Elsevier

International Journal of Cardiology

Volume 277, 15 February 2019, Pages 258-265
International Journal of Cardiology

Cross-sectional associations between Ideal Cardiovascular Health scores and vascular phenotypes in 11- to 12-year-olds and their parents: The Longitudinal Study of Australian Children

https://doi.org/10.1016/j.ijcard.2018.11.020Get rights and content

Highlights

  • Lower child Ideal Cardiovascular Health scores predicted poorer vascular function.

  • In their parents, lower scores predicted poorer vascular function and structure.

  • Parent attainment of ideal health predicted their child's attainment in each metric.

Abstract

Background

Understanding early-life relationships between the Ideal Cardiovascular Health (ICVH) score and vascular phenotypes could inform likely effectiveness and timing of cardiovascular disease prevention strategies. We aimed to describe associations between ICVH scores and vascular phenotypes in 11- to 12-year-old children and their parents.

Methods and results

Cross-sectional ICVH scores (range 0–7, higher indicating better health), derived by summing dichotomized metrics for cholesterol, glucose, blood pressure (BP), body mass index (BMI), diet, physical activity and smoking, were constructed for 1235 adults (89% female, mean age 43 years) and 1028 children (48% female, 12 years). The median scores were 4 and 5 for adults and children respectively. Child ICVH scores were associated with parent scores (0.18 higher child score per additional point in parent's score, 95% CI 0.12 to 0.22, P < 0.001). Each additional point in the adult ICVH score was associated with slower carotid-femoral pulse wave velocity (PWV, −0.32 m/s, 95% CI −0.37 to −0.27), greater carotid elasticity (0.017%/mm Hg, 95% CI 0.014 to 0.020) and reduced carotid intima-media thickness (IMT, −7.3 μm, 95% CI −12.0 to −2.5). An additional point in the child score was associated with functional phenotypes (PWV −0.07 m/s, 95% CI −0.11 to −0.03; carotid elasticity 0.009%/mm Hg, 95% CI 0.004 to 0.015) but not structural phenotypes (IMT −1.8 μm, 95% CI −5.2 to 1.5).

Conclusion

Few Australian children and even fewer parents have ideal cardiovascular health. Lower ICVH scores were associated with adverse adult vascular phenotypes and adverse child vascular function. Family-based interventions optimizing ICVH metrics may delay onset and progression of subclinical atherosclerosis and later cardiovascular disease.

Introduction

In 2010 the American Heart Association (AHA) proposed the concept of Ideal Cardiovascular Health [1]. A 7-point Ideal Cardiovascular Health (ICVH) score (Supplementary Table 1) summarizes an individual's attainment of cardiovascular health metrics and is useful to quantify and monitor population trends in cardiovascular disease (CVD) risk factors [1,2]. In adults, ICVH score is inversely associated with all-cause and CVD-related mortality [3], CVD events [4], and other non-communicable diseases including cancer [5] and depression [6]. Importantly, the ICVH score represents a conceptual shift towards primordial prevention [7], as evidenced by the inclusion of child cut-offs for each metric [1].

Few studies have examined the ICVH score in children. Limited evidence suggests that by late adolescence a lower ICVH score is associated with worse vascular outcomes [8]. In 190 US youth with type 1 diabetes, lower ICVH scores were associated with adverse vascular function (increased pulse wave velocity, PWV), but not vascular structure [[9], [10], [11]] (carotid intima-media thickness, IMT), 5 years later [12]. In the Cardiovascular Risk in Young Finns study, worsening ICVH scores over 21 years from childhood to adulthood were associated with increased adult PWV [13]. In another Finnish study of 15- to 19-year-old adolescents, lower ICVH scores were cross-sectionally associated with increased aortic IMT and lower aortic elasticity [14]. Data from earlier in childhood would indicate when associations between ICVH scores and vascular phenotypes become evident. Understanding parent-child relationships in this context would direct family-based interventions.

Here we used national population-derived Australian data to: 1) describe the ICVH score in 11- to 12-year-old children and their parents; 2) examine the relationship between parent and child ICVH scores; and 3) investigate cross-sectional associations of the overall ICVH score with vascular phenotypes among children and their parents. Secondary aims were to explore associations within the individual metrics.

Section snippets

Study design and participants

Predominantly cross-sectional data were drawn from the Longitudinal Study of Australian Children (LSAC) [15] and Child Health CheckPoint [16]. Details of the initial two-stage random sampling design (with postcode as primary sampling unit) are outlined elsewhere [17]. Briefly, LSAC recruited a nationally representative sample of 5107 infants (age 0–1 years) [16], and followed them up in biennial ‘waves’ of data collection up to 2015 (at child age 10–11 years). At the latest visit, families were

Participants and missing data

The analytical sample contained 1482 of 1874 families who attended CheckPoint (Supplementary Fig. 2). Participants were excluded because they had home visits where carotid ultrasound was not available, or because the attending adult was not a biological parent. The sample characteristics of participants who were excluded were not substantially different to the characteristics of those included (Supplementary Table 4). Within the analytic sample, complete data on all 7 metrics of the ICVH score

Discussion

We report a low prevalence of perfect ICVH scores in this relatively advantaged population of Australian children and adults. Parental and child attainment of individual ICVH metrics were correlated. Lower ICVH scores were associated with adverse structural and functional adult vascular phenotypes. For the first time, we report associations between ICVH and functional phenotypes (PWV and carotid elasticity) in children, and between two specific ICVH metrics (blood pressure and BMI) and adverse

Sources of funding and support

This work has been supported to date by the National Health and Medical Research Council of Australia (1041352, 1109355), The Royal Children's Hospital Foundation (2014-241), Murdoch Children's Research Institute, The University of Melbourne, National Heart Foundation of Australia (100660), Financial Markets Foundation for Children (2014-055: 2016-310) and Victoria Deaf Education Institute.

The following authors were supported by the National Health and Medical Research Council of Australia:

Financial interests and disclosures

The authors have no financial (or otherwise) conflicts of interest relevant to this article to disclose.

Acknowledgements

We thank Greta Goldsmith (Murdoch Children's Research Institute, research assistant) for her significant contribution to data collection, analysis and processing, and Josh Muller (Murdoch Children's Research Institute, research assistant) for his contribution to data collation and cleaning. Some study data were collected and managed using REDCap (Research Electronic Data Capture) electronic data capture tools. REDCap is a secure, web-based application designed to support data capture for

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    M Juonala and DP Burgner contributed equally to this work.

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