Elsevier

Atherosclerosis

Volume 239, Issue 2, April 2015, Pages 496-502
Atherosclerosis

Early childhood hospitalisation with infection and subclinical atherosclerosis in adulthood: The Cardiovascular Risk in Young Finns Study

https://doi.org/10.1016/j.atherosclerosis.2015.02.024Get rights and content

Highlights

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    Severe early life infections were associated with subclinical atherosclerosis in adulthood.

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    There was a significant decrease in brachial FMD over six years in those with early childhood IRH.

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    These associations were independent of age, sex and cardiovascular risk factors.

Abstract

Objective

Most infections occur in pre-school children but the severity of the inflammatory response to common pathogens varies considerably. We examined the relationship between early childhood infections of sufficient severity to warrant hospitalisation, and markers of subclinical atherosclerosis in adulthood.

Methods

We investigated whether infection-related hospitalisation (IRH) in early childhood (0–5 years) was associated with adverse non-invasive phenotypes of atherosclerosis (carotid artery distensibility and intima-media thickness (IMT), and brachial artery flow-mediated dilation (FMD)) in adulthood in participants from the Cardiovascular Risk in Young Finns study. Analyses were adjusted for age, sex, and socioeconomic status and cardiovascular risk factors in childhood and adulthood. 1043 participants had lifetime IRH data with a mean age at adult follow-up of 33 years.

Results

Brachial FMD levels were significantly lower among individuals with early child IRH (mean ± SEM 8.15 ± 0.37 vs. 9.10 ± 0.16%, p = 0.03). These individuals had a 1.84% (95% CI 0.64–3.04, p = 0.002) greater decrease in FMD over a 6-year interval between two adult follow-ups at mean ages 27 and 33 years. Childhood IRH was associated with increased asymmetrical dimethylarginine (ADMA) in adulthood (0.62 ± 0.01 vs. 0.59 ± 0.01 μmol/l, p = 0.04), adjusted for age, sex, adult body mass index, and serum creatinine. Early childhood IRH was associated with lower carotid distensibility levels (1.95 ± 0.06 vs. 2.09 ± 0.02%/10 mmHg, p = 0.02), but not with carotid intima-media thickness (0.601 ± 0.006 vs. 0.596 ± 0.003 mm). All findings remained unchanged after adjustments for age, sex and conventional cardiovascular risk factors in childhood or adulthood.

Conclusion

Infection-related hospitalisation in the pre-school period was associated with adverse adult atherosclerotic phenotypes and increased ADMA. Infection may contribute to causal pathways leading to the development of endothelial dysfunction and early atherosclerosis.

Section snippets

Participants

The Cardiovascular Risk in Young Finns Study is an ongoing prospective study of cardiovascular risk factors from childhood onwards. The study commenced in 1980, when participants were aged 3–9 years, with repeated follow-up assessments [9]. The current sample included 1043 individuals with entire lifetime hospitalisation data extracted from the Finnish national hospitalisation database, which commenced in 1969. Main outcome measures included carotid/brachial artery ultrasound data from 2001

Results

One hundred and forty one (13.5%) individuals had at least one early childhood IRH (Table 1), with a male predominance (54.6%). Early childhood IRH was less common in those with higher family income. In adulthood, individuals without early childhood IRHs had lower BMI levels, lower smoking prevalence and higher education level.

Discussion

This is the first longitudinal analysis of severe early childhood infection and adult cardiovascular risk parameters in the same individuals over a prolonged period. Infection of sufficient severity to warrant hospitalisation in early life was associated with decreased carotid distensibility and brachial FMD in adulthood. In addition there was a significant decrease in FMD over a six-year period in adulthood, and higher plasma ADMA levels, known to be associated with reduced FMD [12], in those

Funding

The Cardiovascular Risk in Young Finns Study is supported by the Academy of Finland (grants 126925, 121584, 124282, 129378 [Salve], 117787 [Gendi], 41071 [Skidi], and 134309 [eye]); the Social Insurance Institution of Finland; the Kuopio, Tampere (grant X51001 for T.L.), and Turku University Hospital Medical Funds; the Paulo Foundation; the Juho Vainio Foundation; the Paavo Nurmi Foundation; the Finnish Foundation for Cardiovascular Research; the Finnish Cultural Foundation, the Finnish Medical

Conflicts of interest

All authors declare that they have no conflicts of interest.

Acknowledgements

We would like to thank Ville Aalto, MSc, for assistance with data cleaning and initial analysis.

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