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Ischemic myocardial necrosis and papillary muscle dysfunction in infants and children

W H Donnelly1

  • 1Department of Pathology, University of Florida, Gainesville.

The American Journal of Cardiovascular Pathology
|January 1, 1987
PubMed

Insights

Ischemic myocardial necrosis (IMN) in infants and children results from underperfusion, not coronary artery occlusion. Pathologists should consider IMN in newborns with specific clinical signs.

Area of Science:

  • Pediatric Cardiology
  • Neonatal Pathology
  • Cardiovascular Research

Background:

  • Ischemic myocardial and papillary muscle dysfunction significantly impacts infants and children, differing from adult causes like coronary artery occlusion.
  • In pediatric populations, myocardial injury stems from underperfusion due to factors like birth asphyxia, congenital heart disease, and premature delivery complications.
  • Unlike adults, infants and children experience ischemic injury with similar frequency in both ventricles.

Purpose of the Study:

  • To highlight the distinct causes and presentations of ischemic myocardial necrosis (IMN) in newborns and children.
  • To alert pathologists to clinical indicators suggestive of IMN in neonates and older infants.
  • To differentiate pediatric ischemic cardiac injury from adult models.

Main Methods:

  • Review of clinical presentations and pathological findings in infants and children with myocardial dysfunction.
  • Analysis of etiological factors contributing to myocardial underperfusion in neonates and children.
  • Comparison of pediatric ischemic injury patterns with those observed in adult models.

Main Results:

  • Ischemic myocardial necrosis in infants and children is primarily caused by underperfusion, with coronary artery occlusion being rare.
  • Clinical signs such as cardiogenic shock, cyanotic heart failure, or persistent fetal circulation in newborns may indicate IMN.
  • Older infants may present with IMN, fibrosis, or calcification, particularly those with ventricular hypertrophy, persistent pulmonary hypertension, bronchopulmonary dysplasia, or complex congenital heart disease.

Conclusions:

  • Ischemic myocardial injury in the pediatric population has unique etiologies and requires specific diagnostic considerations.
  • Pathologists must be aware of the clinical context, including birth asphyxia and congenital heart disease, when evaluating myocardial damage in infants.
  • Existing animal models for adult ischemic heart disease may not accurately represent the pathophysiology in newborns.

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