Cardiac troponins can be useful in monitoring cardiac injury following perinatal distress. We report here an increase of cardiac troponin I (cTnI) to 2.84 microg/l at 3 weeks (age-related median: 0.07 microg/l) followed by normalization in a newborn with an uneventful clinical course after resuscitation at birth. Serial echocardiographs showed normal cardiac function. Such a time course of cTnI, not previously reported, could be due to either a greater sensitivity of biochemical markers than of instrumental tools or birth asphyxia. Larger studies are neede

Biban, P

Caputo, M

Cavalli, C

Dorizzi, Rm

Lanzoni, L

English

Dorizzi, RM

Catalogo dei prodotti della ricerca

Full Terms & Conditions of access and use can be found athttps://www.tandfonline.com/action/journalInformation?journalCode=ijmf20The Journal of Maternal-Fetal & Neonatal MedicineISSN: 1476-7058 (Print) 1476-4954 (Online) Journal homepage: https://www.tandfonline.com/loi/ijmf20How much and for how long does the neonatalmyocardium suffer from mild perinatal asphyxia?C Cavalli, RM Dorizzi, L Lanzoni, M Caputo & P BibanTo cite this article: C Cavalli, RM Dorizzi, L Lanzoni, M Caputo & P Biban (2005) How much andfor how long does the neonatal myocardium suffer from mild perinatal asphyxia?, The Journal ofMaternal-Fetal & Neonatal Medicine, 17:1, 85-86, DOI: 10.1080/14767050400013438To link to this article:  https://doi.org/10.1080/14767050400013438Published online: 07 Jul 2009.Submit your article to this journal Article views: 46View related articles Citing articles: 1 View citing articles CASE REPORTHow much and for how long does the neonatal myocardium suffer frommild perinatal asphyxia?C. CAVALLI1, R. M. DORIZZI2, L. LANZONI3, M. CAPUTO3, & P. BIBAN11Pediatric and Neonatal Intensive Care Unit, Division of Pediatrics, Hospital of Verona, Parma, Italy, 2Clinical Chemistryand Hematology Laboratory, Hospital of Verona, Parma, Italy, and 3Pediatric Cardiology Unit, Department of Cardiology,Hospital of Verona, Parma, Italy(Received 14 November 2003; revised 20 April 2004; accepted 21 April 2004)AbstractCardiac troponins can be useful in monitoring cardiac injury following perinatal distress. We report here an increase ofcardiac troponin I (cTnI) to 2.84 mg/l at 3 weeks (age-related median: 0.07 mg/l) followed by normalization in a newbornwith an uneventful clinical course after resuscitation at birth. Serial echocardiographs showed normal cardiac function. Sucha time course of cTnI, not previously reported, could be due to either a greater sensitivity of biochemical markers than ofinstrumental tools or birth asphyxia. Larger studies are needed.Keywords: Perinatal asphyxia, transient myocardial ischemia of the newborn, cardiac troponinsIntroductionTransient myocardial ischemia (TMI) and myocar-dial damage are relatively common complications ofbirth asphyxia and other perinatal conditions [1–3].In the past, the diagnosis of neonatal cardiac injurywas difficult due to the lack of specific biochemicalmarkers. The recent availability of cardiac troponinswith higher tissue specificity than other markers suchas creatine kinase MB fraction [3–5] suggests theiradoption as reliable indicators of cardiac injury evenin newly born infants [6].We report here the case of a newborn whorequired resuscitation for a short time in the deliveryroom and thereafter presented with an atypical andprolonged rise of cardiac troponin I (cTnI) level.Case reportA female infant was born at term by spontaneousdelivery (birth weight 2780 g). She showed mild birthasphyxia (Apgar score: 1 min= 3, 5 min= 9) andrequired bag and mask ventilation with oxygen. Shewas therefore admitted to our neonatal intensive-careunit (NICU) in good clinical condition. Balancedmild metabolic acidosis (pH= 7.42, arterial pCO2=24 mmHg, HCO3= 15.4 mmol/l, arterial lactate =5 mmol/l) was demonstrated 90 min after birth. Aspart of the standard care of asphyxiated newborninfants, we performed continuous electrocardio-graphic monitoring and serial measurements ofcTnI using an automated analyzer (Dimension RxL;Dade Behring, Newark, DE, USA). The analyticalperformance was similar to that described elsewhere[7]: in particular, day-to-day coefficient of variationwas lower than 10%. No electrocardiographic sign ofTMI emerged in the first 48 h of life according toJedeikin’s criteria [1]. Echocardiography in the firstday of life excluded congenital heart diseases,coronary anomalies and left ventricular segmentaldysfunction. The clinical and laboratory course wasuneventful. Thus, on day 2 of life, the infant wastransferred from the NICU to the normal care unit ofour institution even though cTnI concentrationshowed an upward trend (Figure 1) during the firstdays of life. The latter exceeded the upper referencelimit (Table I) we previously defined for our neonatalpopulation [8]. The patient was discharged on day 3of life, in healthy condition and breastfed. Electro-cardiograms, echocardiographic recordings andCorrespondence: Dr C. Cavalli, Section of Neonatology and Neonatal Intensive Care, Department of Gynecology, Obstetrics and Neonatology, UniversityHospital, 14 via A. Gramsci, I-43100 Parma, Italy.The Journal of Maternal-Fetal and Neonatal Medicine, January 2005; 17(1): 85–86ISSN 1476-7058 print/ISSN 1476-4954 online # 2005 Taylor & Francis Group LtdDOI: 10.1080/14767050400013438blood cTnI assays were therefore scheduled forfollow-up. In the following weeks the infant washealthy and showed normal cardiac function (leftventricular ejection fraction consistently remainedaround 70%). However, cTnI concentration in-creased markedly to a peak value of 2.84 mg/l at 3weeks of life, returning within the reference interval at3.5 months (0.12 mg/l) and falling to below 0.1 mg/l at9.5 months of age (Figure 1).DiscussionTroponins usually show near-zero background levelsin adults as well as newly born infants [5]. Thus, arise of troponin, even in the absence of echocardio-graphic findings or other markers of elevation,reliably indicates cardiac damage or myocardialischemia [9].Interestingly, short-lived cTnI elevations have beenreported in adult patients with chest pain withoutcardiac ischemic disease [10], and troponin level havebeen evaluated for detecting minor myocardialdamage in adult patients with acute non-cardiacdisease [11]. Furthermore, in newborns, severalperinatal conditions can be complicated by TMI ortroponin elevations following a perinatal injury [1–3,6,12]. Even if, according to many authors, TMI is aself-limiting problem, the effects of a long-lastingevent, if any, have been considered a relevant questionsince TMI was first reported [1].In the present case report we describe an episodeof mild perinatal asphyxia followed by a healthyclinical course associated with increased cTnIextending until the 3rd week of life. The lattercourse has been previously reported [3], but theremarkable aspect of our case is that cTnI remainedhigh for a long time (almost until 3 months of life)without any clinical or instrumental sign of cardio-vascular disease (Figure 1). To our knowledge, this isthe first report of such a time course of cTnI in anewborn and we speculate a role of birth asphyxia.The intrinsic mechanism might be due to afragmentation of troponins and/or their intracellularcompartmentation [3,5]. Nevertheless, the phenom-enon remains only partly understood.Both the lack of any evidence of TMI in theclinical course of our case and the lack of anyechocardiographic evidence of left ventricular seg-mental dysfunction in the follow-up could suggestthat cTnI might provide higher sensitivity thaninstrumental diagnostic tools at substantially lowercost. Larger studies are needed to confirm thispotential.References1. Jedeikin R, Primhak A, Shennan AT, et al. Serial electro-cardiographic changes in healthy and stressed neonates. ArchDis Child 1983;58:605–11.2. Panteghini M, Agnoletti G, Pagani F, Spandrio M. Cardiactroponin T in serum as marker for myocardial injury innewborns. Clin Chem 1997;43:1455–7.3. Adamcova M, Kokstein Z, Palicka V, et al. Cardiac troponinT in neonates after acute and long-term tocolysis. BiolNeonate 2000;78:288–92.4. Ghaemmaghami CA, Nooy RV, Ullman E, et al. Troponin Iusurps the role of CKMB in the biochemical diagnosis ofmyocardial injury. Acad Emerg Med 2001;8:552–3.5. Wu AHB, Jialal I. How specific is cardiac troponin? Am J ClinPathol 2000;114:509–11.6. Moller JC, Thielsen B, Schaible TF, et al. Value of myocardialhypoxia markers (creatine kinase and its MB-fraction,troponin-T, QT-intervals) and serum creatinine for therestrospective diagnosis of perinatal asphyxia. Biol Neonate1998;73:367–74.7. Hafner G, Peetz D, Dati F, et al. Analytical and clinicalevaluation of troponin I determination on Dimension RXL-HM. Clin Chem Lab Med 2000;38:355–618. Cavalli C, Dorizzi RM, Caputo M, Biban P. Serendipitousdetection of umbilical venous catheter displacement bycardiac troponin I measurement. Clin Chem 2001;47:1328–99. Menhusen M. Isolated troponin I elevation in acute myocar-dial infarction: a case report. Aviat Space Environ Med2002;72:763–4.10. Wright SA, Sawyer DB, Sacks DB, et al. Elevation of troponinI levels in patients without evidence of myocardial injury. J AmMed Assoc 1997;278:2144.11. Arlati S, Brenna S, Prencipe L, et al. Myocardial necrosis inICU patients with acute non-cardiac disease: a prospectivestudy. Intensive Care Med 2000;26:31–7.12. Trevisanuto D, Zaninotto M, Altinier S, et al. High serumcardiac troponin T concentrations in preterm infants withrespiratory distress syndrome. Acta Paediatr 2000;89:1134–6.Figure 1. Plasma concentration of cardiac troponin I (cTnI)from day 1 to day 294 of life.Table I. Upper reference limits for plasma concentration (mg/l) ofcardiac troponin I in the first month of life.Day of life n MedianLowerquartileUpperquartile1 34 0.07 0.04 0.152 17 0.11 0.04 0.153 12 0.11 0.03 0.188–12 16 0.14 0.05 0.2613–21 10 0.07 0.02 0.122–30 11 0.16 0.08 0.3286 C. Cavelli et al.

How much and for how long does the neonatal myocardium suffer from mild perinatal asphyxia?

https://iris.univr.it/bitstream/11562/1020499/1/How%20much%20and%20for%20how%20long%20does%20the%20neonatal%20myocardium%20suffer%20from%20mild%20perinatal%20asphyxia%20%281%29.pdf

How much and for how long does the neonatal myocardium suffer from mild perinatal asphyxia?

Abstract

Similar works

Full text

Available Versions

Catalogo dei prodotti della ricerca