hemodynamic function complicates severe malaria. The FEAST 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 (CI) and Ejection Fraction (EF) were calculated at T0 and T1. Cardiac Troponin I (cTnI) and Brain-Naturetic-Peptide (BNP) were measured at T0. We compared clinical and echocardiographic parameters in children with and without severe anemia [Hb < 5mg/dl] (SMA) at T0 and T1.
Setting: Mbale Regional Referral Hospital.
Patients: Children aged 3 months–12 years with severe falciparum malaria.
Interventions: usual care
Measurements and Main Results: We enrolled 104 children, median age 23.3 months, including 61 children with SMA. cTnI levels were elevated (>0.1ng/ml) in n=50, (48%); and median BNP was within normal range (69.1pg/ml, IQR 48.4-90.8). At T0, median CI was significantly higher in the SMA vs. non-SMA 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). CI negatively correlated with hemoglobin, r = -0.380 (p<0.001). Four patients (3.8%) had evidence of depressed cardiac systolic function (EF <45%). Overall, 6 children died, none developed pulmonary oedema, biventricular failure or required diuretic treatment.
Conclusions: Elevation of CI, due to increased stroke volume, in severe malaria is a physiological response to circulatory compromise and correlates with anemia. Following whole blood transfusion and antimalarial therapy, CI in SMA returns to normal. The majority (>96%) of children with severe malaria have preserved myocardial systolic function. While there is evidence for myocardial injury (elevated cTnI), this does not correlate with cardiac dysfunction.
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 (CI) and Ejection Fraction (EF) were calculated at T0 and T1. Cardiac Troponin I (cTnI) and Brain-Naturetic-Peptide (BNP) were measured at T0. We compared clinical and echocardiographic parameters in children with and without severe anemia [Hb < 5mg/dl] (SMA) at T0 and T1.
Setting: Mbale Regional Referral Hospital.
Patients: Children aged 3 months–12 years with severe falciparum malaria.
Interventions: usual care
Measurements and Main Results: We enrolled 104 children, median age 23.3 months, including 61 children with SMA. cTnI levels were elevated (>0.1ng/ml) in n=50, (48%); and median BNP was within normal range (69.1pg/ml, IQR 48.4-90.8). At T0, median CI was significantly higher in the SMA vs. non-SMA 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). CI negatively correlated with hemoglobin, r = -0.380 (p<0.001). Four patients (3.8%) had evidence of depressed cardiac systolic function (EF <45%). Overall, 6 children died, none developed pulmonary oedema, biventricular failure or required diuretic treatment.
Conclusions: Elevation of CI, due to increased stroke volume, in severe malaria is a physiological response to circulatory compromise and correlates with anemia. Following whole blood transfusion and antimalarial therapy, CI in SMA returns to normal. The majority (>96%) of children with severe malaria have preserved myocardial systolic function. While there is evidence for myocardial injury (elevated cTnI), this does not correlate with cardiac dysfunction.
Date Issued
2018-03-01
Date Acceptance
2017-10-10
Citation
Pediatric Critical Care Medicine, 2018, 19 (3), pp.179-185
ISSN
1529-7535
Publisher
Lippincott, Williams & Wilkins
Start Page
179
End Page
185
Journal / Book Title
Pediatric Critical Care Medicine
Volume
19
Issue
3
Copyright Statement
Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies. 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.
License URL
Sponsor
Medical Research Council (MRC)
Wellcome Trust
Grant Number
G0801439
100693/Z/12/Z
Subjects
1110 Nursing
1114 Paediatrics And Reproductive Medicine
Pediatrics
Publication Status
Published
Date Publish Online
2017-12-04