Preterm Birth With Neonatal Interventions Accelerates Collagen Deposition in the Left Ventricle of Lambs Without

Bianca Lê1, Mar Janna Dahl2, Kurt H Albertine2

  • 1Department of Anatomy and Developmental Biology and Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.

CJC Open
|May 26, 2021
PubMed

Insights

Preterm birth and ventilation in lambs did not affect cardiomyocyte growth but increased collagen in the left ventricle. This collagen buildup may lead to cardiac dysfunction later in life.

Area of Science:

  • Cardiovascular Physiology
  • Neonatal Research
  • Cardiac Remodeling

Background:

  • Adults born preterm (<37 weeks' gestation) have altered cardiac growth and are prone to cardiac dysfunction.
  • Previous sheep studies indicated moderate preterm birth causes maladaptive cardiac remodeling.

Purpose of the Study:

  • To investigate ventricular structure in lambs born at a greater severity of preterm birth and mechanically ventilated postnatally.
  • To assess the long-term cardiac effects of severe preterm birth and neonatal respiratory support.

Main Methods:

  • Compared former-preterm lambs (128 days gestation, ventilated) with term-born lambs (150 days gestation, unventilated) at 2 and 5 months term-equivalent age.
  • Utilized immunohistochemistry, histology, and stereology to analyze right and left ventricular structure.

Main Results:

  • Cardiomyocyte number, size, proliferation, and apoptosis were unaffected by preterm birth or age.
  • Interstitial collagen increased with age in the left ventricle plus septum, and this was exacerbated by preterm birth.
  • Right ventricle collagen increased with age but was not influenced by preterm birth.

Conclusions:

  • This study is the first to examine the impact of preterm birth and neonatal interventions on lamb ventricular myocardium.
  • No adverse effects on cardiomyocyte growth were observed in early postnatal life.
  • Increased collagen deposition in preterm hearts is a concern, potentially leading to cardiac dysfunction with aging.
Abstract

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