Key result
ApoB correlates strongly with standard lipid fractions, while Lp(a) levels show no clinical or biochemical associations.
Why the study?
What are the clinical, metabolic, and biochemical correlates of lipoprotein(a) and apolipoprotein B levels in adult patients with dyslipidemia and cardiovascular disease?
Cross-Sectional (n=153)
No
What are the clinical, metabolic, and biochemical correlates of lipoprotein(a) and apolipoprotein B levels in adult patients with dyslipidemia and cardiovascular disease?
Answers are grounded in this paper and cite their sources.
Routine clinical and biochemical markers do not independently predict Lp(a) levels after multivariable adjustment, confirming its independence from traditional lipid fractions, whereas ApoB strongly tracks with total cholesterol and triglycerides as a marker of atherogenic particle burden.
Background Atherosclerotic cardiovascular disease remains a major cause of morbidity and mortality worldwide, with residual cardiovascular risk persisting despite optimized lipid-lowering therapy. Lipoprotein(a) [Lp(a)] and apolipoprotein B (ApoB) have emerged as independent, causal biomarkers of cardiovascular risk, reflecting atherogenic particle burden beyond conventional lipid measures. This study aimed to evaluate the clinical, metabolic, and biochemical correlates of Lp(a) and ApoB levels in patients with dyslipidemia and cardiovascular disease. Methods A cross-sectional observational analysis was performed in 153 adults evaluated for cardiometabolic risk. Anthropometric, biochemical, and inflammatory parameters were assessed. Correlation analyses were conducted to identify associations between lipoproteins and metabolic variables. Decision tree regression was used to explore distribution patterns of Lp(a) and ApoB variability. Results The study population exhibited a mean age of 57.9 ± 12.3 years, with a predominance of dyslipidemia (79.1%) and established cardiovascular disease (75.2%). The mean Lp(a) concentration was 30.14 ± 31.50 mg/dL, while ApoB averaged 119.87 ± 36.01 mg/dL. ApoB correlated significantly with total cholesterol ( r = 0.49, p < 0.001), triglycerides ( r = 0.46, p < 0.001), and LDL-C ( r = 0.26, p < 0.01). Decision tree analysis identified GGT, creatinine, and uric acid as factors that influence of Lp(a) variability. Conclusions Both hepatic and renal function markers significantly modulate Lp(a) levels, while ApoB remains a robust indicator of atherogenic particle load. Integrating Lp(a) and ApoB assessment into cardiovascular risk profiling may improve identification of residual risk and guide personalized therapeutic strategies in dyslipidemic populations.
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Alexandrescu et al. (2026) conducted a cross-sectional in Dyslipidemia and cardiovascular disease (n=153). Clinical, metabolic, and biochemical correlates (hepatic and renal markers, lipid fractions) was evaluated on Correlation between ApoB and total cholesterol (r = 0.492, 95% CI 0.361-0.603, p=<0.001). Apolipoprotein B correlated strongly with total cholesterol and triglycerides, whereas Lp(a) levels were not independently explained by routine clinical or biochemical variables in multivariable regression.
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