High Lp(a) in childhood linked to adult ASCVD risk
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High lipoprotein(a) measured during childhood was predictive of atherosclerotic CVD development during adulthood, according to an analysis of two cohorts published in Circulation.
“Elevated Lp(a) levels are causally linked with CVD outcomes. Our data demonstrate that Lp(a) measurements made in childhood can help to identify groups that have increased risk of future cardiovascular events,” Olli Raitakari, MD, PhD, academy professor of cardiovascular medicine at the University of Turku and Turku University Hospital in Finland, told Healio. “Based on all available evidence, including our study, it could be argued that Lp(a) should be measured as part of the pediatric assessment of serum lipids — so-called universal screening that is recommended at ages 9 to 11 years. Lp(a) levels remain stable from early childhood to adulthood, so that levels after age 2 years reflect future adult levels.”
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The YFS and BHS studies
To determine whether high Lp(a) levels, defined as Lp(a) 30 mg/dL or more, during childhood was predictive of adult ASCVD, researchers evaluated subgroups in the Cardiovascular Risk in Young Finns Study (YFS) with replication in the Bogalusa Heart Study (BHS), both International Childhood Cardiovascular Cohort Consortium cohorts (i3C).
In the original analysis of the YFS published in JAMA, researchers found that BMI, LDL level and smoking in children aged 3 to 18 years were each associated with increased adult carotid intima-media thickness. Similarly, findings from the BHS study also published in JAMA showed that high childhood BMI and LDL were both associated with carotid intima-media thickness in adults aged 25 to 37 years.
For the present analysis, Lp(a) was measured in YFS in those aged 9 to 24 years, for which 2.7% of the original 3,596 participants were diagnosed with ASCVD at a median age of 47 years. In the BHS, 587 white participants had data on childhood Lp(a) measured at age 8 to 17 years and had data on CVD events in adulthood.
High childhood Lp(a) and adult ASCVD risk
In YFS, researchers observed that individuals with high Lp(a) level in childhood had an approximately twofold greater risk for ASCVD in adults compared with those with lower childhood Lp(a) (HR = 2; 95% CI, 1.4-2.6).
In BHS, individuals with high Lp(a) in childhood had an approximately 2.5 times greater risk for ASCVD in adulthood compared with participants with lower childhood Lp(a) (95% CI, 0.9-6.8). After researchers adjusted for LDL and BMI, the increased risk associated with high Lp(a) was unchanged (HR = 2.4; 95% CI, 0.8-7.3).
In a multivariable model of pooled data from both the YFS and BHS, individuals with high Lp(a) during childhood had a twofold greater risk for ASCVD in adulthood compared with individuals with lower childhood Lp(a) (95% CI, 1-3.7).
Raitakari and colleagues observed no association between childhood Lp(a) and adult carotid artery thickness in either cohort or pooled data.
“There are currently effective drug treatments being tested to lower Lp(a) levels. Ongoing trials will clarify whether lowering Lp(a) levels is safe and can reduce the risk of CVD outcomes,” Raitakari told Healio. “However, it is unlikely that the newly developed pharmaceuticals would have a major role in the treatment of most children and adolescents with elevated Lp(a) levels. Analogously, pharmaceutical therapies using statins to lower LDL cholesterol are reserved for special high-risk pediatric populations such as children with familial hypercholesterolemia.
“Even if, in theory, effective pharmaceutical lowering of causal risk factors initiated in early life would likely lead to a substantial reduction of CVDs, such a strategy is not feasible because of the potential ethical and health issues related to the long-term use of pharmaceuticals targeted at healthy children,” Raitakari told Healio. “Therefore, interventions to prevent risk factors for CVD beginning in childhood in larger population segments need to concentrate on intervening on diet and lifestyle.”
For more information:
Olli Raitakari, MD, PhD, can be reached at olli.raitakari@utu.fi.
References:
- Li S, et al. JAMA. 2022;doi:10.1001/jama.290.17.2271.
- Raitakari OT, et al. JAMA. 2003;doi:10.1001/jama.290.17.2277.
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