Early survival following in utero myocardial infarction

Peter Cosgrove; Shan Modi; Karla Lawson; Camille Hancock-Friesen; Gregory Johnson

doi:10.1017/S1047951118001105

Early survival following in utero myocardial infarction

Published online by Cambridge University Press: 23 July 2018

Peter Cosgrove ,

Shan Modi ,

Karla Lawson ,

Camille Hancock-Friesen and

Gregory Johnson

Show author details

Peter Cosgrove*: Affiliation:
Department of Emergency Medicine, Boston Children’s Hospital, Boston, MA, USA
Shan Modi: Affiliation:
Department of Medicine, University of Texas Medical Branch at Galveston, Galveston, TX, USA
Karla Lawson: Affiliation:
Department of Trauma and Injury Research Center, University of Texas at Austin, Dell Children’s Medical Center, Austin, TX, USA
Camille Hancock-Friesen: Affiliation:
Department of Pediatric Cardiovascular Surgery Division, Dell Children’s Regional Heart Center, University of Texas at Austin, Dell Children’s Medical Center, Austin, TX, USA
Gregory Johnson: Affiliation:
Department of Pediatric Cardiology, University of Texas at Austin, Dell Children’s Medical Center, Austin, TX, USA
*: Author for correspondence: P. Cosgrove, Department of Pediatric Emergency Medicine, Boston Children’s Hospital, 300 Longwood Ave, Boston, MA 02115, USA. Tel: 512 221 8598; Fax: 617 730 0335; E-mail: Peter.Cosgrove@childrens.harvard.edu

Article contents

Abstract
Case report
Systematic review introduction
Methods
Results
Discussion
Limitations
Conclusions
Supplementary materials
References

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Abstract

Intrauterine myocardial infarction is a rare and frequently fatal diagnosis. It has been presented in the literature only as case reports and short series. We present a case report of a coronary occlusive intrauterine myocardial infarction and survival and present a systematic review of the literature. This is the first summative description of current data on intrauterine and perinatal myocardial infarction. We performed the systematic review based on the guidelines established by the PRISMA statement. Our population of intrauterine and perinatal myocardial infarction included published cases who presented as a live birth within the first 28 postnatal days, and had a diagnosis of myocardial infarction. We conducted descriptive statistics and regression analysis on short-term mortality as the primary outcome. After applying exclusion criteria we described 84 individual cases of myocardial infarction from 63 full-text articles including our own case. Presentation within the first 12 hours was associated with mortality (OR 3.90, p=0.004). Treatment modalities were varied and inconsistently recorded. The aetiologies and comorbidities are varied in our systematic review. We would have a low threshold to perform viral testing, consider anticoagulation early and coronary imaging if feasible. The use of extracorporeal membranous oxygenation may serve as a bridge to cardiac recovery.

Keywords

Myocardial infarction perinatal intrauterine general cardiology

Type: Review Article
Information: Cardiology in the Young , Volume 28 , Issue 10 , October 2018 , pp. 1079 - 1087

DOI: https://doi.org/10.1017/S1047951118001105 [Opens in a new window]
Copyright: © Cambridge University Press 2018

Intrauterine myocardial infarction is a rare and frequently fatal diagnosis. The presentation includes in utero or postnatal ventricular dysfunction, ventricular aneurysm, or postnatal haemodynamic instability. The diagnosis may not be apparent during intrauterine life. We present the case report of a newborn with an intrauterine myocardial infarction related to coronary occlusion and include a systematic review of the literature.Reference Ferns, Khan and Firmin ¹ ^– Reference Lehoullier, Bowers and Harris ⁶⁴

Case report

During routine screening at 48 hours postpartum, a term male newborn was found to have a heart rate of 140 beats per minute by auscultation and 70 beats per minute by pulse oximetry. An electrocardiogram demonstrated ventricular bigeminy, deep Q-waves in the inferolateral leads, ST segment changes, and T-wave abnormalities (Fig 1). He was transferred to a tertiary-level paediatric ICU after identification of decreased ventricular function and a ventricular aneurysm by echocardiography. Upon arrival to the paediatric ICU, he had an intermittent gallop with good peripheral perfusion, frequent premature ventricular contractions, intermittently in a trigeminal pattern, with episodic bradycardia and hypotension.

Figure 1 Electrocardiography showing ventricular bigeminy, Q-waves in the inferolateral leads, and ST segment and T-wave abnormalities.

The newborn was delivered at 37 weeks estimated gestational age to a 29-year-old multiparous mother by caesarean section secondary to fetal bradycardia. The mother had routine antenatal care without concern. The mother’s only medication was a prenatal vitamin and she had no history of illegal drug use. He was vigorous at birth with APGARs of 8 and 9 at 1 and 5 minutes, respectively. There was no family history of thrombosis, miscarriage, early sudden death, or clotting disorders.

The initial echocardiogram revealed a moderately dilated left ventricle with moderately depressed systolic function with a left ventricular ejection fraction of 30.5% (normal ⩾55%). The apex of the left ventricle was dyskinetic and aneurysmal (Fig 2). Left ventricular wall thinning of the distal lateral wall and apex was noted. Right ventricular systolic wall motion was normal with normal origins and appearance of the proximal coronary arteries (Supplementary videos 1 and 2).

Figure 2 Echocardiogram showing a moderately dilated left ventricle and aneurysmal wall.

Laboratory evaluation demonstrated a normal Troponin-I at 0.03 ng/ml (normal<0.04 ng/ml) and an elevated Creatine Kinase-Muscle/Brain at 13.8 ng/ml (normal 0.6–6.3 ng/ml). B-natriuretic peptide was elevated at 534 pg/ml (normal <100 pg/ml). Routine cranial and renal ultrasounds were normal. Cytomegalovirus culture and viral polymerase chain reaction studies were negative. A hypercoagulability work-up consisting of factor V Leiden, PT20210A mutation, anti-phospholipid antibodies, serum homocysteine level, anti-thrombin assay, Protein C, and Protein S was unremarkable.

An amiodarone infusion was started at 5 mcg/kg/minute. Carvedilol and captopril were initiated. The B-natriuretic peptide level decreased steadily from 534 pg/ml on day 1 to 194 and then 26 on days 4 and 7, respectively. The patient remained on low-molecular-weight heparin (enoxaparin) to reduce the likelihood of a left ventricular mural thrombus.

A repeat echocardiogram on day 7 demonstrated improvement in the left ventricular ejection fraction, increasing from 30.5 to 62.4%. Left ventricular systolic thinning and apical dyskinesis persisted. M-mode was used to estimate left ventricular ejection fraction. The same operator and cardiologist reviewed the images.

A cardiac MRI scan on day 7 confirmed normal cardiac chamber sizes with thinning of the mid-distal left ventricular lateral wall/apex with aneurysmal formation (Fig 3). There was severe hypokinesis/dyskinesis of the mid-distal lateral and apical ventricular walls. The MRI confirmed a transmural scar in the mid-distal lateral wall, a total scar burden of 15% of the left ventricle, and an ejection fraction of 38%. Right ventricular systolic function was normal. There were no other intracardiac or great vessel abnormalities.

Figure 3 Cardiac MRI showing the left ventricular (LV) aneurysm and occlusion of the left anterior descending (LAD) coronary artery.

Cardiac catheterisation with angiography was performed on day 14. The study showed normal haemodynamics on room air (Fig 4). The left anterior descending coronary artery showed abrupt occlusion near the mid-septum with two well-formed tortuous collaterals anteriorly and laterally. Angiography of the right coronary artery, left main, and left circumflex arteries was unremarkable. Left ventricular systolic function had improved with a persistent aneurysmal dilation of the apex. Earlier catheterisation was considered, but there was team consensus that early angiography was unlikely to change the clinical course. Normal proximal coronary artery origins and flow had been demonstrated by echocardiography. The patient had been anticoagulated. It was felt that there was a low probability of finding coronary artery pathology that was amenable to catheter-based intervention. The decision to proceed with coronary angiography at 2 weeks after presentation was to more precisely define the coronary artery abnormality and collaterals and to assist with making a decision regarding long-term anticoagulation.

Figure 4 Coronary angiography showing abrupt occlusion of the left anterior descending (LAD) coronary artery near the mid-septum with two well-formed tortuous collaterals anteriorly (Collateral 1) and laterally (Collateral 2). Right coronary artery (RCA) and left coronary artery (LCA) identified.

Premature ventricular contractions resolved by day 13 and the amiodarone infusion was transitioned to oral therapy. The patient was feeding well orally and gaining weight. After team discussion and before discharge on day 18, aspirin was started and enoxaparin stopped. Our choice of aspirin over enoxaparin was based on our impression that the infarct was not acute and that there was a low risk of further coronary thrombosis or left ventricular mural thrombus; thus, the risk of continuing enoxaparin was not justified. He was discharged on oral amiodarone, carvedilol, enalapril, and aspirin. The child remained asymptomatic at the 18-month follow-up visit with a persistent apical aneurysm and good left ventricular systolic function.

Systematic review introduction

Intrauterine myocardial infarction is a rare diagnosis and commonly made on autopsy in the neonatal period. To broaden our literature review, we included all myocardial infarctions diagnosed within the first 28 days after birth. Ravich et al first described neonatal myocardial infarction in 1947 and since then the diagnosis has been presented in the literature only as case reports and short series. To create a summative description of current data on intrauterine and perinatal myocardial infarction, we performed a systematic review of all published case reports.

Methods

We performed the systematic review based on the guidelines established by the PRISMA statement for reporting systematic reviews and meta-analysis of studies. In all, two authors, according to pre-determined inclusion and exclusion criteria, reviewed all studies.

We defined our population of intrauterine and perinatal myocardial infarction as those presenting within the first 28 postnatal days, a live birth, and with a diagnosis of myocardial infarction. This allowed us to exclude series of myocardial infarction diagnosed on autopsy review that would skew our results. We excluded non-English publications owing to our inability to reliably translate the full documents.

Search strategy

We searched PubMed and Ovid Medline using key terms and free text words for “myocardial infarction”, “neonatal”, or “newborn” or “perinatal”. The Cochrane Library revealed no further relevant studies.

There were no existing meta-analyses, systematic reviews, randomised controlled trials, or cohort studies. We identified only case reports and case series. We have included data from these in our descriptive statistics and regression analysis on mortality as the primary outcome.

Studies retrieved were published from September, 1947 through January, 2016. Articles were selected for the study by screening the titles and abstracts and reviewing the full text for reaffirmation. Disagreements in study selection were resolved by consensus of all authors when necessary. Case reports that did not include data pertinent to our study were discarded.

Variables collected include gender, gestation time period (full term was defined as >37 weeks), time and type of presentation, difficult delivery/perinatal asphyxia, echocardiography use, echocardiography parameters including “regional hypokinesia”, “mitral regurgitation”, and “structural abnormality on echocardiography”, presence of anomalous coronary anatomy, presence of dysrhythmia, documented thrombophilia, documented viral testing, presence of thrombosis and its location, use of extracorporeal membranous oxygenation, use of surgical or invasive treatment, presence of cardiac structural abnormality, survival, and co-morbidities. Difficult delivery was defined as the presence of meconium, an emergency caesarean section, abnormal cardiotocography, or the presence of a nuchal cord. We did not report on cardiac biomarkers or electrocardiographic findings owing to their variable reporting and lack of reference standards.

Statistical analysis

STATA version 12 was used to determine odds ratios using univariate regression analysis with short-term survival as the primary outcome measure. Statistical significance was set at the p<0.05 level.

Results

A total of 579 items of literature were retrieved in our initial search of the literature (Fig 5). Two manuscripts were discarded as duplicate records. After screening titles and abstracts, 457 references were discarded owing to irrelevance or not meeting inclusion criteria. The remaining 120 articles were selected for further analysis via full-text review. Upon further review of the 120 articles, 36 articles were not included owing to not meeting inclusion criteria and another 21 articles were excluded owing to transcription in a foreign language. The decision to exclude foreign language studies was because of inadequate resources to properly translate articles for data analysis. The remaining 63 full-text articles contained 83 individual cases of myocardial infarction. We also included our own case report in the qualitative analysis, bringing the total cases studied to 84.

Figure 5 PRISMA Flowchart.Reference Moher, Liberati, Tetzlaff and Altman ⁶⁵

Population characteristics are summarised in Table 1. There is no sex preponderance – 41% were female – and the majority present early – 59% within 12 hours of birth – with profound cardiovascular dysfunction: cardiogenic shock in 56%, cyanosis in 24%, and respiratory distress in 23%. Structural cardiac abnormalities were identified in 20% (Table 2). Anomalous coronary arteries occurred in only two cases.

Table 1 Characteristics of the study population.

ECG=electrocardiography; ECHO=echocardiography; ECMO=extracorporeal membranous oxygenation.

* Gestational age was documented in 78 cases.

** The “other” presentations included apnoea, hypotonia, hypothermia, maternal pre-existing condition, prenatally identified heart disease, asphyxia, and vomiting.

*** Perinatal asphyxia or a difficult delivery was documented in 19 of 82 cases.

**** Difficult delivery was defined as the presence of meconium, an emergency caesarean section, abnormal cardiotocography, or the presence of a nuchal cord.

***** Echocardiography was not available in 31 cases, all published between 1947 and 1986.

****** Confirmation of infarction was by angiography or direct visualisation at surgery or autopsy. Other myocardial infarctions (MI) diagnoses based on one or a combination of the following: ECG, ECHO, and elevated cardiac markers only.

******* Identifiable thromboses were identified during angiography or autopsy in only 32 cases (38%).

******** Dysrhythmia included bradycardia, heart block, wide complex tachycardias, supraventricular, and junctional tachycardias and ventricular ectopics.

********* Thrombophilia testing was documented only in 17 cases.

********** Viral testing was only documented in 15 cases.

*********** Invasive or surgical treatment included intravenous or intracoronary thrombolysis (eight cases), drainage of pericardial effusion, exchange transfusion, congenital heart surgery, valvuloplasty, and balloon septostomy.

Table 2 Identified cardiac structural abnormalities.

There is no dominant identifiable aetiology for perinatal myocardial infarction. Thrombophilia testing was performed in 20% of cases, and 29% of those were positive. Viral testing was documented in only 18% of cases, but 40% of those tested were positive for enterovirus or coxsackie virus.

Documentation of an occluded coronary artery by angiography or direct visualisation of infarcted myocardium at surgery or autopsy substantiated the diagnosis in 61 (73%). The remaining cases were diagnosed based upon a combination of electrocardiogram and echocardiogram findings and elevated cardiac enzymes. Cardiac markers included one or a combination of the following: CK, CK-MB, Troponin-I, and Troponin-T. The reporting was highly variable and was not included in this analysis. Thromboses were identified during angiography or autopsy in 32 (38%). The left coronary was involved in 26 (81%) thromboses. Extracorporeal membranous oxygenation was used in eight cases. Invasive or surgical treatment was described in 24 (29%) and included intravenous or intracoronary thrombolysis (eight cases), drainage of pericardial effusion, congenital heart surgery, valvuloplasty, and balloon septostomy. Severe co-morbidities were described in 29 (35%) (Table 3). Overall, 38 (45%) newborns survived.

Table 3 Identified co-morbidities.

MSSA=methicillin sensitive staphlococcus aureus; RV=right ventricle.

Systematic review analytics: association between patient characteristics and mortality in a series of published case studies.

Presentation within 12 hours and lack of echocardiogram were statistically associated with mortality (p=0.004 and <0.001, respectively). The majority lacking echocardiograms were cases reported in the years before it was standard of care. Mortality was associated with female gender (p=0.051), approaching significance. Perinatal asphyxia has been shown to raise troponin-T and impair systolic myocardial function.Reference Costa, Zecca and De Rosa ⁶⁶ However, among newborns with myocardial infarction, the presence of a difficult delivery or perinatal asphyxia was not associated with increased mortality (Table 4).

Table 4 Systematic review analytics: association between patient characteristics and mortality in a series of published case studies.

ECHO=echocardiography; ECMO=extracorporeal membranous oxygenation.

Discussion

Coleman first described intrauterine myocardial infarction in 1962, with subsequent reports associated with stillbirth and hydrops fetalis in twin gestations.Reference Coleman and Macdonald ³⁰ ^, Reference Marton, Hajdu and Hruby ⁶⁷ ^, Reference Volker, Demmer and Gattenlohner ⁶⁸ Survival has only been described once before in published reports of specifically intrauterine myocardial infarction.Reference Birnbacher, Salzer-Muhar and Kurtaran ⁵¹

Intrauterine myocardial infarction studies (Table 5)

Aetiology

Our data on in utero and perinatal myocardial infarction support the polyfactorial association with thrombus, underlying thrombophilia, viral myocarditis, and those with severe co-morbidities. Anomalous coronary anatomy is a rare cause of myocardial infarction in the perinatal period (Table 5).

Table 5 Intrauterine myocardial infarctions studies.

LV=left ventricle; RV=right ventricle.

Presentation

Common perinatal presentations include acute cardiogenic shock, cyanosis, and/or respiratory distress. Of the cases with identifiable thrombus, 81% involved the left coronary artery and its tributaries. This may not be evident during fetal life because of the relatively lower metabolic demand of the left ventricle. Paradoxical thromboembolism from the umbilical venous system has been suggested in other case reports. Of the 32 cases with identified thrombus, three cases also found thrombi in the ductus venosus or umbilical veins. An additional three cases had thrombi within the cardiac veins, suggesting that the diagnosis of thromboemboli is underestimated.

Diagnosis

Elevated cardiac biomarkers have been described to occur in otherwise healthy term and preterm newborns, peaking on day three.Reference Lipshultz, Simbre and Hart ⁶⁹ ^, Reference El-Khuffash and Molloy ⁷⁰ Elevated Troponin-T levels have been described in respiratory distress syndrome, grade III neonatal encephalopathy, and perinatal asphyxia with variable cardiac impairment.Reference Gunes, Ozturk and Koklu ⁷¹ ^, Reference Boo, Hafidz and Nawawi ⁷² Troponins also appear to be a surrogate marker of global hypoxia/ischaemia.Reference El-Khuffash and Molloy ⁷⁰ Highly sensitive cardiac Troponin-I has not yet been evaluated as an aid for diagnosis in paediatric myocardial infarction. Given the unquantified influence of gestational age, birth weight, gender, and delivery on cardiac biomarker reference ranges in the neonatal population, it remains challenging to separate normal neonatal physiologic myocardial remodelling from either myocardial injury or true infarction. Electrocardiographic criteria for the diagnosis of acute myocardial infarction in childhood have been suggested.Reference Towbin, Bricker and Garson ⁷³ However, the similar confounding issues of myocardial strain during normal physiologic adaptation or relative myocardial injury due to global hypoxia/ischaemia raise concerns over its utility during the perinatal period.

Certain laboratory, electrocardiographic, and echocardiographic findings may suggest a diagnosis of neonatal myocarditis, as well as acute myocardial infarction.Reference de Vetten, Bergman and Elzenga ³² Myocarditis has been postulated as a potential aetiology for intrauterine myocardial infarction. Localised inflammation may result in coronary arteritis and thrombosis. Myocarditis should be considered not only in the differential diagnosis in the setting of a potential intrauterine myocardial infarction but also as a possible underlying cause.

Clinical management focusses on the management of haemodynamic derangements and arrhythmias. Tissue plasminogen activator has been used in the setting of suspected acute infarction. Extracorporeal membranous oxygenation may have a role as a bridge to cardiac recovery. The number of patients treated with extracorporeal membranous oxygenation or tissue plasminogen activator was insufficient to provide the power to detect a statistically significant clinical contribution. Treatment modalities were varied and inconsistently recorded. Limited by the study’s retrospective nature, we found no treatment modality trend in the systematic review. There were no long-term follow-up or neurodevelopmental outcomes recorded.

Our own case highlights the wide differential for ischaemia in a neonate. The aetiologies and associated co-morbidities are varied, as highlighted in the systematic review. Our patient continued to improve with medical management only. We would suggest having a low threshold to perform viral testing, consider anticoagulation early, and coronary imaging if feasible.

Limitations

Systematic reviews of case reports are rarely performed because of the limitations of retrospective data and risk of publication bias. However, the rarity of neonatal/perinatal myocardial infarction would make obtaining meaningful data from a single centre or prospective study difficult. Our systematic review was designed to present summative data and describe clinical and diagnostic characteristics not previously described in large numbers.

We are limited by the retrospective nature of the project on which conclusions we can draw. We would highlight that electrocardiographic and lab values suggestive of infarction may also indicate myocarditis or an alternate diagnosis with associated myocardial dysfunction. We included these more equivocal cases as we were unable to state that ischaemia was not present.

Conclusions

Intrauterine and neonatal myocardial infarctions are extremely rare. The diagnosis should be considered in the setting of cardiovascular instability or arrhythmia in the newborn period. Viral myocarditis may mimic laboratory and electrocardiographic changes of a myocardial infarction. The use of extracorporeal membranous oxygenation may serve as a bridge to cardiac recovery.

Supplementary materials

To view supplementary material for this article, please visit https://doi.org/10.1017/S1047951118001105

Acknowledgement

None.

Financial Support

This research received no specific grant from any funding agency or from commercial or not-for-profit sectors.

Conflicts of Interest

None.

References

1. Ferns, S, Khan, M, Firmin, R, et al. Neonatal myocardial infarction and the role of extracorporeal membrane oxygenation. Arch Dis Child Fetal Neonatal Ed 2009; 94: F54–F57.Google Scholar

2. Deutsch, MA, Cleuziou, J, Noebauer, C, et al. Successful management of neonatal myocardial infarction with ECMO and intracoronary r-tPA lysis. Congenit Heart Dis 2014; 9: E169–E174.Google Scholar

3. Tometzki, AJ, Pollock, JC, Wilson, N, et al. Role of ECMO in neonatal myocardial infarction. Arch Dis Child Fetal Neonatal Ed 1996; 74: F143–F144.Google Scholar

4. Takeuchi, M, Suzuki, T, Nakayama, M, et al. Neonatal myocardial infarction due to thrombotic occlusion. J Matern Fetal Neonatal Med 2006; 19: 121–123.Google Scholar

5. Murugan, SJ, Gnanapragasam, J, Vettukattil, J. Acute myocardial infarction in the neonatal period. Cardiol Young 2002; 12: 411–413.Google Scholar

6. Tillett, A, Hartley, B, Simpson, J. Paradoxical embolism causing fatal myocardial infarction in a newborn infant. Arch Dis Child Fetal Neonatal Ed 2001; 85: F137–F138.Google Scholar

7. Abdurrahman, L, Schwartz, SM, Beekman, RH 3rd. Thrombotic occlusion of the main stem of the left coronary artery in a neonate. Cardiol Young 1999; 9: 189–191.Google Scholar

8. Lucas, VW Jr, Burchfield, DJ, Donnelly, WH Jr. Multiple coronary thromboemboli and myocardial infarction in a newborn infant. J Perinatol 1993; 14: 145–149.Google Scholar

9. Cesna, S, Eicken, A, Juenger, H, et al. Successful treatment of a newborn with acute myocardial infarction on the first day of life. Pediatr Cardiol 2013; 34: 1868–1870.Google Scholar

10. Abbal, J, Paranon, S, Brierre, G, et al. Myocardial infarction in a newborn from a diabetic mother. Cardiol Young 2010; 20: 451–454.Google Scholar

11. Boulton, J, Henry, R, Roddick, LG, et al. Survival after neonatal myocardial infarction. Pediatrics 1991; 88: 145–150.Google Scholar

12. Bernstein, D, Finkbeiner, WE, Soifer, S, et al. Perinatal myocardial infarction: a case report and review of the literature. Pediatr Cardiol 1986; 6: 313–317.Google Scholar

13. Saker, D, Walsh-Sukys, M, Spector, M, et al. Cardiac recovery and survival after neonatal myocardial infarction. Pediatr Cardiol 1997; 18: 139–142.Google Scholar

14. Sandhyamani, S, Chopra, P. Acute myocardial infarction in the neonate. Indian J Med Res 1982; 75: 820–826.Google Scholar

15. Giralt, G, Gran, F, Betrian, P, et al. Acute myocardial infarction in a neonate caused by a coronary thrombosis: a considerable diagnostic and therapeutic challenge. Rev Esp Cardiol 2015; 68: 903–904.Google Scholar

16. Hallbergson, A, Gillespie, MJ, Dori, Y. A case of neonatal myocardial infarction: left coronary artery thrombus resolution and normalisation of ventricular function by intracoronary low-dose tissue plasminogen activator. Cardiol Young 2015; 25: 810–812.Google Scholar

17. Caruso, E, Di Pino, A, Poli, D, et al. Erythrocytosis and severe asphyxia: two different causes of neonatal myocardial infarction. Cardiol Young 2014; 24: 178–181.Google Scholar

18. Ramlogan, SR, McKee, D, Lofland, GK, et al. Neonatal acute myocardial infarction of unknown etiology treated with surgical thrombectomy. Congenit Heart Dis 2014; 9: E158–E162.Google Scholar

19. Hruda, J, Van de Wal, H, Brouwers, H, et al. Survival of a neonate after myocardial infarction complicated by late mitral regurgitation. Pediatr Cardiol 1995; 16: 131–132.Google Scholar

20. Sapire, DW, Markowitz, R, Valdes-Dapena, M, et al. Thrombosis of the left coronary artery in a newborn infant. J Pediatr 1977; 90: 957–959.Google Scholar

21. De Lucia, V, Andreassi, MG, Sabatini, L, et al. Myocardial infarction and arterial thrombosis in identical newborn twins with homozygosity for the PAI-1 4 G/5 G polymorphism. Int J Cardiol 2009; 137: e1–e4.Google Scholar

22. Iannone, LA, Duritz, G, McCarty, RJ. Myocardial infarction in the newborn: a case report complicated by cardiogenic shock and associated with normal coronary arteries. Am Heart J 1975; 89: 232–235.Google Scholar

23. Cabrera, A, Izquierdo, MA, Bilbao, FJ. Myocardial infarction with ventricular aneurysm in a newborn with normal coronary arteries. Int J Cardiol 1991; 31: 243–245.Google Scholar

24. Fletcher, MA, Meyer, M, Kirkpatrick, SE, et al. Myocardial infarction associated with umbilical cord hematoma. J Pediatr 1976; 89: 806–807.Google Scholar

25. Berry, CL. Myocardial infarction in a neonate. Br Heart J 1970; 32: 412–415.Google Scholar

26. Verlaak, R, Backx, AP, Van Heijst, AF. Myocardial infarction in a neonate with left‐sided congenital diaphragmatic hernia. Congenit Anom 2009; 49: 35–37.Google Scholar

27. Peeters, S, Vandenplas, Y, Jochmans, K, et al. Myocardial infarction in a neonate with hereditary antithrombin III deficiency. Acta Paediatr 1993; 82: 610–613.Google Scholar

28. de Moor, MM, Vosloo, SM, Human, DG. Myocardial infarction in a neonate with cyanotic congenital heart disease. Pediatr Cardiol 1986; 6: 219–221.Google Scholar

29. Gault, M, Usher, R. Coronary thrombosis with myocardial infarction in a newborn infant: clinical, electrocardiographic and post-mortem findings. N Engl J Med 1960; 263: 379–382.Google Scholar

30. Coleman, EN, Macdonald, AM. Intrauterine myocardial infarction. Arch Dis Child 1962; 37: 444–447.Google Scholar

31. Fagan, LF, Thurmann, M, LoPiccolo, VF, et al. Myocardial infarction in the perinatal period with long-term survival. J Pediatr 1966; 69: 378–382.Google Scholar

32. de Vetten, L, Bergman, KA, Elzenga, NJ, et al. Neonatal myocardial infarction or myocarditis? Pediatr Cardiol 2011; 32: 492–497.Google Scholar

33. Ravich, RM, Rosenblatt, P. Myocardial infarction in the newborn infant. J Pediatr 1947; 31: 266–273.Google Scholar

34. Farooqi, KM, Sutton, N, Weinstein, S, et al. Neonatal myocardial infarction: case report and review of the literature. Congenit Heart Dis 2012; 7: E97–E102.Google Scholar

35. Patel, CR, Judge, NE, Muise, KL, et al. Prenatal myocardial infarction suspected by fetal echocardiography. J Am Soc Echocardiogr 1996; 9: 721–723.Google Scholar

36. Arthur, A, Cottom, D, Evans, R, et al. Myocardial infarction in a newborn infant. J Pediatr 1968; 73: 110–114.Google Scholar

37. Richard, R, Benirschke, K. Myocardial infarction in the perinatal period: report of two cases in newborn infants. J Pediatr 1959; 55: 706–712.Google Scholar

38. Van der Hauwaert, LG, Loos, MC, Verhaeghe, LK. Myocardial infarction during exchange transfusion in a newborn infant. J Pediatr 1967; 70: 745–750.Google Scholar

39. Kilbride, MH, Way, GL, Merenstein, GB, et al. Myocardial infarction in the neonate with normal heart and coronary arteries. Am J Dis Child 1980; 134: 759–762.Google Scholar

40. Hornung, T, Bernard, E, Howman‐Giles, R, et al. Myocardial infarction complicating neonatal enterovirus myocarditis. J Paediatr Child Health 1999; 35: 309–312.Google Scholar

41. Haubner, BJ, Schneider, J, Schweigmann, U, et al. Functional recovery of a human neonatal heart after severe myocardial infarction. Circ Res 2016; 118: 216–221.Google Scholar

42. Poonai, N, Kornecki, A, Buffo, I, et al. Neonatal myocardial infarction secondary to umbilical venous catheterization: a case report and review of the literature. Paediatr Child Health 2009; 14: 539–541.Google Scholar

43. Bulbul, ZR, Rosenthal, DN, Kleinman, CS. Myocardial infarction in the perinatal period secondary to maternal cocaine abuse: a case report and literature review. Arch Pediatr Adolesc Med 1994; 148: 1092–1096.Google Scholar

44. Muraskas, J, Besinger, R, Bell, T, et al. Perinatal myocardial infarction in a newborn with a structurally normal heart. Am J Perinatol 1997; 14: 93–97.Google Scholar

45. Bor, I. Myocardial infarction and ischaemic heart disease in infants and children. Analysis of 29 cases and review of the literature. Arch Dis Child 1969; 44: 268–281.Google Scholar

46. Rowe, RD, Hoffman, T. Transient myocardial ischemia of the newborn infant: a form of severe cardiorespiratory distress in full-term infants. J Pediatr 1972; 81: 243–250.Google Scholar

47. Fesslova, V, Lucci, G, Brankovic, J, et al. Massive myocardial infarction in a full-term newborn: a case report. Int J Pediatr 2010; 2010: 658065.Google Scholar

48. Hines, AJ, Rawlins, PV. Staphylococcus aureus Septicemia with a fatal transmural myocardial infarction in a 27-week-gestation twin infant: a case study. Neonatal Netw 2010; 29: 75–85.Google Scholar

49. Jones, TK, Lawson, BM. Profound neonatal congestive heart failure caused by maternal consumption of blue cohosh herbal medication. J Pediatr 1998; 132 (Pt 1): 550–552.Google Scholar

50. Brown, NJ. Proceedings: myocardial infarction in the newborn. Arch Dis Child 1974; 49: 494.Google Scholar

51. Birnbacher, R, Salzer-Muhar, U, Kurtaran, A, et al. Survival after intrauterine myocardial infarction: noninvasive assessment of myocardial perfusion with 99mTc-Sestamibi scintigraphy. Am J Perinatol 2000; 17: 309–313.Google Scholar

52. Guller, B, Bozic, C. Right-to-left shunting through a patent ductus arteriosus in a newborn with myocardial infarction. Cardiology 1972; 57: 348–357.Google Scholar

53. Hu, W, Lu, J, Meng, C, et al. Neonatal myocardial infarction: a case report. Zhonghua Yi Xue Za Zhi 1998; 61: 110–115.Google Scholar

54. Rance, NE, de la Monte, SM, Hutchins, GM. Dilatation of the left ventricle in a newborn: probable in utero myocardial infarction. Pediatr Pathol 1986; 5: 463–469.Google Scholar

55. Anderson, BR, Rhee, D, Abellar, RG, et al. Congenital coronary arteriopathy and myocardial infarctions occur with tricuspid atresia. Pediatr Cardiol 2013; 34: 1247–1249.Google Scholar

56. Gadoth, N, Kornmehl, P, Gueron, M, et al. Haemorrhagic infarction of the myocardium in a newborn with haemoglobin H disease and erythroblastosis. Acta Paediatr Scand 1978; 67: 245–247.Google Scholar

57. Hubbard, JF, Girod, DA, Caldwell, RL, et al. Right ventricular infarction with cardiac rupture in an infant with pulmonary valve atresia with intact ventricular septum. J Am Coll Cardiol 1983; 2: 363–368.Google Scholar

58. McCormack, M. Venous infarction of the myocardium in a newborn child: an unusual effect of disseminated intravascular coagulation. J Clin Pathol 1973; 26: 364–366.Google Scholar

59. Saiki, Y, Dyck, JD, Kantoch, MJ, et al. Prenatal right ventricular infarction associated with hypoplastic left heart syndrome. J Thorac Cardiovasc Surg 2001; 122: 180–181.Google Scholar

60. Clapp, JF 3rd, Naeye, RL. Intra-uterine myocardial infarction. JAMA 1961; 178: 1039–1040.Google Scholar

61. Hayashi, Y, Kishida, K, Haneda, N, et al. A case of Bland-White-Garland syndrome with myocardial infarction on the first day after birth. Pediatr Cardiol 1990; 11: 175–176.Google Scholar

62. Sarkola, T, Boldt, T, Happonen, JM, et al. Atresia of proximal coronary arteries in pulmonary atresia with intact ventricular septum - fetal and neonatal findings. Fetal Diagn Ther 2008; 24: 413–415.Google Scholar

63. Hanes, TE, Page, DL, Graham, TB, et al. Regional myocardial infarction of low-flow type in a neonate with tricuspid atresia. Arch Pathol Lab Med 1977; 101: 86–88.Google Scholar

64. Lehoullier, PF, Bowers, PN, Harris, JP. Cardiology casebook. Coysackie virus B myocarditis presenting as a myocardial infarction in a newborn infant. J Perinatol 1996; 16: 403–405.Google Scholar

65. Moher, D, Liberati, A, Tetzlaff, J, Altman, DG. The PRISMA Group. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. PLoS Med 2009; 6: e1000097.Google Scholar

66. Costa, S, Zecca, E, De Rosa, G, et al. Is serum troponin T a useful marker of myocardial damage in newborn infants with perinatal asphyxia? Acta Paediatr 2007; 96: 181–184.Google Scholar

67. Marton, T, Hajdu, J, Hruby, E, et al. Intrauterine left chamber myocardial infarction of the heart and hydrops fetalis in the recipient fetus due to twin-to-twin transfusion syndrome. Prenat Diagn 2002; 22: 241–243.Google Scholar

68. Volker, HU, Demmer, P, Gattenlohner, S. Idiopathic intrauterine myocardial infarction without malformations of the heart or coronary vessels as a cause of stillbirth. Int J Gynaecol Obstet 2009; 107: 251–252.Google Scholar

69. Lipshultz, SE, Simbre, VC 2nd, Hart, S, et al. Frequency of elevations in markers of cardiomyocyte damage in otherwise healthy newborns. Am J Cardiol 2008; 102: 761–766.Google Scholar

70. El-Khuffash, AF, Molloy, EJ. Serum troponin in neonatal intensive care. Neonatology 2008; 94: 1–7.Google Scholar

71. Gunes, T, Ozturk, MA, Koklu, SM, et al. Troponin-T levels in perinatally asphyxiated infants during the first 15 days of life. Acta Paediatr 2005; 94: 1638–1643.Google Scholar

72. Boo, NY, Hafidz, H, Nawawi, HM, et al. Comparison of serum cardiac troponin T and creatine kinase MB isoenzyme mass concentrations in asphyxiated term infants during the first 48 h of life. J Paediatr Child Health 2005; 41: 331–337.Google Scholar

73. Towbin, JA, Bricker, JT, Garson, A. Electrocardiographic criteria for diagnosis of acute myocardial infarction in childhood. Am J Cardiol 1992; 69: 1545–1548.Google Scholar

74. Concheiro-Guisan, A, Sousa-Rouco, C, Fernandez-Santamarina, I, et al. Intrauterine myocardial infarction: unsuspected diagnosis in the delivery room. Fetal Pediatr Pathol 2006; 25: 179–184.Google Scholar