Defining Body Mass Index Using Weight and Length for Gestational Age in the Growth Assessment of Preterm Infants at Birth.

OBJECTIVE: The objectives of this study were to describe (1) body mass indexes (BMIs) using weight and length for gestational age (GA) classifications, and (2) the additional information BMI, as a measure of body proportionality, provides for preterm infant growth assessment and care plans at birth. STUDY DESIGN: Birth weight, length, and BMI of 188,646 preterm infants (24-36 weeks gestation) admitted to U.S. neonatal intensive care units (Pediatrix Clinical Data Warehouse, 2013-2018) were classified (Olsen curves) as small, appropriate, or large for GA (SGA < 10th, AGA 10-90th, LGA > 90th percentile for GA, respectively). The distribution for the 27 weight-length-BMI combinations was described. RESULTS: At birth, most infants were appropriate for weight (80.0%), length (82.2%), head circumference (82.9%), and BMI (79.9%) for GA. Birth weight for GA identified approximately 20% of infants as SGA or LGA. Infants born SGA (or LGA) for both weight and length ("proportionate" in size) were usually appropriate for BMI (59.0% and 75.6%). BMI distinguished disproportionate weight for length in infants with SGA or LGA weight at birth (58.3%, 49.9%). BMI also identified 11.4% of AGA weight infants as small or large for BMI ("disproportionate" in size) at birth; only using weight for GA missed these underweight/overweight for length infants. CONCLUSION: The unique, additional information provided by birth BMI further informs individualized preterm infant growth assessment by providing an assessment of an infant's body proportionality (weight relative to its length) in addition to the routine assessment of weight, length, and head circumference for GA and may better inform care plans and impact outcomes. KEY POINTS: · Most preterm infants were born AGA for all growth measures.. · AGA weight infants may be under- or overweight for length.. · BMI distinguished body disproportionality in SGA/LGA infants.. · Recommend BMI assessed along with weight, length and head.. · Further research on BMI in preterm infants is needed..

Myocardial mechanical dysfunction following endotoxemia: role of changes in energy substrate metabolism.

Cardiovascular depression due to endotoxemia remains a major cause of mortality in intensive care patients. To determine whether drug-induced alterations in cardiac metabolism may be a viable strategy to reduce endotoxemia-mediated cardiac dysfunction, we assessed endotoxemia-induced changes in glucose and fatty acid metabolism under aerobic and post-ischemic conditions. Endotoxemia was induced in male Sprague-Dawley rats by lipopolysaccharide (Escherichia coli 0111:B4c, 4 mg/kg, i.p.) 6 h prior to heart removal for ex vivo assessment of left ventricular (LV) work and rates of glucose metabolism (glucose uptake, glycogen synthesis, glycolysis and glucose oxidation) and palmitate oxidation. Under aerobic conditions, endotoxemic hearts had impaired LV function as judged by echocardiography in vivo (% ejection fraction, 66.0 ± 3.2 vs 78.0 ± 2.1, p < 0.05) or by LV work ex vivo (2.14 ± 0.16 vs 3.28 ± 0.16, Joules min(-1) g dry wt(-1), p < 0.05). However, rates of glucose uptake, glycogen synthesis, glycolysis, and glucose oxidation were not altered. Palmitate oxidation was lower in endotoxemic hearts in proportion to the decreased workload, thus metabolic efficiency was unaffected. In hearts reperfused following global ischemia, untreated hearts had impaired recovery of LV work (52.3 ± 9.4 %) whereas endotoxemic hearts had significantly higher recovery (105.6 ± 11.3 %, p < 0.05). During reperfusion, fatty acid oxidation, acetyl CoA production and metabolic efficiency were similar in both groups. As impaired cardiac function appeared unrelated to depression of energy substrate oxidation, it is unlikely that drug-induced acceleration of fatty acid oxidation will improve mechanical function. The beneficial repartitioning of glucose metabolism in reperfused endotoxemic hearts may contribute to the cardioprotected phenotype.

Tolerance to ischaemic injury in remodelled mouse hearts: less ischaemic glycogenolysis and preserved metabolic efficiency.

AIMS: Post-infarction remodelled failing hearts have reduced metabolic efficiency. Paradoxically, they have increased tolerance to further ischaemic injury. This study was designed to investigate the metabolic mechanisms that may contribute to this phenomenon and to examine the relationship between ischaemic tolerance and metabolic efficiency during post-ischaemic reperfusion. METHODS AND RESULTS: Male C57BL/6 mice were subjected to coronary artery ligation (CAL) or SHAM surgery. After 4 weeks, in vivo mechanical function was assessed by echocardiography, and then isolated working hearts were perfused in this sequence: 45 min aerobic, 15 min global no-flow ischaemia, and 30 min aerobic reperfusion. Left ventricular (LV) function, metabolic rates, and metabolic efficiency were measured. Relative to SHAM, both in vivo and in vitro CAL hearts had depressed cardiac function under aerobic conditions (45 and 36%, respectively), but they had a greater recovery of LV function during post-ischaemic reperfusion (67 vs. 49%, P < 0.05). While metabolic efficiency (LV work per ATP produced) was 50% lower during reperfusion of SHAM hearts, metabolic efficiency in CAL hearts did not decrease. During ischaemia, glycogenolysis was 28% lower in CAL hearts, indicative of lower ischaemic proton production. There were no differences in mitochondrial abundance, calcium handling proteins, or key metabolic enzymes. CONCLUSION: Compared with SHAM, remodelled CAL hearts are more tolerant to ischaemic injury and undergo no further deterioration of metabolic efficiency during reperfusion. Less glycogen utilization in CAL hearts during ischaemia may contribute to increased ischaemic tolerance by limiting ischaemic proton production that may improve ion homeostasis during early reperfusion.

Failing mouse hearts utilize energy inefficiently and benefit from improved coupling of glycolysis and glucose oxidation.

AIMS: To determine whether post-infarction LV dysfunction is due to low energy availability or inefficient energy utilization, we compared energy metabolism in normal and failing hearts. We also studied whether improved coupling of glycolysis and glucose oxidation by knockout of malonyl CoA decarboxylase (MCD-KO) would have beneficial effects on LV function and efficiency. METHODS AND RESULTS: Male C57BL/6 mice were subjected to coronary artery ligation (CAL) or sham operation (SHAM) procedure. After 4 weeks and echocardiographic evaluation, hearts were perfused (working mode) to measure LV function and rates of energy metabolism. Similar protocols using MCD-KO mice and wild-type (WT) littermates were used to assess consequences of MCD deficiency. Relative to SHAM, CAL hearts had impaired LV function [lower % ejection fraction (%EF, 49%) and LV work (46%)]. CAL hearts had higher rates (expressed per LV work) of glycolysis, glucose oxidation, and proton production. LV work per ATP production from exogenous sources was lower in CAL hearts, indicative of inefficient exogenous energy substrate utilization. Fatty acid oxidation rates, ATP, creatine, and creatine phosphate contents were unaffected. Utilization of endogenous substrates, triacylglycerol and glycogen, was similar in CAL and SHAM hearts. MCD-KO CAL hearts had 31% higher %EF compared with that of WT-CAL, and lower rates of glycolysis, glucose oxidation, proton production, and ATP production, indicative of improved efficiency. CONCLUSION: CAL hearts are inefficient in utilizing energy for mechanical function, possibly due to higher proton production arising from mismatched glycolysis and glucose oxidation. MCD deficiency lessens proton production, LV dysfunction, and inefficiency of exogenous energy substrate utilization.