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Preterm birth and cardiac function in adulthood
  1. Charlotte Greer1,
  2. Richard W Troughton1,2,
  3. Philip D Adamson2,3,
  4. Sarah L Harris4
  1. 1 Cardiology Department, Christchurch Hospital, Christchurch, New Zealand
  2. 2 Christchurch Heart Institute, University of Otago, Christchurch, New Zealand
  3. 3 Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, UK
  4. 4 Department of Pediatrics, University of Otago, Christchurch, New Zealand
  1. Correspondence to Dr Charlotte Greer, Christchurch Hospital, Christchurch, New Zealand; charlotte.greer{at}


Preterm birth affects 1 in 10 pregnancies worldwide, with increasing survival rates over the last 30 years. However, as this new generation of long-term survivors approaches middle age, recent studies have revealed increased cardiovascular risk factors and higher rates of ischaemic heart disease and heart failure. Cardiovascular imaging has identified smaller cardiac chamber size, changes in myocardial mass and impaired ventricular function, particularly under physiological stress. Accordingly, this population should be recognised as having a higher risk of heart failure as they age. In this review, we present current evidence for increased rates of heart failure and evidence of alterations in cardiac structure and function in those born preterm. We discuss potential mechanisms to explain this risk including greater frequency of co-morbidities known to be associated with heart failure. We also explore potential mechanistic links specific to the preterm-born population, including the impact of premature birth on myocardial and vascular development and the effects of perinatal haemodynamic changes and chronic lung disease on the developing heart. We highlight gaps in our knowledge and consider implications for patient management relevant to the adult physician.

  • echocardiography
  • cardiac imaging techniques
  • magnetic resonanceimaging
  • epidemiology
  • risk factors
  • heart failure

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  • Contributors CG wrote the initial draft of the manuscript and subsequent revisions. SLH provided revisions and added content. RWT and PDA provided edits and suggested revisions.

  • Funding CG has been supported by the AH Couch Heart Trust. PDA is supported by a Heart Foundation of New Zealand Senior Fellowship (1844). SLH is supported by a New Zealand Heart Foundation Fellowship (1872), which is supported by The Grace EM Kay Estate and The Hilda Curtis Charitable Trust.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Commissioned; internally peer reviewed.