BackgroundSepsis, trauma, and burn injury acutely depress systolic and
diastolic cardiac function; data on long-term cardiac sequelae of pediatric
critical illness are sparse. This study evaluated long-term systolic and
diastolic function, myocardial fibrosis, and exercise tolerance in survivors
of severe pediatric burn injury.MethodsSubjects at least 5 years after severe burn (post-burn:PB) and
age-matched healthy controls (HC) underwent echocardiography to quantify
systolic function (ejection fraction[EF%]),
diastolic function (E/e′), and myocardial fibrosis (calibrated
integrated backscatter) of the left ventricle. Exercise tolerance was
quantified by oxygen consumption (VO2) and heart rate at rest and
peak exercise. Demographic information, clinical data, and biomarker
expression were used to predict long-term cardiac dysfunction and
fibrosis.FindingsSixty-five subjects (PB:40;HC:25) were evaluated. At study date, PB
subjects were 19±5 years, were at 12±4 years postburn, and
had burns over 59±19% of total body surface area, sustained
at 8±5 years of age. The PB group had lower EF%
(PB:52±9%;HC:61±6%; p=0.004),
E/e′ (PB:9.8±2.9;HC: 5.4±0.9;p<0.0001),
VO2peak (PB:37.9±12;HC: 46±8.32 ml/min/kg;
p=0.029), and peak heart rate
(PB:161±26;HC:182±13bpm;p=0.007). The PB group had
moderate (28%) or severe (15%) systolic dysfunction,
moderate (50%) or severe diastolic dysfunction (21%), and
myocardial fibrosis (18%). Biomarkers and clinical parameters
predicted myocardial fibrosis, systolic dysfunction, and diastolic
dysfunction.InterpretationSevere pediatric burn injury may have lasting impact on cardiac
function into young adulthood and is associated with myocardial fibrosis and
reduced exercise tolerance. Given the strong predictive value of systolic
and diastolic dysfunction, these patients might be at increased risk for
early heart failure, associated morbidity, and mortality.FundingConflicts of Interest and Sources of Funding: The authors do not have
any conflicts of interest to declare. This work was supported by NIH (P50
GM060338, R01 GM056687, R01 HD049471, R01 GM112936, R01-GM56687 and T32
GM008256), NIDILRR (H133A120091, 90DP00430100), Shriners Hospitals for
Children (84080, 79141, 79135, 71009, 80100, 71008, 87300 and 71000), FAER
(MRTG CON14876), and the Department of Defense (W81XWH-14-2-0162 and
W81XWH1420162). It was also made possible with the support of UTMB’s
Institute for Translational Sciences, supported in part by a Clinical and
Translational Science Award (UL1TR000071) from the National Center for
Advancing Translational Sciences (NIH).