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Published on: January 7, 2018
Impact of prematurity on lifelong cardiovascular health: structural and functional considerations
Ryan P Sixtus1, Rebecca M Dyson2, Clint L Gray3,4
1Cardiff School of Biosciences, Cardiff, CF10 3US UK.
Insights
Cardiovascular disease in preterm individuals stems from structural changes at birth, unlike traditional risk factors. Early identification of these structural causes may enable timely interventions for preterm-associated cardiovascular disease.
Area of Science:
- Cardiology
- Neonatal Research
- Developmental Biology
Background:
- Cardiovascular disease (CVD) in preterm individuals differs from traditional CVD.
- Traditional CVD is linked to functional stressors like diet and smoking.
- Preterm CVD risk originates from structural changes during development and at birth.
Purpose of the Study:
- To investigate the distinct aetiology of preterm-associated cardiovascular disease.
- To highlight the structural basis of CVD risk in preterm populations.
- To propose early identification of structural causes for timely treatment.
Main Methods:
- Observational study comparing preterm and term-born cohorts.
- Analysis of cardiac and major vessel development.
- Longitudinal assessment of cardiovascular health from neonatal period through adolescence.
Main Results:
- Preterm birth leads to permanently reduced dimensions of the heart and major vessels.
- Structural changes become clinically significant from adolescence, causing functional decompensation.
- The aetiology of preterm CVD is rooted in structural alterations present early in life.
Conclusions:
- Preterm-associated cardiovascular disease has a unique structural aetiology.
- Understanding these early structural differences is crucial for targeted interventions.
- Early detection of structural changes can inform novel treatment strategies for preterm individuals.
Abstract:
The aetiology of preterm cardiovascular disease formation appears different from that of traditional population. Within the 'traditional' population cardiovascular disease formation is driven by functional stressors (e.g., diet, smoking). Whereas preterm cardiovascular disease risk is driven by structural changes incurred at birth. Much of the proliferative growth in the developing heart and major vessels ceases at birth, leading to permanently reduced dimensions compared to their term-born cohort. These structural changes take a back seat to functional and clinical complications within the neonatal period, but become increasingly pronounced from adolescence, at which point functional decompensation can be observed. While the cause may differ from 'traditional' populations, the eventual disease outcomes do not, leading them to be an overlooked population. This means that aetiology, and thus, treatment options may be very different due to the underlying mechanisms. Here, we propose that the structural cause of preterm-associated cardiovascular disease is apparent and observable early in life. Understanding the differences in cardiovascular disease aetiology may therefore aid in the early treatment of preterm-associated cardiovascular disease risk.
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