Elevated non-HDL-c during adolescence, young- and mid-adulthood associated with CAC

Introduction and methods

The underlying causes for heart disease begin early in life before clinical symptoms occur [1,2]. Data from ongoing cohort studies indicate that risk factor levels in adolescents and young adulthood could be better predictors for CVD (elevated carotid intima-media thickness and coronary artery calcification [CAC]) in mid to later life than subsequent levels later in life [3,4]. However, strategies to reduce CVD risk are typically initiated in middle to later life when symptoms have manifested and need for clinical intervention has become more acute.

LDL-c is a risk factor for heart disease and a primary target against adult dyslipidemia [5]. However, other parameters of the lipoprotein lipid profile, such as non-HDL-c that encompasses a greater number of atherogenic lipids and lipoproteins, may be more closely associated with heart disease risk [6,7]. Previous studies among children and adults have demonstrated that non-HDL-c is at least as good as LDL-c for the prediction of subclinical atherosclerosis [8,9]. This has led to a recommendation by the National Heart, Lung, and Blood Institute (NHLBI) to use non-HDL-c for primary screening of dyslipidemia in childhood [10]. However, the relative importance of non-HDL-c at specific life stages for predicting atherosclerotic disease remain unclear. This study assessed the relative importance between non-HDL-c levels in adolescence, young adulthood, and mid-adulthood with CAC in mid-adulthood.

The Cardiovascular Risk in Young Finns Study included in 1980 participants at the age of 3, 6, 9, 12, 15, and 18 who were representatives of the general population at that time. Follow-ups were conducted in 1983, 1986, 1989, 1992, 2001, and 2007. In 2008, participants (n=589) from the 3 oldest baseline age-groups, then aged 40-46 years, underwent a CT scan to measure CAC. CAC scores were dichotomized as 0 (no CAC; Agatston score 0) and 1 (presence of CAC; Agatston score ≥1). Non-HDL-c was calculated as total cholesterol minus HDL-c and life stage average non-HDL-c was calculated for the adolescence (12-18 years), young adulthood (21-30 years), and mid-adulthood (33-45 years) groups. The bayesian relevant life course exposure model was used to calculate the relative importance of non-HDL-c exposure at each of the three age-groups for the presence of CAC in mid-adulthood. Follow-up was 28 years.

Main results

• In total, 113 (19.2%) participants had CAC in mid-adulthood, of which 73 (12.4%) were men and 40 (6.8%) were women (X²=22.9 [n=589], P<0.01).

• In a model adjusted for sex, the accumulated odds for CAC in mid-adulthood were ~1.6 times higher for each 1-unit increase in non-HDL-c (OR 1.59, 95% CI: 1.25-1.99). The strongest life stage-specific association for the presence of CAC in mid-adulthood from non-HDL-c exposure was in adolescence (OR 1.18, 95% CI: 1.01-1.49), followed by young adulthood (OR 1.18, 95% CI: 1.01-1.48) and mid-adulthood (OR 1.15, 95% CI: 1.01-1.40).

• In a fully adjusted model, the accumulated odds for CAC in mid-adulthood were 1.5 times higher for each 1-unit increase in non-HDL-c (OR 1.50, 95% CI: 1.14-1.192). The highest life stage-specific odd for CAC in mid-adulthood was found with non-HDL-c exposure during adolescence (OR 1.16, 95% CI: 1.01-1.46), followed by young adulthood (OR 1.14, 95% CI: 1.01-1.43), and mid-adulthood (OR 1.12, 95% CI: 1.01-1.34).

Conclusion

References

Find this article online at JAMA Cardiol