Abstract
Thirteen percent of infants are born prematurely and this population is at increased risk of cardiovascular disease (CVD) as they age. We hypothesized that compared with term‐born controls (CON), individuals born prematurely would have premature aortic stiffening, indicating greater CVD risk.To test this hypothesis in humans, aortic pulse wave velocity (aPWV) was used to determine aortic stiffness in young adults born preterm between 1989 and 1991 (PT, 21–23 years) and age‐matched controls (CON). Intra‐arterial brachial artery pressure waveforms from 9 PT and 11 CON subjects were converted to central aortic pressure waveforms using a published transfer function. aPWV was then derived from the time delay between the forward and reflected waves and the effective reflecting distance, estimated based on individual anthropometric data. To test the hypothesis in a rodent model that perinatal supplemental oxygen (O2) promotes aortic stiffening, newborn rat pups were exposed to 80% O2 for 14 days, or 21% O2 as a control.aPWV was higher in PT (10.1±2.6 m/s) compared with CON (7.2±0.8 m/s, p=0.025). aPWV did not correlate with systolic blood pressure in either group (PT R2=0.02, p=0.73; CON R2=0.17, p=0.20). At age 12 months, aortic stiffness, determined by aPWV, was higher in 80% O2‐exposed rats (487.1±27.8 cm/s) compared with controls (371.1±13.25 cm/s, p=0.02).These data suggest that individuals born prematurely experience accelerated vascular aging of the aorta and that exposure to supplemental O2 as part of clinical care in premature infants may be a potential mechanism mediating this novel observation.Support or Funding InformationUniversity of Iowa Start‐Up Fund
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