Elevated lipoprotein(a) [Lp(a)] levels are associated with an increased risk of cardiovascular disease (CVD)1,2. With a reported population prevalence of approximately 20%, elevated Lp(a) (>50 mg/dL, corresponding to ≈120 nmol/L) is a prevalent risk factor3. Lp(a) levels are mainly genetically determined and if elevated, individuals are exposed to a high Lp(a)-burden from early in childhood onwards4. Results of a recent follow-up study in children with familial hypercholesterolemia (FH) showed that Lp(a) levels contributed significantly to arterial wall thickening, as measured by carotid intima-media thickness (cIMT), independent of low-density lipoprotein cholesterol (LDL-C) levels and statin use5. These findings suggested that exposure to a high Lp(a)-burden from birth onwards may contribute substantially to the development of early atherosclerosis in young FH patients that are already at high CVD risk. However, it is unknown if this holds true for young individuals without FH. Previous studies yielded inconsistent results6, 7, 8. Therefore, the aim of this study is to evaluate the contribution of Lp(a) to arterial wall thickening, as measured by cIMT, in children without FH that were followed for nearly two decades.
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