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Lipoprotein(a) Levels at Birth and in Early Childhood: The COMPARE Study
Nina Strandkjær1, Malene Kongsgaard Hansen1, Sofie Taageby Nielsen2
1Department of Cardiology, Copenhagen University Hospital - Herlev and Gentofte Hospital, 2730 Herlev, Denmark.
Insights
High lipoprotein(a) (Lp(a)) levels are a risk factor for cardiovascular disease. Early life Lp(a) levels, particularly from birth, can predict future high levels, aiding in early risk identification.
Area of Science:
- Cardiovascular Science
- Genetics
- Pediatrics
Background:
- High lipoprotein(a) (Lp(a)) is a genetically determined risk factor for cardiovascular disease.
- Approximately 20% of adults have elevated Lp(a) levels (>42 mg/dL).
- Understanding early life Lp(a) is crucial for long-term cardiovascular risk assessment.
Purpose of the Study:
- To determine if cord blood Lp(a) levels can proxy for neonatal venous blood levels.
- To investigate if birth Lp(a) levels predict later life Lp(a) levels.
- To examine the correlation between early life and parental Lp(a) levels.
Main Methods:
- Prospective cohort study (Compare study) of 450 newborns in Copenhagen.
- Collected plasma Lp(a) from cord blood, neonatal venous blood, and at 2 and 15 months follow-up.
- Included blood sampling from 705 parents.
Main Results:
- Cord blood Lp(a) strongly correlated with neonatal venous blood levels (R²=0.95).
- Birth levels ≥90th percentile predicted high Lp(a) at 15 months (85-89% PPV).
- Neonatal and infant Lp(a) levels showed weak correlation with parental levels.
Conclusions:
- Lipoprotein(a) levels are low in early life.
- Cord blood is a reliable proxy for neonatal venous blood Lp(a) levels.
- Birth Lp(a) levels can identify newborns at risk for developing high levels later in life.
Background And Objective:
High lipoprotein(a) is a genetically determined causal risk factor for cardiovascular disease, and 20% of the adult population has high levels (ie, >42 mg/dL, >88 nmol/L). We investigated whether early life lipoprotein(a) levels measured in cord blood may serve as a proxy for neonatal venous blood levels, whether lipoprotein(a) birth levels (ie, cord or venous) predict levels later in life, and whether early life and parental levels correlate.
Methods:
The Compare study is a prospective cohort study of newborns (N = 450) from Copenhagen, Denmark, including blood sampling of parents. Plasma lipoprotein(a) was measured in cord blood (N = 402), neonatal venous blood (N = 356), and at 2 (N = 320) and 15 months follow-up (N = 148) of infants, and in parents (N = 705).
Results:
Mean lipoprotein(a) levels were 2.2 (95% CI, 1.9-2.5), 2.4 (2.0-2.7), 4.1 (3.4-4.9), and 14.6 (11.4-17.9) mg/dL in cord, neonatal venous, and 2- and 15-month venous samples, respectively. Lipoprotein(a) levels in cord blood correlated strongly with neonatal venous blood levels (R2 = 0.95, P < 0.001) and neonatal levels correlated moderately with 2- and 15-month levels (R2 = 0.68 and 0.67, both P < 0.001). Birth levels ≥ 90th percentile predicted lipoprotein(a) > 42 mg/dL at 15 months with positive predictive values of 89% and 85% for neonatal venous and cord blood. Neonatal and infant levels correlated weakly with parental levels, most pronounced at 15 months (R2 = 0.22, P < 0.001).
Conclusions:
Lipoprotein(a) levels are low in early life, cord blood may serve as a proxy for neonatal venous blood, and birth levels ≥ 90th percentile can identify newborns at risk of developing high levels.
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