What factors contribute to the elevation of serum free fatty acids (FFA) in newborns in the cardiac surgical setting?

Elevations in serum free fatty acids (FFA) levels during heart surgery have been reported in humans and experimental animals, causing increased arrhythmias, decreased heart function, and contributing to mortality. Factors such as heparin administration, age, cardiopulmonary bypass (CPB) and cyanosis/hypoxia have been implicated but not proven. This study was designed to clarify the contribution of these factors using an experimental pig model as follows: a) adult (n=10) versus 3-day old piglets (n=18) had FFA levels assessed before and after heparin administration; b) 3 day old piglets, the additional effect of CPB (n=8) or just severe hypoxia (PaO2 = 20-25 mmHg; n=6) exposure on FFA levels. This work demonstrated that significant elevations in serum FFA were mainly due to heparin administration, with modest contributions by young age, CPB and hypoxia. Our preliminary clinical investigations also suggest that children undergoing CPB are at risk of being exposed to high FFA levels and that these patients only suffered a decrease in heart function when these elevations were present in conjunction with cyanosis and/or prolonged ischemic time. These initial findings require further confirmation. Given these findings, pharmaco-therapeutics geared towards limiting FFA elevations should be considered, especially in young children undergoing pediatric cardiac surgery.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Does young age really put the heart at risk?

Despite significant advances in the management and treatment of heart disease in children, there continue to be patients who have worse outcomes than might be expected. A number of risk factors that could be responsible have been identified. Evidence based findings will be reviewed including whether young age and/or reduced body weight exacerbate these responses. For example, newborn children undergoing congenital cardiac surgery are known to have worse outcomes than older children. Evidence exists that newborn hearts do not tolerate ischemia as well as adults; developing irreversible injury sooner and exhibiting at risk metabolic profiles. As well, in response to the administration of heparin, elevations in free fatty acids occur during congenital heart surgery in children which can have detrimental effects on the heart. Furthermore, myocardial energetic state has also been suggested to impact outcomes. Unfavorable energetic profiles were correlated to lower body weights in the same age healthy newborn piglet model. Newborn children suffering from congenital heart disease, with lower body weights, also had lower myocardial energetic state and this correlated with longer post operative ventilatory support as well as a trend to longer Intensive Care Unit stay. These findings imply that unfavorable myocardial metabolic profiles could contribute to post operative complications.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Not all neonatal hearts are equally protected from ischemic damage during hypothermia

Despite hypothermia, pediatric cardiac surgeons continue to experience difficulties in providing adequate myocardial protection in newborns. This study examines the effects of deep hypothermia on neonatal heart tolerance to ischemia by measuring metabolic responses and the time to onset of ischemic contracture, or “stone heart.” After control right ventricular biopsy specimens were obtained, hearts of newborn pigs (n = 36) were excised and placed in temperature-regulated baths: 37.5 ° ± 0.5 °C (n = 9), 19.0 ° ± 0.5 °C (n = 14), and 12.0 ° ± 0.5 °C (n = 13). With a compliant balloon in the left ventricle to measure pressure, time to onset of ischemic contracture (> 2-mm Hg rise) was recorded, and sequential biopsies were done. Data indicated hypothermia significantly ( p < 0.001) prolonged time to onset of ischemic contracture from 29.5 ± 1.7 minutes (mean ± standard error of the mean) at normothermia to 150.0 ± 6.4 minutes at 19 °C and to 283.8 ± 46.4 minutes at 12 °C. Lactate buildup at 30 minutes of ischemia was significantly reduced by 70% with hypothermia. Decline in adenosine triphosphate level was significantly reduced by 50% (19 °C) and 75% (12 °C) with hypothermia. More importantly, a subgroup of hearts in each hypothermia group (n = 5 per group) was identified by 38% to 48% lower adenosine triphosphate stores before ischemia compared with the group means. These hearts had a significantly ( p < 0.01) shorter time to onset of ischemic contracture than the group means (19 °C, 65.0 ± 8.0 minutes; 12 °C, 167.0 ± 4.0 minutes). These “at risks” hearts would not be afforded the same safe time for repair expected with hypothermia, and this requires consideration if we are to improve outcomes in this young patient population