The Decline and Fall of the Cardiac Biomarker: A Good Indicator of Resolution of Cardiac Dysfunction following Perinatal Asphyxia

Molloy, Eleanor J.

doi:10.1159/000341865

Cited by 2 publications

(1 citation statement)

References 28 publications

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“…Although the BNP and troponin I results seem to lead to different evidence with regard to cardiac protection by hypothermia, it has been demonstrated that both BNP and cardiac troponin I are suitable parameters to monitor impairment of cardiomyocytes and cardiac function as a valuable alternative to Doppler echocardiography in neonates. The commentary by Molloy [3] underlines the importance of BNP and cardiac troponin I as biomarkers of cardiac dysfunction in general and as an essential result of the Vijlbrief study. In particular, the maximal troponin I level has been considered as an indicator for the degree of perinatal asphyxia.…”

Section: Figmentioning

confidence: 99%

Spontaneous Hypothermia Is Not Able to Completely Counteract Cardiac Arrest-Induced Mitochondrial Impairment in the Rat Heart

Keilhoff

Ebmeyer²,

Schild

2012

Neonatology

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Vijlbrief et al. [Neonatology 2012;102:243–248] reported a beneficial effect of hypothermia on cardiac function after perinatal asphyxia indicated by low levels of B-type natriuretic peptide (BNP). Elevated troponin I plasma levels, however, reflects impairment of cardiomyocytes under hypothermic conditions. The importance of BNP and cardiac troponin I as biomarkers of cardiac dysfunction that may supplement or substitute Doppler echocardiography has been outlined. Using an asphyxia cardiac arrest (ACA) animal model under spontaneous hypothermia, we found a decrease in the activities of NADH-cytochrome c-oxidoreductase and succinate-cytochrome c-oxidoreductase in comparison to normothermic sham-operated controls. This observation indicates the impairment of the respiratory chain of heart mitochondria, which is accompanied by morphological changes in these mitochondria. Changed cardiac troponin I levels and respiratory chain complexes activity represent different but corresponding steps within the process of cardiomyocyte injury. Interestingly, liver and brain mitochondria remained unchanged under this condition. Patients could benefit from the control of mitochondrial function during hypothermic intervention. When indicated, substances could be supplemented that support mitochondrial function, e.g. antioxidative-acting vitamins and ubiquinone.

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Section: Figmentioning

confidence: 99%

Spontaneous Hypothermia Is Not Able to Completely Counteract Cardiac Arrest-Induced Mitochondrial Impairment in the Rat Heart

Keilhoff

Ebmeyer²,

Schild

2012

Neonatology

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Severe myocardial injury and extracorporeal membrane oxygenation following perinatal asphyxia

Ham

Patel

Wise

et al. 2015

Journal of Pediatric Surgery Case Reports

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a b s t r a c tPerinatal asphyxia is a common cause of morbidity and mortality in the newborn and is associated with myocardial injury in a significant proportion of cases. Biomarkers, echocardiography, and rhythm disturbances are sensitive indicators of myocardial ischemia and may predict mortality. We present a case of severe myocardial dysfunction immediately after delivery managed with extracorporeal membrane oxygenation (ECMO) and discuss the role of cardiac biomarkers, echocardiography, electrocardiography, and ECMO in the asphyxiated newborn. Ó 2015 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Perinatal asphyxia is a common cause of morbidity and mortality in the newborn period with an incidence between 0.5 and 2% [1,2]. The newborn myocardium is preferentially spared during the early phase of newborn hypoxemia; however, evidence of myocardial injury is present in 29e78% of newborns diagnosed with hypoxic-ischemic encephalopathy (HIE) [3e5]. Global oxygen deprivation, which is suggested by a 5 min Apgar score less than 7, underlies the pathogenesis of myocardial injury in the newborn period [6,7]. Additionally, biomarkers of myocardial injury (i.e. troponin and CK-MB), echocardiographic abnormalities, and rhythm disturbances are sensitive indicators of myocardial ischemia and may predict mortality [7]. We present a case of an infant who developed severe myocardial dysfunction following emergent Caesarian delivery for fetal decelarations and was managed with extracorporeal membrane oxygenation (ECMO). We discuss the role of cardiac biomarkers, echocardiography, electrocardiography (ECG), and ECMO in the asphyxiated newborn. Case presentationA 22-year-old G 1 P 0 mother presented to a regional hospital with symptoms of labor at 35 weeks gestation. The perinatal history was significant for insulin-dependent diabetes mellitus and chronic hypertension. A normal anatomic ultrasound was noted, however fetal echocardiography was not performed. Following a trial of labor and poor progression, late decelerations were noted and the infant was delivered by Caesarian section. Upon delivery, the 2,700 g infant appeared floppy without spontaneous respiratory effort and persistent bradycardia. Resuscitative efforts in the delivery room included intubation, ventilation, chest compressions (15 min), multiple fluid boluses, and epinephrine. APGAR scores were 1, 3, and 5 at 1, 5, and 10 min, respectively and an initial arterial blood gas provided evidence of severe metabolic acidosis with a pH of 6.81 and base deficit of À23. The patient was transferred to the in-hospital Level III NICU and was noted to have spontaneous respirations and movement with significant hypoxemia (70e80% saturations on FiO2 of 1.0). However, the patient experienced prolonged bradycardia (60e70 b.p.m.) and a corresponding rhythm strip revealed ST segment elevation. A continuous infusion of epinephrine was initiated and the infant was transferred...

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The Decline and Fall of the Cardiac Biomarker: A Good Indicator of Resolution of Cardiac Dysfunction following Perinatal Asphyxia

Cited by 2 publications

References 28 publications

Spontaneous Hypothermia Is Not Able to Completely Counteract Cardiac Arrest-Induced Mitochondrial Impairment in the Rat Heart

Spontaneous Hypothermia Is Not Able to Completely Counteract Cardiac Arrest-Induced Mitochondrial Impairment in the Rat Heart

Severe myocardial injury and extracorporeal membrane oxygenation following perinatal asphyxia

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